TEXTBOOKOI

PEDODONTICS
ET w .. ,...............................................................
Eg

Khobha Tandon
K)ean
Frof. and Head
kept, of Pedodontics & Preventive Dentistry
fcollege of Dental Surgery
■MAHE, a deemed university)
l/lanipal
India.

Foreword by:
R. S. Nanda

fPreviews:
A. K. Munshi
Subba Reddy
CONTRIBUTORS

• Usha Paul, BDS, MDS ■ Nirmala Rao, bds, mds

Dept, of Pedodontics & Preventive Department of Oral Pathology,
Dentistry College of Dental Surgery,
College of Dental Surgery, Manipal Manipal, MAHE

■ Rakhee Goel, BDS, MDS ■ Shyam Bhat, BDS, mds

# 3 Mere Court, Chelford, Department of Pedodontics,
Macclesfield, Cheshire. SK11 9EB Yenopoya Dental College,
Mangalore.
« Soni Stephen. BDS, MDS, FRACDS
Department of Children,s Dentistry, ■ Radhika Muppa, BDS, MDS
United Dental Hospital of Sydney, Former Assistant Professor,
2 Chamers Street Surry Hills , College of Dental Surgery,
NSW 2010 Manipal, MAHE

« Nagesh Kumar G Rao, mbbs, md ■ Amit Van'ka, bds, mds

Department of Forensic Dentistry, Asssistant Professor,
Kasturba Medical College, Manipal Department of pedodontics,
MAHE Dental College,
Humnabad
 CONTENTS

Foreword
Preview
? Preview
Preface
Acknowledgements

SECTION 1 : CHILD AS A PATIENT

1J Introduction to pedodontics........ ................................ 1
1.2 Case History, diagnosis and treatment planning.......................................................... 6
1.3 Radiographic examination of pediatric dental patients............ ..................................... 19
1.4 Practice management....................................... 29

SECTION 2 : NORMAL GROWING CHILD

2.1 Stages of human growth and development (pre-natal).............. ........ 36
2.2 Pedologic anatomy........................... ......45
2.3 Stages of growth and development (post-natal)................. ..60
2.4 Growth assessment............ ............. ................ . —........................................... .75

SECTION 3 : DEVELOPING DENTITION AND IT’S DISTURBANCES

3.1 Development of dentition ....?...... 85
3.2 Common developmental disturbances of teeth............... ...... .................................... 97
3.3 Development of occlusion................................... 106

SECTION 4 : PSYCHOLOGICAL DEVELOPMENT AND

V- «fiHAVIOURMANAGEMENT
4.1 Theories of child psychology.............. 121
4.2 Emotional development...... ............................. ..130
4.3 Behavioural science and its application in pediatric dentistry ...... 139
4.4 Pharmacological means of patient management.................................. 154
4.5 Ephebodontics - Dentistry for adolescents................................. 168

i SECTION 5 : DENTAL CARIES IN EARLY CHILDHOOD

5.1 Introduction ........................................................ 178
5.2 Caries risk factors...................................................................... 185
5.3 Early diagnosis of caries ................ ......196
5.4 Nursing caries and rampant caries ................. ..201
 SECTION 6 : PREVENTIVE APPROACH TO CARIES CONTROL
6.1 Infants oral health care........................... ,............................................................................... 210
6.2 Parent counselling.................................................................................................................... 218
6.3 Diet counselling ........... ,224
.fi^KPit and fissure sealants....................... 233
6.5 Fluorides ........... 240
6.6 Methods on the horizon..................................... 267

SECTION 7 : PEDIATRIC RESTORATIVE DENTISTRY

7.1' Introduction ......................................................................................... 273
7.2 Principles and concepts of cavity preparation....... ......................... 278
7.3 Procedures required for restoration........................ 283
7.4 Modern restorative materials and techniques..................... ...292
JZ/5 Semi-permanent restoration.......................................................... ....314
(Stainless steel and polycarbonate crowns)

SECTION 8 : PEDIATRIC ENDODONTICS

8.1 Objectives and diagnostic procedures......... ...................................... 328
8.2 Treatment modalities .......................................... 335

SECTION 9 : DEVELOPING MALOCCLUSION AND IT’S MANAGEMENT

9.1 Incipient malocclusion....... .................................... ................................ ................ v..,....... 364
9.2 Orthodontic prevention............... ............................................................................. ?........... ,381
9.3 Early orthodontic interventions................... 402
9.4 Commonly occurring oral habits in children and their management.......................... ..
*
427

SECTION 10 : PEDIATRIC CONSIDERATIONS FOR ORAL SURGERY

10.1 Local anesthesia........................................ .....461
10.2Extraction ...................... 471
10.3 Minor oral surgical procedures.............................................................. 476
10.4 Oral and maxillo facial injuries in children............................................................................ 490
10.5 Commonly used drugs in children...................... 526

SECTION 11 : DENTAL CARE FOR THE SPECIAL CHILD

11.1 Introduction ....................................................................................................................... 535
11.2 Management of developmentally disabled child................................................................ 538
11.3 Management of medically compromised patients...................................... 547
11.4 Cleft lip and palate....................................................................................................................574
11.5 Common craniofacial syndromes seen in children................................................. 591
11.6 Pediatric prosthodontics.......................................................................................................... 601

SECTION 12 : GENETICS IN PEDIATRIC DENTISTRY

12.1 Basic concepts in genetics......................................................................................................614
12.2 Chromosomal abnormalities...................................... 622
12.3 Single gene disorders.......................................................................................................... 632
12.4 Genetic counselling.............................................................................................................. 638
12.5 Human gene therapy...................................................................................... 643
12.6 Latest advances in genetics............................................................................................... 648

SECTION 13 : SOFT TISSUE ORAL LESIONS IN CHILDREN

13.1 Periodontal diseases ............................................................................... 654
13.2 Commonly seen other oral lesions.......................... 675

SECTION 14 : ESSENTIAL RESEARCH METHODOLOGY,

EPIDEMIOLOGY AND BIOSTATISTICS
14.1 Research methodology.................................................. ....687
14.2Epidemiology and biostatistics ................. 691

SECTION 15 : FORENSIC PEDODONTICS

15.1 Introduction .................................... ........................... ....697
15.2Child abuse............................ 700
15.3 Bite marks............................... .706
15.4Dental age assessment............................................. ;................ 713

APPENDIX
1. Clincial diagnosis of opacities of enamel.......................... .718
2. Causes of tooth discolouration ................. 719
3. Causes of intra oral bleeding....... ...... ..................... .......... .720
4. Endocrine growth axis................... 721
5. Comparison of normal diagnostic values....................... *................................................ ..722
6. a. Chronology of permanent and deciduous dentition.................... ..723
b. Chronology of deciduous dentition............................................ :............ I*?..... 724
7. Common abnormalities of deciduous dentition .................................. 725
8. Comparison of psychological theories................................................................................ 726
9. Stages of nursing-bottle caries.............................. 727
1G. Comparison of conventional and recent model of caries management ....... :............ .727
11. Treatment protocol for nursing caries ...’.......................................................................... 728
12. Preventive protocol for dental caries...................................................................... .........729
13. a. Vaccination schedule (Indian Academy of Pediatrics) ................... 730
b. Vaccination schedule at KMC, Manipal..................................................... ’.............. 731
14. a. Effects of different fluoride concentrations on enamel formation ............... 732
b. Reports on slow release fluoride dental material^................. 732
c Reports on slow release fluoride in humans......................................... 733
15. Deans index............................................................................................................. .733
16. Material guidance in pediatric dentistry............................................................................ 734
17. Relative characteristics for posterior restorations...................................................... ....734
18. Preventive protocol for periodontal diseases .............................................. 735
19. Major exanthemas in children ...... ......73S

index........................................................................................................................................
 SECTION - 1

Child as a Patient
1.1 Int rod uction to Pedodontics
Tandon S

Child is nature’s most benevolent creation. The child care for special patients who demonstrate mental,
i s not just a miniature adult but a dynamic organism physical or emotional problems.”
undergoing constant mental, physical and emotional
changes. Pedodontics is the branch of dentistry con­ « American Academy of Pediatric Dentistry (1985):
cerned with providing comprehensive dental care and “Pediatric dentistry, also known as Pedodontics
treatment for the child patient, making it the most and as Dentistry for adolescents and children,
satisfying and rewarding type of dentistry. The is the area of dentistry concerned with pre­
Pediatric dentist has the privilege of being entrusted ventive and therapeutic oral health care for
with the commencement ofa lifetime of optimal oral children from birth through adolescence. It also
health to the child patient includes special care for special patients
beyond the age of adolescence who demon­
The word pedodontics is made of two words i.e. pedo strate mental, physical or emotional problems.”
+dontics. Pedo is derived from "pais” which in Greek ■ Boucher’s Dental terminology’s (1993):
means child, “dontics” stands for the study of the “Pedodontics is the branch of dentistry, that
tooth. It has become increasingly difficult to define includes having a child to accept dentistry,
exact boundaries and limitations of pedodontics with prevention, detection, restoration of primary and
continuous development and advancements. There­ permanent dentition; applying preventive meas-
fore, the need to acknowledge the definitions evolv­
ingwithtimeis obligatory. lence, intercepting and correcting various
areas of malocclusion.”

American Academy ofPediatric Dentistry (1999)

■ Stewart, Barber, Trimtman, Wei (1982): “Pediatric dentistry is an age-defined specialty
“Pediatric dentistry? is the practice and teach­ that provides both primary and comprehen­
ing bf cbrnprehensive preventive and thera­ sive preventive and therapeutic oral health|^|^
peutic oral health care of child from birth for infants and children through
through adolescence. It is construed to include including those with special health care^^^g
 TEXTBOOK OF PEDODONTICS

■ Thereto re with the experience of the Author: 1967- CDH

"Pedodontics can be defined as a science International Symposium on Child Dental Health is
which deals with laying down the foundation conducted at London Hospital Medical College
of healthy dentition and oro-facial complex
1969- IADC
from the prenatal period through adolescence”
International Association of Dentistiy for Children
is established
WORLD-WIDE HISTORY OF PEDODONTICS
1984 - AAPD
1800 BC- Ancient Egypt American Academy of Pedodontics is renamed to
No caries in children’s teeth the American Academy of Pediatric Dentistry

1563-64 Eustachius PEDODONTICS IN INDIA

Described and showed illustrations of both primary
and permanent dentition In India (Table 1.1) the first Dental College, ‘"Calcutta
Dental College and Hospital” was started in the year
1737-Gerauldy 1920 by Dr. Rafiuddin Ahmed in his private chamber.
Writes about theories regarding tooth eruption and Dr. Ahmed, the Father of Dentistry7 in India is also
exfoliation known as "The Grand Old Man of Dentistiy”. He is
credited with the first edition of "The Indian Dental
1763- Joseph Hurlock Journal” in October 1925, foundation of the “All In­
Publishes 1st book on children’s dentistiy dia Dental Association” in the year 1927, drafting
and passingof the Bengal Dentist Act in 1939, and
1764- Robert Bunon the passing of the Dentist Act in 1948.
‘"Father of Pedodontics” reiterates the importance
of deciduous dentition Dentistry as a subject was introduced as a 2 years
diploma course to “Licentiate in Dental Science
1926 - Detroit Pedodontics Study Club (LDSc)”. It was changed to the 3yr. course in the
Dr. Samuel D. Harris - "Father of Children’s Den­ year 1926 and further modified to the present 4yr.
tistry Organizations world-wide, starts the Detroit D.S. course in 1935.
B.
Pedodontics Study Club
The foundation of Pedodontics was laid down in
Government Dental College, Amritsar, in 1950.
1927 - AAPDC
Pedodontics did not exist as an independent specialty
Detroit Study Club is now named the American
in the initial years.. of development of Dentistry in
Academy for Promotion of Dentistry for Children
India, but was includedas a mere one or two ques­
tions inthe OperativeDentistry paper. Later it was
1940 - ASDC
recognized as the section -B of the question pa per of
American Academy for Promotion of Dentistiy for
Orthodontics. In the year 1988 as per D.C.L rules it
Children renamed as the American Society of
got iWWe importance and was treated as a separate
Dentistiy for Children
Amritsar thertext to introduce this
K G.M.C. Lucknow (1967), PG.L
i^^toft<1978)andG.D.C.Bombay(1982). The fifth
^^^^sSionand first in south India wasthe C.O.D.S.
I^^pal in the year 1985 under Dr. Shobha Tandon.
 SECTION 1 : CHILD AS A PATIENT |

Fig. 1.1 World-wide foundation of PedodonOc Societies.

Table 1.1: Evolution of Pedodontics in India.

1920 - Calcutta Dental College and Hospital
1 st Dental College started bv Dr. Rafiuddin Ahmed "Father of Dentistry in India”

1935-B.D.S.
Licentiate in Dental Science becomes Bachelor in Dental Suigeiy

1950 - Pedodontics is introduced

Government Pental College, Amritsar starts Pedodontics as a specialty

1978 - Pedodontics for Undergraduates

Pedodontics is introduced as a specialty in the undergraduate curriculum

wt 1979 - Indian Society of Pedodontics &

■'2:

The Association of Indian Pedodontists holds the 1st conference. Dr.B .R Vacher is
1- made the “Father of Pedodontics in India”

1982- Affiliated to IADC

Indian Society of Pedodontics and Preventive Dentistry becomes an affiliate
■ member of IADC
 4EW I TEXTBOOK OF PEDODONTICS

The Associati on of Indian Periodontists held its first

conference on the 24th of November 1979 where it
was first named as the Indian Society of Periodontia
(now Periodontics) and Preventive Dentistry Its con­
stitution was drafted by Dr. Mrs. AmritTewari. Con­
tributions made by Dr. B.R. Vacher, the Father of
Periodontics in India, was recalled and thus he was
unanimously made the life patron of the society.

MX. Gauba was elected first president of the soci­

ety; Dr. Mrs. A Tewari the first General Secretary and
Dr. H.S.Chawla was the first editor of the journal. In
1982ISPPD became an affiliate member of I ADC, the
International Academy for Dentistry for Children.

DIFFERENCES BETWEEN THE CHILD AND THE Fig. 1.2 Periodontic triangle
ADULT PATIENT the dental needs of the child patient, basics in the
Hippocrates in the 5th Century B.C. talked about the pediatric medicine, general and oral pathology,
differences between the child and the adult. In the growth and development and child psychology also
4th Century A.D. Celsius recognized that the child need to be known.
must be treated differently from adults. The discov­
ery of childhood began around the 13 th century. (By Changing trends in the scope of Pedodontics
the Middle Ages, children started getting more at­ In 1942 when Pediatric Dentistry was recognized as
tention especially as the heirs and sons of the ruling a speciality, the common needèof the children were
houses and had belief not die while "teething’").. restoration of the cari ous teeth, treatment of dental
Childhood compared to adulthood is a transitional pulp, and maintenance of tooth spaçe. Preventive
Stage characterized by many changes. Rapid changes modalities of treatment were limited in practice. Di­
agnostic techniques and materials for pediatric use
in childhood affect every aspect of dental care be­
needed to be developed.
ginning from the first step of diagnosis till the peri­
odic recall following treatment. A child differs from
With the changing trends and development there
an adult in various ways:
has been a tremendous increase in the scope of
1 physical pedodontics. Various factors responsible for this
2. emotional and psychological change are:
3. consideration of behaviour ■ Professional and public recognition of dental
4. type of treatment (different dentition considerations) health for the general well being of the child.
5. dentist-patient relationship This indicates the increased knowledge in the
6. parent-dentist relationship (Fig. 1.2) public sector regarding child dental health care.
■ Wide recognition of fluorides as the most effec­
SCOPE OF PEDODONTICS tive health agent in the prevention of dental
caries. This is gaining momentum even in India.
In order to handle majority of the needs of the child,
■ Introduction of high-speed technology in the
the periodontist requires interaction with many
preparation of teeth requiring restoration.
specialities (Fig. 1.3). The scope refers to the range
■ Great improvement of various anesthetic agents
of activities considered in the practice of
in clinical use.
Periodontics. In addition to be knowledgeable about
 SECTION 1 : CHILD AS A PATIENT |

Fig. 1.3 Scope of Periodontics

■ Introduction of * the
system.of sophisticated she provides comprehensive health in total to the
plastics i.e. composites, ionomer cements, patient, prevents the onset of the disease right from
compomer, pit and fissure sealants - what are now the beginning while considering the psychological
popularly called "the invisible fillings” need of the child patient thus instills a fiositive atti­
■ Radical changes to control virulent infections in tude to dental health in future vears to come. With
any clinical content.' the increasing range of activities one must realize
■ Recognition of the child as an individual. the need for knowledgeable and skilled practition­
ers as the pedodontist
The present trends in Pediatric dentistry comprises of:
1. Preventive Dentistry
Self-Assessment
2. Public health dentistry
3. Child psychology and management 1. Define Pedodontics.
4. Clinicaldentistry 2. Who is the father ofdentistiy in India?
5. Preventive and Interceptive Orthodontics 3. When was the American Academy of Periodontic
6 Special care dentistry formed?
7. Child abuse and neglect ( Forensic Pedodontics) 4. When and where was the first P.G. program in
8. Genetics in Pediatric Dentistry. pedodontics started?
Preventive practice has now become the dominant 5. What is the difference between a child and adult <
branchin pedodontics. patient? /JW"
6. What is the periodontic triangle? j .
The characteristic that differentiates the pediatric 7. What is the scope of pedodontics?
dentist from the other dentists is the fact that he/
 1.2 Case History, Diagnosis and
Treatment Planning
Tandon S

One can treat and cure only those diseases or signs HISTORY
and symptoms .that are diagnosed in the first place.
This art and science of the patient evaluation is the L Health history:
key to treatment planning. Health history is a structured format and must be
recorded as such. The interview conducted should
A few terminologies need to be classified before go­ have a few guidelines to be followed such as:
ing on with the case history recording. « Various questions need to be asked depending
• Diagnosis - The determination of the nature of on the type of information needed. It may be
the disease. open-ended questions (encouraging a detailed
» Differential diagnosis * The process of listing explanation) or close ended (specific 4 Yes’ or
out two or more diseases, having similar signs 4No’ answers). Leading questions are well
and symptoms of which only one could be attrib­ avoided.
uted to the patient’s suffering.
■ To obtain history in infants and children, under
« Provisional diagnosis - A general diagnosis
5 years of age, the parent or legal guardian is
based on clinical impression without any labora­
interviewed.
tory investigations.
■ The questionnaire should be accommodative
to the various problems encountered and not
■ Final diagnosis - A confirmed diagnosis based
stereotype.
on all available data.
■ Often, the symptoms are aptly described by
■ Symptom - Any morbid phenomenon or depar­
ture from the normal in structure, function, or the patient and should be recorded in his own
sensation experienced by the patient and words, (e.g. Doctor, I have a sudden ‘shooting’
indicative of a disease. type of pain).
• Sign - Any abnormality indicative of disease, ■ The dentist should be an empathetic listener
discovered on examination of the patient (an for the patients may often pour out their
objective symptom of a disease). grievances to him/her and this will go a long
way in establishing a good rapport.
Accurate diagnosis can only be achieved by sys­
tematic and methodical collection and evaluation of From the pedodontist’s point of view the dental
data. Rarely does one come across diseases that have visit serves as a positive attitude instilling process
just a single symptom or sign. Each component of for further dental treatment. Thus behavior
case evaluation has its own significance and should shaping should be started from case history taking
HJbe allotted the same. and even before.
 SECTION 1 : CHILD AS A PATIENT |
i

IL Vital statistics omatitis from 6 months to 6 years,

It can be defined as a systematic approach to collect nursing caries is seen in the preschool age
and compile in numerical form the information group only). Depending on the age the
related to vital events. live births, deaths, behaviour management'techniques also vary
recognition, social structure and legislation. and this should be kept in mind.
Uses: It is essential to -
■ Maintain records 6. Sex : Girls mature faster than boys and
■ To create administrative standard of health thus their treatment may be required earlier.
activities Some diseases are more common in females than
■ To direct or maintain control during execution in males, e.g. anorexia is more common in
of programs. females while hemophilia may be found
■ To disseminate reliable i nformation on hea 1th exclusively in males. A combination of age and
situation and programs. sex can sometimes give an indication of the
occurrence of a disease, e.g. pubertal gingivitis
1. Date: It records the time the patient reported is commonly encountered in adolescent
and can be referred back to during the follow­ females.
up visits.
7. Race/Ethnic origin : Some diseases may be
2. Hospital numher/Case number: For the common in certain races. Oral hygiene practices
purpose of maintaining a record, billing the may be common in some religions or races.
individual and for legal considerations (in view
of the Consumer Protection Act) one should 8. Address: Theaddress is used for all comnmni-
note the hospital number. cations sometimes even before the first visit.
By knowing the locality, along with the EHily
3. School and class : To know the economic income and parents occupation, the socio­
status, to communicate with the teacher. It also economic status can be assessed.
helps in assessing the IQ of the child and to
If the patient is coming from a far distance, the
establish effective communication at his own
appointments can be modified to complete
IQ level.
treatment in fewer visits.
Name: Name asking is a verbal communication Living area may indicate diseases endemic to
that establishes a rapport with the patient. the particular areas.
Further communication by means of the name
gives a sense of importance and acceptance. 9. Source of information : The source of infor­
(Nickname helps make the environment mation and relationship with à child should be
informal). ascertained. The reliability of the information
BEI
provided may also need to be evaluated.
5. Age : The chronological age (date of birth)
should be noted to compare with other ages 10. Source of referral: In multidisciplinary set
(dental, skeletal) so as to know whether growth ups, day to day referrals are seen. The chief
and development is normal in the child. complaint in these cases may be non-dental.
Thus stress on dental awareness arid
Certain diseases are known to occur motivation may be needed.
frequently at particular ages, which should ■ In certain cases, just an opinion may be
be kept in mind (e.g. primary herpes gingivost- required and the patient’s treatment can be
 tfiWl I TEXTBOOK OF PEDODONTICS

'carried out only in consultation with 1. Rh incompatibility: May result in the condition
pediatrician or physician. The patient care termed 'erythroblastosis fetalis’. The sensitized
can be optimized by being in constant touch antibodies of the mother cross the placental
with physician or pediatrician. barrier and a immune reaction takes place. The
(e.g. Dental procedures may be performed effects may be seen in the dentition, with wetb
along with any. other general anesthesia described entities such as Hump’ on the tooth
procedure in an uncooperative child). and the characteristic blue-green discoloration.

III Chief complaint: 2. Neonatorum Jaundice: The immature RBCs

A detailed history of the same goes a long way in in an infant are rapidly destroyed in the spleen.
establishing the diagnosis. Several factors need The increased bilirubin cannot be sufficiently
to be evaluated regarding the chief complaint. For cleared by the liver leading to a transient
example, the most common presenting illness can jaundice’ in the child.
be evaluated as:
1. The onset Other problems such as
2. The duration Blue baby
3. The location Forceps delivery7
4. The quantity;- quality; severity; and frequency Any other problems
of occurrence
5. Aggravating and relieving factors VIL Postnatal historv:
6. Associated symptoms As discussed elsewhere, significance is attached
to the amount of time the child was breast fed,
Medical History: History of any medical condi­
bottle fed, if the bottle was misused, and the type
tions should be asked, including recent hospita­
of nipple used etc. as given in the chart.
lization, blood transfusions, etc.
■ Vaccination status needs to be assessed along
IV Parent history:
with the present medical illness if any. Presence
A dental visit and the treatment performed would
of any habit/its duration, frequency# intensity
point towards the attitudes of the parents. An
need to be evaluated.The behavioral status,
unpleasant experience may be transmitted
a general assessment as to whether the child is
unknowingly to the child and it should be kept in
cooperative or unco-operative and if any deep-
mind. Any genetic/inherited abnormalities should
rooted problems are present, have to be found
be interviewed into.
out.
■ Any previous experience with the dentist and
V Prenatal history :
what bearing it has on the present visit should
Prenatal history (mainly maternal) may disclose
be noted.
information that can be linked to the present
■ Progress in school, how he interacts with other
condition (e.g. tetracycline stains on teeth) and
children will indicate the development of the
may indicate when an antibiotic can be
child’s emotions.
administered.
Diet chart. A detailed diet history should be recorded.
VI Birth History:
The diet chart shows whether it is adequate. More
Suggests if any problems were encountered at
importantly it can indicate the cariogenicity of diet
birth, as:
(refer to diet counseling).
 SECTION 1 : CHILD AS A PATIENT | CB

EXAMINATION Gingiva: The normal gingiva in a child is different

from an adult. Inflammation of the gingiva and
accumulation of the plaque on the teeth are seen
by respective indices.

C Hard tissue evaluation

The teeth present have to be recorded so that the
dental age can be assessed along with the stage
of development of the dentition.

FDI scoring system : It is one of the commonly used

numbering system. Quadrants are allotted initial num­
bers as:
Upper right Upper left
Fig. 1.4 Knee to knee position of the Dentist and Primai}7 5 6
the parent while examining the child.
8 7
A. The general examination and evaluation of the
Upper right Upper left
patient begins with the first appearance of the
child and the parent themselves. A child hiding Permanent 1 2
behind the parent, child inquisitively looking at
4 3
the equipment, a smiling and laughing child, will
give a fair indication of the response to be ex­
pected.
Then the tooth in each quadrant is numbered as:
The build up of the child (whether normal for his
age), height, and posture while standing can also Primaiy:
be evaluated simultaneously. 555453 5251 616263,6465
858483 8281 7172737475
The child, walking along with the parent should
be checked for the gait as well. Sometimes the
Permanent:
way the child walks can be associated with a par­
181716 151413 12 11 2122 23 2425 26 27 28
ticular disease.
48 47 46 45 44 43 42 41 3132 33 34 35 36 37 38
B. Local examination: Apart from the facial features
soft tissues need to be evaluated. (Fig. 1.4) Indices: The most commonly used indices are die
Skin/Lips: For presence of any sinus/fistula plaque index, gingival index and caries index:
Mucosa:. Any ulcerations, growths, Pallor of
mucosa may indicate anemia, yellowish discolou- Caries index: In pedodontics department, Manipal
ration - jaundice (rarely seen). we use the WHO criteria on each tooth surface.
Systemic manifestations of diseases may be Table 1.2)
present (Koplik’s spot as in early measles).
Nodes: Palpation of commonly involved lymph ■ Plaque Index (Silness and Loe, 1964)
nodes (sub mental and sub mandibular) shows
Plaque has been defined as:
an acute or chronic infection. A specific, highly selective entity resulti^g^^^|t
Palate: The hard and soft palate may also show sequential colonization of microorganw^J^^^/;
manifestations of systemic diseases.
 MTÏ> I TEXTBOOK OF PEDODONTICS

Table 1.2: WHO (1987) criteria for primary and permanent teeth.
Permanent tooth code Condition/status Primary tooth code

0 Sound A
1 Decayed B
2 Filled, with decay C
3 Filled, no decay D
4 Missing as a result of caries E
5 Missing due to any other reason -
6 Sealant, Varnish F
7 Bridge abutment or special crown G
8 Unerupted tooth -
9 Excluded tooth
__________________________ :--------- -—. __ _______________ ,____

Surface of the teeth, soft tissues, restorations and 2 - Moderate accumulation of soft deposits within
appliances. (Silness and Loe included materia alba the gingival margin and/or adjacent tooth sur­
ànd debris under the plaque). face that can be seen with naked ejre.
3 - Abundance of soft matter within the gingival
Rather than examine the whole dentition, a few4 In­ pocket and/or on tire gingival margin and ad­
*
dex teeth are selected jacent tooth surface.

Permanent Dentition - 16,12,24,36,32,44

Calculations *
Primary Dentition - 55,52,64,75,72,84

In cases of mixed dentition, sometimes, depending A. Plaque index for a tooth =

on the teeth present, the Index teeth may be as: Add scores from 4 areas of tooth
16,52,64,36,32,84, or such combinations where the
deciduous counterpart, if present is considered. 4
W Should both the primary and permanent teeth be
present, the permanent one is to be considered. B. Plaque index for a individual =
■ Should both be absent, the tooth distal to them
Add scores for each tooth
may be considered or only 5 teeth are considered.
• Each tooth is divided into 4 parts.
No. of teeth examined
Scoring criteria
Interpretation scale
0 * No plaque in the gingival area
0.0 - Excellent
1 - A film of plaque adhering to tire free gingival
0.1-0.9 - Good
margin and adjacent area of the teeth. Only
1.0-1.9 - Fair
running a probe across the teeth surface may
2.0-3.0 - Poor
recognize the plaque.
 SECTION 1 : CHILD AS A PATIENT I CXB

■ Gingival Index (Loe and Silness, 1967) This probe detects pocket temperature differ­
ences of 0.1 °C from a referenced subgingival
It has been developed for the purpose of assessing
temperature
the severity of gingivitis and its location in four pos­
Higher temperature pockets a re signaled with a
sible areas of an individua l tooth.
red-emitting diode
Same teeth are examined as in plaque index

Each tooth is divided in to 4 parts b) Fluoride Probe

t Disto - facial papilla - used to measure pocket depth
2. Mid - facial papilla
3. Mesial facial papilla Advantages:
4. Entire lingual gingival margin 1. Constant probing force
2. Digital readout
Score Criteria 3. High degree of accuracy
0 - Normal gingiva
1 - Mild inflammation, slight change in colour, It is a computerised peridental probe consists
slight edema; No bleeding on probing of a probe, handpiece, a digital readout, a foot
2 - Moderate inflammation, redness, edema, and switch, a computer interface and a computer. *
glazing; bleeding on probing
3 - Severe inflammation, marked redness and c) Foster-Miller Probe:
edema, ulcerations, tendency to spontaneous Couples pocket depth determination with
bleeding detecting of CEJ from which clinical attaclunent
level is automatically detected.
Calculations
d) Toronto Automated Probe:
Gingival index score per tooth = To measure clinical attachment levels
Total score Sulcus is probed with a Ni-Ti wire that is
extended under air pressure
4
Gingival index score for a person = e) DNA Probe:
Total of all scores Helps to identify the organism associated with
periodontal disease.
No. of teeth examined It identifies species-specific sequences of
Interpretation nucleic acids that make up DNA, thereby
1. 0.1-1.0 Mild permitting identification. The DNA library
2. 1.1-2.0 Moderate includes probes for A.actinomycetum-
3. 2.1-3.0 Severe comitans, P.gingivalis, B.intemiedius, C.rectus,
E.corrrodens, F.nucleatum andT.denticola.
ADVANCED DIAGNOSTIC AIDS
II. OTHER AIDS
Following diagnostic aids may be used as per the
need of patient. a) Xeroradiography: is an x-ray imaging system
PROBES that uses the xerographic copying process to
a) Perio temp probe record images.
- helps to detect early inflammatory changes
in the gingiva by detecting temperature rise.
 SOI I TEXTBOOK OF PEDODONTICS

b) CADIA: Computer Assisted Densitometric ■ Keeping in mind the systemic condition, pre
Image Analysis system. A video camera meas­ medication (as in antibiotic prophylaxis,
ures the light transmitted through a radiograph sedation) needs to be given to the child, again
and the signals from the camera are converted with the consent of the pediatrician or
into gray levels. The camera is interfaced with physician.
an image processor and a computer that allows
storage and manipulation of images. 2. Preventive phase:
Caries risk assessment (as described elsewhere)
c) Computers: In diagnosis by computers, it is Assessment for various preventive measures
necessary to store facts associated with symp (fluoride application, pit and fissure and sealant,
toms of patients with known diseases in field diet counseling).
of study. Computers help us by retention of
facts about many patients and selection of rel­ 3. Preparatory phase:
evant facts to give a diagnosis. Computers a) Behaviour management: The child’s behav­
also help in comparati ve digital study of radio­ iour shaping should start right from the
graphs eg. Cephalograms. reception itself.
b) O ral prophylaxis - It presents a clearer view
of the caries process which facilitate its
diagnosis. It also gives an idea whether the
patient will cooperate.
c) Caries control - Further progress of carious
lesions should be controlled. Sometimes
multiple lesions may need to be temprorized.
d) O rthodontic consultation - Minor orthodon­
tic correction should be carried out before
evaluating the space maintenance program.
e) Oral surgery - Gross caries may necessitate
the removal of teeth.
Fig. 1.4a Use of computers in comparative
f) Endodontic therapy - Sometimes, a tooth may
digital study of radiographs
need to be saved with endodontic treatment.
d) Ultrasonics: The fundamental use of high fre­
quency sonic vibrations is to define areas of Corrective phase:
differing physical properties by reflection of a) Restorative dentistry - permanent fillings,
waves from the surfaces of adjacent areas of stainless steel crowns would be included
tissues. Helps in defining the pulp anatomy, under this phase.
shape of soft tissue neoplasms etc. b) Prosthetic Rehabilitation - tooth replacement,
jacket crowns etc.
PHASES OF TREATMENT PLANNING c) Early orthodontic intervention is to be car­
1. Systemic phase: ried out.
■ A patient with a medical disease background
may require the condition to be stabilized and 5. Maintenance phase:
then dental treatment to be carried out. In Depending on the risk of the individual and his
this respect the patient may have to be oral hygiene status, a 3-6 month recall visit can
referred to the physician or pediatrician as be established.
required.
 SECTION 1 : CHILD AS A PATIENT | ŒEB

FORMAT OF A CASE RECORD

DEPARTMENT OF PEDODONTICS AND PREVENTIVE DENTISTRY
COLLEGE OF DENTAL SURGERY, MANIPAL
DENTAL CASE SHEET

VITAL STATISTICS

Date : Hospital No.: Pedo Reg. No.

Name : Age : Sex :
School : STD: Examiner :

CHIEF COMPLAINT

History of Present illness :

Medical History:

Past Dental History :

Oral Hygienic Habits :

ORAL HABITS FREQUENCY INTENSITY DURATION

Digit sucking

Nail biting/Lip biting

Tongue thrusting

Mouth breathing

Bruxism

Postural

DIET HISTORY

Time Type of Food Quantity Method of Quantity of

Preparation Sugar Added
 CEB I TEXTBOOK OF PEDODONTICS

CLINICAL EXAMINATION

GENERAL

Build: Height: Weight:

Gait: Posture: Body type:

Examination of Head & Neck:

Shape of Head:

Facial form -

Facial Symmetry:

TMJ:

Lymph Nodes:

LOCAL EXAMINATION:

ORAL SOFT TISSUES:

Skin/Lips: Mucosa: Palate: \

Floor of Mouth: Tongue: Tonsi Is / Adenoids:

Any other:

Oral Hard Tissue Examination:

Teeth present (FDI coding)

Caries Status:
DMFT/dinft
55 54 53 52 51 61 62 63 64 65
r *

1
18 17 16 15 14 13 12 11 21 22 23 24 25 26 27 28

48 47 46 45 44 43 42 41 31 32 33 34 35 36 37 38

85 84 83 82 81 71 72 73 74 75
contd.
 SECTION 1 : CHILD AS A PAT,'ENT |

Score D= d=
M= IB =
F= f-
DMFT = dmft =

Oral hygiene Plaque Index - Silness and Loe

B B
D| |M
dlZZJm
P p

B
D| IM
L

Score: ~ Comment:

Gingival Index = Loe and Silness

B
DI IM
P

B B
D| |M D| |M
L L

Score:

Occlusal Review:

Molar Relationship:
Primary. Permanent:
«

Canine Relationship;

Over jet mms

contd.
 ffEB | TEXTBOOK OF PEDODONTICS

Over bite nuns.

Midline Normal / Deviated

Cross bite

Any other

Provisional Diagnosis

Lab Investigations if any:

Final Diagnosis:

TREATMENT PLAN:

Date Treatment Done Name of the Student Sign, of Staff Grade

ASSESSMENT OF THE EFFECTIVENESS OF THE ■ Has the dental IQ improved? (of the child and
COMPREHENSIVE TREATMENT PLAN the parent)
■ Were the expectations reached?
After completion of the scheduled treatment plan, it ■ How would you change the treatment plan
is important to-assess all aspects of care provided knowing the results achieved?
and the anticipated follow up programs. The clini­
cian should always assess by the following queries 2. Evaluation of restorative care
to himself. ■ Were the restorative techniques used success­
ful?
1. Effectiveness of the preventive program: ■ Were the teeth restored as planned?
■ Was the program appropriate?(for the age of ■ Were there any changes of major conse
the patient and for the parent) quences?
■ Was the program effective?
SYSTEMIC APPROACH TO ORAL DIAGNOSTIC AND TREATMENT PLAN FOR A CHILD PATIENT
 »1« I TEXTBOOK ÔF PEDODONTICS

■ What are the problems that could be antici­ S elf-Assessment

pated?
1. What do you understand by differential diagnosis?
■ What would you like to do differently?
2. How does the provisional diagnosis differ from
the final diagnosis?
3. Evaluation on tooth guidance treatment
3. What is vital statistics and its importance?
■ Was the case diagnosed properly?
4. What are the factors needed to evaluate the chief
■ Were the expected results achieved?
complaint?
■ Is treatment complete?
5. Why is the recording of prenatal history impor­
■ Is the necessary follow-up care arranged?
tant?
6. What is neonatorum jaundice?
4. Assess behavioral management approach used
7. Why should the extra oral examination be per­
■ Effective?
formed?
■ Appropriate for the chi Id?
8. What is the FDI coding system?
■ Was the child’s behavior altered? Yes/No
9. Define an Index.
10. What are the different phases of a treatment plan?
5. Development of plan for the follow-up
11. What do you understand by recall?
« Establish proper referral
■ Establish recall( Time and treatment )
■ Establish home care program that will work
for the particular child and the parent.
 1.3 Radiographie Examination of Pediatric
Dental Patients
John P, Tandon S

Radiographic examination plays a vital role in the Intra-oral films

diagnosis and treatment planning of both children
and adults. It has to be stressed that radiographs Intra-oral films arc meant for positioning inside the
have an additional importance in the evaluation and mouth during exposure. There are three types of
treatment planning of pediatric dental patients. A intraoral radiographic projections:
complete examination of the dentition and associ­ ■ Intraora 1 periapical (ЮРА) radiographs
ated structures should include a radiographic sur­ ■ Bitewing radiographs
vey as well. In pediatric dental practice, radiographs ■ Occlusal radiographs
also play a significant role in the assessment of
growth and development. Radiographs, at the sim­ Size of intraoral films
plest level, help in the detection of dental caries and
at the most complex level, in the diagnosis of cysts,
tumours or any other ma jor craniofacial disorders.

The work of many scientists culminated in the dis­

covery of X-rays by Roentgen on November 8,1895.
The then unknown and invisible rays were given the
name X-rays by Roentgen because of the simple fact
that the nature of these rays were not known at the
time of the discovery. However’ discovery of X-rays (-------------

changed the medical science rapidly, bringing in a 0

great revolution. X-rays have also been widely used
in dentistry and have a special place in pediatric den­
tistry where the growing child with a developing den­
tition needs to be assessed carefully.

Types of radiographs:

The radiographs taken of a child patient can be

broadly grouped into two categories, intra-oral and
extra-oral radiographs. Accordingly, the film used in
pediatric dental practice for radiographic examina­
tion can be grouped into: Fig. 1.5 X-ray Films
i Intra-oral films
ii. Extra-oral films
 | TEXTBOOK OF PEDODONTICS

■ Size 0 is used for bitewing and periapical radio 3. Film emulsion: The film emulsion is the main
graphs of small children. image receptor system of x-ray film, as this is
■ Size 1 is used for radiographing the anterior teeth sensitive to both light and x-rays. The emulsion
in adults. This film is not routinely used. mainly consists of silver bromide crystals with
« Size 2 is the standard film used for anterior occlu­ some amount of silver iodide.
sal radiograph, periapical radiograph and bitewing
survey in mixed and permanent dentition. As it has already been mentioned, when the film is
exposed to x-rays, a latent image is formed in the film
Occlusal films have a size of57 x 76 nun and are taken which gets converted to a visible image only when
for visualizing the entire maxillary or mandibular chemically processed.
arches. (Fig. 1.5)
For a radiograph to be of proper diagnostic quality, it
Extraoral films should be free from technical or processing errors
and it should give sufficient information pertaining
Most of the extra-oral films are used in intensifying to the area radiographed or for which purpose the
screen-film combinations. The extra-oral films used radiographic projection is made.
in dental practice vary in their sizes depending on
the individual projection for which they are employed. Intraoral radiographs
• 1.5 x 7 inches films - these films are used for
temporomandibular joint (TMJ) views and lateral As it has already been mentioned, there are three
oblique views. types of intra-oral projections, intra-oral periapical
• 8x10 inches films: These films are used for lateral (ЮРА) radiographs, bitewing radiographs and oc­
cephalograms, paranasal sinus veiw, etc. clusal radiographs.
« 6 x 12 inches film: These films are used for
orthopantomography. Intraoral Periapical Radiographs (IOPA)

Composition of films ЮРА radiographs are useful in the evaluation of teeth

and their associated structures. ЮРА radiograph can
A radiographic film is an image receptor system. On be taken by using two techniques; short cone tech­
exposure to x-rays, there is formation of an invisible nique or bisecting angle technique and long cone
image or latent image which when chemically proc­ technique or paralleling technique. Though the par­
essed transforms into a visible image which can be alleling technique provides an image of teeth with
viewed under trans-illumination. minimal magnification, there is an inherent disadvan­
tage of using this technique as special holders or
An X-ray film consists of the following components. position indicating devices are required to take the
1. Base: The base of x-ray film is made up of a poly­ radiographs.
ester, polyethylene terepthalate. The base helps
in supporting the emulsion which gets chemi­ Paralleling technique cannot be employed in chil­
cally activated when exposed to x-rays. The base dren with a shallow palate and a shallow floor of the
also provides rigidity to the film. mouth. In small children, with primary dentition, size
2, Adhesive layer: An adhesive layer is present over 0 film should be used. In older children or in situa­
the base to attach the film emulsion to the film tions where a larger area has to be visualised, size 1
base. film should be used.
 SECTION 1 : CHILD AS A PATIENT |
I

Indication Projections (Fig. 1.6) i

ï

The indications for taking periapical radiographs in For projection of the maxillary teeth, the head of the
children are given below patient should be kept upright. The vertical angula­
■ To determine the status of the periapical region tion used are:
in the deciduous and young permanent teeth. For the anterior teeth +50
■ In the evaluation of pulp treatment or endodon­ For the premolars +30
tic treatment. For the molars +25
■ In the detection of developmental anomalies such
as supernumerary teeth, unerupted teeth or mal The film is positioned on the palatal aspect of the
formed teeth. teeth by using film holders. The tooth/teeth to be
■ To identify any pathology involving the primary radiographed should come in the center of the film.
teeth such as periapical pathology or internal
resorption. The central x-ray beam is directed in such a way that
■ To evaluate the status of the periodontal it liits the film almost perpendicularly. This principle
ligament should be followed to prevent magnification of the
• In the diagnosis of pulp calcification, root image and also to avoid a cone-cut appearance im­
resorption or root development age formation.
■ Ana lysis of space in mixed dentition
■ Diagnosis of traumatic injuries effecting For projection of mandibular teeth, the following ver­
pathologic changes tical angulations are used.

Technique For the anterior teeth -20

For the premolars -10
Obtaining Child's Co-operation for
For the first and second molars -5
Radiographs:
For the third molar

The following have been suggested for achieving

For the lower anterior projection, the film is kept on
better co-operation from the child patient during the
the floor of the mouth, on the lingual side of the
radiographic procedure:
teeth. For the posterior projection, the film is kept on
1. Acquaint the child with the dental X-ray machine
the lingual sulcus. Care should be taken while taking
and explain the procedure to him. Use words the
the radiographs of mandibular teeth to avoid soft
child can understand.
tissue trauma due to the sharp margins of the film.
The central x-ray beam is directed almost perpen­
2. Pre-set the timer and position the cone in the
dicular to the film.
approximate angulation prior to placing the film
when intra-oral radiographs are taken.
While employing the long cone technique, the cen­
tral x-ray beam is directed perpendicular to the long
3. Obtain the confidence and the co-operation of
axis of the tooth and the long axis of the film, whereas,
the child. Take the easiest film for the patient first
while employing the short cone technique, the cen­
(e.g., upper anterior films).
tral x-ray beam is directed perpendicular to an imagi­
nary bisector that bisects the angle formed by the
4. Talk to the child so that you distract his attention
long axis of the tooth and the film.
and establish rapport and confidence.
 Ψ 1 TEXTBOOK OF PEDODONTICS

Posterior teeth

MAXILLARY REGION

Horizontal plane

Central ray

Anterior teeth Posterior teeth

MANDIBULAR REGION • J

Fig. 1.6 Angulation of X-ray tube for different regions of Oral Cavity.

Bitewing radiograph ■ Observation of location and position of retained

primary roots
Bitewing radiograph is a very usefid intrapral radio­ ■ Observation of relationship of opposing teeth
graph, especially to detect incipient proximal caries. ■ Observation of location and position of
Bitewing radiographs can be taken by using film sizes permanent tooth bud and its relationship, to
No 0 or 1 for younger children and No.2 for older the primary root.
children. The coronal portion of both the maxillary
and mandibular teeth of the required area can be visu­ Bitewing radiographs can be taken with paper hold­
alized on the film. ers to which a tab is attached. The central x-ray
'beam is directed between the contact points of the
Indications teeth.

• Detection of interproximal caries with respect to Occlusal radiographs

depth and relationship to pulp
• Detection in incipient interproximal caries Occlusal radiographs are used in the evaluation of
• Observation of boundaries of the pulp chamber the entire maxillary arch or mandibular arch. Occlu­
and the height of the pulp horns sal radiograph are indicated in the localisation tech­
• Observation of primary resorption pattern nique (for example to determine the buccolingual
 SECTION 1 : CHILD AS A PATIENT |

position of impacted teeth), to evaluate cortical plate 2. The presence of residual primary roots.
expansion, to evaluate fraction displacement, to 3. The possibility of removal of a primary tooth
evaluate the maxillary sinus or submandibular sali­ because of interference with the eruption of the
vary gland calculi. A larger film is used to cover the permanent tooth
larger area in one film. 4. Proper sequence of eruption
5. Evaluation of old restorations and detection of
Visualization of radiographs recurrent lesions
6. In emergency situations, thé degree of pulpal
Visualization of a radiograph requires a good source involvement, the amount of alveolar bone loss or
of extraneous light. A thorough knowledge of the the presence of periapical pathosis is detected
basic anatomy and the radiographic appearance of 7 Finally, in the ca se of traumatic injury, the possi­
various osseous structures is very essential in the bility of a root fracture, and the type and area of
proper interpretation of radiographs. Radiographs the fracture, are evaluated.
should be examined in a quiet area that is free from
multiple extraneous stimuli. Recommended radiographic examination of
children and adolescents
Conditions and Areas routinely Evaluated
Radiographs shoul d be taken judiciously and only
■ The degree and variation of calcification of the after thoroughly evaluating the patient clinically. The
teeth, and the size, shape, position and angula­ following guidelines can be employed while advis­
tion of the unerupted teeth: ing radiographs for a child patient or an adolescent
■ The presence or absence of teeth, including patient.
anomalies in number, delayed eruption, or impac­
tion. 1. Child patient (before the eruption of the first
■ Carious lesions and interproximal carious lesions permanent tooth)
in particular. Incipient lesions on the facial and ■ New patient: 2 bitewing projections of the
lingual surfaces are not seen in a radiograph and posterior region
are more readily found with an explorer. Radio­ ■ Recall patients: Bitewing examination at 6
graphic evidence of caries is seen only when sub­ months interval.
stantial amounts of decalcification has occurred Clinically no caries or no increased suscepti-
and a change in density is noted. bility to caries: Bitewing radiograph at 12 to
■ Degree and variation of root resorption of the 24 month intervals
primary teeth, as well as the root development of ■ Deep caries: SelectedIOPA radiograph
the permanent teeth.
• The presence of any periapical pathosis or bone 2 Child patient after the eruption of the first perma­
lesion nent tooth
■ New patient: Selected IOPA radiographs,
Conditions and Areas for Evaluation on Peri­ posterior bitewings, occlusal views, and OPG
odic Visits: ■ Recall patient: Bitewing radiographs and
selected IOPA radiographs, if indicated.
All previously mentioned areas and conditions are ■ Clinically no caries: Posterior bitewing radio­
and should be part ofa periodic examination. In addi­ graphs
tion, the following should be evaluated: ■ Deep caries: Selected IOPA radiograph
1 Ectopic eruption.
 <EEB I TEXTBOOK OF PEDODONTICS

3. Adolescent (permanent dentition and before the structures that come within a “zone of image
eruption of the third molars) layer' are clearly visualized, whereas the stru­
■ New patient: Posterior bitewing radiographs ctures outside the image layer are blurred out.
and a selected 1OPA radiograph.
■ Recall patient: Posterior bitewing radiograph ■ With an advanced panoramic radiographic
at 6 to 12 month intervals. system and by using panoramic scanography,
■ Clinically no caries: Posterior bitewing radio programs are available for imaging selected
anatomical areas such as the maxillary sinus,
graphs
■ Deep caries: A selected ЮРА radiograph and nasal fossae, and so on.
or bitewing radiograph. ■ Panoramic radiography is used in the evalua­
tion of traumatic injuries as well as dental age
Extraoral and specialized radiographs evaluation as it gives a good information
about the eruption status of the teeth,. OPG
1. Rationale of panoramic radiograph (Fig. 1.8,1.9) can also be used for patient education.
■ A panoramic radiograph or orthopanto­
mogram (OPG) helps in the visualization of 2. Cephalometric radiography (Fig. 1.10,1.11)
both the maxilla and mandible together with Pediatric dentists, orthodontists, and maxillofa­
their associated structures in one film with cial surgeons, use cephalometric radiographs or
considerably less radiation exposure thana cephalograms for facial and jaw growth analysis.
routine full-mouth radiographic survey. Cephalometric radiographs are mainly used for
г
conventional cephalometric measurements and
■ In panoramic radiography, the X-ray source cannot be used in case of evaluation of craniofa­
and the film rotate, with the result that the cial anomalies.

Fig. 1.7 Cephalometric tracing on lateral Cephalogram.

 SECTION 1 : CHILD AS A PATIENT | dklA

A typical tracing of lateral cephalogram with high resolution. It is very helpful in the diagno­
planes and constructed points is shown in Fig. 1.7 sis of disorders involving auditory ossicles,
neonatal maxillae and temporomandibular joint
Cephalometric radiographs can be traced manu­ (TMJ). CT provides a comprehensive view of
ally or can be digitized on a computer aided the dental arches, especially the positioning of
software device and television based system. the supernumerary teeth, extent of cysts or
tumours. For easily identifiable problems, when
3. Lateral oblique view the conventional radiographs would suffice, it is
A lateral oblique view can be takèn by using a 5 x 7 better to avoid CT.
inches screen film combination. Projections are TACT (tuned aperture computed tomography)
made separately for the right and left sides. for the diagnosis of the external root resorption
Lateral oblique view can be taxen either to visu­ * in which a new type of imaging digital radiographs
alize the body of the mandible or the ramus and subtraction radiographs are used. This has
region. This radiograph is of good use to identify an advantage over the current radiographic
any pathology extending from the body of the modalities in viewing an object while decreasing
mandible to the ramus region. the superimposition of the overlying anatomical
strucutres.
4. Wrist radiography
Wrist radiography is taken for bone age estima­ 7. Magnetic Resonance Imaging
tion. In the radiography of the wrist, a plain film Magnetic resonance imaging, popularly known
of the left wrist is taken and the carpal and meta­ as MRI, is a non-invasive technique in which high
carpal bones are studied for the degree of ossifica ­ strength, static magnetic field pulsed radio waves
tion. Using Gruilich and Pyle scale, and compar­ and switched gradient magnetic fields are used
ing with the standard ossification patterns at to create an image. The magnetic resonance
different stages, the degree of ossification is signal is generated primarily from the hydrogen
. assessed. The skeletal age can be compared with nuclei of water and lipid molecules. MRI is widely
the Demirijian 'dental age', estimated from the used to image the head, neck and the musculo
stage of crown and root development (maturity) skeletal system. MRI is also a useful technique
of premolars and molars . in case of neoplasm ofthe maxilla and mandible,
study of the vascular structures and evaluation
5. Sialography of lymph nodes. MRI cannot distinguish between
Sialography is a specialized radiographic benign and malignant neoplasms.
technique in which a dye or contrast medium is
introduced in a retrograde fashion into the duct 8. Ultrasound
of the salivary gland and then a radiograph is Diagnostic ultrasound, which makes use of sound
taken to study the pathology of the major waves to generate an image is cohimonly used in
salivary glands. Mainly iodine-based contrast obstetrics. Of late, ultrasound has found its
agents are used. Sialography is contraindicated application indbe examination of the floor of the
in acute infection of the salivary glands. Sialog­ mouth and salwaiy glands.
raphy is mainly indicated in the case of stones
within the duct or Sjogren's syndrome. 9. Postero-anteriarvieW
A postero-antenor view or PA view is taken with
6. Computerized tomography a 8 x 10 inchesscreen film combination. As the
Computerized tomography or CT is an advanced name implies, the central x-ray beam is directed
radiographic system. An advantage of CT is its from behind aad through the skull. 4t is used to
 I TEXTBOOK OF PEDODONTICS

Fig. 1.8 Orthopantomogram (an extraorai Fig. 1.10 Patient position on Cephaiostat.
radiograph)

Fig. 1.9 Taking of an O.P.G Fig. 1.11 Lateral Cephalogram (an extraoral
radiograph)
 SECTION 1 •: CHILD AS A PATIENT | tfgfafc

evaluate the skull for any pathology, trauma or 13. Direct digital radiography (Fig. 1.12)
developmental anomalies. It gives a good view Direct digital radiography or digital intra-oral ra­
of the skull in the medio-lateral direction. diography is popularly called radio-visiography
(RVG). Though this technique makes use of the
10. Paranasal sinus view " y " x-ray machine, it differs from the conventional ra­
Paranasal sinus view or PNS view or Waters diographic technique in that here an intensifying
projection is a variation of the PA view and is screen charged coupled device (CCD) is used as
mainly indicated in the visualization ofparanasal the.image receptor system. The signal from the
sinuses, orbits and zygomaticofrontal sutures. CCD is digitalized to form an image in the monitor.
In this projection, the central x-ray beam enters In this technique the image is obtained immedi­
the skull tangentially to exit at the chin region. ately and contrast enhancement is possible to
This view is taken with a 8 x 10 inches screen film achieve better results. The image obtained can
combination. also be stored in the computer for future refer­
ence. It is also possible to obtain print outs from
11. Reverse - town projection
the image recorded in the monitor.
This radiograph is taken on a 8 x 10 inches screen
film combination. It is indicated in suspected cases
Probable technical errors while taking
of condylar neck fractures. This radiograph is
radiograph for a child patient:
taken in an open mouth position. This projection
is similar to the PNS view with the difference that
In general there is no scientific difference in the tech­
the head is tilted downward.
nique applied for the child and that for the adult pa­
12. Submentovertexview tient, but there is a high probability of technical er­
A submentovertex view is also taken with a 8 x 10 rors while taking radiographs for the child patients.
inches screen film combination. This radiograph These errors may distract or destroy the radiographs’
is taken by directing the central x-ray beam diagnostic value. The most commonly observed tech­
through the floor of the mouth to exit at the nical errors are: .
vertex of the skull. This radiograph helps in the ■ Improper placement of films.
visualization of the condyles, sphenoid sinus and ■ Cone cutting,
curvature of the mandible. ■ Incorrect horizontal angulation, for example in
case of interproximal caries this improper angula­
tion showstheoverlappingof the contact area
and makes the diagnosis impossible.
■ Improper vertical angulation projects the cap of
the enamel of the crown over the interproximal
surface and obliterates the carious lesion
■ Over exposure due to defective devices.
■ A high exposure of the patient to radiation
because of repetition of taking X-rays due to an
uncooperative child '

Radiation hygiene measures:

It is imperative that the radiograph should be taken

Fig. 1.12 Radiovisuography. by following proper radiation hygiene measures.
These measures are:
 I TEXTBOOK OF PEDODONTICS

■ Proper registration of radiographic units ■ Proper sterilization of objects used in radiogra­

■ Proper maintenance of radiographic units phy that can get contaminated by the patient’s
saliva.
• Training of personnel who are associated with
radiography Self-Assessment
« Dosage monitoring
• Radiation protection of the child patients by us­ 1. Which sizes of films are used in children?
ing lead apron with a thyroid collar. 2. What are the intra-oral projections ?
« Use of long lead-lined cylinders and cone posi­ 3. What are the indications for using IOPA and bite
wing films in children ?
tioning devices
4. What are the advantages of an OPG ?
■ Use of electronically controlled exposure timer
5. Name new techniques which can be utilized for a
• Use of high speed films radiographic diagnosis.
• Use of automatic processing machines that give 6. What measures will you adopt to make radio­
good consistent results graphic procedures more acceptable to children ?
• Employing proper technique to avoid the chances 7. Prepare a chart of angulations used for different
of repeating the exposure. regions of the mouth.

I
 1.4 Practice - Management

Tandon S, Paul U

The special developmental characteristics of the The receptionist should speak clearly in a natural
pediatric patients and the important relationship and well modulated tone and should converse in
these patients establish with their parents, the prac­ an efficient but unhurried manner. The patient’s
titioners and stciff members call for a unique environ­ full name and nickname, boththe parents’ names,
ment and establishment. Those who treat children address and telephone number should be re­
should periodically review various aspects of prac­ corded by the receptionist.
tice management such as initial communication with
the parents, management of time, the child’s first visit 2. Dental clinic environment
evaluation of guidance and education in home health The ideal office/clinic should be easy to approach
measures. for self, staff and patients withampie car parking.
A dental office serving pediatric dental practi­
Each decision taken by a dentist that has a bearing tioner should consider the age range of the per­
on office environment procedure or the assignment sons using the facilities. An attractive and com­
of staff responsibility should be directed towards fortable environment should be designed for both
children and parents. The interest of patients of
the goals of rendering effective and pleasant service
preschool age through the late teenage period
for children.
also need to be considered as well as the interest
of their parents. Therefore the decor of the re­
A thorough oral examination, an accurate diagnosis
ception and dental clinic requires careful plan­
and effective treatment supported by preventive
ning. Neutral colors, such as beige or light shades
measures are essential in the treatment of a child
of green or blue for the wall decor promote a tran­
patient. Emotional guidance is provided as needed,
quil feeling and will permit the use of attractive
and dental services are conducted in the most effi-
color accessories.
I cfent and pleasant manner commensurate with the
If i^bd’s behavior and parent’s attitudes.
Decorations and accouterments depicting defi­
>' ■ ■ . ■ V
nite settings meh as the circus, the outerspace,
f l. Initial communication with parents
or nursery rhymes add to the warmth and fantasy
| fAt the time the parents make an initial contact by
of the office and tend to dispel fear. An aquarium
U=; telephone, the receptionist should project the den-
is always a source of entertainment and may be
! OWstaff’s true interest in the child patient.
placed either in the reception room or in the treat­
way to accomplish this is by offering correct ment room where it is visible to the child in the
information in a friendly manner in response to chair (Fig. 1.13). Soothing, muffled music in the
tiie inquiries. A friendly telephone voice con­ reception room has a comforting effect on both
veys a cordial feeling towards the parent the parent and the patient and dispels the cold­
 ifcfiü I TEXTBOOK OF PEDODONTICS

ness often felt in a si lent room. Objects of inter­ ■ It decreases the length of the dental appoint­
ests for all ages of children will provide an invit­ ment thus aiding in child management.
ing atmosphere^ Children are attracted to books ■ The denti st practices more efficiently a nd more
or magazines. If adults are to bring children to rapidly thereby becoming more productive.
the dental office, reading material should be avail­ from the assistant decreases the number
able for them. Cookery books affefMtisy moth­ of steps and movements necessary resulting
ers interested in reading. in less fatigue to the dentist. Statements re­
garding the assistants’ role in periodontics are
Selected toys, preferably of large size, including generally limited to the need for this individual
building blocks, and wall attached activity centers to be a warm, caring person who must genu­
have proved to be main attractions for children of inely portray a friendly attitude to the child.
all ages? (Stewart 1982). Finn (1973) has emphasized
that dental care of the handicapped child can
Certain dental drawings used in conjunction with only be accomplished through the well coor­
the different procedures undertaken in the clinic dinated teamwork of the dentist and his/her
can also be included and this has shown to alle­ auxiliary personnel.
viate anxiety or fear of child patient (Fig. 1.14)
5. Establishing a suitable record system
3. Management of time and appointment This must cover the medical history, chief com­
■ To guide the parents in choosing the most plaints, investigation advised and carried out, di­
desirable hour for their child’s appointment the agnosis plan and treatment plan, appointment
receptionist must be prepared with informa­ schedule, and fee chargeable and recovered. For
tion to justify the scheduling. this computer and good software can have a re­
■ Morning appointments are preferable in a markable use. It is legally mandatory for the den­
young patient because the child will be fresh tist to keep proper records. *
and active. The length of the appointment
»
should be as short as possible (preferably less 6. Establishing professional fees
thanTO min). Children should not be made to ■ The fees must be revised from time to time.
wait top long in the reception area before the This can either be done by reference to the
dental procedure, as this wil 1 make them rest­ schedules employed by other colleagues in the
less. There are certain other factors that affect locality or by applying the principles of cost
the child’s behavior,5which are under the con­ accountancy.
trol of the dentist. ■ A rational method for determining the fee and
■ An appointment book should be well planned payment system should be followed with a few
and effectively designed with the layout for important factors in mind such as the patient
the entire week. Longer appointments may be work load, annual production hours, working
scheduled first with shorter appointments days per year, and the average monthly fore­
around the longer ones. A definite schedule cast per year.
should be set for starting and finishing the
clinic. 7. Effective infection control measures
■ To protect the dentists’ self by using good
4. Ancillary personnel
quality gloves, masks, protective eye glasses,
The efficient utilization ofchairside assistants is
etc.
extremely important in pedodontic practice be­ ■ To protect the patients from cross contamina­
cause: tion by making sure that all the instruments
 SECTION 1 : CHILD AS A PATIENT

¡¡W W iK -
Fig. 1.13 Initial contact with the child. Fig. 1.15 Patient sitting comfortably on
contoured dental chair.

Washing the mouth with Cleaning the teeth with

Toooth brushing vacuum and 3 way syringe. brush in handpiece.

Drilling a vital tooth with air Infiltration anaesthesia by Motivating patient towards oral
turbine. injection. health.

Fig. 1.14 Portrayal of dental procedures to allay dental anxiety of children - KOYOT01988.
 ik» I TEXTBOOK OF PEDODONTICS

are properly sterilized. Thus infection control 12. Consent

should be given utmost importance. Consent, before any complicated diagnostic or
invasive procedures, anesthesia and surgery, is a
8. Proper maintenance of clinic must except in rare circumstances such as life
The flooring, walls, ceilings and all the surfaces threatening medical emergencies, on a court or­
of the equipment apdTnstruments and cabinets der or on request of the police. The consent
* must be made of such materials so that they can should be in local language and signed by the
be very easily maintained clean. parents or his close relatives or guardians.

9. Health education room : NEVER DO IT

Space should be allocated in the dental office 1. Never operate a patient without consent
where the child and the parents can be given 2. Never lose your temper even on provocation
proper instructions in preventive procedures. In­ 3. Don’t neglect updating your knowledge
struction in oral hygiene procedures should be through training courses/conferences etc. and
explained fully and participation by the child keep proof of it.
should be used until tooth brushing and flossing 4. Never experiment on patients
become an established habit pattern. Dietary 5. Never forget your limitations
counselling can also be given here. The dentist 6. Never hesitate to refer the case if it cannot be
should keep in touch with the current develop­ managed by you
ments; it is imperative that he participates in the 7. Never give general anesthesia without an
activities/deliberations of professional bodies. anesthetist
8. Never use outdated medicines
10. Consultation with the parents: 9. Never resort to UNETHICAL practice
■ During the consultation with the parents the
dentist may review the major diagnosis or may Right from diagnosing the incipient caries and
elaborate on specific details such as the type checking margins of restorations, a good vision
of infection, severity of dental caries, reasons is critical in numerous aspects of clinical dentistry
for pain, nature of oral defects, objectives of
guiding the developing occlusion and any oth­ 13. Handling the Child in the Dental Chair (Fig. 1.15)
ers. Selection of a dental contour chair has been found
■ If consultation period is to be conducted effi­ to be most effective in children’s practice
ciently, control of the parents’ conversation is ■ The patient rests in a supine position with his
important. body parallel to the floor and feet slightly el­
■ If the parents are argumentators or demanding evated:
or have a low level of dental information, the ■ The assistant’s arm is held slightly above the
dentist will require additional time and patience child’s chest, which affords a comforting feel­
to communicate the findings and propertreat­ ing of security to him. The assistant sits across
ment program. the chair from the dentist completely.
■ The dentist operates in a sitting position on a
11. Accountability comfortable, contoured stool. All equipment
Dental profession is morally, ethically and legally is conveniently located near the dentist and
accountable to the patient in particular and the the assistant; high and low speed handpiece,
society in general. In no way can we get out of suction, air and water syringes are mounted
the obligation. This aspect has to be kept in mind on a bracket extending partially over the chair,
every time you treat a patient.
 SECTION 1 : CHILD AS A PATIENT |

and well integrated instruction makes it possi­ appointment to allow the development of the pa­
ble for these complements to be handed to the tient trust and confidence.
dentist as needed.
■ Everything needed for any specific procedure Step four: Following the completion of the re­
is within easy reach without leaving the chair, storative phase of treatment, orthodontic and
c.g. the amalgamator is kept in a portable cabi­ prosthodontic care may be rendered if needed.
net nearby the chair. Although minor oral surgical procedures are ac­
■ All instruments are handed to and removed complished during the restorative phase of treat­
from the dentist’s hand by the assistant. ment, complex surgical endeavor should be de­
■ The concept of ' four handed dentistry'7 im­ layed until this phase.
plies that the assistant’s hands are constantly
employed in the treat ment of the child. Step five: No treatment plan is completed until
provision is made to provide a recall appointment
14. Sequence of procedures for evaluation and necessary follow-up care.
After a thorough diagnosis of the problem is es­
tablished, a sequence of appointments must be Special considerations while managing
incorporated. This area encompasses personal the child
preferences and individual treatment philoso­ • Direct physical contact with the child during all
phies. However, there are certain guidelines, procedures provides security to the child. It also
which can be utilized. helps the doctor to better control the patient. Ob­
servation of the patient’s hands during their
Step one: Emergency procedures must be dealt evaluation allows a critique for genetic anoma­
with immediately. This implies rendering only the lies, medically compromised signs of the systemic
minimal necessary treatment to relieve pain and etiology and specific oral habits.
or infection.
If possible, delay extraction or extensive pulpal ■ Sight considerations are also a major part of doc­
therapy provided that the pain can be relieved by tor-patient transactions. The doctor should ap­
some other means. proach small children at the eye level and talking
with child in the chair at eye level is helpful in
Step two: A prevention plaque control program maintaining rapport. Instruments including sy­
should be introduced. This program includes ringes, la rge bur blocks, or forceps should be kept
plaque identification and removal, diet counseling, away from sight of the child to reduce his anxiety.
topical fluoride application and child parent edu­
cation on home care arid oral hygiene practices. ■ The senses of taste and smell are also important
The advantage of this approach is the opportu­ considerations in treating a child patient The
nity to place emphasis upon prevention, devel­ , child can react rather adversely to the bitter taste
opment of rapport with the patient, evaluation of of local anaesthetic solutions or to the taste of
patient behavior, and introduction of an initial trau­ phosphoflouride solutions. Topical anesthetics,
matic experience to the childpatient. The empha­ topical fluorides, oral premedications. and impres­
sis on prevention should be reinforced at every sion materials which are flavored for taste and
future appointment. smell are of great benefit in the patients reception
of dental care. The hands and breath of the doc­
Step three: Restorative therapy usually begins tor and staff should not only be clean but also
at the third visit. A procedure which is short and relatively free of offensive odors.
simple should be selected first during this initial
 I TEXTBOOK OF PEDODONTICS

Table 1.3: Attitudes of children towards dentistry.

Likes Dislikes
■ An interesting waiting room with background ■ Being kept waiting
music ■ Unattractive waiting room
■ Be truthful, do not lie to the patient ■ Untruthfulness of a painful procedure
■ To be called by the first name ■ Being made fun of
■ Have everything ready before the child arrives ■ Using fearprovoking words
■ Educate both the child and the parent ■ Using undesirable mannerisms or facial
■ Dentist to talk while working expression
■ To watch in a mirror while the dentist is working ■ Using words such as drill, sharp,
■ To be told repeatedly that he or she is a needle etc.
good patient ■ Scolding by the dentist
■ Allow the child to get into the dental chair ■ Being compared to other children
unassisted and adjust the chair for comfort ■ Adjusting the chair without consulting
■ Giving the child a preview of what will occur the child
at the next appointment, and postoperative gift.

Attitudes of children towards dentistry are Further Suggested Reading For Section -1
given in Table 1.3
1. AAPD; Guidelines for prescribing dental radio­
Essentials of Pedodontists’ attitude: graphs. Ped. Dent. Reference manual 21(5), 60,
1999-2000.
For a successful pedodontic practice, one should 2. Bauden, J. W : The use of radiographs in pediatric
have the following qualities in one’s own personal­ dentistry: The challenge of the eighties. Pediatric
ity or attitude projecting to a child patient. Dentistry 3(2):455,1982. ,
Î » Self-confidence with a positive mental attitude. 3. Beoun L.R and Akerman, WY. Jr. : Intraoral or pano-
* Goal orientation with clarity ramic radiography? Dental clinics of North
» Patience while handling children America 28(1):47,1984. ‘
■ Gentle approach with tender, loving care. 4. Bodner L., Sarnad H, Jacob B.Z. Computed tom­
■ Art of developing a friendly rapport. ography in pediatric oral and maxillofacial sur­
« Cheerful and being honest with chi Idren gery. JDC. 32-38.1996.
■ Sincere and emphathetic. 5. Bragger U Pasquali L, Rylander H et al. Computer
assisted densitométrie image analysis in peri­
.... Self-Assessment
odontal radiography to methodological study. J.
1. What are the objectives of practice management? Clin. Periodontal 15:27,1988.
2. What is most desirable time for child patient ap­ 6. Caplan C M : Practice Expansion • The decision­
pointment? making process and related strategies.
3. Why should a suitable record system be main- DCNA32(1), 1988.
; tained? 7. Curcio R J : The art of the dental examination
4. How should be the dental clinic environment for DCNA 22(2), 209-28.1978
JI children? 8. Curcio R J : The first phone call. DCNA 22(2) 197-
g 5. What is the rational method to determine the fee 208,1978.
structure? 9. Fechtner L J; Mallin R J : Recall : The philosophy,
È 6. What are the essentials of a pedodontist’s atti­ Methods and Results. DCNA 22(2),285-306,1978.
tude?
 SECTION 1 : CHILD AS A PATIENT |

10. GelbierS: History of International Association of 18. Lewin B : Appointment Book Control: DCNA
Pediatric Dentistry, Part 6; Int. Jr. of Ped. Den., 22(2)307-312,1978.
June, 6.2.143.1996. 19. MC Culloch CA, BirekP. Automated probe: Fu­
11. Gelbier S.-History of the International associa­ turistic technology for diagnosis of periodontal
tion of Pediatric Dentistry. Part LNational and disease. Univ. Toronto Dent. J. 4:6,1991.
society of dentistry for children; International 20. Me Donald- The dental literature: A reflection of
Journal of Pediatric Dentistry Dec., 4.4.281.1994. changesinDentistry for children: Jr. of Den for
12. Gelbier S.-History of the International Associa­ Children, 253-254.1993.
tion of Pediatric Dentistry, Part 3 : Samuel D Harris 21. Mittleman S J. Getting through to your patients:
Psychological jnotivation. DCNA32(1) 29-
and some early pressure for International devel­ *
1988.
34
opments; Int Jr. Of Ped. Den., 1'2.123,1995
22. Myers R.D. Dental radiology for children DCNA.
13. Gibbs CH, Hirsch feld JW, Lee JG et al. Descrip­
28(1)37-461984.
tion and clinical evaluation of a new computer­
23. Norman H. Oslen- Four decades of change: Jr. of
ised periodontal probe - the fluoride probe. J.
Den. for Children, July-Oct, 253-254.1993.
Clin. Periodontol 15:137, 1988
24. Schwartz S H : Dental staff motivation, DCNA
14. GrattBM, Sickles EA, Armitage GC. Use ofdental
32(1), 1988.
xeroradiographs in periodontics comparison with
25. White and Tsantsouris. The use and abuse of
conventional radiographs. J. Periodontal 51:1,
radiographs of the primary dentition. Quintes­
1980:
sence Int’L Dent. Digest 59-62,1977.
15. Gupta S. Chada M.K. Sharma A. Assessment of
26. White and Weissman, Relative discernment of
puberty growth spurts in boys and girls- a dental
Lesions by Intra-oral and Panoramic Radiogra­
radiographic method J- Indian Soc- Pedod-Prev- phy 99 JADA 1117-1121,1977.
dent 13(11), 4-9,1995. 27. Zappa U. In vivo determination of radiographic
16. Jeffcoat MK. Diagnosing periodontal disease. projection errors produced by novel film holder
New tools to solved old problems. J. In. Dent. and x ray beam manipulatorJ- Periodontol. 62( 1),
Asso 122:54,1999. 674-83;1991.
17. Kahn M A : The initial interview. DCNA 22(2),
231-242.1978.
 SECTION - 2

Normal Growing Child

2.1 Stages of Human Growth and
Development (Pre-natal)

The complexity of cranio-facial growth is of great 5. Growth signifies an increase, expansion or exten­
importance for a pedodontic understanding. Every sion of any given tissue (Pinkham 1994).
pedodontist should be an applied biologist and
Therefore, growth is not a random process. It is a
should keep in mind the fact that the child is in a
dynamic process with a stable pattern of changes
dynamic, changing state and presents no static pic­
resulting in the increase in physical size and mass
ture. The fully developed cranio-facial skeleton rep­
during its course of development This can be pre­
resents the sum of its separate parts, in which growth
dicted with reasonable certainty.
is highly differentiated and occurs at different rates
and in different directions and is thus a complex con­ Development
cept. Growth and development can be divided into
Growth is often used as a synonym for development.
three aspects.
In the biologic sense development is a process of
We grow - increase in size, with a few exceptions continuous changes occurring in a predetermined
every dimension of the body gets larger with age order. x
through the first two decades of life. i

We grow up - changes in proportion, different areas Development is an increase in complexity (Todd 1931)
grow at different rates at different times. Development is used to indicate an increase in the
We grow older - maturation skill and complexity of functions (Lowrey 1951).
1. Development is in complexity (Proffit 1986)
DEFINITION
2. Development embraces other aspects of differ­
Growth entiation of form, but principally involves
Has been defined in many ways by different authors. changes of function, including those largely
1. Growth may be defined as a developmental in­ shaped by interaction with the structural, emo­
crease in mass, in other words it is a process that tional or social environment (Vaugham 1987).
leads to an increase in the physical size of cells, 3. Development refers to all the naturally occurring
tissues, organs or organisms as a whole (Stewart unidirectional changes in the life of an individual
1982). from its existence as a single cell to its elabora­
2. Growth refers to an increase in size or number tion as a multifunctional unit terminating in death
(Proffit 1986). (Moyer 1988).
3. Growth may be defined as the normal changes in 4. The act or process of natural progression from a
the amount of a living substance (Moyer 1988). previous, lower or embryonic stage to a later, more-
4. Growth is an increase in the size of a living being complex, or adult stage (Stedman 1990).
or any of its parts, occurring in the process of
development (Stedman 1990).
 SECTION 2 : NORMAL GROWING CHILD | CEB

5. Development addresses the progressive evolu­ Primitive streak initiates the formation of
tion of a tissue (Pinkham 1994). embryo.
Notochord is formed.
Therefore, development comprises all the normal
sequential series of events which result in the Embryonic disc is slightly curved as the
increased complexity or maturity in the course of head and tail folds appear.
natural progression from a single cell to the multi­ Paraxial mesoderm condenses from the
functionalorganism ending at death. somites.
By the end of the 3rd wk primitive endothe­
Prenatal period lial cells are formed which fuse into the
primitive heart tube.
The total period of prenatal life consists of forty Cardiovascular system is the first to reach
weeks and after 28 weeks. The fetus is considered its functional stage.
viable. The period of intra-uterine life can be divided Head forms 1/2 of the body length.
into two principle developing organs, the embryo
and the fetus. 4 wk Neural tube is formed
(Fig. Embryonic disc assumes a C-shape as the
TIME PERIOD OF OVUM (Fig. 2.1) 2.6B) head, tail aid lateral folds form. (Fig. 2.5)
All major oxgans and systems of the body
0-1 wk Secondary oocyte fuses with the sperm start developing from the 3 germ layers.
within 24 hrs after ovulation forming the Formation of the foregut, midgut and
zygote. The zygote undergoes cleavage hindgut takes place.
after 30 hrs to form the Morula and finally By die 24th day, 3 pairs of branchial arches
the Blastocyte, which gets implanted in the are present
endometrium by 3-5 days Dental lamina too is formed.
On die 27di day the upper limb buds appear
PERIOD OF EMBRYO (Fig. 2.2) Crown rumplengdi is 4-5 mm

l-2wk Embryonic period begins with the 5wk Major development occurs in the head
pre-somite embryo. (Fig. region
Appearance of bilaminar embiyonk disc 2.6D) 4 branchial arches present
consisting of the ectoderm and endoderm 2nd pharyngeal arch overgrows the 3rd
Amniotic cavity and the yolk sac are and 4di arches to form cervical sinuses.
formed separated by the embryonic disc. Upper limbs differentiate into hand plates.
Prochordal plate is formed indicating Otic placodes and optic vesicles are seen.
the fixture cranial region and the primi­ Heart beat can be detected
tive mouth ultrasonographically.
By the end of the 5th wk, 42-44 pairs of
3 wk First missed menstrual period, (mother) somites are formed.
(Fig. 2.3, Morphogensis begins. Lower limb buds appear.
2.4) Gastrulation results in the formation of the Spontaneous movement of the embryo
intra-embryonic mesoderm thus forming such as twitching of the trunk and limbs
the trilaminar disc. seen.
I TEXTBOOK OF PEDODONTICS

Polar body
Zona pellucida
- Blastomeres

ZYGOTE (24 Hrs.) 2 CELLED STAGE

Inner cell mass

Degenerating Zone

Blastocyst cavity

: Trophoblast

MORULA (72 Hrs.) BLASTOCYST

Endothelial stroma
Inner cell mass
*
. Cystotrophoblast
Hypoblast
Uterine cavity

. IMPLANTED BLASTOCYST
(3rd to 5th day)

Fig. 2.1 Transformation of Zygote into Embryo.

 SECTION 2 : NORMAL GROWING CHILD |

Syncitic trophoblast
Amniotic cavity

Bilaminar; Embyonic disc

Yolk sac

Fig. 2.2 Transverse section of the embryo.

Fig. 2.3 21 days old embryo

ME I TEXTBOOK OF PEDODONTICS

Oropharyngeal
membrane

Neural fold

Notochord

Primitive streak
17th Day
21st Day

Fig. 2.4 Dorsal view of embryonic disc-origin ally egg, then pear shaped and
finally slipper like.

2nd Week
6th to 7th Weeks

Fig. 2.5 Appearance of the head and tail folds.

 SECTION 2 : NORMAL GROWING CHILD | CI*

Stómodium

A - 24th Day Brachial

•arches
——

Heart prominence
Lens placode
Nasal placode
B - 28th Day
Stomodium

Nasal pit
C - 31st Day
Nasolacrimal
groove

Medial Nasal
Lateral promi­
D - 35th Day nence
1st Brachial
arch groove

Medial & lateral

nasal promine­
E - 48th Day nces merge with
each other and
with lateral nasal
prominences

Intermaxillary
segment
forming
F -14 Wks philtrum
" of lip —...

Fig. 2.6 A-F Development of face in intrauterine life.

 , | TEXTBOOK OF PEDODONTICS

6 wk Formation of primitive nose, philtrum 12 wk Erythropoiesis decreases in the liver and

and primary palate. begins in the spleen.
Development of auricular hillocks around By the end of the 12th wk primary7 ossifica­
the facial groove. tion centers appear in the skeleton espe­
Formation of retinal pigment in the eye. cially in the skull and long bones.
Increase in head size which is more bent According to clinicians convenience the
over the heart prominence. 1st wk to 12t,‘ wk mark the 1st trimester of
Embryo shows reflex response to touch. pregnancy. During this period the embryo
Tooth buds of primary7 teeth develop. is sensitive to genetic, intra and extrauter-
Cranium to face ratio is 40:1 ine insults which could result in miscar­
Crown ramp length is 21-23 mm. riage or termination of pregnancy. Various
deformities like deafness, mental retarda­
7 wk Eyelid formation begins. Midgut herniation tion, congenital heart diseases, cataract,
( Fig. occurs Change of the blood supply to face orofacial anomalies result from radiation,
2.6E) from the internal to external carotid artery7 infection, mechanical or psychological
and is characterized as the critical period. trauma.

8 wk At the beginning of the 8th wk 13-15 Breathing & swallowing motions appear,
Hands are short and webbed. wk Crown calcification of primary' incisors and
Eyes are open. (Fig. 1st molar begins.
Tail still present but stubby. 2.6F) Condyle, coronoid and the angle of
Scalp vascular plexus occurs as a band mandible become distinct.
around the head.
By the end of the 8th week 17-20 Primordial follicles form oogonia in the
Gross structure of the nervous system has wk ovaries.
been established. Tail has disappeared. Brown fat is formed which generates heat
Eyes unite by epithelial fusion. for the infant. 1
Vascular plexus forms a band near the Sucking reflex develops.
vertex of the head. Calcification of canines and the second
Ovaries and testes are formed respectively molar begins.
but the external genitalia are not yet dis­ Myelination of the nerves begins.
tinguishable.
Purposefill limb movements first occur but 20 wk Lanugo head and hair appear.
are too slight to be felt by the mother till Skin is coated with vernix caseosa
about 17th wk. This period is the usual lower limit of
foetal viability.
PERIOD OF FETUS
24 wk Secretory epithelial cells secrete surfactant
*4 wk Fetal period begins.
in the lungs.
Crown rump length is 3cm weight 8gm.
Histo differentiation of enamel organ and
This a period of rapid proliferation and
dental lamina forms ameloblasts and
differentiation
odontoblasts
10 wk External genitalia distinguishable Second trimester ends. This period is
relatively safe for dental treatment for the
mother.
 SECTION 2 : NORMAL GROWING CHILD | €*EB

Table 2.1: Events taking place during embryonic period

Days Length Clinical Features

14-15 0.2 mm Appearance of the primitive streak.

16-18 0.4 mm Notochordal process appears.

Haemopoietic cells appear in the yolk sac

19-20 1-20mm Intra embryonic mesoderm.

Primitive streak complete
Umbilical vessels and cranial neural folds form

20-21 2.0-3.0mm Cranial neural folds develop.

Elevated embryonic bud.
Formation of primitive heart
22-23 3.0-3.5mm Fusion of neural folds in cervical region.
Anterior and posterior neuropores open.
The first and second visceral arches formed
Heart tube begins to fold.
24-25 3.0-4.5mm Cephalocaudal folding develops.
Cranial neuropore closes
Optic vesicles are formed and optic placodes appear
Formation of dental lamina
26-27 3.5-5.0mm Caudal neuropore closed.
Upper limb buds appear
3rd pair of visceral arches are formed
.th . ,
28-30 4.0-6.0mm 4 visceral arch seen
Hindlimb buds appear
Optic vesicle and lens placode present
31-35 7.0-10.0mm Forelimb pads paddle shaped.
Nasal pits seen.
Embryo C-shaped
35-42 9.0-14.0mm Brain vesicles prominent.
Umbilical herniation present
External auricle visible
43-49 13.0-22.0mm Pigmentation of retina seen.
Eyelids formed?
Maxillary swellings fuse with medial nasal swellings as upper lip
50-56 21.0-31.0mm Limbs elongate with bending of the elbows and knees.
Face becomes human like, tail disappears.
 tf № I TEXTBOOK OF PEDODONTICS

Third trimester begins. Length is 45-50 cm (30 inches).

Weight 900 g. Weight is 3200 gm or 2.5 - 4.5 kg (5.5 to
Length 25 cm 10 lbs).
Head circumference 35 cm.
28 wk Eyes begin to reopen. At the end of 3rd trimester there is
Grasp reflex well developed. increased risk of hypoxia or its complica­
Fetal head turns down. tion to the foetus.
Fetus weighs 1000 gm -1300 gms. Patient should not be subjected to dental
Length of fetus is 35 cm (14”). treatment without taking utmost care

30 wk Fetus appears reddish and wizened since Self-Assessment

skin is thin and there is relative absence of
1. Defi ne growl h a nd development.
subcutaneous fat
2. When does the first and second visceral arches
form?
36-38 wk Fat develops rapidly resulting in red,
3. When does the formation of dental lamina take
smooth, plump appearance This period is
place?
devoted mainly to building up of tissues
4. What wi 11 be t he length of embryo when it is 20 to
and to preparing systems involved in the
21 days old?
transition from intrauterine to extrauterine
5. When does face appear human like?
environment primarily the respiratory and
6. What is the significance of pre-natal period?
the cardiovascular systems
Hand forms 1/3 of the body length,
cranium to face ratio is 8:1.
 2.2 Pedologic Anatomy

Tandon S

A child may appear as a miniature adult to the lay­

man but the details of the anatomy reveal that a child
is entirely different from an adult. The miracle of
growth and development are more evident here than
in the anatomical changes taking place in a growing
child. These changes vary progressively till puberty,
after which permanent features are established. The
knowledge of comparative anatomy of an adult and a
child is essential for the dentist for a correct diagno­
sis and to recognize some of the developing charac­
teristics of a child which may be mistaken for an ab­ 3rd month 5th month At birth
normality or a pathologic condition that may cause Fig. 2.7b Prenatal changes upto birth
concern to the parents of a child patient and also
mislead the clinician for a successfill treatment.
End of first month:
FETAL GROWTH CHANGES (Fig. 2.7a, b)
The head is less flexed and the neck longer and
clearly defined. The development of the face with
the formation of the upper lip and nostrils takes place.
The palate is still incompletely formed. Enamel or­
gans are developed from dental lamina. The external
ears and eyelids are developing and limbs are form­
ing. Skeletal and visceral tissues begin to form. Kid­
neys begin to form with tubules; The backbone and
the vertebral canal form small buds that will develop
inner and upper extremities. Heart forms, starts beat­
ing, and the body systems begin to form.

End of second month:.

Eyes are far apart with eyelids fused, the nose is flat.
Ossification begins and limbs become distinct as
Fig. 2;7a Stages of growth from, the end of the the upper and lower extremities. Digits are well
third week to the end of eighth week in the utero
formed. Major blood vessels form. Many internal
organs continue to develop.
 C33I I TEXTBOOK OF PEDODONTICS

End of third month: cheesy covering over the skin. Fetal movement so
called‘quickening; can be seen
Eyes almost fully develop but eyelids still remain
fused. Bridge of nose develops and external ears are
End of sixth month:
formed. Ossification continues, nails develop. Head
flexion increases and the neck becomes proportion­
Head becomes even less disproportionate to the rest
ately larger. The umbilical protrusion of the gut is of the body. Eyelids separate and eyelashes form.
reduced with a proportionate abdominal volume. Skin is wrinkled and pink. Increase in the growth of
Heart beat is detectable. the cutaneous and subcutaneous tissues occurs.

End of fourth month: End of seventh month:

Head is large in proportion to the rest of the body. Head and the body become more proportionate. Skin
Face takes on human features and hair appears on is wrinkled and pink. Eyebrow hairs and eyelashes
the head. Skin is bright pink. Many bones are ossi­ developed. The eyelids separate and the papillary
fied and joints begin to form with continued devel­ membrane separate. Body is more plump.
opment of the body systems. The eyes have moved
further into an anterior position but are still relatively End of eight month:
wide apart. The external ear is formed on the side of
the head and is no longer in the upper part of the Sub-cutaneous fat deposition takes place. Skin is
neck. less wrinkled. Testes descend into the scrotum. Bones
of the head are soft.. There is a progressive loss of
End of fifth month: lanugo, except for the hair on eyelids, eyebrows and
scalp. The bodily shape is more infantile. The tho­
Head is less disproportionate to rest of the body. rax broadens relative to the head and the abdomen
Fine lanugo hairs covers the body. Rapid develop­ also increases. The umbilicus is gradually centrally
ment of body systems takes place. Skin is bright located. Chances of survival are much greater by
pink and sebaceous glands become active forming a this period.

Table 2.2: Growth of length and weight during fetal period.

Weeks Months Crown-rump length (cm) Weight (gm)

9-12 3 5-8 10-45

13-16 4 9-14 60-200

17-20 5 15-19 250-450

21-24 6 20-23 500-820

25-28 7 24-27 900-1300

29-32 8 28-30 1400-2100

33-36 9 31-34 2200-2900

At birth 35-36 45-50 3400+

 SECTION 2 : NORMAL GROWING CHJLD |

End of ninth month: ■ The sphenoid bone is made up of 3 parts (the

body, lesser and greater wings) at birth, which
Additional sub-cutaneous fat accumulates. Lanugo fuse during the first year. Sinuses do not develop
sheds. Nails extend to the tips of the fingers and in the sphenoid till the 5 year.
even beyond. ■ The ethmoid bone at birth is in 3 pieces (median
plate and a right and left labyrinth) which fuse by
Growth of length and weight during fetal the 5th or 6th year of life.
period are given in Table 2.2 • Each temporal bone consists of 4 parts which
completely fuse by puberty
GENERAL POSTNATAL CHANGES IN DIMENSIONS ■ Mastoid process is absent in the neonate, thus
AND PROPORTIONS the stylomastoid foramen lies superficial .

Neonatal Skeleton Body Proportions (Fig. 2.8)

The body proportions are a result of the differential

• The neonate has 270 bones as compared to an
rates of growth of the cephalic and the caudal ends.
adult who has 206 bones.
Massive changes in the body proportion occur from
« The ratio between the calvarial and facial portion
the fetal life to adulthood.
is 8:1 at birth whereas it is 2.5:1 in an adult female
■ Mid point: The mid-point of stature of a twe
and 2:1 in an adult male.
month-old embryo is at the chest, closelo the chin
■ Skull bones in the neonate are 45 (due to incom­
• At birth:This may shift tojust above the umbilici
plete ossification) and in the adult 22.
■ In adult: It is at the pubic-symphysis region.
■ The frontal bone at birth is in 2 halves, which
■ The length of the head doubles by adulthoo«
fuses at 2 years.
but the rest of the body grows still more, hence
« There are 2 parietal bones
birth 22% of the body area is coveredby the 1k«~.
« The occipital bone at birth consists of 4 pieces,
■ This decreases to 13% at 12 years and only 10%
which fuse by 3-4 years of life.
in an adult.

In utero
2 mo 5 mo New born 2 yr 6 yr 12 yr 24 yr
 <331 I TEXTBOOK OF PEDODONTICS

■ There is an axis of increased growth extending ■ At this stage the abdomen is quite protuberant
from the head towards the feet. This increased but soft.
growth is the cephalo-caudai gradient. ■ Ci rcumferencc of the abdomen is equa 1 to the chest
■ The cephalo-caudai gradient can be observed in until two years.
the growth of the head. In the face, the mandible, ■ After two years the abdominal circumference is
which is the farthest from the brain, grows more less than the chesf s.
as compared to the maxilla, which is closer.
• I n t he early period of development, the cranium is Extremities:
larger in relation to the face. Later, this propor­
tion changes due to increased growth of the face.
■ At birth: Legs arc short, arms long.

Posture:
■ Arms: Birth to 2 years - length increases by
6.75%
• The newborn is usually kept in a supine posture
At 8 years - 50% longer than at two
but can be literally folded' to its most comfort­
years
able posture i.e., the posture simulating the fetal
posture of partial flexion. By 16 to 18 years - slow growth,
• Mild lordosis and protuberance of the abdomen increased development takes place
is a common finding at 2-3 years of age, but this Thus an early maturer has shorter arms
disappears by 4 years. than a late maturer

The Neck: ■ Legs: At birth - short and curved

Birth to 2 years - length increases 40%
• The neck is relatively short at birth and its mus­ A lot of fat on the anedial aspect of
cles are not developed for supporting the head. the foot gives the appearance of a flat
• Functional development of these muscles begin foot
from two months onwards. 6 years - straight, the knock-knee and
flat foot appearance gets corrected
The Chest: 8 years - 50% longer than at two years
s

•3
Adolescence - 4 times longer than at birth
1 ■ The girth of the chest at birth is smaller than the Early maturer - shorter legs than the
L head circumference. late maturer
f ■ It becomes equal at two years and, by fifteen years
CHANGES IN CRANIOFACIAL COMPLEX
its ratio becomes 3: 2.
« The final ratio in adults is 5:3.
The skeletal portion of craniofacial complex devel­
■ ■ The chest is rounded in the newborn.
ops as a blend of morphogenesis of primary skull
■ Its final shape is attained by the time puberty is
components.
reached.
1. The neurocranium: This consists of two parts
■ The desmocra nium which comprises the vault
Abdomen:
of the skull or calvarium. It evolved in response
to need for protection of the brain and is formed
* The umbilicus of a newborn is shed-off around
of the intra-membranous bone.
the 12<}1 to 15th day.
■ The chondrocranium forms the base of the
* The umbilicus is everted and in some cases um-
skull, which ossifies as a endochondral bone.
bilical hernia may be present.
 SECTION 2 . NORMAL GROWING CHILD I CEB

■ At birth:
Craniofacial skeleton undergoes between 30%
and 60% of its total growth.
Head makes up about a greater part of the total
bod\' length whereas in the adult it accounts for
about one-eighth of the total body height.
This change reflects the early development and
attainment of the final size of the head compared
with the rest of the body.
The remaining dimensional increase is not equal
in all parts of the cranium.
■ Afterbirth:
While the size ofthe cerebral cranium will increase
by about 50%. the facial skeleton will grow to
more than twice the original size.
Fig. 2.9a Comparison between adult and
Cranial circumference is an indicator of cranial
neonatal skull - Frontal view
i volume and therefore is often used in young in­
fants fora rough measure of brain development.
■ By four years:
This growth is almost completed.
Cranial circumference thus increases from about
33 cm (at birth) to 50 cm at 3 years after which it
only increases by 6 cm.
■ Four years onwards:
Facial skeleton increases in all dimensions dur­
ing postnatal growth period, tiie increase in height
being the greatest, (approximate!}7 200%).
In depth, the increase is somewhat smaller (ap­
proximately 75%).
Increase in width is the smallest (approximately
15%).
The height of upper and lower face are highly
Fig. 2.9b Lateral view
independent. The upper anterior face height
seems to be primarily correlated with cranial base
2. The viscerocramum is formed by the bones of
changes. Hie lower face height seems to be more
facial skeleton which develop by intramembra-
dependent on muscular function, environmental
nous ossification. This is derived from the
factors interfering with the airway and the pos­
branchial arches
ture of the head.
tMfhehsional changes in craniofacial ■ Because of the above changesdn the craniofacial
skeleton (Fig. 2.9a, b) complex, general features of th^head and the face
arc observed to be different at different ages.
These changes can be appreciated even in intrauter­
ine life. Head:
■ Third month to birth: ■ At birth:
The entire cranium becomes longer and wider in The head circumference is around 35 ems (13.75
its relation to height. inches), (Fig. 2.10a)
 I TEXTBOOK OF PEDODONTICS

Head shape is rounded but sometimes it may get 3. Anterior fontanelle serves as a landmark for with­
molded during parturition as over-riding of the drawal of blood for analysis from the superior
parietal bone takes place when the head gets en­ sagittal sinus.
gaged in the birth canal. 4. Depressed level of fontanelle indicates dehydra­
» Six months: tion and increased level indicates an increased
It increases to 44 cms intracranial pressure.
• One year:
Head circumference may be more than the chest Closure time of fontanelle:
circumference.
A total four inches increase takes place (2 inches ■ Anterior fontanelle (frontal): 18-24 months after
first 4 months and then 2 inches next 8 months) birth
By the end of the year head circumference be­ ■ Posterior fontanelle (occipital): 2 months after
comes equal to trunk dimension and the trunk's birth
may even exceed. ■ Anterolateral fontanelle (sphenoid) : 3 months af­
•» One vear onwards: ter birth (paired)
Between one to two years 4 inches increase takes ■ Posterolateral fontanelle (mastoid): begins to
place. close 1-2 months after birth, closure completely
• At 10 years: by 12 months (paired)
95% of total head growth completes with the width
of the head completed by 3 years while the length Cranial synchondroses
of the head completes by 17-18 years.
Cranial synchondroses play an important role in
craniofacial growth.
Fontanelles: They bridge the gap between the
bones that limit them. They are made up of the
Sphenoccipital: closes by 17-20 years
duramater, the primitive periosteum and the aponeu­
■ Sphenoethmoidal: closed by 2-4 years; may per­
rosis from inside outwards. (Fig. 2.10b)
sist and fuse later in adolescence but is of little
importance in postnatal growth
Fontanelles present at birth are:
■ Mid sphenoid: closes shortly after birth
a) Anterior fontanelle, between the two parietal
bones and the frontal bone. Other synchondroses:
b) Posterior fontanelle, between the two parietal ■ Intraoccipital
bones and the occipital bone. ■ Sphenopetrosal
c) Sphenoid fontanelle, between the frontal, pari­ ■ Petrooccipital
etal, temporal and the sphenoid bone.
d) Mastoid fontanelle, between the parietal, occipi­ Craniotabes or soft skull due to paper-thin bones is
tal and the temporal bone. palpable in premature infants.

Clinical importance of fontanelles Sutures of Cranium

1. Enables the fetal skull to modify its size and shape 1. Coronal suture: Between the frontal and parietal
as it passes through the birth canal and permits bones
rapid growth of the brain during infancy Closes: 24 years to 35 years of age
2. Helps the physician to gauge the degree of brain 2. Sagittal suture: Between two parietal bone
development by their state of closure. Closes: 22 years - 30 years of age
 SECTION 2 : NORMAL GROWING CHILD | C33

Measuring the height of new born child Measuring the head circumference
of new born child
Fig. 2.10a
Metopic sutrue

Lateral view

Superior view

Fig. 2.10b Fontanelle and sutures ir> neonatal skull.

 <SFB-| TEXTBOOK OF PEDODONTICS

3. Lambdoidal suture: Between two parietal and ■ During the early phase of fetal development the
occipital bone sagittal interrelation of the jaws is characterized
Starts to close around 29 years of age. by mandibular protrusion, which is gradually
4. Squamous sutures and lateral anteroposterior su­ reversed.
tures: between the squamous portion of the tem­ ■ At birth the maxilla is placed more anteriorly giv­
poral bone and the parietal bone. The squamous ing class II relationship of the jaws.
sutures closet late in life. ■ Later, in the course of post-natal development,
both maxilla and mandible with their.associated
Face
soft tissues grow forward and downward and es­
tablish a normal class I relationship.
■ At birth, the lower third and the middle third of
■ Maxillary sinuses at birth are not well developed
the face are underdeveloped due to the absence
and are present like slits.
of teeth.
■ Development of the orbita 1 cavities is practically
• The forehead is high and bulging.
complete at birth.
• The face of the newly born baby is round and
■ Nasal cavity is located between the two orbits of
flat.
• The eyes dominate and owing to the absence of the eyes and its floor, is roughly level with their
the root of the nose, appear to be widely sepa­ bottoms.
rated. • The alveolar process can only be faintly dis­
■ After the onset of puberty the forehead flattens cerned and the palate has a weak transversal cur­
and widens, lips thicken and the face acquires an vature.
oval shape, mainly due to growth of the jaws. ■ The maxillary body is almost entirely filled with
■ The child's convex facial profile is straightened the developing teeth.
out, owing to the more anterior position of the
jaws, Mandible
■ The development of chi n prominence and deeper
position of the eyes through growth of .the or­ ■ Although still separated by a symphysis in the
bital ridges and the ridge of the nose increases midline, the two halves of the mandible fuse into
this impression. a single bone by the age of 1-2 years.
■ At birth
Nasomaxillary Complex - The 2 rami are short
- Condylar development is minima 1
■ The maxilla develops in the membranous tissue - A thin line of fibrocartilage and connective tis­
at the end of the sixth fetal week sue exists at the midline of the symphysis to
• The maxilla proper is a result of a highly complex separate the right and left mandibular bodies.
growth pattern with many different components. - The symphysial cartilage is replaced by bone
• The maxilla is attached to the neurocranium di­ (Between 4 months of age and end of the 1st
rectly with the fronto-maxillary sutures and indi­ year)
rectly by means of various other facial structures - Growth is quite general, with all surfaces show­
such as, the nasal, lacrimal and ethmoid bones, ing bone apposition, especially at the alveolar
the nasal septum including vomer, the palatine border, at the distal and superior surfaces of
the ramus, at the condyle, at the lower border
bone and the zygomatic arch.
of the mandible and on its lateral surfaces.
■ Most of the structures mentioned are joined to­
gether in an edge-to-edge fashion.
 SECTION 2 : NORMAL GROWING CHILD |

- The alveolar processes and the muscles are ■ Mandibular condyle grows in a constant poste­
poorly developed at this age, so that its basal rior, superior and lateral direction and attains a
arch mainly determines the shape of the man­ mature contour by late mixed dentition period.
dible in the neonate.
- At birth the structure of mandible is shell like ORAL FEATURES OF THE NEONATE:
with the 10 alveolar sockets for the develop­
ing tooth gum. The edentulous arches of a child vary from an
- Of all the facial bones, the mandible shows not edentulous adult.
only the largest amount of postnatal growth, The alveolar arches of an infant are called gum
but also the largest individual variation in mor­ pads which are firm and pink structures with a
phology. definite form.
- The position of the mandibular foramen Each gumpad is divided into ten segments by
changes by remodeling, to a more superior transverse grooves, and, of these, the groove be­
position from the occlusal plane as the child tween the deciduous canine and the deciduous
matures into an adult. first molar segments are prominent and called the $

- The foramen is below the occlusal plane in a lateral sulci.

The upper gum pad (Fig. 2.12a): It is horseshoe
very young child, slightly at the occlusal plane
shaped and shows:
during the period of primary dentition. It aver­
- Gingival groove - It is the groove-separating
ages 7 mm above the occlusal plane in the adult.
the gum pad from the palate.
- Angle of the mandible is more obtuse in young
• Dental groove - It originates in the incisive
children.
papilla region and extends backwards to touch
- Mental foramen is placed very close to the
the gingival groove in the canine region and
border of the mandible in young children.
then laterally to end in the molar region.
- Lateral sulcus -It is a deepened groove sepa­
Temporomandibular joint
rating the canine and deciduous first molar
segments.
Three phases of development are seen in the intrau­
The lower gumpad: (Fig. 2.12b)
terine life period (Velasco Merida et. al 1999)
•- Differs from the upper.
■ Blastemic stage (7 to 8 weeks of development)
- It is U-shaped, with its anterior portion everted
corresponds with the organization of the condyle
labially.
and articular disc and capsule.
■ It also shows the gingival groove that demar­
■ Cavitation stage (9 to 11 weeks of development)
cates the lingual extent of the gumpads.
corresponds to the initial formation of inferiorjoint
- Dental groove
Mtci] running from the mandible back­
cavity and then start of condylar chondrogenesis.
wards, laterally to join the gingival groove in
» Maturation stage (after 12 weeks of development)
the canine region.
“ Lateral sulcus - a deepened groove separating
Post natal changes in TMJ (Fig. 2.11)
the canine and deciduous first molar segments.
» At birth the articula r disc is flat and develops an
accentuated S-shaped profile as the articular tu­ Relationship of gumpads (Fig. 2:12c)
bercle develops.
At rest the gumpads are separated by the ton J
■ Condylar cartilage is approximately 1.5mm thick
at birth but soon thins down to about 0.5mm. By lying over the lower gumpad.
20 to 30 years of life, it is completely replaced by There is no definite antero-posterior relatip
endochondral ossification. of the gumpads on occlusion, btft ?||||
C® I TEXTBOOK OF PEDODONTICS

Fig. 2.11 Development of mandible and the T.M.J.

gumpad being smaller, the lateral sulcus of the Growth of gum pads
lower gumpad lies distal to that of the upper.
There is a variable overjet with contact only in ■ At birth the width of the gum pads are inadequate
the first molar segments. to accommodate all the incisors.
During function the mandibular movements at this ■ The growth of gum pads is rapid in the first year
stage are mainly vertical and to a very small ex­ after birth.
tent in the antero-posterior direction. Lateral ■ Growth is more in a transverse direction and in
movements are absent. the labio-lingual direction.
During the .early phases of foetal development ■ Due to growth ,the segments of each gum-pad
the sagittal interrelationship of the jaws is char­ become prominent.
acterized by a mandibular protrusion, which is ■ Eruption of deciduous teeth commences at six
gradually reversed. months of age.
At birth the lower jaw is often situated posteriorly.
This relationship has some clinical significance Tongue
as disturbed post-natal forward growth of the
mandible may result in malocclusion. ■ It is comparatively large in relation to the small
mouth.
 SECTION 2 : NORMAL GROWING CHILD |

Medial incisor segment Papilla

Lateral incisor segment Central incisor
Canine segment Lateral incisor
1st molar segment Canine

Dental groove ■ 1st molar

Gingival groove
2nd molar

Fig. 2.12a Upper Gum Pad.

Fig. 2.12b Lower gum pads

Fig. 2.12c Gum pad relationship

 <EEB I TEXTBOOK OF PEDODONTICS

■ The tongue is flat, thin and blunt tipped, prob­ O i HER EXTERNAL FEATURES OF A NEWLY
ably due to the short frenunu BORN CHILD:
■ The tongue, at this stage performs only one func­
Skin
tion, i.e., acts as a piston while suckling.
■ The ski n of a neonate is often reddish. Described
Tonsils and Adenoids to be like that of a lobster, it shows various nor­
mal variations.
■ At birth: The tonsils and adenoids are small in ■ A child may have an appearance of cyanosis due
size. Clusters of white-yellow follicles with ery­ to the thin skin and a high hemoglobin content of
thematous borders may appear initially. A few the blood even when CO is high, while a deep
days after birth these may regress. red purplish appearance may be the result of a
■ First few months: transient anoxia resulting from a closed glottis
The growth of tonsils and adenoids takes place prior to a vigorous cry. Cyanosis of hands and
as the lymphoid tissue starts proliferating and feet also occurs upon exposure to cold.
establishing function. This growth is more in the ■ The cause of acrocyanosis is an imbalance in
presence of infection. autonomous regulatory mechanism, and also, pe­
« Six months to two years: ripheral vascular sluggishness. Another effect of
Maximum growth occurs as the primary physi­ this is the ’Harlequin color change' (Harlequin­
armour).
ological enlargement.
■ ‘Mongolian Spots' are slate blue colored well-
[ • At six years:
| The next hypertrophy, after a period of quies- circumscribed patches of pigmentation over the
back, buttocks and sometimes over the other parts
I cence, occurs especia liy when the child is exposed
occurring in more than 50% of black infants and
I to infection at school. This is the secondary
occasionally in white infants,
I physiological enlargement.
■ Vernix caseosa, a whitish covering over the skin
« At puberty:
formed by sebaceous secretion and exfoliated
The regression and atrophy of the nasopharyn­ epithelial cells around the end of the^fifth month

1
geal lymphoid tissue finally occurs by the time of gestation, may persist even after birth or may
the child attains puberty. be stained with the amniotic fluid contaminated
with meconium.
Buccal Pad of Fat (‘Corpus adiposum’ or ■ Deep red skin with fine, soft, immature, lanugo
Bichat’s fat pad): hair is characteristic of a premature infant.
■ Post-term infants may show a whitish, peeling,
f ■ It is the child's reserve of energy. It is nothing parchment like skin.
but the cheek prominence giving the infant a ■ Erythema toxicum is a rash of w hitish, vesiculo-
chubby-cheek appearance. It is formed of a firm pustular papules w ith erythematous base that may
encapsulated mass of fat lying between the sub­ appear soon after birth, lasting for 1 week on the
cutaneous fat and the muscles of the cheek. trunk, face and extremities.
• Its exact role in suckling is not known. It prob- ■ Pustular melanosis is a similar, benign vesiculo-
abty plays no role in suckling but it has been papular rash at birth in some blacks, around the
found to regress once the suckling has ceased. chin, back and extremities, palms and soles.
 SECTION 2 : NORMAL GROWING CHILD |

Eyes Ears

■ Size: The eyes of a neonate a re small at birth, the ■ The ears of a child arc almost completely devel­
size being one-third of the adult size. Maximal oped.
growth occurs in the first year and continues at a ■ The external auditory canal is short, straight and
rapidly decelerating rate till three years, and fur­ fall of secretion.
ther slows down till puberty. ■ The tympanic membrane has a dull gray translu­
« Cornea: At birth, the cornea is relatively more cency and the structures of the middle ear can be
(10mm) and nearly fills the palpebral fissures. It easily studied through it.
reaches an adult size (12mm) by two years. After
2 years, the posterior aspect of the eye grows, REFLEXES PRESENTAT BIRTH:
giving the eyeballs their final spherical shape.
■ The Lens: The lens of a child is more or less 1. Moro reflex: Any sudden movement of the neck
spherical and has greater refracting power. initiates this reflex. A satisfactory way of eliciting
■ Thefundus: It is less pigmented than the adult’s. the reflex is to pull the baby half-way to a sitting
The fundus acquires its adult form by 4-6 months. position from the supine and suddenly let the
■ The retina: Has a fine peppery mottling. The pe­ head fall back to a short distance. The reflex con­
ripheral retina appears pale or grayish since the sists of a rapid abduction and extension of the
peripheral vasculature is immature. arms with the opening of hands. The arms then
come together as in an embrace.
Nose Clinical importance: Its nature gives an indica­
tion of the muscle tone. The response may be
■ The nose of a neonate is small and flat with nar­
asymmetrical if muscle tone is unequal on the two
row nostrils.
sides, or if there is a weakness of an arm or an
■ The bridge of the nose is depressed. Maximal
injury to the humorous or clavicle. This reflex
growth of the nasal cartilage occurs till puberty,
usually disappears in 2 or 3 months.
after which it attains its final form.
■ The hair within the nose becomes thicker around
2. Startle reflex: It is similar to moro reflex, but is
puberty.
initiated by a sudden noise or any other stimulus.
In this reflex, the elbows are flexed and the hands
Lips
remain closed, there is less of the embrace, less
■ The 1 ips of a new-born are reddish pink, soft and outward and inward movement of the arms.
supple.
• The midline of the upper lip has a small projec­ Grasp reflex: When the baby’s palm is stimu­
tion * the labial tubercle (suckling callus), which lated, the hand closes. There is also a correspond­
is said to disappear after the cessation of suck­ ing plantar reflex. Both normally disappear by 24
ling. months.
■ Another feature of the lip similarly found to be
Walking/stepping reflex: When the sole of the
related to suckling is the abrupt separation of the
foot is pressed against the couch, the baby tries
mucosa covering the inner aspect of the lips from •I
to walk. It persists as voluntary standing.
the outer aspect by a thin single line, parallel to •■

the free border of the lip. Limb placement reflex: When the front of tl^ l||g 'I
.yâ
■ It may undergo a slow transformation to form the below the knee, or the arm below the.;^^^^^
transition zone between the outer and inner as­ brought into contact with the edge.' Ml -f
I

pects after one year. the child lifts the limbs over
 ME® 1 TEXTBOOK OF PEDODONTICS

6. Asymmetric tonic neck reflex: When the baby onwards, the child tends to swallow with the teeth
is at rest and not crying, he lies at intervals with brought together by the masticatory’ muscle ac­
his head on one side, the arm extended to the tion, without a tongue thrust.
same side, and often with a flexion of the contral­
ateral knee. This reflex normally disappears after 11. Cry: It is a non conditioned reflex which accounts
2 or 3 months, but may persist in spastic children. for its lack of individual character and is of spo­
radic nature. It starts as early as 21-29 weeks I.U
7. Rooting reflex and sucking: When the infants
life.
cheek contacts the mother’s breast, the baby’s
mouth results in vigorous sucking movements
12. Mastication: It is a conditioned reflex, learned ini­
the baby rooting for milk. When corner of mouth
tially by irregular and poorly coordinated’ chew­
is touched, the lower lip is lowered, the tongue
ing movements. The proprioceptive responses of
moves towards the point stimulated. When the
the TMJ and the periodontal ligament of the
linger slides away, the head turns to follow it.
erupting dentition establishes a stabilized chew­
When the center of upper lip is stimulated, the lip
ing pattern, aligned to the individual dental
elevates.
Swallowing begins around 12 1/2 weeks of in­ intercuspation.
trauterine life.
Full swallowing-and sucking is established around 13. Blink reflex: Various stimuli provoke blinking.
32-36 weeks I.U life. Whether the child is awake or asleep, pupils of
the eye react to changes in the intensity of light.
8. Gag reflex: It is seen at 18 1/2 weeks I.U life. In
the buccal cavity and pharynx, the ectoderm / 14. Doll’s eye reflex: Through a complex mechanism,
endoderm zone is towards the posterior third of infants hold fixation of faces, piovements or chang­
the tongue. Touching here elicits a gag reflex, a ing intensity of light within their visual fields.
protective reflex. During the Ist week they are able to maintain these
fixations against passive movement of their bod­
9. Nasal reflex ies.
Stimulation of the face or nasal cavity with water
or local irritants produces apnea in neonates.
15. Babinski’s reflex: Stroking of the lateral surface
Breathing stops in expiration with laryngeal clo­
of the planter surface of the foot from the heel to
sure and infants exhibit bradycardia and lower­
the toe results in flexion of the toe.
ing of the cardiac output.
Blood flow to the skin, splanchnic areas, muscles 16. Parachute reflex: It appears at about 6-9 months
and kidney decreases, whereas the flow to the and persists thereafter. The reflex is elicited by
heart and brain is protected. Midwives have for holding the child in ventral suspension and sud­
many years blown on the face of neonates to in­ denly7 lowering him to the couch. The arms ex­
duce the first breath. tend as a defensive reaction. In children with
cerebral palsy, the reflex may be absent or abnor­
10. Infantile swallow: Until tile primary molars erupt, mal. It would be asymmetrical in spastic hemiple­
infant swallows with the jaws separated and the
gia.
tongue thrust forward using facial muscles (or­
bicularis oris and buccinator). This is a non-con- 17. Landau reflex: It is seen in vertical suspension,
ditional congenital reflex. with the head, spine and legs extended. If the
Acquired congenital reflex: After eruption of the head is flexed, the hip knees and the elbows also
posterior primary teeth, from 18 months of age flex. It is normally present from 3 months and is
 SECTION 2 : NORMAL GROWING CHILD |

Self Assessment
difficult to elicit after 1 year. Absence of reflex
occurs in hypotonia, hypertonia or severe mental 1. What is the period of embryo and foetus?
abnormality. 2. Which are the fontanelle and when do they close?
3. Which are the sutures and when do they close?
18. Tendon reflexes: They are present in the neonate. 4. Explain how the moro’ reflex is elicited and what
They are of great value for the diagnosis of cer­ is it’s clinical importance?
ebral palsy, for, in spastic children, the tendon 5. What are Gum pads? Give the features of the up­
jerks are exaggerated. per gum pad.
6. What is the head circumference of the child at
19. Abdominal reflexes: They are also present in most
birth.?
of the newborn babies.
 2.3 Stages of Human Growth and
Development (Post-natal)
Tandon S, Radhika M

Singes of post natal growth and development are Smiles on social contact.
based on the average fluctuation in growth and de­ Listens to voice and coos.
velopment The followi ng developmental periods till
adulthood are generally considered. 12 wk Lifts the head and chest.
Lifts head above plane of body on ventral
suspension.
POST NATAL PERIOD (Fig. 2.13a, b) Early head control with bobbing motion.
Makes defensive movements.
1-4 wk In prone position child 1 ies flexed and turns Listens to music.
| Neonatal head from side to side, head sags on
period ventral suspension. 16 wk Lifts head and chest, head in approximately
Motor response, grasp reflex are active. vertical axis.
Shows visual preference to human face. Symmetric posture predominates, hands in
Face is round and mandible small. midline.
Abdomen is prominent with relatively Enjoys sitting with full truncal support.
short extremities. Laughs out loud. 1
Criteria to assess premature newly Excited at sight of food.
horn is -
born between the 28th to 37th week of 28 wk Rolls over, crawls.
gestation. Sits briefly.
birth weight 2500 grams (51bs-81bs) or less. Reaches out for and grasps large objects.
birth length 47 cm (18 1/2 inches) or less. Transfers objects from hand to hand
head length below 11.5 cm (4 1/2 inches) Polysyllabic vowel sounds formed
and Prefers mother, babbles
head circumference below 33 an (13 inches). Enjoys mirror

4 wk Holds chin up. 40 wk Sits up alone, without support.

Head lifted momentarily to the plane of Pulls to standing position; “cruises” or
the body on ventral suspension. walks holding on to furniture.
Watches person, follows moving object. Grasps objects with the thumb and fore
Beginning to smile. finger; pokes at things with forefinger.
Repetitiveconsonantsounds (mama, dada).
8 wk Head sustained in plane of body on Responds to sound of name.
ventral suspension. Plays peek -a- boo, waves bye-bye.
 SECTION 2 : NORMAL GROWING CHILD | 4CTB

Stands alone
Walks with support
Cruises

Pulls up
Creeps
Sits briefly
Transfers objects
Rolls over
Holds head
Turns head
Smiles
Regards

Birth 1 2 3 4 5 6 7 8 9 10 11 12 13 14
Age in Months

Fig. 2.13a Cephalo-caudal growth - Aldrich 1972.

Fig. 2.13b Normal Milestones in Development

New born: Prone Supine Puled to sit

Ventral suspension Held sitting

NEWBORN
 1 TEXTBOOK OF PEDODONTICS

Pulled to sit

Held sitting (Momentarily lifts head)

4 TO 6 WEEKS

Prone Ventral suspension Pulled to sit

4

Held sitting

10 T011 WEEKS

5TH MONTH
 SECTION 2 : NORMAL GROWING CHILD |

Lifts head
Sits without being held

Transfers object from one Palmar grasp of cube Held standing bears
hand to other full weight

6TH MONTH

Palm and thumb grasp

support

Forefinger and thumb grasp Bear like crawl

Walks with hand held

1YEAR
 I TEXTBOOK OF PEDODONTfCS

52 wk Walks with one hand held, rises independ­ 36 Mo Rides tricycle.

ently takes several steps. .Stands momentarily on one foot.
Releases object to other person on request Imitates a cross, copies a circle.
or gesture. Knows age and sex.
Increase in vocabulary by a few words, Counts 3 objects correct 1\
besides ’mama. dada’.
Makes postural adjustments to dressing. 48 Mo Hops on one foot.
Uses scissors to cut out pictures.
PRESCHOOL PERIOD Tells a story;
Plays with several children.
15 Mo Walks alone, crawls upstairs. Goes to toilet alone.
Inserts pellet in bottle.
Jargon; follows simple commands, may 60 Mo Skips.
name a familiar object. Dresses, undresses.
Indicates some desires or needs by point­ Asks questions about meaning of words
ing; hugs parents. Domestic role-playing.

18 Mo Runs stiflly. SCHOOL PERIOD (6-12 yrs)

Walks up stairs with one hand held.
Explores drawers and waste baskets. 6-10 yrs Steady growth until the pre-pubertal
Imitates scribbling (vertical strokes). growth spurts.
Dumps pellet from bottle.
Vocabulary consists of about 10 words, 10-12 yrs Usual peak height velocity in girls.
identifies one or more parts of the body.
Feeds self: seeks helps when in trouble. 13-14 yrs Usual peak height velocity in boys.
Lymphatic tissues are at their peak devel­
24 Mo Runs well; walks up and down the stairs opment during these years.
one step at a time. Girls reach their peak height velocities
Opens doors. earlier than boys on an average and have
Jumps. a lower peak.
Circular scribbling. Growth rate declines after the peak height
Imitates horizontal stroke. velocity period to about the same as
Puts 3 words together (subject, verb, during the infantile period
object). Average weight gain during this period =
Handles spoon well. 3-3.5kg(71bs)
Helps to undress. Average height gain during this period = 6
Listens to stories with pictures. cm (2.5 inches)

30 Mo Goes upstairs with alternating feet. PUBERTY AND ADOLESCENCE

Refers to self by pronoun T, knows full
name. There exits a considerable variability in the
Helps put things away. chronologic ages in which this pubertal
Pretends in play. period begins
 SECTION 2 : NORMAL GROWING CHILD |

10 vrs On an average it begins in female child. There is an increase in the mass of muscles.
Redistribution of body fat.
12 «•vrs Adolescence begins in male child.
Increase in skeletal growth.
13 vrs Puberty coincides with development of Average height gain from 5 yrs to puberty
secondary sexual characteristics ie. is +3 inches (annually) and by 13 years in
breasts in female child, pubic hair? voice females is 63 inches while 62-65 inches in
change in male child. mates.
It is also marked by menarche in females.
The sooner the puberty occurs the sooner Events of Puberty are given in Table 2.3
the rate of growth declines and finally
stops. Predicting adult height and weight:
In females maximum growth in height
occurs the year before the menarch. Boys 2 x height at 8 years = adult height
Giris 2 x height at 7 ’/2 years = adult height

Table 2.3: Events of Puberty

In males In females
Onset of the height spurt Major growth phases concern development
of adult female appearance.
Age of maximum spurt Breast development.
Achievement of adult height Changes in body contour.
Genital changes begin within one Genital development
year of beginning of accelerated
height growth
At about 12 14 years there is increased Height spurt usually 2 years earlier
amount of androgen (17 ketosteroid) than males 8 14 to 9 14 years)
found in urine
Changes in pubic, auxiliary facial Secondary sex changes occur
and body hair begins shortly after this time
Height growth attains its maximum Menarche appears earlier than
velocity in the early genital and hair the average age most likeiy due to
change period better health
Height spurt peaks at about 14 years Sterile period of 3 years from menarche
until reproduction possible
Strength spurt peaks at end of Early sexual maturation is accompanied by
height spurt an advanced skeletal age compared to
chronological age
Voice change correlates with Early menarche - taller,
skeletal age and occurs at about the heavier and advanced developmentally
time of spermatogenesis
(14-16 years).
 <îÏÏB I TEXTBOOK OF PEDODONTICS

(3 years to puberty slow gain in weight)

Body weight is probably the best index of nutrition
and growth

Predicting adult weight:

Boys 5 x weight at 2 years = adult weight

Girls 5 x weight at 1 V? years = adult weight

At different ages Weight in Ihs

Birth 6-8 lbs

1 month Regain birth weight
4 months 2 x birth weight
2-3 years 3 to 5 lbs yearly
5 years 5 x birth weight
Puberty 80 to 90 lbs

DIFFERENTIAL GROWTH Age in years

Fig. 2.14 Pattern of growth in Man-Tanner 1962
Changes from birth to adulthood (Scammon’s curve)
Head 2 x birth size
3 x birth size Head At birth 22% total body length
Trunk
, 10 years 95% total head growth complete
Limbs, arms 4 x birth size
15 years 98% total head growth complete
Legs 5 x birth size
Width of the head complete by 3 years 1
Length of the head complete by 17-18 years
• Changes in body proportions occur due to asyn­
chronous growth i.e. ' split growth”. Body parts
Scammon’s Growth Curve
grow at their own rate and reach maturity inde­
pendently, but in a coordinated fashion.
■ Generally, growth is more rapid in height than Scammon’s growth curve indicates that growth rate
weight. Hence, one "grows taller before growing of different tissues are different at different ages. For
heavy”. example, lymphatic tissue grows and reaches its maxi­
■ Less developed body parts grow more like mus­ mum growth rate at 10-12 yrs after which there is a
cles, lungs, bones, genitals increase approximately decline in growth rate. Genital organs reaches its peak
twice the original size.
at the time of puberty (Fig. 2.14)
■ More developed body parts grow less like eyes,
Growth Spurts
brain, which complete development early.

Eye Completes growth by 5 years Growth does not take place uniformly at all times.
Brain Completes growth by 10 years There seems to be periods when a sudden accelera­
Heart Completes growth by 20 years tion of growth occurs. This sudden increase in growth
is termed " growth spurt”
 SECTION 2 : NORMAL GROWING CHILD |

The growth spurts in the prenatal period and the ■ Pubescent phase: Very rapid growth p hase.
infantile period differ in that they are more of a bio­ ■ Postpubescent phase: Decelerating height ve­
physical process, involving the division of the cells. locity. Finally, linear growth comes to a stop
with the fusion of the epiphyses.
On the other hand, the physiological alteration hi Growth modification by means of functional and
hormonal secretion is believed to be the cause for orthodontic appliances elicit better response dur­
the accentuated growth associated with the pubertal ing growth spurts. Surgical correction involving
period. The timing of the growth spurts differ in boys the maxilla and mandible should be carried out
and girls. only after cessation of the growth spurts.

Growth trends
cm/yr
By overlapping consequent Cephalograms, Tweed '
discerned a pattern of growth and termed it as
Growth trends'. He thus divided the individuals into
the following groups:

• TVPEA
The maxilla and mandible grow together and thus
the ANB angle remains basically unchanged.
Should this be accompanied with a class 1 rela­
tionship and in the mixed dentition does not ex­
ceed 4.5°, no treatment is indicated. It is seen in
25 % of the cases.

■ TYPE A Sub-division
The maxilla is protruding with the ANB angle more
Fig. 2.15 Growth in boys and girls (modified
from Bjork 1975) than 4.5. The treatment is to restrict the growth
ofthe maxilla while allowing the mandible to catch
up. The prognosis is good, but may sometimes
The following are the timings of growth spurts (Fig. require the extraction of the premolars.
2.15):
a. Just before birth ■ TYPEB
b. One year after birth The maxilla and the mandible are found to grow
c. Mixed dentition growth spurt forwards and downwards with the growth of the
• Boys : 8-11 yrs maxilla exceeding that of the mandible. This type
■ Girls:7-9yrs of growth trend has a poor prognosis asthe treiid
d Adolescent growth spurt. indicates that the point B will not catch up with
■ Boys : 14-16 yrs point A. Growth of the middle and lower face is
• Giris: 11-13 yrs predominantly in the vatical direction.

The Adolescent growth spurt has been divided into ■ TYPE B Subdivision
three phases: The ANB angle is large and continues to grow,
■ Pre pubescent take offstage: Moderate incre- indicating an unfavourable growth trend,
ment in the height velocity.
 <4:11 I TEXTBOOK OF PEDODONTICS

■ TYPEC
The maxilla and the mandible grow forwards and
downward with the mandible growing forward
more rapidly than the maxilla. The ANB angle is
seen to be decreasing w ith the mandible catching
up with the maxilla. This indicates a favourable
growth trend and treatment is not indicated until
the eruption of the canine.

« TYPE C Subdivision
The mandible is found to be growing more for­
ward as compared with the maxilla. With this the
mandibular incisors touch the lingual surface of
the maxillary incisors. Thus
1. either the mandibular incisors are tipped lin
gually or
2. maxillary incisors are tipped labially. Fig. 2.16b Diagramatic representation of the drift
and displacement (Chilander et al 1985)
The prognosis is good and the mandibular inci­
sors need to be retained from one cuspid to an­
2. Cartilage has the capacity for interstitial growth.
other.
3. Continuous remodelling i.e. deposition of bone
on external bone surface (appositioned) and se­
Principles of bone growth and growth theories
lective breaking down of bone on other surface
(resorptive) serves to maintain the shape and pro­
L Any dimensional change in bone is restricted to
portion of bone. %
appositional growth on the external surface (pe­
4. Remodelling leads to migration, known as drift
riosteum) and internal surface (endosteal) (Fig.
and movement, known as translation^ displace­
2.16a,b).
ment.

Resorption A knowledge of these separate process in the bone

tissue movement is essential for a proper understand­
ing of growth events and the effects of various forms
of treatment, e.g. an orthopedic force may prevent
normal growth through displacement, but need not
necessarily prevent drift continuing or even increas­
ing to compensate for this absence of displacement
growth.

Enlow’s ‘V’ Principle

Enlow has explained the significance of the interplay

between deposition and resorption for the shape of
Fig. 2.16a Relocation of Maxillary Palate various bones in the form of4 V’ shape. Deposition
(Enlow 1966)
on the internal surface of 4 V’ in the direction of
 SECTION 2 : NORMAL GROWING CHILD |

led by thyroxin and steroids. Pubertal growth spurt,

is a primary function of the steroids and human
growth hormone Any increase in the above hormones
brings about an accelerated bone maturation.
Ossification and Ca4"* level in blood are interrelated.
While parathormone brings about increased osteo­
clastic activity to compensate for decreased Ca++
blood level, calcitonin is responsible for enhancing
bone deposition.

In females, prolactin also brings about growth hor­

mone like effects, though its primary effect is on breast
development.

GROWTH THEORIES: ASSUMPTIONS AND

CLINICAL IMPLICATIONS (See table 2.4)

Fig. 2.17 V-Principle of growth POST NATAL DEVELOPMENT OF THE MAXILLA

(Chilander et al 1985). (Fig. 2.18)

growth and absorption on the outer surface allows The mechanisms involved in the growth of the
the bone to retain its characteristic shape during nasomaxillaiy complex are the sutures, the nasal
growth, is the growth of the head of the mandible septum, the periosteal and endosteal surfaces, and
(Fig.2.17). the alveolar processes.

Physiology of growth Growth of the maxilla, has two interrelated mecha­

nisms, i.e.
Growth takes place due to the effect of the hormones 1. the shift in position of the maxillary complex and
on the bone tissue. In one way or another, all the 2. the enlargement of the maxillary complex itself..
hormones affect growth, with the growth hormones,
thyroxin, corticosteroids and insulin bringing about This mechanism can be assessed from three param­
changes in the growth rate and parathormone, vita­ eters, the height, width and length.
min D (and it’s various forms) and calcitonin affect­
ing skeletal maturation and pubertal growth. Maxillary height

Growth hormone brings about changes in carbohy- Maxillary height increases because of sutural growth
drate and lipid metabolism. It also stimulates towards the frontal and zygomatic bones, and appo­
stomatomedin release, which causes cartilage growth. sitional growth in the alveolar process. The nasal
Apart from growth hormone, insulin may also inciease floor is lowered by resorption while apposition oc­
production of stomatomedin, while thyroxin can have curs on the hard palate. Alveolar remodeling con­
a modulating effect on it. Glucocorticoids, on the tributing to significant early vertical growth helps in
other hand, are seen to suppress stomatomedin. the attainment of width because of die divergence of
the alveolar processes. As they grow vertically, their
The effect of growth hormone is indirect (through divergence increases the width.
stomatomedin). Skeletal maturation is mainly control-
 COB I TEXTBOOK OF PEDODONTICS

Table 2.4: Growth Theories: Assumptions and Clinical Implications.

Theory Assumption Applications

Genetic ■ The assumption was ■ The external factors have a significant,

(Brodie, 1941) that genes controlled modifying effect on it, thus reducing its effect
all aspects of growth. vastly. The inheritance that does take place
is polygenic in nature. For example the pre­
disposition of an individual to class III
malocclusion.
Scott’s • Cartilage grows actively, ■ Mandibular growth has been explained that the
Hypothesis bone later replaces it. condyles act as the diaphysis of a long bone
(1953) Thus cartilage has innate with growth occurring at both the ends. Recent
growth potiential. studies have proven that growth at the condyle
■ Transplantation and extir­ is mostly reactive and not of primary nature.
pation experiments prove ■ Maxillary growth can be explained due to the
that some innate potential translation of the nasomaxillary complex as
is evident though results a unit , I
are equivocal.
Sutural « Proliferation of sutural ■ Explains maxillary growth as the result of
dominance connective tissue causes pressure created by growth at the sutures.
theory appositional growth. ■ Limitation being it could not explain.
(Sicher, 1955) ■ Genetic factor was - Lack of growth in suture transplantation.
accepted. - Growth occurs in cleft palate cases.
- Sutures respond to external influences.
■ Membranous bones were
considered as growth
centers.
Moss’s « Functional matrices, which ■ Several examples can be cited such as the
Functional can be further divided into excessive growth of the cranial vaultMn cases
theory capsular and periosteal of Hydrocephalus.
(1962) matrices have the primary
control for the growth of
the craniofacial structures.
■ Bone responds to the
matrices in a passive
manner and does not
have any primary growth
potential
. Van ■ Factors controlling skele­ ■ Explains the interaction between the genetic
Limborgh’s tal morphogenesis are: and environmental factors. Thus what may be
theory 1. Intrinsic genetic factors. environment for the bone (muscle & soft tissue)
(1970) 2. Local epigenetic factors. is in turn dependent on the growth and function
3. General epigenetic of the soft tissues. The growth of the muscle
factors and soft tissue has a genetic component
4. Local environmental ■ Even if there were genetic disposition, it is
factors polygenic, multifactorial in nature, thus pre-;
5. General environmental eluding any predictions of the facial dimensions
factors. of children from the study of their parents.
. - 1
contd.
 SECTION 2 : NORMAL GROWING CHILD |

Theory Assumption Applications

Petrovic’s ■ Primary cartilage, in which ■ It explains the mode of action of the functional
Hypothesis growth occurs by differenti­ appliances directed at the condyle.
1974, ation of chondroblasts, ■ The upper arch acts as a mould into which the
Cybernetics can be modified with lower arch adjusts itself, such that optimal
factors which affect the occlusion is established.
direction only and not the
amount of growth.
■ Secondary cartilage has a
direct cell multiplication
effect but more importantly
indirect effects also play
an important role.

Neurotropism ■ The nerve impulse • Effect has been reported to be negligible.

(Work done by involving axoplasmic
Behrents 1976) transport has direct growth
includes potential.
epithelial ■ It also has an indirect effect
visceral and on the osteogenic growth
muscular by influencing soft tissue
components growth.

Maxillary width areas which proceed away from each other, thereby
drawing out the dimensions of the maxilla in several
Growth in the median suture is more important than different directions. Thus it would be inporrect to
appositional remodelling in the development of max­ assume that growth occurs only in a forward and
illary width. downward direction.

Maxillary Length As the maxillary complex is joined to the cranial base,

Length increases in the maxilla after about the sec­ it naturally influences the development of maxilla.
ond year and this occurs by apposition in the maxil­ There is no sharp line of demarcation between the
lary tuberosity & by sutural growth toward the pala­ cranial and maxillary growth gradients. The position
tine bone. Surface resorption occurs anteriorly on of the maxilla is dependent on the growth at the
t he bony maxillary arch. spheno-occipital and sphenoethmoidal synchon­
droses.
The postnatal growth of the maxilla parallels that of
the mandible in that forward & downward movement Age changes in maxilla
of growing bone as a whole is a result of growth
which takes place in a posterior direction with corre­ At birth the transverse & anteroposterior diameters
sponding repositioning of the entire bone in a for­ of the maxilla are greater than the vertical diameter.
ward direction. The frontal process is well marked but the body of
the bone consists of a little more than the alveolar
The overall size of thé face increases by a series of process. The tooth socket reaching almost to the
specific growth movements in several individual floor of the orbit. The maxillary sinus is a mere furrow
 I TEXTBOOK OF PEDODONTICS

on the lateral wall of the nasal cavity. In the adult the rami and the alveolar ridges. These areas of bone
vertical diameter is greater owing to the development deposition account grossly for increase in the height,
of alveolar process and increase in size of the sinus. length, and width of the mandible.

The palatine processes of the maxilla grow in a gen- At birth, the mandible generally consists of two
—------ orally downward direction by a combination of sur­ halves generally ossifying by 12 month of life. The
face deposition on the entire oral side of the palatal coronoid process is relatively large and projects well
cortex with resorptive removal from the opposite na­ above the condyle. The body has tooth buds, man­
sal side, as well as from periosteal labial surfaces of dibular canal running low' in the body.
the anterior maxillary arch.
Condylar growth (Fig. 2.19)
The premaxillary part of the maxilla grows in a down­
ward direction. The surface orientation of this area is
such that a downward movement is brought about by
resorptive removal from the periosteal surface of the
labial cortex which faces away from the direction of
growth. The endosteal side of its cortex and the pe­
riosteal surface of the lingual cortex receive new bone
deposits. This growth pattern also produces a slight
’’recession’* of the incisor area in a posterior direc­
tion, a situation also present in the human mandible.

10 yrs.

Fig. 2.19 Vertical growth of the condyles.

(Bjork & Skieller 1972)

The condylar cartilage of the mandible serves the

uniquely dual roles of an articular cartilage in the
Fig. 2.18 Comparative growth of the upper and
TMJ, characterized by fibrocartilage surface layer,
lower jaw
and as a growth cartilage analogous to the epiphy­
seal plate in a long bone. It would be wrong how­
POST-NATAL DEVELOPMENT OF MANDIBLE ever to accept this per se, as the condyle is not
(Fig. 2.18) considered the primary growth centre any more. Stud­
ies that have evaluated the growth in cases of con­
The main sites of post-natal mandibular growth are dylar fractures show that the growth of the mandi­
at the condylar cartilage, posterior borders of the ble may still continue in these cases.
 SECTION 2 : NORMAL GROWING CHILD I C£B

Growth of the ramus Change in the width

The ramus of the mandible lengthens by the growth The mandible increases in width following the ‘V’
of the condylar cartilage and by the periosteal bone principle wherein bone deposition takes place on the
formed at the posterior borders of the ramus. outer aspect of the mandible and resorption on the
. The ramus increases in height by growth of con­ inner aspect.
dylar cartilage and by the bone deposited at the
base of the sigmoid notch, at the posterior bor­ , Age changes in mandible
der and at tip of coronoid process. The growth
of bone at the angle of the mandible leads to a ■ The body elongates especially behind the mental
change in mandibular angle from about 135 de­ foramen providing space for permanent molars.
grees in the new born to about 100 degrees in ■ The mental foramen changes direction from ante­
the adult, although it is variable. The main in­ rior to posterosuperior and then almost horizon­
crease in height of the body is due to develop­ tally, accommodating a changing direction ofthe
ment of alveolar bone. emerging mental nerve. When teeth are present,
■ The ramus is also translated posteriorly by the mental foramen is located midway between
resorption of the anterior border and deposition the upper and lower borders of the mandible.
on the posterior border [ which also creates space ■ The angle of the mandible diminishes with age.
for the permanent molars to erupt]. ■ During post-natal development, growth in man­
dibular width is completed, this is followed by
Thus the combination of condylar and ramus growth growth in length, and then in height. The growth
brings about: in width including the dental arches completes
a) Backward transposition of the entire ramus, before the adolescent growth spurt.
thereby elongating the mandibular body.
b) Displacement of mandibular body in an anterior Maxillo-mandibular relation
direction (in a downward and forward direction)
c) Vertical lengthening of the ramus as the mandible At birth the mandible tends to be retrognathic to the
is displaced. maxilia, although the twojaws may be of equal size.
d) Movable articulation during these various growth This retrognathic condition is normally corrected
changes in the alveolar region above it creating early in the postnalal life by rapid mandibular growth
the submental concavity. and forward displacement to establish orthognathic
or an angle class I maxillomandibular relationship.
Alveolar process This yet again conforms to the cephalocaudal gra­
dient of growth pattern. Inadequate mandibular
The growth of the alveolar process is primarily re­ growth results in angle class II, overgrowth of man­
lated to the presence and eruption of the teeth as it is dible produces angle class HI relation.
the increase in height and thickness.
Self-Assessment
Chin
1. What are the growth spurts? In which age it is
The chin develops as a separate subunit of the man­ seen and what is its significance?
dible. It is poorly developed in the infant and 2. What is cephalocaudal growth gradient?
achieves its prominence only during pubertal growth. 3. What are growth trends?
The resorption of the alveolar process above it a lso 4. Describe the physiology of growth
accentuates the chin. 5. What is functional matrix theory?
 CEB I TEXTBOOK OF PEDODOMT1CS

6. What is differential growth and Scammon’s 10. What are the age changes take place in mandi­
growth curve? ble?
7. What is Enlow’s ‘ V’ principle? 11. How does chin develop?
8. What are the assumptions of 'petrovic’s hypoth­ 12. What maxillo-mandibular relationship exists at
esis? birth?
9 Which theory explains the interaction between
genetic and environmental factors?

4
 2.4 Growth Assessment

Paul U. Tandon S

Craniofacial growth comprises the phenomena fall­ iii) Semi longitudinal method: is sometimes used
ing within the scope of a number of disciplines and in an attempt to reduce the aforesaid disad­
occurring at several levels, including the molecular, vantages. Hiis means monitoring age-groups
cellular tissue and organ levels. No specific method or subgroups at different levels of develop­
can therefore be assigned to the study of these ment only forthat period which separates one
events. In clinical pedodontics, however, data on group from the next. Suitable selection criteria
craniofacial growth usually serve to describe dimen­ are a prerequisite for obtaining representative
sional changes, relations between different bones results with all these methods. However, when
and growth mechanism. Some of the methods com­ studying facial dimensions, the importance of
monly used for this purpose are described here. race, sex, etc., must be taken into considera­
tion.
1. Biometrics: is defined as the science of statisti-
calbiology, the collection and statistical analysis
2. Craniometry: The metric study of cranial dimen-
of data regarding a living orga nism. Hie biometric
sions in dry skulls is less suitable for descriptive
methods used for recording dimensional changes
purpose where growth in children is concerned.
in the cranium during growth are:

i) Longitudinal methods: These imply serial meas­ 3. Somatometry: The metric evaluations of facial
urements in the same individual or population dimensions, including soft tissues, is limited mainly
over a long period of time. Their advantages by lack of reliable methods for recording the data
lie in the fact that individual patterns can be and is therefdre used very little in pedodontics.
defined and the variation within a group can
be analyzed, which is of special importance 4. X-ray cephalometry: Enables longitudinal inves­
when the individuals are to be compared with tigations to be carried exit, and the information of
standards or norms. These studies are expen­ human craniofacial growth which has accumu-
sive and time consuming, however, and the läted during recent year is mainly based on this
dropout rate may be so high that statistical technique. This method does not describe attirai
significance of the observations is lost. growth changes but usually depicts only how
the radiographic structure has changed in rela­
ii) Cross-sectional method: Groups of varying
tion to a certain reference structure. This prob­
ages or at varying stages in development are
lem is because x-ray cephalometry describes
examined only once. This method requires large
growth as a two dimensional phenomenon in
populations in order to yield statistical obser­
which growth of structures is simplified to
vations, and it tends to mask or exclude indi­
positional changes in a system of
vidual variations, e.g. in the age of the puber­
The x-ray film does not distingui^^^^^^^g||
tal spurt.
 Æ5B I TEXTBOOK OF PEDODONTICS

changes in the position of a structure per se and 9. Animal experiments: are used to study specific
changes due to remodeling of its external sur­ pathological conditions, malformations or ac­
faces. quired defects and events at the cellular level of
5. Metal indicators: The x-ray cephalometry can be histological, histochemical and biochemical tech­
used to overcome the above mentioned problem nique. More detailed information on growth
by implanting metal markers in a bone to act as a changes thus can be obtained by the use of bone
reference point and changes in the external con­ labeling with the substances that are incorporated
tours of the bone can be studied. into newly formed bone. Embiyological research
6. Superimposition: By taking a series of x-ray films has been made possible due to these experiments.
by using the above method to superimpose an
anatomical reference structures; the positional 10. Vital staining: Belchier (1736) stated that the
changes can be studied. bones of animals who had eaten madder plant
were stained a red color due to alizarin, an essen­
7« Steriopairs images: In computer analysis tial dye of the plant which was incorporated into
positional changes can be studied in a three di- the bone. The bones contained a band of red
* mensional system.
stain followed by an unstained band. The vital
staining method depicts the pattern of the post­
8. Electromyography: Allows the action potentials
natal bone deposition over an extended time pe­
of the muscles of mastication to be correlated with
riod. It also gives the growth sites, the direction
morphological data and normalization of muscle
function in the treatment of malocclusion. The and amounts of growth, as well as the timing and
role of functional factors in craniofacial morpho­ relative duration of growth at different sites. Ali­
genesis is commonly accepted and has potential zarin, and other vital dyes like procion and tetra-
to elucidate the important factors of hereditary cj'dine are used extensively in hone research.
and environmental factors in the twin studies.

i
Normal
Deviation from normal i
I

Fig. 2.20 Anthropometric measurements.

 SECTION 2 : NORMAL GROWING CHILD |

L Radioisotopes: Radioisotopes of certain elements child’s date of birth. Since each child has his own
and compounds are used as invivo markers for characteristics growth time clock, i.e., there are
studying bone growth. With injection the iso­ early, middle and late maturation chronological
topes, after a time get located within the growing age, neither accurate indicators of stage of devel­
bones: Growth is measured by means of Geiger opment: nor it is a good predictor of growth po­
counters or autoradiographic techniques. tential.
An emitting isotope 99mTc is used to detect ar­
eas of rapid bone growth in humans where bones 2. Somatotypic age: In the overall assessment of a
or sections of bones are placed against photo­ child, a general body type which is also called as
graphic emulsions and then exposed by emission somato type, is usually considered. Sheldon di­
of radiation from the radioactive substance. vides somatotype into three categories; ecto­
morph, mesomorph and endomorph. The endo­
2. Natural markers: There is a persistence of cer­ morph is stocky, has-abundant subcutaneous fat
tain developmental features of bone which are and has digestive viscera that are highly devel­
used as natural markers. Trabaculae, nutrient oped; somatic structures are relatively underde­
canals and lines of arrested growth can be used veloped. The mesomorph is upright, sturdy and
for reference to study deposition, resorption and athletic; muscles; bones and connective tissue
remodeling. predominate. The ectomoiph is tall, thin and frag­
ile; his extremities are long and slender with mini­
3. Anthropometry: Various landmarks established mal subcutaneous fat and muscle tissue. In gen­
on dry skull are measured viewing individuals by eral, the ectomorph is a late maturer (adolescent
using soft tissue points overlying the bony land­ growth spurt about 1 year after that of
marks. Farkas (1987) in his anthropometric stud­ mesomorphs), whereas an endomorph is anearly
ies have provided new data for the human facial maturer in terms of chronologic age. Although
proportions and change in time. (Fig. 2.20) somatotype may give a gestalt about the child’s
developmental pattern, it is not an accurate
irowth assessment parameters predictor.

Why assessment should be done”? 3. Height and weight age: Height has been consid­
: is done for: ered as an convenient determinant of develop­
Identification of grossly abnormal growth or even mental age. The standard growth commonly em­
pathological growth. ployed to characterize a child’s height compared
Recognition and diagnosis of any significant de­ to that of children of some chronological age is
viation from normal growth. used to assess developmental age. It is generally
Planning of orthodontic/orthopedic treatment seen that after age 2 each child tends to follow
Determining efficacy of the treatment modality the same percentile on the growth curve until the
puberty, when deviation may occur because bf
’ rogman defines five ages >f childhood which may timing of the spurt differs among adolescents.
e considered as growth assessment parameters in an Since each child’s height is related to genetic and
iterdisciplinary team evaluation of the patient with environmental factors as well as to chronologic
arious types of short stature, endocrino/metabolic age, it is clear that a single height measuremait is
isorders, syndrome identification and forensics. limited as a predictor of developmental age. Not
, Chronologic age : The most commonly and easily all the children have same height at the same per­
determined developmental age parameter is the centile.
chronologic age, which is simply figured from the
 TEXTBOOK OF PEDODONTICS

Similarly weight standard curves have been con­ 5. Sexual age:

structed. Although in the average child weight With the onset of puberty, differential hormonal
may be correlated with height, it is clear that ab­ action give characteristic body changes. Second­
normal variation in weight in otherwise normal ary sexual characters like hair growth, accelera­
children limits the use of these curves as a sole tion of growth of genital organs and height spurt
indication of developmental age. occurs in males. In females, appearance of breast
buds and distribution of body fat with menarche
4. Dental age which follows the maximal height velocity is seen.
The simplest but least accurate dental age indica­ In females, the peak height velocity is a relatively
tor involves recognizing teeth clinically present early event whereas in males it is a relatively late
and comparing them to the dental eruption charts. event. The correlation of coefficient between the
But a wide variation of eruption time along with age at menarche and skeletal age at 13 years is
environmental and local influences do not make 0.85.
this a reliable parameter. Therefore, it is thought
that dental age should be replaced by a scale of 6. Facial age:
maturity, between immaturity and complete matu­ ■ The ultimate goal of developmental growth
rity, which can be expressed by a figure. assessment of children is the facial age in or­
der to identify where they are on their own
Gieiser and Hunt (1955): He was the first who ad­ facial growth curve and use this as a predictor
vocated the calcification of a tooth as a more mean­ .of future growth.
ingful indication of somatic maturation than its
clinical emergence. Whilethe emergence of a tooth In addition to the developmental age assessment,
is a fleeting event and its exact time is very diffi­ the most commonly used method of analysis be­
cult to determine, its calcification is a continuous tween the normal versus abnormal facial devel­
opment is cephalometric analysis. Other meas­
process, which can be assessed by permanent
urements for assessing craniofacial developments
records such as x-rays.
are: 1
Head circumference
Demirjian (1973): A new approach has been
Eye measurements
adopted which is based on absolute values, for
■ inner canthal
the lengths of the crowns or roots by using a new
■ interpupillary
technique ofpanoramic radiographs. Eight stages
■ outer canthal
of development, from calcification of the tip of
Ear length
the cusp to the closure of the apex closure, were
Philtrum lengths
designated by 0 (for no calcification) and letters
Width of the commissures
A to H, corresponding to the eight stages. Let­
ters rather than numbers were selected so as not
Change in facial proportions:
to leave the false impression that each stage is
Increase in facial proportions are seen as:
equidistant from other. Each stage was then given
1. General facial growth from infancy to adoles­
a numerical score, according to the mathematical
cence and increase in size of dental arches.
technique by, the sum of which provides an esti­ 2. Increase in size of the muscles of mastication
mate of an individual’s dental maturity on a 0 to and facial expression.
100 scale. 3. Growth of alveolar processes of the maxilla and
the mandible with development and eruption
of deciduous and permanent dentition.
 SECTION 2 : NORMAL GROWING CHILD |

4. I ncrease in maxilla size and growth of maxillary hand and wrist has been chosen as a stand­
sinus ard. Dreizenetal 1957 stated that a 3 months
5. Increase in mandible discrepancy occurred between the right and
6. Increase in size of nasal area and paranasal left hand wrists in 13% and more than 6 months
sinuses. in only 1.5%:
7. Enlargements of orbits.
The radiograph of the hand and wrist of the child
8. Expansion of ethmoid and sphenoid bones.
is compared to the atlas standards with the same
sex and nearest age. The bones are assessed in a
7. Skeletal age:
regular order: Distal radius, Ulna, the carpels
The assessment of skeletal maturation has been
(Capitate, hammate triqetral, lunate, scaphoid,
used as an indicator of the developmental age -
trapezium, trapezoid, psiform) metacarpals - the
Stanecu 1977.
proximal, middle, ilistal phalanges. Each center is
Advantage: given a skeletal age. An overall average age is
1. A characteristic pattern of progression of os­ then taken. The carpel bones are taken as a reli­
sification can be identified i.e., each endochon­ able assessment parameter.
dral bone begins with a primary ossification
Tanner and Whitehouse et al (1975) gave a method
center which changes in shape, size and con­
of scoring maturity of indi vidual bone to get the
tour until the ultimate fusion.
skeletal age:
2. Easily recognizable at ages of ossification 1. RUS (Radius Ulnar Short bones) score rates
The hand and wrist radiograph is easily the radius, ulna, metacarpels of the digits 1,3
radiographed with minimal radiation exposure and 5 proximal, middle and distal phalanges of
(Fig. 2.21a, b). The PA radiograph of the left digits 1,3 and 5.

Fig. 2.21a Schematic representation of

hand wrist X-ray
 tfîhfc I TEXT BOOK OF PEDODONTICS

2. The carpel bone method score rates the carpel ■ In 1 to 2 years post-natal shift has a significant
bones. Here only 97% of the carpel score is relationship to the genetic background of the
reached by 13 years in females age 11 in males. child, reflective of mid parental height.
3. The TW2 method scores all the bones. Each
growth center is given a maturity rating on a ■ During adolescence, growth correlates with the
scale of 8 (A to H) except the radius which has parental size more strongly, being 0.7 to 18
9 (A to 1) "^ number is then given to each years. Hence the size of the parents can be
center in an attempt to allow biologic variabil­ considered as a best indicator of the eventual
ity. A total is got and this gives the overall predicted size of a newborn baby.
maturity rating.
2. Extra cranial and intra cranial pressure:
8. Basal metabolic rate: There is a direct relation-, Any factor affecting the physical growth is ex­
ship between BMR (Basal Metabolic rate) and pected to be associated with a profound and wide
growth. A mathematical expression can be de­ spread effect on the size and shape of the cranial
veloped by means of which, it is possible to con­ vault.
struct ideal curves of cumulative gain in height
and basal heat production from fetal stage to the « Artificially induced reshaping of the cranial
adulthood. vault has been practiced in many cultures. The
baby’s skull is molded by wrapping it in a bond­
Factors affecting the physical growth age by using a cradle board. According to the
mythology of the Maya culture, the skull shape
The regulation of growth in terms of rate, timing, symbolized the social class. Extra cranial me­
| character as well as its ultimate form largely depend chanical forces exerted during the period of
| on a combination and interaction of genetic and en­ growth can effect the size and shape of the
vironmental factors. part. It is observed that symmetrically deformed
skulls have significantly short cranial base and
1. Genetic factors: The genes contained within the the maxilla than underformed.
nucleus of each cell are said to be necessary to
produce an entire organism and primarily respon­ « The signs and symptoms related to increased
sible for orchestrating the phenomenon of nor­ intra cranial pressure depend on the age of the
mal growth. A genetic control influences the size patient at the onset. During infancy rapid ven­
of the organism to a great extent and the rate of tricular dilatation and increased cranial circum­
the onset of growth event Not all the genes are ference results. If the raised pressure is
active at birth. longstanding, sutural margins develop deep
interdigitation with spiky appearance. Later
• It is believed that size at birth relates to about when the sutures are closed, the volumetric
18% to the genome of the fetus, 20% to the expansion in the neurocranium results in an
maternal genome, 3 2% maternal environmen­ excessive resorption of the inner table of the
tal factors, and the remaining 20% to unknown cranial vault. This manifestation is quite when
factors. hydrocephaly occurs in conjunction with
pathologic sutural obliteration, as in Crouzon
■ After birth infants growth rate is no longer and Apert syndrome, for instance.
dependent on maternal factors but increas­
ingly related to his own genetic makeup.
 SECTION 2 : NORMAL GROWING CHILD J

3. Nutrition: Lack of nutrition delays growth and Hormones responsible for growth -
niay^ffcct size of parts, body proportions, body Group I
chemistry, quality and texture of some tissues. It Hormones influencing skeletal growth bone:
may delay growth and the adolescent growth 1. Growth hormone (anterior pituitary)
spurt. For example, lodiacdcficient diet effect 2. Insulin (p cells of langerhans)
the craniofacial growth in relation to all the di­ 3. Thyrotropic hormone
mensions. Soft diet has been found to show re­
tarded craniofacial growth in comparison to body Group II
growth. The height, depth of the distal part of the Hormones responsible for ossification of long
mandible were seen to be retarded during a study bones:
of 3 weeks to 20 week of growth in male mice. As 1. Parathormone
the distal areas of both the craniofacial complex
and the mandible are closely related to jaw func­ GroupIU
tion, growth retardation of this area could be ex­ Hormones responsible for pubertal growth
plained as the skeletal adaptation to the soft diet. spurt
1. Androgens
In children, during rather short periods of malnu­ 2. Progesterone and oestrogen
trition, they exhibit fine recuperative powers where
growth slows up and waits for a better time, and Group IV
with the return of good nutrition growth takes Prolactin hormone (anteriorpituitary)
place unusually fast until the genetically deter­ 5. Muscular functions: The close relation between
mined curve is neared once more. This catch up the muscles and the bone growth is seen due to
growth is seen in both sexes but females are bet­ the fact that the muscles influence the growth
ter buffered against the effects of malnutrition. both as a tissue affecting the vascular supply
and as a force element. The importance of the
4. Hormones: It is seen that 20 micrograms/kg b.w masticatory muscle function has been observed
of thyroxine injection daily for 28 days decreases in anthropologic studies, in which a low fre­
the length of the visccrocranium after 14 days, quency of malocclusions was found in
whereas cranial base growth increases between populations with primitive living conditions. The
14 to 28 days. Thus, the craniofacial growth pat­ frequency of malformation seems to have in­
tern is influenced by variation in the scrum level creased since these populations came under the
of hormones. Similarly, anabolic steroids therapy influence of industrialized civilization. The in­
was found to significantly increase all measures creased loading of the jaw due to masticatory
muscle hyperfunction may lead to an increased
of the craniofacial complex. The low dose exhib­
sutural growth and bone apposition resulting in
ited proportionate increases in most craniofacial
turn in an increased transverse growth of the
dimension, but the high dose produced overt
maxilla and broader base ofthe dental arches. Fur­
shape changes, notably a maxillomandibular, an­
thermore, an increase in the function of the mas­
teroposterior jaw discrepancy due to maxillary
ticatory muscles is associated with the anterior
excess. About 20% increase in body weight was
growth rotation pattern of the mandible and with
noted with elongation of the maxillary and man­ a well developed angular, coronoid and condylar
dibular incisors and an increase in depth of the process. For example, wrestlers who are in gen­
antegonial notch. eral, characterized by a well developed muscular
 | TEXTBOOK OF PEDODONTICS

system and have undergone heavy resistance and in weight of the newborns are present. There
training, have wide and well developed dental is no direct effect of climate on the rate of growth.
arches with a low frequency of malocclusion. The
excessive attrition observed on the teeth of the 9. Adult physique: Certain correlation between adult
medieval skulls indicated an extensive function physique and earlier developmental events
of the masticatory muscles. In contrast, the cranio­ present e.g. tall women tend to mature later. Vari­
facial morphology was found to be deteriorated ations in the rate of growth are associated with
in a group of patients with myotonic dystrophy. differing somatotypes.
The patients had a vertical growth pattern and a
high incidence of malocclusion such as distal oc­ 10. Socio-economic factors: These factors e.g. nutri­
clusion, anterior open bite, lateral cross bite and tion obviously play a role as a growth factor. Chil­
crowding. This group was characterized by a low dren living in favourable socio-economic condi­
bite force level and a reduced masticatory tions tend to be larger, display different types of
electromyographic activity. growth (height, weight ratio) and show a varia­
tion in timing of growth. The lower the socio
(u Growth factors: Growth factors are peptides (pro­ class or socioeconomic status of the mother, the
teins factors) that transmit signals within and be­ smaller is the baby and subsequently the child.
tween cells and play a comprehensive role in the
modulation of tissue growth and development. 11. Exercise: Exercise may be useful for development
They were first discovered in early 1960 as growth of motor skills, for an increase in the muscle mass,
stimulants. These factors regulate cell activity for the general well being and fitness but has no
by a number of mechanisms such as mitogenic, favorable effect on the linear growth.
migration, differentiation and gene regulation,
which may occur simultaneously and in different 12. Family size and birth undey: There are differences
tissues w here the effects may be different depend­ in the size of individuals, in their maturational lev­
ing upon the condition. These factors have els of achievement and in their intel ligence that
greater significance in the treatment of oral and can be correlated with the site of the family from
dental conditions. For example, recently they which they come. First bo rife usually weigh less
have been used to promote regeneration of sup­ at birth, have less stature and a higher I.Q.
port tissues after a periodontal surgery; It is also
seen that a single application growth factors such 13. Secular trends: Size and maturational changes in
as bone morphogenic protein (BMP) around ex­ large populations can be shown to occur with
traction socket implants increased osseous tis­ time, e.g., 15 years old boys are 5 inches taller
sue formation. than 15 years olds of 50 years back. The average
onset of menarche has steadily become earlier.
7. Illness: Systemic disease has an effect oh child
When race, socio-economic levels, nutrition, cli­
growth. The usual minor illnesses do not show
mate and other differences which lead to a change
much of an effect on growth. Serious prolonged
in growth are called secular trends.
debilitating illnesses have a marked effect on
growth and growth processes.
14. Psychological disturbance: Can lead to an inhibi­
8. Climate and seasonal effects: Those living in cold tion of growth by various methods. Children ex­
climate usually have a greater proportion of adi­ periencing stressful conditions display an inhibi­
pose tissue. A large amount of skeletal varia­ tion of growth hormone. These may also happen
tions associated with ^variations in climate sea­ under less extreme conditions and thus amount
sonal variations in the growth rate of children for lesser variations in individual growth.
 SECTION 2 : NORMAL GROWING CHILD | <*EB

15. Maternal factors: Size of a full term infant is re­ Further Suggested Reading For Section -2
lated to the size of the mother. With adipose tis­
sue development at 7 months IUL, there is an 1. Bishara-SE; Jakobsen-JR; Treder-J; Nowak-A:
increase weight gain the fetus fills the uterine cav­ Arch width changes from 6 weeks to 45 years of
ity where the uterine size constraint is a factor for age. Am-J-Orthod-Dentofacial-Orthop. 111(4):
the fetal growth. The role of placenta must also 401-9,1997
be considered. The placenta grows by cell number 2. Dahllof-G: Craniofacial growth in children treated
occurs till 35 weeks IUL after which increases in for malignant diseases.Acta-OdontoI-Scand.
cell size till 38-40 weeks. Thereafter, signs of de­ 56(6): 378-82,1998
terioration are seen in which a postmature infant 3. Enlow et al : Handbook on facila growth. WB
may become underweight for the length. Sunders company 1982
4. Frankenburgh WK et al: The Denver II: A major
Incremental increase in height revision and restandardization of Denver devel­
opmental screening test. Pediatrics. .4.1411992
Age Increment Height 5. Friede-H: Growth sites and growth mechanisms
at risk in cleft lip and palate. Acta-Odontol-Scand.
Birth 20 inches 56(6): 346-51,1998
0-6 months 1 inch/month 26 inches 6. Gosh S.: Second thoughts on growth monitoring.
6-12 months 1/2 inch/mbnth 32 inches IndianPediatr.:30.449,1993
1-7 years 3 inches/year 50 inches 7. Graber T.M. :Growth and Development. Orthodon­
8-15 years 1 inches/year 62 inches tics Principles and Practice. W.B. Saunders and
Company 1988
Incremental increase in w eight 8. Illingworth R.S.: General development .the
neonatal child - some problems of early years and
Age Increment Weight their development Churchil Livingstone. 191,1991
9. Kjaer-I: Human prenatal craniofacial development
Birth - 7 to 8 lbs related to brain development under normal and
0-4 months 2 Ibs/month 15 to 16 lbs pathologic conditions. Acta-Odontol-Scand. 1995
4-12 months 2 Ibs/month 23-24 lbs Jun; 53(3): 135-43,1995
1-2 years 1/2 Ibs/year 29-30 lbs 10. Moore K.L. Developing Human. WB Saunders
2-10 years 5 Ibs/year 69-70 lbs Co., 1992
11. Moyers Robert E.: Basic Concepts of Growth
and Development. Handbook of Orthodontics.
Self-Assessment Year Book Medical Publishers. 1988
12. Nanda-SK: Growth patterns in subjects with long
i What are the different growth assessment param­ and short faces [see comments]. Am-J-Orthod-
eters? Dentofacial-Orthop. 98(3): 247-58; 1990
2. What are the methods of assessing the dental 13. Needleman Robert D.: Growth and development.
age of the child? Textbook of Pediatrics. W.B. Saunders.30-67,1996
3. Which are the measurements performed at birth 14. Ranly-DM: Early orofacial development. J-Clin-
to assess the child? Pediatr-Dent. 22(|): 267-757,1998
4. What is dental age? How will you assess it? 15. Seow-WK: Effects of preterm birth on oral growth
5. What are the approximate heights of 2,5 and 10 and development Aust-Dent-J. 42(2): 85-91,1997
yea r old children?
 CE» I TEXTBOOK OF PEDODONTICS

15. Salzmann J A: Practice of Orthodontics JB crosomia and Nager syndrome. Acta-Odontol-

Lippincott compaly. 1966 Scand. 56(6): 331-8 1998
16. Sejrsen-B; JakQbsen-J; Skovgaard-LT; Kjaer-I: 19. Vinter-I; Krmpotic-Nemanic-J; Ivankovic-D;
Growth in the external cranial base evaluated on Jalsovec-D: The influence of the dentition on the
human dry skulls, using nerve canal openings as shape of the mandible. Coll-Antropol. 21(2): 555-
references. Acta-Odontol-Sea nd. 55(6): 356-64, 604997
1997 20. Wasserman E., Gromosch D.S.: Growth and de­
17. So-LL: Skeletal maturation of the hand and wrist velopment. Survey of clinical pediatrics. Me Graw
and its correlation with dental development Aust- Hill International company. 1-39,1981
Orthod-J. 15(1): 1-9,1997 21. Williams P.L.: Embryology and development.
18. Vargervik-K:Mandibular malformations: growth Gray’s Anatomy. 91,1995
characteristics and management in hemifacial mi­
 SECTION - 3

Developing Dentition and

its Disturbances
3.1 Development of Dentition
Tandon S, ShayamBhat

Introduction Stages of tooth evolution

The purpose of this chapter is to discuss the main Graphically there are four stages of tooth evolution.
course of the normal development of human denti­ i) The reptilian stage (Haplodont)
tion, together with the concept of evolution of tooth ii) Early mammalian stage (Triconodont)
development, clinical features of the dentition and iii) Triangular stage (Tritubercular molars)
the most common developmental disturbances. iv) Quadri tubercular molars
Knowledge of the normal development of the denti­
tion and an ability to detect deviation from the nor­ The Reptilian stage
mal are essential prerequisites for pedodontic diag­ This stage is represented by the simplest form of
nosis and a treatment plan. tooth, the single cone type. It includes many teeth
in both jaws which limit jaw movement. Thus the
Definition jaw movement is confined to that of a single hinge
movement.
■ Dentition means a set of teeth *

■ Teeth in the dental arch are used to designate the Early mammalian stage
natural teeth in position in their alveoli. This stage exhibits three cusps in the line of devel­
opment of the posterior teeth. The larger or anthro­
Evolutionary concept pologically original cusp is centered with one smaller
cusp located anteriorly and another posteriorly.
During evolution several significant changes took
place in the jaws and teeth. When the Reptilian . Tritubercular stage
evolved to mammalian, the dentition went from According to the recognized theories explaining evo­
“potyphydont” (many set of teeth) to “diphydont” lutionary tooth development, three triconodont limes
(only two sets of teeth) and then to "homodent” (all are changed to three cone shaped with the teeth still
of same teeth) to heterodent (different types of teeth by-passing each other more or less, when the jaw
like incisor, canines, premolars and molars). There opened or closed. These types are found in dogs
also arose a necessity for the teeth and bones to and other carnivorous animals.
develop somewhat synchronously in order that the
function of occlusion.could be facilitated. Finally, Quadritubercular stage:
the number of cranial and facial bones has been re­ The next stage of development created a prQ^|bM
duced by loss or fusion and the dental formula has on the triangular form that finally occlud^^^^^g
also undergone changes. antagonist of the opposingjaw Durii^^^^^n
 tfiïSB i TEXTBOOK OF PEDODONTICS

an accommodation to the changes in the tooth form Characteristic of human dentition

and anatomy, the articulation of the jaws changed
accordingly. Teeth of the vertebrates are characterized depending
upon:
The animals with dentition similar to that of humans ■ Mode of attachment
arc anthropoid apes. These include Chimpanzee, ■ Number of successive sets
Gibbon,Gorilla and Orangutan. The shapes of indi­ ■ Shape of teeth
vidual teeth in these animals are very close to their
counterparts in human mouth. Nevertheless, devel­ L The way teeth are attached to the jaws.
opment of canines, arch form and jaw development a) Acrodont: Teeth attached to the jaw by a con­
arc quite different. nective tissue.
b) Pleurodont: Teeth are set inside the jaws
Common evolutionary trends in the primates c) Thecodont: Teeth are inserted in a bony socket

1. There was shortening of the jaw due to the de­ II. Depending on the number of teeth of successive
crease in the size of the olfactory organs, upright sets.
body position and wide angle of the head to the a) Polyphyodont: Teeth replaced throughout the
body. life, eg. shark.
2. There was decrease in the tooth size to be accom­ b) Diphyodont: Two sets of teeth, eg. human be­
modated in these jaws, with subsequent elimina­ ing.
tion of some teeth from the dentition. c) Monophyodont: One set of teeth, eg. sheep,
3. There was progressive shortening of the arch (in goat.
front) and relative widening.
4. Canines reduced in size III. According to type or shape of teeth
5. Lower premolar crowns became more symmetri­ a) Homodont: A single type of teeth
cal from oval. b) Heterodont: Various types of teeth, eg. human
6. First molars became the dominant cheek teeth. being.
7. In the upper second and third molars, the
distolingual cusp reduced and often disappeared. Dental formula
8. Third molars, which were larger than the first
molars, were reduced in size and often eliminated. Original formula of mammals was:

In modern man: Permanent dentition: r

13/3, C 1/1, PM4/4, M 3/3 J 11 x2 = 44 teeth

■ There is a decrease in the tooth-bearing portion
of the face. This decrease is partly due to a reduc­ 11
tion in tooth size.
3 incisors, 1 canine, 4 premolars, 3 molars.
■ In some primitive and pre historic human skulls
the second permanent molars usually succeeds
Deciduous dentition:
the 1st molar.
12/2, C 1/1, M 2/2 5x2 = 20 teeth
« The occlusal length of the lower molars is reduced
in modern man and the ramus width is even more 11
reduced, less than the occlusal length of the lower
molars.
 SECTION 3 : DEVELOPING DENTITION AND ITS DISTURBANCES |

Pteient-dental formula: Teeth nuntber reduced in oro-denial development, involve a scries of interac­
tions not only between specific cell components, but
Permanent dentition: r also between the different varieties of cells which
2 1 2 3 8 arise during organization of the various tissues
c —-PM—. M —
/■ 2 1 2 3 8 The formation of the primitive oral cavhy or
stomatodcum and the perforation of the buccopha­
2 incisors, 1 canine, 2 premolars. 3 molars ryngeal membrane depend upon the contact between
the oral ectoderm and the pharyngeal ectoderm The
Deciduous dentition: r odontogenic epithelium is derived fiomthis ectoderm
1 2 5 It is believed that ectoderm, ecto-mesenchymc which
. ;Q C --- M 'S — is contributed by the primitive streak through the
2 1 2 5 notochord and adjacent tissue and the mesoderm
arc involved in tooth formation. The inductive dif­
ferentiation of the cell layers of a tooth germ results
Origin of teeth from both cciodcrmal-ectomesenchymal and
cctomcscnchymal - mesodermal interaçtioiis.
Theories: Each tooth whether primary or permanent
is believed to develop from theepithelial primary germ Prenatal development
cell: Varions theories regarding mammalian dentition
are reported. I n humans, odontogenic epithelium which is the all­
iage of the dentitions, can be identified in 28-30 day
!• The theory of concrescence: The mammalian den­ (ovulation age) embryo.
tition was produced by the fusion of two or more
primitive conical teeth and each tubercle with its 28-30 days The epithelium proliferates, giving the
corresponding root originated as a single tooth appearance of epithelial thickening
located on the i nferior border of the max-
2. Theory of tritubercul v: Each of the mammalian illary process and the superior borders
teeth was derived from a single reptilian tooth by ofthe mandibular arches in the area form­
a secondary differentiation bf tubercles and roots. ing the lateral margins of the stomato-
This theory is widely accepted. deum

3. Theory of multituberculy: The mammalian denti­ 30-32 days The odontogenic epithelium is 3-4 cell
tion is the result of reduction and condensation thick, the cells being ovoid to cuboid
of primitive tuberculate teeth. with little cytoplasm.

Tooth Development 32-34 days The mesenchyme immediately beneath

the odontogenic epithelium can be
In the developmental process specialized structures distinguished from the adjacent mesen­
such as teeth, differentiate as part of a closely inte­ chyme. The odontogenic epithelium
grated pattern of events. These progress from the becomes invaginated relative to the
initial genetic potential of the fertilized ovum to be underlying mesenchyme and a dental
influenced later by the prenatal and postnatal envi­ lamina from which individual tooth
ronment. The complex mechanisms, concerned with buds arise.
 i TEXTBOOK OF PEDODONTICS

4thweek The formation of dental lamina tion stages, namely bud, cap and bell stages. This
commences around and the tooth buds basic configuration of the future tooth crown is fixed
for the deciduous teeth begin to form at the morphological differentiation stage. The
about two weeks later. The dental lamina enamel organ produces the enamel by a process of
marks out the position of the future cell proliferation, cell differentiation and later miner­
dental arches. The tooth buds for the alization, and the dental papilla produces the dentin
corresponding permanent teeth develop and pulp of the tooth in a similar way. The dental sac
from the same arch. produces the cementum and the periodontal ligament.

Stages of tooth bud development (Fig. 3.1) Enamel formation ceases once the tooth crowns is
complete, but dentine formation continues with root
1» Initiation:
development. A layer of cementum is laid down on
« Phase of deciduous tooth - 5th month in utero
the surface of the root dentine, and incorporates peri­
« Phase of permanent tooth - 6th month
odontal fibers that support the tooth through its at­
■ Phase of accessional tooth - spaced from 4th
tachment to the bony wall of the tooth socket. Once
month in utero to 4-5 years
histo-differentiation of the cells has progressed suf­
2. Proliferation
ficiently far, mineralization commences. This occurs
3. Histo-differentiation
in the deciduous teeth during the 14th intrauterine
4. Morpho-ditferentiation
week on average and begins with the central inci­
5. Apposition
sors. The permanent tooth buds appear in the fourth
A tooth germ (tooth bud) consists of three parts: An and fifth intrauterine months, at about the same age
enamel organ, which is derived from the oral ectoderm, at which mineralization of the deciduous teeth com­
a dental papilla and a dental sac, both of the latter mences. Mineralization of the permanent teeth is
being derived from the mesenchyme. Each swelling initiated around the time of birth on average, begin­
of the lamina which is destined to be a tooth germ ning with the first permanent molar. Stages of tooth
proliferates and differentiates, passing through development as classified by Nolla»can be referred
various histological and morphological differentia­ from Fig. 3.2

A B DEF
Initiation Proliferation Morpho- Apposition (Before (After
(Bud stage) (Cap stage) differèntiation emergence) emergence)
Histo-
differentiation
(Bell stage)

| GROWTH CALCIFICATION ERUPTION

Fig. 3.1 Life cycle of tooth. (Sharawig, Bhusary 1990).

 SECTION 3 : DEVELOPING DENTITION AND ITS DISTURBANCES |

10 - Apical end of root completed.

9 - Root almost completed.

8 - 2/3 of root completed.

7 -1/3 of root completed.

6 - Crown completed.

5 - Crown almost completed.

4 - 2/3 of crown completed.

3 - 1/3 of crown completed.

2 - Initial calcification.

1 - Abscence of crypt.

Fig. 3.2 Stages of tooth development (NoIla 1952)

 d»> I TEXTBOOK OF PEDODONTICS

Chronology first dental tissue laid down to the emergence of tooth

into the oral cavity and its completion of calcifica­
An intimate relationship exists between tooth devel­
tion (completion of root formation).
opment and bone growth since teeth develop either
within a bony crypt or within a bony trough. Each Deciduous dentition
tooth passes through various progressive stages,
Originally chronology for dentition is based on the
continually evolved with a physiologic process in
data of Logan and Kronfeld reportéd in 1933. Later, a
which histoïogïc, biochemical changes are simulta­
careful review of the data was done by various re­
neously taking place. The stages of development
searchers like Massier and Shour in 1941, Moorrees
are growth, calcification, eruption, attrition,
and Fanning and Hunt 1963, Kraus and Jordan in
resorption and exfoliation.
1965, and Nystrom in 1977 etc.

Definition
ERUPTION STATUS OF DECIDUOUS TEETH IN IN­
Chronos - Time DIAN AND WHITE CHILDREN
Logos - Study
Initiation of hard tissue development for all decidu­
Therefore, chronology may be defined as the study ous teeth occurs between 3.5 and 4.5 intrauterine
which deals with the timings of the various stages of months. The crowns have been seen to get mineral­
tooth development, starting with the initiation of the ized about halfway by birth and become folly formed

Table 3.1: Eruption status of deciduous teeth in Indian and white children

MAXILLARY ARCH

Teeth South India Central India North India West Bengal Western
(Tandon 1998) (Kharbanda (Narinder (Mukerji, Country (C.
1988) et al, 2000) 1973) data 1964-84)

Male Female Male Female Male Female Male Female Male Female

Central Incisor 11-14 '10-14 10-14 10-14 9-11 9-11 10-12 10-13 7-9 9-12 i
Lateral Incisor 12-15 14-16 12-16 14-18 11-14 11-14 11-14 12-15 8-11 12-14
Canine 19-24 22-24 20-24 24-26 20-24 20-24 19-24 19-24 17-20 20-24
First molar 18-20 16-20 18-21 18-24 13-19 13-19 16-18 16-19 15-20 16-28
Second molar 28-36 26-32 26-32 20-36 20-30 20-30 29-32 29-32 23-36 30-32

MANDIBULAR ARCH

Central Incisor 10-12 10-12 10-12 10-13 7-9 7-9 10-12 10-13 7-9 6-6
Lateral Incisor 12-14 11-14 10-14 12-16 10-14 10-14 14-18 15-20 8-11 14-15
Canine 20-24 20-24 18-24 24-26 20-24 20-24 20-24 20-24 16-19 20-24
First molar 18-20 18-20 16-18 18-12 15-19 15-19 10-18 16-18 15-20 15-16
Second molar 26-30 26-32 26-32 26-32 20-30 20-30 29-32 29-32 20-26 30-32
 SECTION 3 : DEVELOPING DENTITION AND ITS DISTURBANCES | CD

during first 12 months of postnatal life. Root forma­ relatively rapid under normal function, increases
tion continues and is completed after eruption, be­ whenever the velocity of the wear increases or
tween the ages of 1.5 and 3 years (for complete chro­ when the antagonist tooth is removed. Examples
nology, refer table 3.1). (Fig. 3.3) of these teeth are the incisors of rodents and
lyomorphs.
Root completion Root completion
ii) Continuously extruding: Teeth stop forming once
root formation is complete. These teeth have a
1 year 3 years well-defined anatomic crowns and root and are
usually associated with moderate occlusal wear.
The height of the clinical crown is maintained by
Eruption Eruption
eruption of the tooth and apical migration of the
surrounding epithelial attachment, without simul­
Canines
taneous deposition of the alveolar bone. As oc­
and 6-12 months 3 years
clusal wear progresses, the tooth eventually loos­
incisors 4-6 months ens and exfoliates completely from its alveolar
housing. Examples are the check teeth of cattle
Crown completion Crown completion
and sheep.

Time requirement for - Time requirement for

iii) Continuously invested teeth: Human teeth belong
development of priman7 development of perma­
to this type of eruption. These teeth also stop
teeth. nent teeth.
forming after a predictable amount of root devel­
Fig. 3.3 Timing of Crown and Root Development opment has occurred and have distinct anatomic
crown and root structures, but the alveolar bone
Clinical eruption. Eruption is derived from the Latin remodels in response to eruption. With normal
word erumpere’ i.e., to break through. It is defined, attrition in the absence of periodontal disease,
as the movement of the tooth from its position within the clinical crown shortens as the tooth erupts to
the jaws to its functional position in an occlusal plane, maintain vertical height and occlusal function and
in vertical/axial direction. Tooth eruption is intimately brings the alveolar bone with it.
associated with normal dentofacial growth and oc­
clusal development, and the knowledge of eruption Stages of human tooth eruption
is essential for a clinician to diagnose a dental prob­
lem correctly, to plan his treatment successfully. Human tooth eruption occurs in two major stages
which can be further divided into six phases.
Types of eruption
1. Pre-emergence eruption:
Three distinct types of teeth are differentiated by During the early part of tooth formation, called
their eruption pattern: the follicular phase of eruption, the follicle en­
larges concentrically in eveiy direction. It may
i) Continuously growing: Tooth formation ana erup­ slightly move facially within the alveolar bone,
tion occur throughout the life. The dental tis­ but there is little or no eruptive movement. The
sues are formed from a proliferative base, and the tooth starts to enipt, and the pre-emergent spurt
anatomic crown and root are very similar mor­ phase of eruption begins, when crown formation
phologically. Typically, these teeth have exten­ is complete and root development starts.
sive wear. The eruption velocity, which is
 I TEXTBOOK OF PEDODONTICS

Theories of eruption: Vascular pressure has long been considered a lead­

■ Root growth theory ing possibility but the pre-emergent eruption
■ Constriction of pulp mechanism remains an enigma.
« Pulp growth
■ Bone growth 2. Post emergent eruption
« Tissue fluid pressure ■ The post-emergent stage of eruption begins
■ Shrinkage of collagen with the prefunctional eruptive spurt, as the
tooth emerges through the gingiva and moves
For a tooth to erupt intra-osseously, following into occlusal contact with its antimere. During
two factors are necessary: this phase, a tooth typically erupts about 4
■ The overlying tissue (bone, primary tooth root, nun in 14 weeks.
and gingiva) must resorb to provide an erup­ ■ The juvenile occlusal equilibrium, circump-
tive path, and ubertal eruptive spurt and adult occlusal equi­
■ A force must be generated to move the tooth librium phases that follow are characterized by
vertically. Resorption over the tooth seems to a slower velocity of eruption.
be dependentonly on the presence of the coro­ ■ After the teeth are in function, they continue
nal portion of the dental follicle. to erupt at the same rate as vertical growth of
the jaws unless there is occlusal wear or loss
The timing and development of the eruption path­ at the opposing tooth, in which case additional
way is independent of eruption pressure or even eruption occurs.
the presence of a developing tooth. ■ Throughout the post-emergent stage of erup­
tion the PDL seems to be the major contributor
Recent studies show that resorptive process may to the eruptive force. The principal fibers are
be regulated by local growth factors such as trans­ now well oriented and attached firmly to the
forming growth factor beta 1 (TGF-B1 ) and epi­ alveolar bone.
dermal growth factor (EGF) produced within or « The primary eruption mechanism is thought to
around the dental follicle. These growth factors be either contraction of collagen As it matures
seem to chemoattract monocytes from the periph­ or (less likely) traction from contractile
eral blood vessels around the dental follicles. The fibroblasts.
resorptive process begins with the formation of ■ Vascular effects similar to pre-emergent erup­
osteoclasts from the coalescence of the tion may also contribute.
monocytes.
It seems reasonable to presume that forces op­
How the eruptive force is generated in the pre- posing the eruption mechanism control post-emer­
emergent stage remains unclear. Although meta­ gent eruption, analogues to the control of pre-
bolic activity within the PDL probably plays an emergent eruption by the resorption mechanism.
important part, it is unlikely to be a source of the There are two points of evidence to support this
pre-emergent eruptive force, because the major­ view:
ity of the principal periodontal fibers are sparsely i) in continuously erupting rodent incisors, the
formed and incompletely linked with the alveolar rate of eruption slows as an erupting tooth
bone at this stage. comes into function and
ii) in teeth of all types, if the opposing tooth is
Deposition of the bone beneath the erupting tooth removed, eruption occurs at a faster rate. Hu­
is associated with eruption, but this seems to be man teeth wilt erupt beyond their normal posi­
a result of eruption rather than its cause. tion if the antagonist is removed.
 SECTION 3 : DEVELOPING DENTITION AND ITS DISTURBANCES |

Eruption rhythm post-emergent eruption almost surely reflects a

rhythm in PDL activity7. The cellular activities of
The circadian rhythm, in eruption is potentially sig­ periodontal fibroblasts have a periodicity similar
nificant in clinical practice. Studies indicate that cir­ to eruption and orthodontic movements are also
cadian rhythm exists during the pre-functional stage related to cellular activity in PDL. Therefore, at
of eruption of human teeth. The teeth intrude the time of treatment planning clinician should
transiently in conjunction with masticatory activity explore fully this periodicity ofperiodontal cellu­
and then erupt significantly overnight. The mean lar activity for the control of pain and hyaliniza-
daily eruption velocity was seen to be 71pm/day. It tion or undermined resorption.
is also believed that the effect on eruption of a su­
pine position versus an upright position during the Teething
night could be due to a change in intra-oral pressure
against the erupting tooth from either resting soft Teething is a term limited by common usage to erup­
tissue pressure (cheek and tongue) or functional tion of primary dentition. Since the time of
intraoral pressures (e.g. swallowing). Hippocrates (460-377 BC) teething is blamed for ail­
ments such as fever; convulsions, bronchitis, otitis
CLINICAL SIGNIFICANCE OF ERUPTION RHYTHM media and diarrhea for causing 12% of the death in
children under four years. Complete opposite views
i) Timing of eruption - controlling intervention. Ex­ are also available. It is seen that these local and
cessive eruption of the posterior teeth is a major systemic factors are associated with the disease
characteristic ofthe long face, and control of erup­ somewhere also and just as a coincidence appear
tion during growth seems to be the key to suc­ with teething.
cessful treatment. The amount of force, its direc­
tion, and the total hours of wear of the appliance Eruption of primary dentition usually begins in the
often are consideredthe most important clinical fifth or sixth month ofa child’s life. The appearance
factors that affect treatment outcome. If teeth of normal teeth is eagerly awaited by the parents
erupt primarily during the night with little or no since it represents an important early milestone in
net eruption during the day, it is quite possible development. In mosteases eruption of teeth causes
that wearing an appliance (functional appliance, no distress to the child or parents but sometimes the
bite blocks^ high pull head gear etc) is effective process causes local irritation, which is usually mi­
during the night and early morning period when nor but which may be fewer enough to interfere with
the Eruption is most active is sufficient. the child’s sleep.

ii) Daily rhythm in skeletal growth: Ample evidence CONICAL FEATURES OF TEETHING
demonstrates the skeletal growth requires an ad­
equate level of HGH which increases in the night. Local signs:
The rhythm in tooth eruption also reflects this ■ Hyperemia or swelling of the mucosa overlying
increase soon after the child goes to sleep. The the erupting teeth.
clinician should be aware that there is a rhythm in ■ Patches of erythema on the cheeks
skeletal growth and modification of treatment may ■ Flushing may also occur in the skin of the adja­
be more effective at the night than during the day. cent cheek.

iii) Effect of tooth movement more generally: Be­ Systemic signs:

cause eruption depends on metabolic activity ■ General irritability and crying
within the PDL, the rhythmicity associated with « Loss of appetite
 CEB I TEXTBOOK OF PEDODONTICS

■ Sleeplessness, restlessness Resorption of the deciduous incisors takes place

■ 1 ncreased salivation and drooling more rapidly (lasting 1.5-2 years on average) than
■ Insanity that of the canines and molars (2.5 - 5.7 years). The
■ Meningitis permanent successor may be visible immediately af­
■ Increased thirst ter exfoliation of a deciduous tooth, or there may be
■ Circumoral rash a latent period of 0.1 to 0.5 years before the perma­
• Cough nent successor erupts. The resorption process is
not continuous, but is interrupted by periods of rest
Associated problems: and periods of repair. This intermittent resorption
and repair explains the variation in mobility of the
Svstemic: deciduous teeth prior to exfoliation.
« Fever
■ Convulsions Premature loss of deciduous tooth has been found
■ Diarrhea to accelerate the clinical eruption of the subsequent
• Vomiting permanent tooth if the deciduous tooth is lost shortly
a Bronchitis before normal tooth exfoliation time i.e., 1-2 years
■ Cholera before, whereas there is evidence both for and against
« Tetanus a retarding effect in the case of very early tooth loss
■ Infantile paralysis e. , 2-5 years before exfoliation. The explanation for
i.
this is that the dense fibrous connective tissue which
Local: forms in place of the extracted deciduous may hinder
■ Eruption hematoma the eruption of its permanent successor.
« Erupt sequestrum
■ Ectopic eruption Permanent teeth
■ Transmigration
« Transposition Mineralization of the first permanent molar com­
mences at birth on average, and is fallowed by the
Exfoliation other teeth (except third molars) in a given order
during the first 3.5 years of postnatal life.
The physiologic process resulting in the elimination
■ The crown completion takes place at an age of
of deciduous dentition is called exfoliation or shed­
about 7 vears.
ding. This shedding or exfoliation is due to progres­
■ Mineralization ceases at an average age of 15-16
sive resorption of the roots of the deciduous teeth
years with the completion of the roots of the sec­
and their supporting tissue, the periodontal ligament.
ond molars.
In general, the pressure generated by the growing
■ The respective mineralization stages for the third
and erupting permanent tooth dictates the pattern of
molar are:
deciduous tooth resorption.
1. initiative at about 9 years
The first sign of root resorption is seen in the de­ 2. crown completion at about 13 years
ciduous medial incisors and the first molars by the 3. root formation is completed arouod-2t) years
age of 4-5 years. Resorption of the incisors begins 4. chronology of permanentteeth is presented in
primarily on the lingual side with horizontal resorp­ table (refer table 3a&b in appendix).
tion of the apical parts commencing at a la ter sta ge. ■ The process from the initiation of crown minerali­
Root resorption in the deciduous molars starts from zation to the closure of the root apex, takes from 8
the inner surfaces of the developing permanent tooth to 14 years.
germ.
 SECTION 3 : DEVELOPING DENTITION AND ITS DISTURBANCES |

■ The development of the medial incisors is more monarch are best suited for the determination of the
rapid and that of the canines and second molars biological developmental stage of the individual, as
the slowest. they display the least variation.
■ Root development alone takes on average from 6
to 7 years. Estimation of dental age
■ The mandibular teeth develop earlier than maxil­
lary teeth. Different methods for the assessment of dental age
■ A marked difference has been seen in tooth min­ have been introduced.
eralization, girls being ahead of half a year on 1. Number of teeth erupted in the oral cavity or the
average, except in the case of the third molars. last tooth erupted. This method is rather rough,
■ The sex difference increases witli age and towards however, as individual variations in eruption age
the later formation stages. are extensive and endogenic and local factors may
■ Tooth eruption begins upon the completion of affect tooth eruption.
crown formation and/or the beginning of root for­ 2. Tooth formation stage of every tooth or of only
mation. 4-5 selected teeth may be recorded from a radio­
■ At the time of clinical eruption, root formation is graph, preferably orthopantamograph and corre­
approximately three quarter complete. sponding age for each child. The tooth formation
« There is always variations can be seen in the se­ age of the child is then obtained by calculating
quence of eruption, the most frequent order is the mean of the age estimates for the defined tooth
mentioned in detail in section 3.3 formation stage. The four teeth recommended
for this purpose:
Dental age a) from birth to 9 years: teeth 46,44,43,11
b) from I (» years onwards: teeth47,44,43,13
Dental age has been used for centuries as a param­
eter for expressing biological maturity. It is of par­ A tooth cannot be used, however, once it reaches
ticular interest to the pedodontists and orthodon­ full maturity (the apex closed stage) as it no longer
tists in planning of different types of malocclusions gives any developmental information. Choice ofthe
in relation to maxillo-facial growth. It also plays a teeth from the left side or rigid side does not make
great role in forensic odontology and pediatric en­ any difference.
docrinopathies.
FACTORS AFFECTING DEVELOPMENT OF
Dental age is estimated by comparing the dental de­ DENTITION:
velopment status in a person of unknown age with
published dental developmental surveys. A. Systemic factors:
An accelerating effect: on the whole dentition is
The dental age of an individual as defined from the very rare, but lias been reported to be due to:
radiographically observable tooth mineralization ■ Hyperthyroidism
stages, is a good index and can serve as one index of « Hyper pitutarism
biological age, having certain advantages over many ■ Turner’s syndrome
other such indices. Tooth formation can be defined
throughout the growth period from birth to adoles­ A retarding effect: Delayed eruption in both the
cence, and tooth formation is less responsive to both primary dentition and permanent dentition, but
nutritional modification and hormonal disturbances more especially in the later has been attributed to
than many other developing tissues in the body. many diseases, syndromes and systemic factors,
Krogman believed that tooth formation age and the the most common are:
 <!ÏîB I TEXTBOOK OF PEDODONTICS

Hypopitutarism ■ Supernumerary tooth

■ Hypothyroidism ■ Tumor
■ Cleidocranial dysostosis ■ Cyst
■ Downs syndrome ■ Abnormal habit exerting muscular forces
■ Achondroplasia
« Hypovitaminosis (A and D) S elf-Assessment
• Amelogenesis imperfecta
■ Osteopetrosis 1. Classify developmental dentition periods.
2. What is natal and neonatal teeth?
B. Local factors: Some local factors which may in­ 3. What are the important considerations to be kept
fluence the developing dentition are while removing natal or neonatal teeth?
■ Aberrant tooth position 4. What is teething?
■ Lack of space in the arch
5. What is the chronology of deciduous and perma­
i Very early loss of predecessor
nent dentition?
« Ectopic eruption
6. At what age maximum number of teeth are present?
■ Congenital absence of teeth
7. How does exfoliation take place?
« Ankylosis of predecessor
8. Name few associated local problems to teething.
■ Retained tooth or persisting deciduous root
9. What are the causes of delayed eruption?
remnants
• Arrested tooth formation (trauma) 10. What do you understand by dental age and how
will you assess it?
 3.2 Common Developmental Disturbances
of teeth
Shyam Bhat, Tandon S

COMMON DEVELOPMENTAL DISTURBANCES in the permanent dentition than in the deciduous

OFTEETH dentition. Heredity is believed to be most frequent
cause of these developmental disturbances. Com­
Developmental disturbances in tooth eruption age, monly occuring disturbances are discussed in table
size, shape, number and position are more comfhon 3.2to3.5

Table 3.2: Common Developmental Disturbances of Teeth

Developmental Alteration of Number

Hypqdontia Hyperdontia (Fig. 3.4a, b)

Definition The developmental absence of multiple An excess number of teeth when

teeth usually in association with systemic compared to the normal dental
manifestations (Stewart 1982). formula.

Etiology Autosomal dominant with incomplete Recessive, autosomal or sex

penetrance. linked.
Trauma, infection of the developing ■ Cleft lip and palate 28%
tooth bud, radiation overdose, ■ Cleidocranial dysplasia
glandular dysfunction, systemic ■ Gardiner’s syndrome
conditions such’ as rickets or syphilis, Continued activity of the dental
German measles during pregnancy lamina after the formation of the
and severe intrauterine disturbances. normal number of tooth buds,
Absence of appropriate dental lamina. or result from complete division
of an early developing bud.

Clinical Missing tooth: primary or permanent: Rudimentary or may be of normal

features Other abnormalities include fusion, size.
ankylosis and short roots. Erupted or impacted. May cause
Syndromes: hereditary ectodermal displacement of adjacent teeth.
dysplasia. Types include mesiodens,
supplemental tooth, para molar
and disto molar.

Treatment Orthodontic closure of the space or a Surgical removal

prosthesis can be given. . Orthodontic alignment if needed.
Control of caries.
Crown recontouring. II
1i j
CEB I TEXTBOOK OF PEDODONTICS

Fig. 3.4a Palatally erupting supplemental teeth causing crowding.

Fig. 3.4b Labially erupting supplemental tooth.

Fig. 3.5 Microdontia involving single tooth (Right maxillary central incisor)
 SECTION 3 : DEVELOPING DENTITION AND ITS DISTURBANCES |

Table 3.3: Developmental alteration in the size of teeth

Microdontia (Fig. 3.5) Macrodontia

Description Teeth smaller than normal. Teeth larger than normal.

Classification ■ True generalized microdontia. All • True generalized macrodontia.

teeth are smaller than normal. « All teeth are larger than normal.
■ Relative generalized microdontia. « Relative generalized macro­
Normal or slightly smaller than dontia. Here normal or slightly
normal. Teeth are present in jaws larger than normal teeth are
that are somewhat larger than normal. present in smaller jaws.
■ Microdontia affecting a single tooth. ■ Macrodontia affecting a single
This is a rather common condition tooth. This is occasionally seen
most often affecting the maxillary and is of unknown etiology.
lateral incisor and the third molar.

Treatment No specific treatment is indicated for No specific treatment is indicated

this condition. for this condition.

Table 3.4: Developmental alteration of shape

Anomalies Definition Etiology Clinical features Treatment

Gemination Gemination can A single tooth bud The normal no. of Close monitoring
be defined as divides resulting in teeth may be
counting the bifid the formation of present in the arch.
crown as one tooth with the bifid The tooth has two
tooth, the normal crown and a crowns but only
no. of teeth are common root and one root canal.
present and the root canal.
anomalous tooth
has probably only
one root canal.
(Levitas 1965)

Fusion Fusion can be Union of two Two crowns Surgical division

defined as an normally reported joined by enamel and selected
incomplete tooth buds with the or dentin but two shaping of
attempt of two resultant formation separate roots crown have been
tooth buds to of a joined tooth or root canals. tried.
fuse into one. with confluence of May either be
dentin: Some complete or
physical force or incomplete.
pressure is thou­
ght to produce
contact between the
developing teeth &
their subsequent
fusion.
contd.
<îtïï> I TEXTBOOK OF PEDODONTICS

Anomalies Definition Etiology Clinical features Treatment

Concres­ A form of fusion Traumatic injury or Radiographically No therapy unless
cence which occurs after crowding of teeth it can be seen the union
root formation, with resorption of that the roots of interferes
has been£ _ the interdental bone two adjacent with eruption when
completed. so that the two teeth are fused surgical removal
roots are in appro­ by cementum of the tooth can
priate contact and whereas crowns be considered.
become fused by are separate.
the deposition
of the cementum.

Dens A tubercle or May be due to the The tubercle of Removal of

evaginatus protuberance proliferation and dens, evaginatus enamel of the
from the involved évagination of part appears as a tubercel and
surface of the of the inner enamel pronounced placement of
affected tooth. epithelium into the elevation on the calcium hydroxide
stellate reticulum occlusal surface of dressing to
of the enamel organ the posterior teeth stimulate the
during development. and may occur in odontoblasts to
Continued tooth the form of a drop, produce reparative
development a pointed or dentin. If the dens
creates a tubercle cylindrical cone. invaginatus
of enamel and In anterior teeth a becomes pulpally
dentin containing conically shaped involved endo­
a horn of pulp extension of the dontic procedures
tissue. cingulum is is the treatment of
observed. choice.

Talons cusp The talons cusp Talons cusp occurs Appears as an If the talons cusp
(Fig. 3.6) is an uncommon during the morpho- additonal cusp interferes with
dental anomaly differentiation stage that prominently occlusion then it
referring to an of tooth develop­ projects from the should be
accessory cusp ment It may occur palatal surface of removed by
like structure as an outward a primary or periodic grinding
projecting from the folding of inner permanent anterior of the cusp. If
cingulum area or enamel epithelial tooth and extends deep fissures are
cementoenamel cells and transient at least half present between
junction of the focal hyperplasia distance from the the cusp and tooth
maxillary or of the peripheral cementoenamel then it should be
mandibular cells of the junction to the sealed using pit
anterior teeth. mesenchymal incisal edge. and fissure
dental papilla. Some talon cusps sealant.
are quite sharp
and spike like,
while others have
rounded and
smooth tips.
contd.
 SECTION 3 : DEVELOPING DENTITION AND ITS DISTURBANCES | <!?!>

Fig. 3.6 Talon’s cusp present on right

maxillary lateral incisor’ Fig. 3.7 Ra raph showing
taurodontism.

Fig. 3.8a Types of amelogenesis imperfecta. Fig. 3.8b Hypomaturation amelogenesis

Hypoplastic amelogenesis imperfecta. imperfecta.

Fig. 3.9 Dentinogenesis imperfecta showing severe attrition.

<ft>4 i TEXTBOOK OF PEDODONTICS

Anomalies Definition Etiology Clinical features Treatment

Taurodon- Taurodontism is Genetically or The third molars No special therapy
ttsm the enlargement hereditary most affected is required for
(Fig. 3.7) of the body and transmitted. Error in unilateral or such a tooth.
pulp chamber of a the function of the bilateral single
multi rooted tooth Hertwig's epithelial tooth or at other-
with apical dis­ root sheath. The times several
placement of the epithelial sheath molars. A taurodont
pulpal floor and begins to form has a long body I
bifurcation of the from the cervical with short roots:
roots. Neville ring. This tends to the pulp chamber
1994. limit the pulp is elongated in the-
mesenchymal apico-occlusal
tissue by an apical direction and lacks
diaphragm. constriction at the
cervix.

Dilacera­ Abnormal An injury that The most frequent Grossly deformed

tion angulation or displaces the involved teeth are teeth require
bend in the root calcified portion of the permanent surgical removal.
or less frequently the tooth germ and maxillary incisors,
the crown of a the remainder of the followed by the
tooth. tooth is formed at mandibular
an abnormal angle. anterior dentition.
Secondary to the The abnormal
presence of an angulation may be
adjacent cyst, tumor, present anywhere
or odontogenic along the length i

hamartoma. of the tooth.

--------------------------- i----------------------------------

Table 3.5: Developmental alteration of structure.

Anomaly & I
I

classificat­ Definition Etiology Clinical features Treatment

ion
Amelogene- Amelogenesis Gene mutations in ■ Hypoplastic « For poor esthe­
sis imperfe­ imperfecta is a the enamel matrix The teeth lack tics: Primary
cta (3.8a,b) group of here­ produces one of the normal enamel teeth restored
Type I ditary disorder following results: thickness. with glass
IA - hypopl­ characterized by Hypoplasia Inadequate ionomer cement
astic pitted alteration of the Hypocalcification deposition of and composite
autosomal quantity and Hypo maturation enamel matrix. veneer
dominant quality of enamel isolated defect The enamel may ■ Dentinal
IB - hypopl­ in humans and with autosomal be pitted, have sensitivity: Full
astic local is frequently dominant horizontal or coverage with
autosomal associated with a autosomal vertical ridges. stainless steel
dominant significant dental recessive and ■ Hypomaturation crowns.
IC - hypopl­ disease as stated x-linked inheritance Normal ■ Dental caries:
astic local by Witkop and also occur. deposition of Dietary advice,
autosomal Sauk 1976. enamel matrix fluonde therapy,
_ . . ii________ ___________ I
contd
 SECTION 3 : DEVELOPING DENTITION AND ITS DISTURBANCES |

1 »
i

Anomaly & 1
classificat­ Definition Etiology Clinical features Treatment |
I
ion
recessive Defective crystal glass ionomer
ID 7 hypopl- structure miner­ and composite
astic alisation. The affe­ restorations,
smooth cted teeth show stainless steel
dominant. mottled, opaque crowns.
IE - hypopl­ white brown ■ Gingival
astic yellow discolora­ inflammation
x-linked tion. The enamel Increased
dominant is softer than preventive
IF - hypopl­ normal & tends oral health
astic to chip from the care practices.
rough underlying dentin
autosomal • Hypocalcified
dominant Enamel matrix i
IG - Enamel is laid down
agenesis, appropriately
autosomal but no signi-
recessive cant minerali­
Type 11 zation occurs.
11A - hypom­ Enamel is
aturation, orange yellow at
pigmented eruption and
autosomal consists of
recessive poorly calcified
IIB - hypom­ matrix, which is
aturation, rapidly lost
x linked leaving dentin
recessive cores.
IIC - snow « Hypomaturation
capped hypoplastic with
teeth X taurodontism.
linked The enamel is
HD - snow mottled yellow ~
capped brown; thin with
F teeth, 'S
areas of hypomat-
autosomal uration.Molar teeth
j dominant. have a taurodont
Type HI shape and other
fitA - auto- teeth may have
\ somal enlarged ptrip
dominant champers enamel
j IIIB- auto- hypoplasia in
; somal combination with
recessive hypomaturation.
Type IV
IV A- hypom­
aturation

contd.
CED I TEXTBOOK OF PEDODONTICS

Anomaly &
classificat­ Definition Etiology Clinical features Treatment
ion
hypoplastic
with tauro-
dontism,
autosomal
dominant
IVB - hypo­
plastic
hypomatu­
ration with
taurodont-
ism. auto­
somal
dominant
■. ........................ I__________
j

Dentinogenesis imperfecta (Fig 3.9)

Typel Dentinogenesis Genetically « All the teeth in The entire dentit­

Autosomal imperfecta is a inherited both the dentit­ ion is at risk
dominant hereditary develo­ disease. ions are affected. because of the
Freq. 1 in pmental disturba­ Autosomal The deciduous numerous
8-10,000 nce of the dentin dominant teeth are affected problems. The
Type II that may be seen most severely root canals
Autosomal alone or in conju­ followed by the Kbecome thread like.
dominant nction with the permanent Overlay dentures
Freq. 1 in systemic heredi­ ■ The dentitions placed on teeth
1,25,000 tary disorder have a blue to that ate covered
Type III of the bone, brown discolor­ with fluoride
Autosomal osteogenesis ation, often with releasing glass
dominant imperfecta. a distinctive ionomer cement
Freq. 1 in translucence. Preventive
3,00,000 ■ Enamel measures ought
Type IV frequently to be undertaken
Autosomal separates from at the earliest.
recessive the underlying
Frequency defective dentin.
unknown ■ The pulps are
usually
obliterated by
excess dentin
produciton.

contd.
 SECTION 3 : DEVELOPING DENTITION AND ITS DISTURBANCES | tfBEl

Anomaly &
classificat­ Definition Etiology Clinical features Treatment
ion
Regional odontodysplasia (Ghost teeth)

Regionaf " Etiological factors ■ These teeth are

odontodysplasia suggested include typically discol­
is a localized a somatic mutation ored yellow,
disorder of the affecting the dental yellowish-brown
tissues of dental lamina in the area, or brown.
origin resulting activation of latent ■ The enamel of
in characteristic­ viruses, local both the primary
ally bizarre circulatory disorders, and permanent
clinical and radio- pharmaco-therapy teeth has been
raphic during pregnancy, reported to be ■

appearances. neural disorders, soft on probing.

Rh incompatibi­ ■ Rough surface
lity or failure of texture.
migration and ■ Teeth affected
differentiation of include perman­
neural crest cells. ent anterior
teeth.
■ Maxilla is pre­
dominantly
involved than the
mandible.
« Occlusion,
drifting and over­
eruption of
adjacent or
opposing teeth
may be found
where affected
teeth have failed
to erupt. •
* 4
Self-Assessment

1. Wha t is the difference between fusion and concrescence?

2 What are ghost teeth?
3. What is the difference between Amelogenesis imperfecta and Dentinogenesis imperfecta.?
4. What is gemination?
5. . Classify microdontia,
6. What is the etiology of Talon Cusp?
7. What are the clinical features of Taurodontism?
8. What treatment is suggested for Dilaceration?
 3.3 Development of Occlusion

Tandon S

Introduction Periods of occlusal development

Development of occlusion is a genetically and envi­ The occlusion of the teeth may be divided into the
ronmentally conditioned process which shows a following developmental periods.
great deal of individual variations, and consequently, 1. Predental jaw relationship (Neonate’s mouth)
for the development of an acceptable occlusion, 2. The deciduous dentition
quite a remarkable co-ordination of different events 3. The mixed (transitional) dentition
is necessary. Failure in one part of the developmen­ 4. The permanent dentition
tal process may lead to anomalies, or else may be
compensated for by other developmental process. PREDENTATE PERIOD

In order to facilitate the understanding and compre­ Predentate refers to the period from birth to the erup­
hension of the developmental process in the face, a tion of the first deciduous teeth in the oral cavity. At
three-dimensional structure, this chapter is an attempt birth the alveolar arches, also called gum pads, are
to concentrate mainly on clinical features of devel­ horseshoe shaped in the maxilla and V-shaped in the
oping dentition and establishment of their relation­ mandible. They are firm and pink in colour. These
ship, because, the ultimate goal of the pediatric den­ gum pads develop in two parts.
tist is to develop a perfect and healthy occlusion in ■ Labial portion (differentiates first)
the permanent dentition by guiding the developing ■ Lingual portion (differentiates later)
occlusion.
These two portions are separated from each other by
The term occlusion is derived from the Latin word,
a dental groove which is the site of origin of the
“occlusio” defined as the relationship between all
dental lamina. (Refer chapter 2.2 pedologic anatomy
the components of the masticatory system in normal
for details)
function, dysfunction and parafunction. An ideal
occlusion is the perfect interdigitation at the upper
Longitudinal observations on occlusal development
and lower teeth, which is a result of developmental
suggest that the oral structural features of the new­
process consisting of the main three events, jaw
born child do not seem to provide a reliable basis for
growth, tooth formation and eruption.
predicting the interaction between the teeth. At birth
Although the interrelation between the teeth essen­ distal relationship of the mandible to the maxilla makes
tially becomes established in childhood, it continues for this difference in the course of the first 3 -4 months.
to change to some extent throughout life. Thus the The greater the anteroposterior dimension of the
occlusion is regarded as a dynamic rather than a static gumpads, the greater the possibility of the child de­
interrelation between the facial structures. veloping malocclusion.
 SECTION 3 : DEVELOPING DENTITION AND ITS DISTURBANCES |

Precociously erupted teeth: Sometimes an infant The maxillary central mcisors erupt at 9 months of
may be born with teeth which are precociously age with spaces between them followed by the lateral
erupted. If these teeth emerge before the first three mcisors at the age of 1 year. By 1 to 1 1/2 years, the
months of life, they are classified as premature teeth. first molars enipt, resulting in a vertically supported
Those that are present at birth, are called natal teeth, occlusal contact between the two arches. The man­
those that erupt during the neonatal period, from dibular canines erupt at 16 months and themaxillaiy
birth to 30 days are designated neonatal teeth. Al­ canines follow at around 18 months. By the age of 2
most 90% of these precociously erupted teeth are 1/2 months to 3 years the full compliment of decidu­
primary teeth of which 85% are mandibular incisors ous dentition is present.
and 10% are supernumerary calcified structures fre­
quently, referred to as predeciduous teeth. Natal During the first year of life the infant does not seem
teeth appear more frequently than neonatal teeth (Fig. to have a definite centric occlusal relationship or rest
3.10). position of the mandible. There is a limited anterio­
posterior movement of the mandible but no lateral
Etiology of neonatal and natal teeth: Superficial po­ movements. With the beginning of deciduous inci­
sition of tooth germ, increased rate of eruption due sors eruption the alveolar mucosa presents an ap­
to febrile incidents, hormonal stimulation and hered­ pearance of having receded on the erupting teeth.
ity. Eruption could be dependent on osteoclastic ac­ The primary incisors erupt into the anterior space of
tivity within area of the tooth germ. the gum pads, thus accounting for the apparent
ovcrbitc. This overbite (usually in incisor region)
Association with syndromes: These teeth are report­ gets reduced as the posterior deciduous teeth come
edly associated with syndromes like chondroecto- into occlusion.
dermal dysplasia, Hallermann-StrcifT syndrome and
pachyonychia congenita, Ellisuan Creveland and, Clinical features of deciduous dentition
Rigafede syndrome.
1. General characteristics
Incidence: The incidence of natal and neonatal teeth ■ Both the dental arches are half round in shape
has been estimated to be 1:1000 and 1:30000. It is or ovoid
seen that 85% of natal or neonatal teeth arc man­ « Almost no curve of spee is present
dibular incisors, 11% are maxillary incisors, 3% man­ ■ Shallow cuspal interdigitation
dibular cuspids or molars and only 1% are maxillaiy ■ Slight overjet and overbite
cuspids or molars. ■ Vertical inclination of the incisors
■ Little or no crowding
DECIDUOUS ORPRIMARYbENTITION
2. Spacing: Two types of dentition are
At birth, the dental arches are small with a subse­ A Spaced dentition
quent crowding of tooth germs which are within the Spaced dentition is supposed to be good as
jaw bone. This is overcome by increased jaw growth spaces inbetween the teeth can be utilized for
and the buccal placement of tooth germs. adjustment ofpermanent successors which are
always larger in size compared to the decidu­
The mandibular incisors are the first teeth to erupt ous teeth. These spaces present are of two
into the oral cavity around six months after birth. types:
■ Primate spaces (Fig. 3.11 and 3.13a):
During this period there is increased anterior posi­ These spaces are very prominent spaces
tioning of the lowerjaw with relation to the upperjaw. 1 present in the primate species in
CT>F> I TEXTBOOK OF PEDODONTICS

Fig. 3.10 Mandibular arch showing natal tooth

Fig. 3.11 Primate space and deciduous first molars in mesial step relation

Fig. 3.12 5 year old child showing physiolgoic spaces in upper and lower dentition
 SECTION 3 : DEVELOPING DENTITION AND ITS DISTURBANCES |

Fig. 3.13a Mesial step

Fig. 3.13b Distal step Fig. 3.13c Flush terminal plane

Fig. 3.13a,b,c Mesial step (44%), Distal step (04%), Flush terminal (52%), (Tancfon, Sajid 2000)

human they exist between the upper lateral be due to the narrowness of the dental arches
incisors and the canines (present mesial to or teeth are wider than usual. This type of den­
maxillary deciduous canines) and lower tition usually indicates to crowding in devel­
canines and first deciduous molars (present oping permanent dentition, but, it is not al­
distal to mandibular deciduous canines). ways the case. It may depend on the individu­
These spaces are also called as anthropoid al’s growth of the jaws.
or simian spaces.
3. Occlusal relationship
■ Physiologic/developmentai spaces
Primary dentition develops quite independantly
These spaces (Fig. 3.12) are present in
of other morphologic process Le., there is little
between the primary teeth and play an
relationship between primary tooth development
important rôle in normal development of the
and skeletal maturation. This dentition is com­
permanent dentition. The total space
plete after the eruption of the second primary mo­
present may vary from 0 to 8 mm with the
lars, indicating that location for permanent teeth
average4 nmi in the maxillary archand 1 to7
in future has already been determined at this stage.
mm with the average of 3 mm in the man­
In other words, the dental arch circumference
dibular arch.
(roughly half circular in shape) that connects the
B. Non-spaced dentition most distal surfaces of the right and left second
Primary teeth are present without any spaces primary molars should be preserved for the per-
in between the teeth. This lack of space may iîjSÏIf
 TEXTBOOK OF PEDODONTICS

Primary molar relationship The prevalence of various types of terminal planes:

The relationship of the distal surface of the max­
illary and mandibular second primary molars is, Distribution Type Present (%)
therefore, one of the key factors that influences Bilateral Flush terminal plane 59.1
the future occlusion of the permanent dentition. (Vertical type)
Mesial step 19.1
The posterior primary teeth occlude so that the Distal step 4.8
mandibular cusp articulates just ahead of its cor­ Unilateral Flush terminal plane 9.1-
responding maxillary cusp. The maxillary canine Mesial step
occludes distal to the mandibular canine arid me­ Distal step 8.1
sial to the first molar. The maxillary first molar oc­
cludes between the disto-occlusal aspect of the iv) Anterior teeth relationship
first primary molar and the mesio-occlusal aspect Overbite: It is the distance which the incisal
of the second molar in the mandible. The mesio- edge of the maxillary incisors overlap vertically
lingual cusp of maxillary7 molars occludes in the past the incisal edge of the mandibular inci­
central fossa of the lower molars. sors. The average overbite in the primary den­
tition is 2mm and is sometimes expressed in
The mandibular second molar being somewhat terms of the percentage of the mandibular inci­
wider mesiodistally, gives rise, typically, to a flush sors crown covered.
terminal plane at the end of the primary dentition. Over jet: It is the horizontal distance between
As the distal surface of the second primary mo­ the lingua! aspect of the maxillary7 incisors and
lars guides the first permanent molars into occlu­ the labial aspect of the mandibular incisors,
sion, it is important to know how the upper and when the teeth are in centric occlusion. The
lower deciduous molars are related to each other average in primary dentition is 1-2 mm with a
(Fig. 3.16). The mesio-distal relation between the normal range of 2-6 mnt At the age of 2 years
distal surface of the upper and lower second pri­ it is seen often to be 4 mm with
* a fairly steady
mary molars usually can be classified into the three decrease upto the age of five years. Concur­
types: rently with the excessive wear of the primary
canines and molars, the whole lower dental
i) Flush terminal or vertical plane type arch may7 move anteriorly, the incisors may
The distal surface (Fig. 3.13c) of the upper assume an edge-to-edge interrelationship by
and lower teeth are in a straight plane (flush) the age of six years.
and therefore situated on the same vertical
plane. Usually it is a favourable relationship v) Canine relationship: The relationship of the
to guide the permanent molars. maxillary7 and mandibular deciduous canines
ii) Mesial step type (Fig. 3.11 and3.13a) is one of the most stable in primary dentition.
It is classified as class I when mandibular ca­
The distal surface of the lower molar is more
nine interdigitates in embrasure between the
mesial to that of the upper. Invariably it is
maxillary7 lateral and canine and class II where
favourable to guide the permanent molars into
mandibular canine interdigitates distal to em­
a class I relationship.
brasure.
iii) Distal step type (Fig & 13b)
The distal surface of the lower molar is more vi) Arch dimensions (Fig. 3.14) The size of the
distal to that of the upper. This relationship is primary dental arch can be measured by the
prognostically unfavourable as it guides the dental arch width between the primary canines
permanent molars into distal occlusion. and between the second primary molars.
 SECTION 3 : DEVELOPING DENTITION AND ITS DISTURBANCES |

Arch length and circumference Arch height

■ The terms arch length and arch circumference are Increase in the Iieight of the alveolar bone takes place
often incorrectly used interchangeably as it grows with time.
■ A small a mountof decrease takes place from the ■ There is little or no increase in the arch height
eruption of the second molars until the eruption during the period of the primary dentition
of the first permanent molars due to the mesial ■ It is difficult to measure and is of theoretical value
migration of the second primary molars, or the arch
can also be shortened due to interproximal caries. Spaces

The dental arch length can be measured from the ■ Spaced dentition does not have any change in
most labial surface of the primary central incisors to the spaces present until the eruption of the per­
the canines and to the second primary molars. Arch manent molars.
circumference is determined by measuring the length ■ Non-spaccd dentition does not show any devel­
of the curved line passing over the buccal cusps or opment of spaces in the primary dentition.
the incisal edges of the teeth, from the distal surface
of the primary second molar around the arch to the THE MIXED DENTITION PERIOD
distal surface of the other primary molar.
The period during which both the primary and per­
manent teeth are in the mouth together is known as
mixed dentition. The permanent teeth erupting in
place of previous deciduous teeth are the succès-
sional teeth, whereas those erupting posteriorly to
the primary teeth are called the accessional teeth.

Transition from the-primary to the

permanent dentition
C C
Fig. 3.14 Arch dimension « Calcification of the permanent dentition begins
between birth and three years of age. Second
Arch dimensions premolars may not begin calcification until five
A - Arch length years of age. *
B1 - Bicanine diameter ■ Eruptive movement does not begin before crown
B2 - Bimolar diameter calcification is complete.
C - Arch perimeter / Arch circumference « Enamel calcification is usually complete three to
four years before eruption into the oral cavity
Changes from 3 years to six years: Not many changes (mandibular incisors are the exception).
take place till the eruption of the permanent teeth. ■ Tooth crowns pierce the bony alveolar crest when
approximately 2/3 of root development is com­
Arch width
plete.
■ The primary dentition does not show any sub­ « Teeth emerge into the oral cavity when approxi­
stantial increase in width across the alveolar arch. mately 3 /4 of root development is complete.
■ Both maxillary and mandibular arches increase in ■ Root development is complete approximately 2-3
width by growing posteriorly to accommodate the years after eruption.
eruption of the permanent molars.
 <ilk> I TEXTBOOK OF PEDODONTICS

Phases of mixed dentition can he divided into three In both the jaws, the first permanent molars erupt
i) The first transitional period: more or less in a perpendicular orientation to the
■ emergence of the first permanent molars occlusal plane. They originate one above the other
■ incisors transition in the ramus and come downward with the maxillary
■ establishment of occlusion permanent molars being accommodated by additions
ii) Intertransitional period: at the tuberosity.
■ containing both sets of dentition
■ four permanent incisors, left and right first per­ The antero posterior relation between the two op­
manent molars posing first molars after eruption depends on:
■ deciduous canines and deciduous first and ■ their positions previously occupied within the
second molars jaws
iii) Second transitional period: ■ the sagittal relation between the maxilla and man­
■ emergence of bicuspids, cuspids and the sec­ dible.
ond permanent molars. ■ ratios of the mesiodistal crown dimensions of the
■ establishment of occlusion U/L deciduous molars.
■ The occlusal relationship is established by the
The important aspects of the mixed dentition are uti­ ‘cone and funnel’ mechanism with the upper pala­
lization of the arch perimeter which is used for align­ tal cusp (cone) sliding into the lower occlusal
ment of the permanent incisors and in the adaptive fossa (funnel).
occlusal changes that occur during the transition
Ideally, the eruption of the permanent molars into a
from one dentition to the other.
class I relationship is desired. Since the flush termi­
nal relationship is more common in deciduous denti­
THE FIRST TRANSITIONAL PERIOD (Fig. 3.15)
tion, it is more common for the permanent molars to
By the time of first permanent molars eruption any erupt into an end-to-end relationship. The desired
initial spaces between the deciduous molars and ca­ class I relationship is established by the following
nines will generally have diminished or disappeared. ways: .

Fig. 3.15 Position of unerupted permanent teeth in relation to deciduous teeth

 SECTION 3 : DEVELOPING DENTITION AND ITS DISTURBANCES | CTEl

PRIMARY PERMANENT

Class II

End - End

Class I

Class III

differential
> Forward growth
of mandible

DISTAL STEP CLASS II

Fig. 3116 Occlusal relationships of primary and permanent molars

 €ED i TEXTBOOK OF PEDODONTICS

a) Early mesial shift INCISAL TRANSITION

If the deciduous dentition is spaced dentition
with flush terminal relationship of second decidu­ The period of transition (ages 6 1/2 to 8 1/2) is critical
ous molars, the eruptive force of the permanent for the development of the dentition. During the
molars causes a closing of any existing spaces transition there are a number of factors that deter­
between the ¡primary molars or primate spaces ef­ mine the successful alignment of the permanent teeth
fectively causing a decrease in arch length. toward an ideal arch form.

b) Late mesial shift a) Interdental spacing of primary incisors:

Interdental spacing averages 4 mm in the maxil­
When no spaces exist, the erupting first perma­
lary arch and 3 mm in the mandibular arch. The
nent molar is not able to close spaces. In these
amount of anterior spacing in the primary denti­
cases when the primary molar exfoliates the per­
tion is one of the first clinical observations made
manent molar migrates mesially to use up the “Lee­
in examining a young child. Lack of interdental
way space” (the difference between the mesio-
spacing must be considered a serious handicap
distal width of the primary canine, first and sec­
toward normal incisor alignment.
ond molars and their permanent successors). This
averages 1.8 mm in the maxilla and 3.4 mm in the b) Inter canine arch width growth:
mandible. Only negligible amounts of growth occur from
three years (completion of primary dentition) to
6-7 years when the permanent mandibular inci­
sors begin to erupt. Notable amount of growth
occurs with the eruption of the incisors and ca­
nines.
Initial *Distal Cusp to Normal Mesial
Occlusion 23.3% Cusp 26.7% 0.8%
49.2% Sex Dental arch Width increase
between 2-18 years
Occlusion in Class II Class 1 Class III
permanent 38.6% 58.9% 2.5% Males Maxilla 6 mm
dentition
Mandible 4 mm
Fig. 3.17 Final establishment of permanent Females Maxilla 4.5 mm
molar relationship. Mandible 4mm

c) Primary molar guidance of permanent dentition

The primary second molar relationship can give c) Intercanine arch length increase:
clues to the eventual permanent molar relation­ When the permanent incisors erupt, they assume
ship. If the deciduous arches terminate in a a somewhat more anteriorly inclined position (la­
mesial step, the permanent molars may erupt di­ bial inclination) than the deciduous incisors. This
rectly into a normal, angle class I occlusion (mean­ position of the incisors averages 2.3 mm and re­
ing that the mandibular first molar is half a cusp sults in an increase in intercanine arch length of
mesial to its antagonist), in few cases it may de­ approximately 3 mm without any change in
velop into class III relationship. A definite distal intercanine width. This makes another character­
step guides the molars into distal relationship istic difference in tooth axis. The interincisal
which generally does hot improves with age, in­
stead deteriorates. (Fig. 3.16 and 17)
 SECTION 3 : DEVELOPING DENTITION AND ITS DISTURBANCES |

angle between the maxillary and mandibular inci­ in relation to the upper ones, which consequently
sors is about 150° in primary dentition, whereas it results in a change from a possible cusp-to cusp
is about 123° in permanent dentition which makes molar relationship to a normal molar interrelation.
permanent dental arch circumference wider (Fig.
3.18) ~

Fig. 3.18 Comparison of the angulation of the Fig. 3.19a The size difference between the
permanent and primary teeth primary molars and the permanent premolars

I) Favourable variations in the size ratio between

the primary and permanent teeth:
The permanent incisors are usually larger in total
width than the primary incisors they replace (the 5 years 5 years
difference is iiicisal 1 iajtnlity). —
Permanent canine, premolars are usually smaller
in total width than primary canine and molar they
replace (the difference isjLeeway spaceLUHS-
3.19a, b).

The sum of the mesio.-distal width of the perma­

nent lateral incisors is generally smaller thanbf
the primary lateral incisors by about 1 mm in the
maxilla and 3 mm in the mandible. This carries out
the smooth exchange of the lateral incisors.

The Leeway space, in addition to providing space 6 years 7 years

for the permanent canine, also allows the perma­
Fig. 3.19b Maxillary molar erupts into normal
nent molars to move mesially when the decidu­
occlusion after the mandibular first permanent
ous molars are replaced with the mesio-distally molar migrates mesially to obliterate the
smaller premolars. Moreover, the fact that the mandibular diastema between primary first
Leeway space is greater in the mandible than in molar & cuspid. (Baume, 1950)
the maxilla and facilitates a greater mesial
movement of the lower permanent molars
 CTF» I TEXTBOOK OF PEDODONTICS

BROADBENT PHENOMENON (Fig. 3.20)

(at age 5 1/2 years and 13 1/2 years)
School children tend to look unusual during the ex­ Spacing in deciduous Crowding in permanent
change of their incisors, especially in the upper arch dentition dentition
when the permanent incisors erupt. These appear to
be much larger compared with the primaiy teeth with <0 nun (crowding) 10 out of 10 children .
their longitudinal axes-flared out like as an inverse 0mm 7 out of 10 children
4 V’. As for the colour of the primaiy teeth, it is chalky
0-3 nun 5 out of 10 children
white, whereas permanent teeth tend to be more yel­
lowish. Because of the pressure of erupting perma­ 3-6 mm 2 out of 10 children
nent canines in the developing roots of lateral inci­ >6 mm 0 out of 10 children
sors, the crowns of erupting incisors flare more later­
ally producing diastema. Many parents worry about
INTER TRANSITIONAL PERIOD
these conditions. The transitional mal-alignment dur­
ing the exchange period of the upper anterior teeth is
■ In the intertransitional period which lasts about
called as “the ugly duckling stage’’ (Broadbent in
1.5 years, asymmetry in emergence and associ­
1937). This phenomenon is self correcting and nor­
ated differences in height levels and lengths of
mally, the incisors gradually straighten with the erup­
clinical crowns of the corresponding left and right
tion of the lateral incisors and canines. teeth are made up.

■ Under the influence of the tongue, the mandibu­

lar lateral incisors attain the proper sites within
the dental arch and their initial lingual location is
eliminated. *

■ Small rotations are corrected by the pressure ex­

erted by the tongue and lips if the spatial condi­
tions in the dental arches permit these movements.

« There is wearing of deciduous teeth with attrition

of the cusp tips and occlusal morphology ap­
proaching that of a plane.
Fig. 3.20 7 year old child showing ugly
duckling stage ■ The antero-posterior relation between 2 jaws is
not fixed in occlusion. A fixed intercusp relation­
Sum of spaces in the mandibular deciduous denti­ ship is absent. No interferences from the occlusal
tion and corresponding probability of crowding in contacts are present so the mandibular teeth at­
the permanent dentition tain a slightly more mesial position.
 SECTION 3 : DEVELOPING DENTITION AND ITS DISTURBANCES |

SECOND TRANSITIONAL PERIOD prior to eruption of the second molar by the me­
sial force.
■ At around 9 to 10 years of age, the second transi­
tional period starts with shedding of the poste­ ■ The arch circumference may also become short­
rior teeth. The alignment of the erupting perma­ ened than that of the primary dental arch by the
nent teeth depends a lot on the order of exchange utilization of the leeway space with the exchange
of the lateral teeth which takes about one-and- of the second primary molar to the second premo­
halfyears to complete the exchange of all the lat­ lar.
eral teeth.
■ Therefore, it is quite possible that eruption of
■ After the eruption of incisors, there follows a second molar may accentuate the crowding if it
pause of about one to two years, and the next was already present in the dentition.
tooth to erupt is the lower cuspid and the first
bicuspid at 9-10 years. The maxillary cuspid and « Proximal carious lesions or early extraction of sec­
second bicuspid then erupt, at 11 to 12 years, and ond primary molais, which are very common be­
the period is terminated by the appearance of the cause of high prevalence of caries for this tooth,
second molars at 12 years. will cause further loss of dental arch space. This
space decreases substantially during the erup­
• Transition from the ugly duckling to a mature stage tion period of the second permanent molar and
of dentition is also called as prepubertal period. will significantly affect occlusal relationship.
This is correlative with the maturation of the child
as a whole. ■ In some cases the permanent molar erupts prior
to the second premolars. If the space after the
■ During this period, the child tends to lose the extraction ofthe second primaiy molar is not main­
roundness of childhood and advances noticeably tained that space will be lost rapidly. A carefol
toward adolescence. monitoring is required.

■ The most common sequence of eruption of per­ ■ In the permanent dentition, the overbite and over­
manent lateral teeth in the maxilla is 4-3-5 and in jet decrease throughout the second decade of
the mandible 3-4-5. As mentioned previously, life probably due to relatively greater forward
because permanent canine is larger than the pri­ growth of the mandible.
mary canine, crowding is very con non immedi­
ately after the exchange of the canines. This phe­ SELF-CORRECTING ANOMALIES (see below)
nomenon is more prevalent in the mandible but
this crowding get alleviated after the exfoliation Definition
of the second primary molar. If this sequence of
eruption is changed to 4-3-5 or 4-5-3, the Leeway « Anomaly is defined as marked deviation from
space will not be utilized as efficiently and in such normal.
cases, the dentition will become crowded with­
out the Leeway space helping to improve. ■ Selfcorrecting anomalies are the anomalies which
arise in the child’s developing dentition during
■ After the exchange of the lateral teeth has been the period of transition from that of gum pads
completed and dental arch upto the first molar is stage to the onset of permanent period and get
established, the second permanent molars begin corrected on their own without any dental treat­
to erupt. The dental arch length is reduced just ment
 I TEXTBOOK OF PEDODONTICS

Clinical considerations and should be explained in brief the physiology

behind these transitional changes in the dentition.
Therefore, self correcting anomalies are part of de­
veloping dentition and should not be considered as
The permanent dentition
any developmental or pathological abnormality. If
any apprehension on part of the parents (which is The permanent dentition is considered when all the
often seen) the child should be removed promptly ^permanent teeth (all 28 teeth) are seen in the dental

correcting anomalies Correction (Timing / Factors involved in)

1. Pre-dentate period
a) Retrognathic mandible Corrects with differential and forward growth
of the mandible.
b) Anterior open bite Eruption of primary incisors
c) Infantile swallowing pattern During the first year of life with introduction of
solid foods in diet.

II. Primary dentition

1) Anterior deep bite Correct with:
■ Eruption of deciduous molars
■ Attrition of incisal edges
■ Forward and downward growth of mandible
2) Flush terminal plane (Early shift)
■ Eruption of the first permanent molar
■ (Late shift) Leeway space
3) Spacing ■ Eruption of first permanent molar t
4) Edge to Edge (due to attrition) ■ Eruption of permanent inciors

III. Mixed dentition

1) Anterior deep bite ■ Proprioceptive response condition of patient
(with the eruption of first permanent molars
and premature contact of the pad of tissue
overlying them as natural bite opener)
2) Mandible anterior crowding ■ Tongue pressure
■ Increase in intercanine width
3) Ugly duckling stage ■ Maxillary canine eruption
4) End-on relation ■ With eruption of first permanent molars
« Late mesial shift in non spaced dentition

IV. Permanent Dentition

1) Overjet and overbite ■ Decreases with eruption of all permanent
molars
■ Differential growth of mandible
 SECTION 3 : DEVELOPING DENTITION AND ITS DISTURBANCES |

arches, often by the age of 12 to 14 years of age. The

established interrelationship between permanent « Most frequent sequence of eruption in the per­
dental arches is by no means the final step in occlu­ manent dentition (Fig. 3.21 ) is:
sal development. After the occlusion of the denti­
tion has been established fairly minor changes re­ Upper teetliô 12 4 53 7 8
lated to teeth take place in sagittal, transverse and
vertical interrelationship. Lower teeth 1 2 34 57 8
« Horizontal overbite decreases 6
■ Dental arches become shorter due to proximal wear
and often crowding develops in ‘mandibular inci­ 6 8 10 12 20
sor region by 14 years of age.
Age in years
■ Vertical overbite decreases upto the age of 18
years by 0.5 mm.
Self-Assessment
■ The alveolar process may grow in height beyond
16 years of age.
1. What is the period of gumpads and what are the
■ Ox erjet decreases by 0.7 mm between 12 and 20
self conecting anomalies seen during this period?
years of age.
2. What are the intraoral findings seen in a neonate?
■ Individual variations are considerable
3. What are the different types of deciduous denti­
■ The increase in the dental arches is generally not
tion?
continuous.
4. What are the different features of deciduous den­
■ Functional variations influences the occlusal de­
tition ?
velopment.
5. What is flushterminal, mesial step and distal step?
« The most common sequence of eruption for de­
6. What are the self correcting anomalies present
ciduous teeth is: (The values for boys and girls
during the period of deciduous dentition?
are combined)
7. What is the characteristic feature of first transi­
tions period?
Upper teeth
8. What is the characteristic feature of the second
transitional period?
Lower teeth
9. What is the importance of first permanent molar?
10. What is the significance of early mesial shift and
late mesial shift? ~
Age in months 11 . What is incisal liability?
«
12. What are the self correcting anomalies of mixed
dentition period?
13. What is the leeway space of the Nance?
14. What is intertransitional period?
15. What is conefunnel mechanism?

Further Suggested Reading For Section -3

sequence 1. Anton-SC: Developmental age and taxonomic af-

finity of the Mojokerto child, Java, Indonesia. Am-
Fig. 3.21 Favourable eruption sequence. J-Phys-AnthropoL Apr, 102(4): 497-514,1997
 I TEXTBOOK OF PEDODONTICS

2. Ash M.M.:Development of teeth, calcification, 11. Rizzuti-N; Scotti-S: A case of hyperodpntia with
and eruption. Wheelers Dental Anatomy and Oc­ twenty-two supernumeraries: its surgical-ortho­
clusion. W.B. Saunders Company 1988 dontic treatment. Am-J-Orthod-Dentofacial-
3. Bishara-SE; Khadivi-P; Jakobsen-JR: Changes in Orthop. 111(5): 471-80,1997
tooth size-arch length relationships from the de­ 12. Saleemi-MA; Hagg-U; Jalil-F; Zaman-S; Timing
ciduous to the permanent dentition: a longitudi­ of emergence of individual primary teeth. A pro-
nal studyAm-J-Orthod-Dentofacia 1-0rthop. Dec; spective longitudinal study of Pakistani
108(6): 607-13,1995
children. Swed-Dent-J.; 18(3): 107-12,1994
4. Gazi-Coklica-V; Muretic-Z; Brcic-R; Kern-J;
13. Seow-WK: A study of the development of the
Milicic-A: Craniofacial parameters during growth
permanent dentition in very low birthweight
from the deciduous to permanent dentition—a
children.Pediatr-Dent. 18(5): 379-84,1996
longitudinal study Eur-J-Orthod. 19(6): 681-9,1997
14. Shapira-L; Tarazi-E; Rosen-L; Bimstein-E: The
5. J-Clin-Pediatr-Dent. Spring; 21(3): 205-11,1997
relationship between alveolar bone height and
6. Kieser-JA; Groeneveld-HT; Da-Silva-PC: Dental
age in the primary dentition. A retrospective lon­
asymmetry, maternal obesity, and smoking. Ant-J-
Phys-Anthropol. 102(1): 133-9,1997 gitudinal radiographic study. J-Clin-Periodontol.
7. Lewis-AB : Comparisons between dental and skel­ 22(5): 408-12,1995
etal ages. Angle-Orthod. 61(2): 87-92,1991 15. To-EW: A study of natal teeth in Hong Kong
8. Manzi-G; Santandrea-E; Passarello-P:Dental size Chinese. Int-J-Pediatr-Dent 1(2): 73-6,1991
and shape in the Roman imperial age: two exam­ 16. Tollaro-I; Baccetti-T; Franchi-L: Floating norms
ples from the area of Rome. Am-J-Phys- for the assessment of craniofacial pattern in the
Anthropol. 102(4): 469-79,1997 deciduous dentition.Eur-J-Orthod. 18(4): 359-65,
9. Pahkala-R; Laine-T; Lammi-S: Developmental 1996
stage of the dentition and speech sound produc­ 17. Vedtofte-H; Andreasen-JO; Kjaer-I :Arrested
tion in a series of first-grade schoolchildren. J- eruption of the permanent lowei second molarEur-
Craniofac-Genet-Dev-Biol. 11(3): 170-5,1991 J-Orthod. 21(1): 31-40,1999
10. Peretz-B; Nevis-N; Smith-P: Morphometric analy­ 18. Wölfel J.B., Schied R.C.: Primary Derttition. Den­
sis of developing crowns of maxillary primary sec­ tal Anatomy - Its Relevance to Dentistry. Williams
ond molars and permanent first molars in and Wilkins. 1997
humans.Arch-Oral-Biol.'43(7): 525-33,1998
 .SECTION - 4.

Psychological Development
and Behaviour Management
4.1 Theories of Child Psychology
Tandon S

Introduction Emotion
■ An effective state of consciousness in which joy,
Psychological development is a dynamic process, sorrow, fear, hate or the likes are expressed.
which begins at birth and proceeds in an ascending ■ A feeling or mood manifesting into motor or glan­
order through a series of sequential stages manifest­ dular activity.
ing into various characteristic behaviour. These Behaviour - is any change observed in the function­
stages are governed by genetic, familial, cultural, in­ ing of the organism.
terpersonal and interpsychic factors. The profes­ Behaviour management
sional dentist who deals with children and takes the
■ The means by which dental health team effec­
responsibility of their health care, is a parent surro­
tively and efficiently performs treatment for a child
gate and can discharge certain aspects of the parent
and simultaneously instills a positive denfajatti-
care to the child, as do the physician and the teacher.
Therefore, a dental clinician needs to understand tude in the child (Wright, 1975).
several dimensions of child psychological develop­ ■ It can also be considered as an attempt to alter
ment in order to relate effectively and to guide the the child’s behaviour and emotion in a beneficial
child patient. The clinician should know what emo­ manner according to thelaws of society.
tional and social behaviour to expect from children in
different age groups, and also be able to communi­ . Importance of Child Psychology
cate on a level consistent with the child’s view of the
world. ■ To understand the chikfbetter.
■ To know the problem of psychological origin.
The aim of this discussion is to understand the vari­ ■ To deliver dental services in a jneaningful and
ous aspects of child psychology, applied to the den­ effective manner.
tal situation for the successful management of the
■ To establish effective communication with the
cliild in dental clinic.
child and the parent.
■ To gain confidence of the child and of the parent.
Definitions
■ To teach the child and the parents importance of
Psychology - is the science dealing with human na- primary and preventive care.
ture, function and phenomenon of his soul in the main. ■ To have a better treatment planning and interac­
tion with other discipline.
/Child psychology - is the science that deals with the ■ To produce a comfortable environment for the
mental power or an interaction between the conscious dental team to work on the patient
and subconscious element in a child. >
 <FE> I TEXTBOOK OF PEDODONTICS

Theories of Child Psychology with memory andjndgement. It is developed after

birth, expands with age_anditdelays, modifies
Child psychology theories can be broadly classified and controls Id impulses on a realistic level, (real­
into two groups ity principle).

1 Psychodynamic theories 3. Super Ego: It is the prohibition learned from en-

- Psychosexual theory - Freud vironment (more from parents and authorities). It
- Psychosocial theory - Eric Erickson
acts as a censor of acceptability of thoughts, feel­
- Cognitive theory - Piaget
ings and behavior. It is determined by regulations
imposed upon the child by parents society, and
fl. Behavioural theories
culture, (ethics & morals). It is the internalised
- Hierarchy of needs - Maslow
control which produces the feeling of shame and
- Social Learning theory - Bandura
guilt.
- Classicalcpnditioning - Pavlov
- Operant conditioning - Skinner
The expression of disôomfort as a result of conflict
PSYCHOANALYTICAL THEORY between the three components of the psychic struc­
Sigmond Freud (1905) (Table 4.1) ture is defined as anxiety.

Sigmond Freud (1905) was the originator of psycho- Oedipus complex.

| analytical approach. Freud’s interest in development
I arose from his desire to explain the disorders of per- Abung boys have a natural tendency to be attached
I sonality in adults. Freud thought the personality to to the mother and they considertheir father astheir
I originate from biological roots, as a result of satis- enemy. Hence they strive to imitate their father to
| faction of a set of instincts of which sexual instinct ggtfTthe affection of the mother. Freud has also de­
| was the most important. He described five psycho- scribed oedipal complex as a desire to have sexual
I sexual stages. At each stage sexual energy is invested relation with the mother. The name of the oedipal
I in a particular part called an erogenous zone. complex comes from Greek mythology. Oedipus the
King of Thebe, unwittingly slew his father and mar­
| ¿"Psychic struciurejproposed by Freud in Psycho dy- ried his mother. The little boy adopts his father’s
| nami^Weory^composed of three parts manners, his attitudes and interests thinking that by
becoming like his father he can win his mother’s sexual
f
| L Id: It is the basic structure of personality, which love.
serves as a reservoir of instincts or their mental
representative. It is present at birth, inyulse rid­ Electra complex
den and strives for immediate pleasure and grati-
fication. (pleasure principle). Similarly the young girls develop an attraction to­
wards their father and they resent the mother being
2. Ego: It develops out of Id in the 2nd to 6th month close to the father. Freud has reported that little girls
of life when the infant begins to distinguish be­ have a comparable Electra complex to resolve this. In
tween itself and the outside world; it is the media­ Greek mythology, Electra helped her brother slay the
tion betweenId and super Ego. Unlike Id, Egois lover of their father Agemennou, in order to win her
governed by the reality principle. It is concerned father’s love.
 SECTION 4 : PSYCHOLOGICAL DEVELOPMENT AND BEHAVIOUR MANAGEMENT | <FE1

Table 4.1: Freud’s Stages of Development

BIRTH ORAL STAGE ANAL STAGE

I ■ Is the 1st experience to ■ In infants the oral ■ During this stage, maturation
N effect personality cavity is the site for of neuromuscular coritmP^ —-
T development identifying needs. occurs.
R ■ It therefore serves as an « Control over sphincters
O erogenous zone. particularly anal sphincter
D results in increased voluntary
U activity.
C
T

o
N
C ■ Abrupt change at birth « This is a dependent _ « Development of personal
H result in psycho­ stage since the infant autonomy and independence.
A physiological emergency is dependent on adults ■ Child realizes his control
R reactions (protective for getting his oral over his needs and practices
A shell) similar to fear needs fulfilled. it with a sense of shame or
C and anxiety. self-doubt.
T ■ The characteristics are
E observed in later life
R during personality
development and depend
S on child’s susceptibility
T during this period.
h « If the neonate gets used
c to the stimuli he is no.
s longer anxious.
o ■ These reactions help the ■ Satisfaction of oral ■ The child realizes the
B child to learn some desires e.g. suckling of increasing voluntary control,
J adaptive mechanisms milk by mother, help in * which provides him with the
E against anxiety development of trust. sense of independence and
generating stimuli. ■ In later period of life *
autonomy.
T results in successful
achievements of needs.
V
E
S
P ■ Neonates who fail to ■ If child's needs are not ■ Anal eroticism and defenses
A adapt to abrupt changes adequately met in this against it result in fixation on
T get startled easily. stage the following anal function.
H ■ This results in a more traits develop. ■ It is characterized by various
O protective mechanism Excessive optimism, abnormal behaviours like:
L which is maladaptive in Narcissism, Pessimism, Disorderliness, Abstinence,
0 later life. Demandingness, Envy, Stubbornness, Willfulness,
G Jealousy. Frugality.

contd.
 <Eg> I TEXTBOOK OF PEDODONTICS

Uretheral Stage PhallicJitage Latency Stage Genital Stage

■ It is a transition ■ The stage begins ■ Resolution of any ■ Psychosexual

between the anal during the 3rc[year defects occufsTn development"
stage and the of life till the 5th this phase. extends from 11
Phallic stage. year. ■ The phase ends jn to 13 yrs. tg_ _
puberty. young adulthood.

■ The child derives It is characterized by: • Maturation of ego ■ Sense ofjdentity

pleasures from ■ Oedipus complex tatesjjJace. develops.
exercising « Castration anxiety ■ There develops a ■ Child has a matured
control over the ■ Penis envy greater degree of personality.
urinary sphincter. ■ Electra^complex control over ■ He can satisfy
■ There is an increase in instinctu.al impulses. genital potency
genital masturbation, • Child gains better and realizes his
accompained with sense of initiative & goals for
unusual fantasies starts adapting to the reproduction
about opposite sex. adverse environment. and survival

■ The objectives are « The child realizes the ■ The goal of this phase ■ Matures the
similar to those of sexual qualities with is the further develop­ personality of the
anal stage. out embarrassment. ment of personality. individual.
• Resolution of the ■ Consolidation of sex ■ Helps to separate
stage in regulation of roles occurs. from the depende­
drive impulse. ■ These result in nce on parents.
maturation of ego ■ Their acceptance
and mastery over of adult role,
skills. functions with social
expectations and
cultural values.

■ Loss of urethra ■ If the above mentioned ■ Lack of inner control ■ Unresolved traits
control results in characteristics are or excessive inner from previous
shame. not resolved the control result in a phases are seen
■ Competitiveness balance between male pathological trait. in a modified
• Ambition and female roles ■ Lack results in an form.
does not develop. immature behaviour
and decreased
development of skills.
 SECTION 4 : PSYCHOLOGICAL DEVELOPMENT AND BEHAVIOUR MANAGEMENT | CTO

CLASSICAL CONDITIONING MAHLERISJ'HEORY (1933)

Pavlov (1927)
This theoiy categorises the early childhood object
Russian psychologist, Ivan Petrovich Pavlov was relations to understand personality development.
one of the first to study conditioned reflexes expe ri­
mentally The period of childhood is thus divided into three
stages:
The crucial element of the conditioning is the rela­ 1. Normal autistic phase
tion between the conditioned stimulus and the un- 2. Normal symbiotic phase
conditioned stimulus. The more frequent the pairing 3. Separation individualisation phase
of the conditioned and unconditioned stimulus, the
stronger is the conditioning. Normal autistic phase (0 -1 yrs)
■ It is a state of half - sleep, half - wakefulness.
The principles involved in the process are: ■ This phase involves achievement of equilibrium
with the environment
1. Generalisation wherein the process of condition-
I
ing is evoked by a band of stimuli centered
Normal symbiotic phase (3-4 wks. to 4-5 mths.)
around a specific conditioned stimulus. Thus a
• The infant at this stage is slightly aware of the
test stimulus similar to training stimulus results
caretaker but they both are still undifferentiated.
in a response, e.g. a child who has had a painful
experience with a doctor in a white coat always
Separation individualisation process (5 to 36mths)
associates any doctor in white coat with pain
■ This phase is divided into 4 subphases (Table4.2)
2. Extinction of the conditioned behaviour results 1) Differentiation (5 - 10 mths)
if the association between the conditioned and 2) Practicing period (10-16 mths)
the unconditioned response is not reinforced, e.g. 3) Rapproachment (16 - 24 mths)
in the above mentioned example subsequent vis­ 4) Consolidation and object constancy (24 - 36
its to the doctor without any unpleasant experi­ mths)
ences results in extinction of the fear.
OPERANT CONDITIONING
3. Discrimination is the opposite of generalisation. Skinner (1938)
If the child is exposed to clinic settings which are
J»-
different to those associated with the painful ex­ The principles of operant conditioning arises from
periences the child learns to discriminate between the experimental work of Skinner. It has been consid-
the two clinics and even the generalised response ered as an extension of classical conditioning. Indi­
to any office will be extinguished. viduals response is changed as a result of reinforce­
ment or extinction ofprevious responses. Hence, sat­
The principles of classical conditioning can be used isfactory outcome will be repeated while unsatisfac­
in the following areas of animal and human behav­ tory outcomes will diminish in frequency. According
iour: to this theoiy, the consequence of behaviour itself
■ Developing goodJiabits acts as a stimulus and affects future behaviour. Since
■ Breaking habits and elimination of conditioned the behaviour acts upon the environment it is called
fear an operant. Skinner described four basic types of
■ Psychotherapy, to decondition emotional fear operant conditioning distinguished by the type of
■ Developing positivejattitiides consequences:
■ Teaching alphabets
 <FIî> I TEXTBOOK OF PEDODONTICS

Table 4.2: Characteristic of Separation Individualisation Sub-Phases.

Differentiation PracticingJ’eriod Rapproacbement Consolidation and

ObjectGonstancy

■ The infant ■ Beginning of this ■ The infant, now a ■ The child achieves a
becomes alert phase is marked toddler is more definite sense of
as cognitive and by upright aware of the individuality and is
neurological locomotion. physcial able to cope up with
maturation ■ The child learns to separateness. the mother’s absence.
occurs. separate himself ■ The child tries to ■ He does not feel
■ Characteristic from mother by overcome this by uncomfortable on
anxiety at this crawling. showing mother his being separated from
period is - « Separation anxiety newly acquired skills. the mother since he
stranger is present as the ■ The mother’s efforts to knows that she will
anxiety. child still requires help toddler are not return.
« He differentiates the mother for successful resulting ■ He develops an
between self safety. in temper tantrums. improved sense of
and other. ■ Rapproachement crisis time and can tolerate
develops as the child delay.
wants to be soothed by
the mother but is unable
to accept her help.
■ ■ This crisis is resolved
as the child’s skill
improves.

1. Positive reinforcement occurs if a pleasant con­ Positive and negative reinforcements are the most
sequence follows the response, e.g. a child re­ suitable types of operant conditioning for a dental
warded for good behaviour following dental treat­ office while the other two types of operant condi­
ment. tioning should be used with caution. One mild form
of punishment that can be used for children is the
2. Negative reinforcement involves removal of un­
“voice control“.
pleasant stimuli following a response, e.g. if the
parent gives in to the temper tantrums thrown by
COGNITIVE THEORY
the child, he reinforces this behaviour.
Jean Piaget (1952)
3. Omission refers to removal of the pleasant re­
sponse after a particular response, e.g. if the child Piaget formulated his theory on how children and
misbehaves during the dentalprocedure, his-fa­ adolescents^think and acquire knowledge. He de­
vourite toy for a short time result­ rived his theories from direct observation of children
ing in the omissionofthe undesirable behaviour. by questioning them about their thinking. Accord­
ing to Piaget, the environment does not shape child
4. Pimishmeiit of an aversive behaviour but the child and adult actively seek to
stimulus into à sîtuÎtfeBio decrease the undesir­ understandthe environment. This process of adap­
able behaviour, eguBbfpalatalrake incorrec­
tation is made up of 3 functional variants -
tion of tongue thrusting habit.
 SECTION 4 : PSYCHOLOGICAL DEVELOPMENT AND BEHAVIOUR MANAGEMENT | Ckfri

limitation concerns with observing, recogniz- tions following adjustments in assimilated knowl­
g, taking up an object and relating it with earlier edge so that the facts fit better.
periences or categories.
The sequence of development has been categorized
xommodation accounts for changing concepts
into 4 major stages (Table 4.3):
d strategies as a result of new assimilated in-
1) Sensorimotor stage (0 to 2 yrs) . -
rniation. Piaget calls the strategies and mental
2) Pre-operational stage (2 to 6 yrs)
tegories as 'schemes’.
3) Concrete operation stage (6 to 12 yrs)
|u ilib ration refers to changing basic assump­ 4) Fonnaloperation stage (11 to 15 yrs)

•le 4.3 : Sequence of development

isorimotor Pre-Operational Concrete Operation Formal Operation
Stage Stage Stage

Every child is ■ Primitive strateg­ « The thinking process ■ The child now a
>orn with certain ies change as the becomes logical. teenager is able to
trategies for child assimilates « He develops the think still more
iteracting with new experiences ability to use abstractly.
he environment, and accommod­ complex mental w He can consider
’hese primitive ates original operations such as a hypothetical
•trategies mark strategies. addition and situation.
he beginning ■ The child uses subtraction. ■ Uses inductive or
•f the thinking symbols in » The child is able to deductive logic to
irocess. language and understand others make decisions
‘he child does play. point of view. and solve problems.
iot yet have the • He learns to ■ Concrete operations ■ He thinks of ideas
apacity to classify things develop based on and has developed
epresent ■ He solves the level of under­ a vast imagination.
•bjects or people problems as a standing achieved
? himself result of intuitive so far.
lentally. thinking but
<s maturation cannot explain *
•rogresses the why
imple reflexes
•egin to be
oordinated e.g. 1
joking along
/¡th arm move-
lents resulting
r hand watching,
ly 10th mth, veri­
ty of elementary
chemes develop
Jbject permane-
ce develops in
ourse of co-ord-
lating actions &
9peated contacts
rith environment
 I TEXTBOOK OF PEDODONTICS

HIERARCHY OF NEEDS Erickson described 8 stages of life cycle which are

Masler (1954) marked by internal crises defined as the turning
points /periods.
Masler believed in the self-actualisation theory, i.e.
the need to understand the totality of a person. He Table 4.4 Comparison between Erickson’s and
gave forward the following thoughts Freud’s Psycholbgicâf stà^es.
« The needs are arranged in a hierarchy and as one "" ■■■■■■ - ........—1

general type of need is satisfied another higher Age Erickson’s Psychological Freud’s
Stages Psychological
order need will emerge. The desires from most
Stages
basic biologic needs to the more psychological
ones become important only after basic needs 0-1 Basic trust versus Oral stage
have been satisfied. mistrust - The infant forms
« Motivation is constantly required and is a never the first trusting relationship
with the caregiver.
ending, fluctuating complex present in almost all
organisms. 2-3 Autonomy versus shame, Anal stage
■ Pain avoidance, tension reduction and pleasure doubt - toddler begins to
act as sources of motivating behaviour. push for independence.

4-5 Initiative versus guilt - Phallic stage

The child becomes more
assertive, resulting conflict
causes guilt.

6-12 Industry versus Latency stage

inferiority - The child must
learn basic cultural skills
such as school skills.

13-18 Identity versus role Genital stage

confusion - The child a
teenager now must realize
who he is and what he
shall become.

19-25 Intimacy verus isolation -

The adult realizes the
PSYCHOSOCIAL THEORY need for one truly
Eric Erickson (1963) intimate relationship.

26-50 Generativity versus

Erickson concentrated on childjjgvelopmentcov^
stagnation - The adult
ering the entire span of life cycle from infancy to rears children or performs
childhood through old age. UnlikeTreud, Erickson creative act failing which
emphasis the conscious self as much as unconscious stagnation occurs.

instincts. Despite differences, Freud and Erickson

50+ Ego integrity versus
share some important assumptions. despair - The adult
• Development depends upon child's instincts and integrates earlier stages
responses of those around him. and achieves sense of
■ 11 n resolved is sues Trom early stages of life affect integrity.

person’s ability to deal with subsequent stages.

 SECTION 4 : PSYCHOLOGICAL DEVELOPMENT AND BEHAVIOUR MANAGEMENT |

SOCIAL LEARNING THEORY process but requires cognitive factors and in

Bandura (1963) volves 4 processes which are:
- Attentional processes ~
Social learning theory is thought to be the most com­ - Retention processes
plete, clinically useful and theoretically a sophisti­ - Reproduction processes
cated form of behaviour therapy. As compared to - Motivational-processes
Operant and Classical conditioning this theory is: 4 Self-re^alation - thisjvstem involves a process
■ Less r cductionistic of self-regulation, judgement and evaluation o
■ Provides more explanatory concepts individual’s responses to his own behaviour.
■ Encompasses a broader range of phenomena
Self Assessment
The learning of behaviour is affected by 4 principle
elements: 1. What is psychic structure?
1. Antecedent determinants - the conditioning is af­ 2. What is Oedipus complex?
fected if the person is aware of what is occurring. 3. What is Electra complex?
2. Consequent determinants - Person’s perception 4. What is psychosocial theory?
and expectancy (cognitive factors) determine be­ 5. What is Jean Piaget theory?
haviour. 6. What is operant conditioning?
J^Moddling - Learning through observation elimi­ 7. What is social learning theory?
nates the trial - error search. It is not an automatic
 4.2 Emotional Development

Tandon S

Emotion is a state of mental excitement characterised system, directly influence muscles and internal
by physiological, behavioural changes and altera­ organs to initiate body changes.
tions of feelings. Emotional expressiveness through ■ Indirectly stimulating adrenal hormones to other
bodily movements, facial expressions and body charges and prepare the body for fight or
vocalizations are within a human being reported to flight response.
be present in an infant through maturity.
Characteristics of commonly seen emotions
Different Emotions at Different Stage of in a child
Life are given in table 4.5
L Distress or Cry:
■ At Birth: Primary emotion present at birth with
Physiology of Emotion
vigorous body expressions usually due to hun­
ger, colic or any other internal cause.
Development of emotions depends on maturation in
■ At six month: It is greatly replaced by a milder
the nervous system and the endocrinal system. Dif­
expression of fussing or vocalization.
ferences in emotional responsiveness between chil­
■ During preschool: It is seen less, only for the
dren and adults appear to be partly due to cortical
reasons of physical pain as he is thwarted by
immaturity and partly due to difference in endocrine
his environment.
output.
■ During school years: Pressure helps him to
• At birth cortex development is completed, frontal
outgrow the crying habit which decreases rap­
lobe is immature and has little influence on the
idly. After this till 15 years crying occurs very
functions of the lower parts of the brain resulting
seldom.
in unbalanced emotions. Hence, emotional re­
■ In young adult: Ultimately it becomes a limited
sponse of the child is quickly aroused but short
quiet cry ing in private only for reasons of grief
lived.
or other intense emotions.
■ In 2 to 5 years and 11-12 years adrenal glands
gain weight rapidly and liberation of adrenaline Different types of cry seen in children:
in blood is vigorous, as a result of which a Sometimes, the different types of cries can be an
preschooler is highly emotional' and emotional asset in diagnosing the behaviour of a child. Fol­
outbursts are prolonged too, giving rise to physi­ lowing four types of crying are usually seen in
ological signs of emotional disturbance. children (Elsbach, 1963).
■ As emotion subsides, parasympathetic energy
1. Obstinate Crv:
conserving system takes over and returns the or­
■ The child throws a temper tantrum to
ganisation to normal.
thwart dental treatment.
• Activities of the brain in certain regions, includ­
■ It is loud, high-pitched.
ing hypothalamus and other parts of nervous
 SECTION 4 : PSYCHOLOGICAL DEVELOPMENT AND BEHAVIOUR MANAGEMENT |

Table 4.5: Different emotions at different stages of life.

Infancy Maturity Old age

Distress Anxiety Mature emotions Grief

Startle Fear Sensitiivity and control Wony

response Shame Minimum differentiation Self pity
Anger of response of esthetic Guilty feeling
Disgust feeling Depression
Jealousy Irritability
Disappointment Boredom
Restlessness
Joy

Delight Elation Mystical

Hopeful anticipation Ecstasy
Affection Possessive
Sex Satisfaction
Benevolence
Sensuousness

■ Characterized as a siren like wail. ■ Usually the ciy sound is slow, monotone.
■ This form a belligerent cry, represents the ■ It is a sort of coping mechanism to unpleas­
child’s external response to anxiety. ant auditory stimuli, finding himselfuncom­
fortable in the situation.
2. Frightened Cry
■ Usually accompanied by a torrent of tears. IL Anger
■ Convulsive breath-catching sobs. Outburst of the emotion is caused by the child’s
■ Usually the child emitting this type of cry lack of skill in handling the situation. Infants and
has been over-whelmed by the situation. * young children respond in anger in a direct and
primitive manner but as they develop the re­
3. Hurt Cry sponses become violent and more symbolic, for
■ May be loud, more frequently. t example
« Frequently accompanied by a s 111411 ■ 15 months children express anger by throwing
whimper. objects.
■ Initially a child in discomfort shows a ■ Two year olds attack other children with an
single tear filling from the comer of the eye intention to hurt.
and running down the child’s cheek with ■ Four years old express their anger through beg­
out making any sound or resistance to the ging-
treatment procedure. ■ Five years old, have less expression of anger.
■ Six years old have a renewa l of violent meth­
4. Compensatory Cry ods of expression of anger.
■ It is not a cry at all. ■ Seven year ones display less aggressiveness,
■ It is a sound that child makes to drown out though kicking, throwing objects is observed.
the noise for example a drill.
 €E©| TEXTBOOK OF PEDODONTICS

■ 8-9 years old’s anger is expressed through feel­ ■ -Sometimes, the smells and sounds of equip­
ings. It becomes directed towards a single per­ ment or even the appearance of dentist with
son. glasses and mask may be frightening.
■ 10 years old’s anger may become violent and
may be expressed physically. h. Pre schooler(2-5 years)
■ 12 year olds express anger verbally. ■ Fear of animals or being left alone or aban­
■ 14 years olds may take out his anger on some­ doned.
one else. ■ More apprehensive about failures, learns
to fear his prestige.
HL Fear
Fear is a reaction to a known danger (augmenting c Early schooler
the fight or flight response). Its source is the con­ Fear of the dark, staying alone. Shows fear of
sciousness. supernatural powers like ghosts and witches,
imaginary objects and situations such as fear
It may be defined as an unpleasant emotion or of war, spies, beggars, etc.
effect consisting of psychophysiological changes
in response to realistic threat or danger to one’s d. Late schooler
own experience. ■ By age of 9, fear of bodily injury may be
present.
Prevalence of Fear • Fear of failure, not being liked, competition,
«. Various studies have found the incidence of fear of punishment.
dental fear to be 3-21%, depending on the age ■ Fear of crowds, heights.
of the child.
■ Girls have been reported to have more fears e. Adolescent
than boys. Fear of social rejection and fear of perform­
ance (peer group pressures, academic pur­
Several reasons suggested are suits). t
■ An inherent timidity in girls.
« Girls are encouraged to display fear while boys Fear of Dental Situation
are encouraged to hide it. It is observed that fearful patients usually report
■ The fears have also been reported to increase a history of traumatic dental experiences. Unfa­
from infancy to young childhood. At the same vourable family attitudes and transmission of
time, the type of fear varies at different ages these may also result in fear. Thus, various types
such as: of fears can be observed in the clinic as:

Development of fear L Innate fear (without stimuli or previous expe­

a. At birth: rience): It is thus also dependent on the vul­
■ This is a primary response acquired soon nerability of the individual.
after birth such as a startle response, how­
ever, the newborn is unaware of the BL Subjective fear: Fears transmitted to the indi­
stimulus. vidual are termed subjective fears. They may
■ With age he starts becoming aware of fear due to:
producing stimuli and can adjust to the - Family experiences, peer (friends), informa­
isolated experience by resorting to flight if tion media (TV, papers, comics).
he cannot solve the problem.
 SECTION 4 : PSYCHOLOGICAL DEVELOPMENT AND BEHAVIOUR MANAGEMENT |

ffl. Objective fear: Fears due to events, objects ■ Anger

and specific conditioning. Previous experience ■ Weakness
(dental trauma) or generalization (medical ex­ ■ Sense of unreality.
perience).
Chronic fear leads to —■ ,
Fear Evoking Dental Stimuli ■ Tiredness.
Various dental stimuli evoke fear. It is observed ■ Difficulty in sleeping and bad dream
that the most feared events in the dental clinic ■ Restlessness
can be ranked as: ■ Loss of appetite
■ Anaesthetic administration locally by injection. ■ Aggression
■ Extraction. ■ Avoidance of tension producing situation.
« Sound of drill.
Physiological Sign of Fear
Factors Causing Dental Fear ■ Pale sweaty skin.
An interaction of various factors occurs in the ■ Hair standing on end
existence of dental fear such.as: ■ Dilatation of pupils.
1. Fear of pain or its anticipation. ■ Rapid breathing.
2. A lack of trust or fear of betrayal. ■ Increased heart-rate.
3. Fear of loss of control. ■ Rising blood pressure.
4. Fear of the unknown. ■ Increased blood flow through muscles.
5. Fear of intrusion. ■ Contraction of the bladder and the rectum.

Features of Fear Biochemical Changes in Few Minutes

Fear is a package of reactions that tend to occur ■ Secretion of adrenaline.
together simultaneously or sequentially. About ■ Secretion of noradrenaline.
70% children acquire dental fear at early age. This ■ Increase in free fatty and corticosteroids in
emotion may present the following main two plasma.
expressions:
1. Tendency to freeze which reaches its extreme Response to fear
in the form of death. It can be described at three level:
2. Startle, scream, run away from the scene of
danger, i.e. flight. 1. Intellectual levelz Where the child is reatty to
It turns, a shift from freeze reaction to flight. accept the situation and face the difficulties to
I
achieve results and benefits (usually seen at
Symptoms of Intense Fear: adolescent age).
■ Unpleasant feeling of terror.
« An urge to cry or hide. 2. Emotional level: Usually the child shows the
■ Pounding of the heart. fight or flight response, which acts as an in­
■ Tense muscles. stantaneous response (seen in school age).
■ Liability to startle
■ Dryness of the throat and mouth. 3. Hedonic level: Usually reflected as self
■ Sinking feeling. centeredness, thereby accepting what is com­
■ Nauseous feeling. fortable and rejecting what is not without too
■ Urge to urinate (very common in children). much concern for the outcome or nature of the
■ Irritability. treatment (may be seen in a very young
 <EE> | TEXTBOOK OF PEDODONTICS

children). It may be expressed through so­ first visit or the learning involved in dental anxi­
matic complains or chronic fatigue in the eld­ ety may have been more indirect, depending upon
erly group. the experience of other people. Maternal anxiety
plays an important role in the chi Id’s anxiety level
IV Anxiety determinant. A mother with higher anxiety, will
« Is an emotion similar to fear but arising with­ have a child usually showing a negative behav­
out any objective source of danger. iour as a result of his high level of anxiety.
« Is a reaction to unknown danger.
« It is often been defined as a state of unpleas­ Biological difference
ant feeling combined with an associated feel­ Some people are ’more predisposed to become
ing of impending doom or danger from within more anxious or to learn about anxiety responses
rather than from without. than others due to the innate biological mecha­
■ It is a learned process being in response to nism.
one’s environment. As anxiety depends on
the ability to imagine, it develops later than
Types of anxiety7
fear.
Trait anxietv
Sub-types of anxiety
Is a lifelong pattern of anxiety7 as a temperament
feature. These children are generally jittery, skit­
Association
tish, hypersensitive to stimuli.
This is a process of classic conditioning whereby
previously neutral stimuli become the cause for
State anxietv
arousal and anxiety by pairing them with pain or
Are acute situationally bound episodes of anxi­
the negative experiences of others.
ety that do not persist beyond the provoking situ­
ation.
Attribution
Arousal in the biological sphere.
Free floating anxiety s

Appraisal is a condition of persistently anxious mood in

Here anxiety is concerned with cognition or the which the cause of emotion is unknown and many
way we think. It involves reconstruction of nega­ other thoughts or events trigger the anxiety.
tive experiences rather than positive happenings
that account for the arousal of anxiety. Situational anxiety
Seen only to specific situations or objects.
Cause of Anxiety
General anxiety
Uncertainity Where the individual experiences a chronic per­
Fear of unknown is anxiety provoking. In dental vasive feeling of anxiousness wha tever the exter­
clinic, new patient’s anxiety can be due to the nal circumstances.
uncertainity they feel about what awaits them af­
ter initial first appointment Check up. Anxiety Rating Scale

Previous learning The patient’s anxiety can be evaluated through

In such cases anxiety is present due to their pre­ the following scales:
vious learning experiences of trauma during the
 SECTION 4 : PSYCHOLOGICAL DEVELOPMENT AND BEHAVIOUR MANAGEMENT

2 - Feeling scared but co-operates

3 - Feeling scared reluctant

4 - Feels very scared
to co-operative
un-cooperative, requires
physical restrains
Fig. 4.1 Anxiety Scale
 CEE) I TEXTBOOK OF PJEDODONTICS

L Pictorial and Response Card Characteristics of phobia

The scale evaluates the child’s fear in the den­ ■ Being out of proportion to the stimulus or situ­
tal set-up in different situations such as: ation (not age appropriate).
- appointment with the dentist ■ Cannot be reasoned with
- waiting for his turn in the dentist’s office ■ Being out of voluntary control
- dental procedures ■ Persistent and unadaptable.
- lying on bed dreaming about the dentist, etc.
Types of Phobia
The scale gives 5 options graded 0 to 4, from Shelhan (1982) divided'anxiety and phobia into
relaxed to panic behaviour depicted by vari­ two major groups.
1. Exogenous (non-endogenous)
ous pictures (Fig. 4.1)
2. Endogenous
0- relaxed
1 - uneasy
Non-endogenous:
2 - Feeling scared but cooperative
This is a psychologically affected group who
3 - feeling scared and uncooperative
involve a situation related anticipatory anxiety
4 - feeling ven’ scared, uncooperative, requires symptoms such as:
physical restrain. ■ Moist palms
■ Flattery stomach
The child is shown pictures and encouraged ■ Fine hand tremors
to represent his feelings. ■ Shaky inside
■ Rapid heart beat
Verbal Questions
The child is asked questions or given “sen­ These are the symptoms seenwhen normal indi­
tence completion tasks” to verbalize his fear. viduals are stressed or threatened. The main cause
Negative or reluctant answers imply fear while is in the external environment. It is an anxiety or
positive opinions imply non-fearful child. phobia due to a factor “to be produced from the
outside”. Thus, the individual can readily iden­
K Questionnaire tify the etiological agent.
Anxiety can also be evaluated by answers to
the questionnaire given to the child patient Endogenous
and the parent. The questions help to deter­ This anxiety is present without any prior warning
mine the attitude and experiences of both the or the presence of any detectable stress situa­
patient and parent. tion. The cause is “to be produced from within”.
This type of anxiety has a more Severe cluster of
symptoms such as:
V Phobia
■ Light headedness or dizziness.
■ Is an irrational fear resulting in the conscious
■ Difficulty in breathing
avoidance of a specific feared object, activity
■ Parasthesia
or situation.
■ Hyper-ventilation
■ It may be defined as a persistent, excessive,
■ Chest pain
unreasonable fear of a specific object, activity
■ Losing control
or situation that results in a compelling desire
to avoid the dreaded object.
 SECTION 4 : PSYCHOLOGICAL DEVELOPMENT AND BEHAVIOUR MANAGEMENT |

Other causes of Phobia ■ Another common phobia is of darkness, a fear

Based on the causative factor they can be experienced by children between the age of 4
classified into three major categories: and 6 years. This is most likely due to the
imagination of the child as to various creatures
L Simple Phobia lurking out in the dark.
Is an isolated fear of a single object or situa­ « School phobia is an exaggerated fear of attend­
tion leading to avoidance of the object of tile ing school and occurs in all children peaking
situation; The fear is irrational and excessive around 11-12 years. A fearof the various ac­
but not always disabling. Some of the phobias tivities connected to school such as new faces
are: and challenges, fear of leaving home.
Acrophobia Height ■ In 12 years children of both sexes, previous
Agoraphobia Open space aversive dental experiences are more closely
Arachnophobia Spider related to dental phobia than general fear.
Anthropophobia People ■ At adolescent period most children outgrow
Aquaphobia (hydro) Water their fear. Two phobias commonly seen are
Astraphobia Lightening fear of blushing and fear of being looked at.
Claustrophobia Closed space
Cynophobia Dog FEAR ASSESSMENTS
Zoophobia Animals
Nyctophobia Darkness The children’s Dental fear picture test
Pyrophobia Fire (Klingberg, 1994)
Xenophobia Stranger
The children’s dental fear picture test (CDFP) con­
2. Situational Phobia sists of three different subtests:
Is popularly interpreted as a fear of open space, ■ The dental setting pictures (CDFP-DS)
but has wider implications. It usually refers to ■ The pointing pictures (CDFP-PP)
a cluster of complaints. In addition to open or ■ A sentence completion task (CDFP-SC)
crowded places they also fear public transport,
bridges, tunnels, being alone at home or being The dental setting pictures contain a set of ten pic-
away from home etc. * tures (ISO A4 size papers) of animals in different
Characteristics progressively more stress evoking dental care situa­
Dizziness, loss of bladder control or bowel con­ tions. The pictures are presented to the child in nu­
trol, cardiac distress. 4 merical order and the child is encouraged to tel l a
story about each picture. The following instructions
X Social Phobia
are given: Tell me a story about what is happening in
Is basically phobia due to the fear of being
the picture.
looked at and the concern about appearing
shameful or stupid in presence of others. Main
The cards depict the following themes:
types of social phobia are public speaking, fear
■ A baby bear brushing his teeth in the bathroom,
of eating, fearof blushing.
supervised by an adult bear.
Phobia in Childhood ■ A puppy and an adult dog walking in the street,
■ The most common phobia in childhood is the one of the houses in the street accomodates a
fea r of animals. This usually comes on between dental office.
the age of 2 and 4 and is gone before the age of ■ A baby lion and an adult lion in the dentist’s wait­
10 years. ing room.
 ŒLJ I TEXTBOOK OF PEDODONTICS

■ A baby bear shaking hands with the dentist. verbally as well as by pointing to the ring represent­
■ A baby cat sitting alone in the dental chair. ing the child’s choice. The answers represent scores
« A bear lying in the dental chain opening his mouth ranging from 1 (veityliappy and not the least afraid)
wide, and looking at the dental .instruments. to 4 (very much afraid). Thus, the test can give a
« A dentist examining the teeth and holding instru­ possible score rattgingfrQin 5 to 20.
ments in the mouth of a puppy.
■ A dentist drilling a tooth of a puppy, dental as­ The child is encouraged to give an answer on how
sistant standing beside the chair. he or she would feel, being in the same situation as
■ A dentist giving a dental hygiene instruction to a the child in the picture. Each set of pictures is con­
kitten. structed in two versions; one for boys and one for
■ A puppy being rewarded by the dentist after the girls.
treatment.
The sentence completion task contains fifteen in­
The pointing pictures contain a set of five pictures complete sentences, which are read to the child con­
- (ISO A4 size papers) showing a (human) child in five secutively. The child is instructed to complete the
different dentally related situation. sentences by saving the first word or words that
« Just before going to the dentist come to mind.
« The dentist examining the mouth
« The dentist giving an injection The above method can also be used with computer
■ The dentist drilling aided hand mounted display of virtual realities.
■ Ly i ng in bed about to fa II asleep/dreaming about
dentists. Self-Assessment
1. What is the emotion present at birth?
Each card shows two different reactions; one happy, 2. Define fear?
non-fcarful child, and one sad and fearful child. Four 3. What is imitative fear?
rings of different sizes are situated below each pic­ 4. What is the difference between anxiety and pho­
ture. representing four different feelings or answers bia? i
to'the picture: very happy and not the least afraid; 5. What are the different types of cries?
feeling very much afraid; feeling somewhat afraid; 6. How does a two year old boy express his anger
-*
feeling very very much afraid. Answers are given
 4.3 Behavioural Science and its Application
in Pediatric Dentistry
PaulU, TandonS

Introduction Classification of child’s behaviour observed in

dental clinic (Table 4.6) —-
Behavioural dentistry is an interdisciplinary science
which needs to be learned, practiced and reinforced
Wilson’s classification (1933)
in the context of clinical care and within the commu­
nity oral health care delivery system. The objectives a) Normal or bold: The child is brave enough to
of this science is to develop in a dental practitioner face new situations, is co-operative, and friendly
an understanding of the interpersonal, intrapersonal, with the dentist.
social forces that influence the patients behavior. b) Tasteful or timid: The child is shy, but does not
The clinician must acquire this knowledge to develop interfere with the dental procedures.
appropriate behavioral skills with an improved qual­ c) Hysterical or rebellious: Child is influenced by
ity of communication and management of patients. home environment - throws temper-tantrums and
Behavioral dentistry also teaches to develop a rec­ is rebellious.
ognition and understanding that the body and mind <5 Nervous or fearful: The child is tense and anx­
are not separate entities, and focuses on patients so­ ious, fears dentistry.
cial, emotional and physiological dental experiences.
Frankel’s classification (1%2) -
Definitions (Frankel’s behaviour rating scale)
Behaviour: is an observable act, which can be de­
scribed in similar ways by more than one person. It Rating Behaviour
is defined as any change observed in the function­
ing ofan organism. Learning as related to behaviour 1. Definitely Refuses treatrnenf cries forcefully,
is a process in which past experience or practice re­ negative. extremely negative behavior
sults in relatively permanent changes in an individu­ (--) associated with fear.
al’s behaviour. 2. Negative Reluctant to accept treatment and
(-) displays evidence of slight
Behavioural science: is the science which deals with
negativism
the observation of behavioural habits of man and
3. Positive Accepts treatment, but if the child has
lower animals in various physical and social envi­
(+) a bad experience during treatment,
ronment including behaviour pedodontics, psychol­
may become uncooperative
ogy, sociology and social anthropology.
4. Definitely Unique behavior, looks forward to and
Behavioural Pedodontics: It is a study of science which positive understands the importance of good
helps to understand development of fear, anxiety and preventive care
anger as it applies to child in the dental situations.
 <EH> I TEXTBOOK-OF PEDODONTICS

Table 4.6: Classification of child’s behaviour observed in dental clinic

Co-operativelsehavioT Lacking co-operation Disruptive behavior

■ Positive ■ Disabled physically ■ Seductive or demanding

■ Potentially cooperative ' J ■ Medically compromised ■ Obsessive or resistant

■ .Cooperative with « Mentally disabled ■ Angry or aggressive

reservation (timid ■ Somatizing behavior
child) ■ Dissociation or psychotic
behavior
■ Depressed behavior
■ Addictive behavior (now-a-days
very common in adolescents)
- Drug abuse
- Eating disorder

Lampshire (1970) b) Lacking cooperative ability

Usually seen in young child, (0-3 yrs.), disa­
1. Cchoperative: The child is physically and emo­ bled child, physical and mental handicap.
tionally relaxed. Is co-operative throughout the c) Potentially cooperative
entire procedure. Has the potential to cooperate, but because of
2. Tense cooperative: The child is tensed, and co­ the inherent fears (subjective/objective) the
operative at the same time. child does not cooperate.
3. Outwardly apprehensive: Avoids treatment ini­
B. Un-cooperative (Negative behaviour)
tially, usually hides behind the mother, avoids
a) Uncontrolled/Hysterical/Incorrigible
looking or talking to the dentist. Eventually ac­
Usually seen in: <
cepts dental treatment.
- Preschool children at their first dental visit
4. Fearful: Requires considerable support so as to
- Temper tantrums i.e., physical lashing out
overcome the fears of dental treatment.
of legs and arms, loud crying and refuses
5. Stubborn/Defiant: Passively resists treatment by
to cooperate with the dentist.
using techniques that have been successful in
b) Defiant behavior/obstinate behavior
other situations.
- This type can be seen in any age group.
6. Hypermotive: The child is acutely agitated and
- Usually in spoilt or stubborn children.
resorts to screaming kicking etc.
- These children can be made co-operative.
7. Handicapped: Physically/mentally, emotionally
c) Tense co-operative
handicapped.
- These children are the borderline between
8. Emotionally immature
positive and negative behavior.
- Does not resist treatment but the child is
Classification given by Wright (1975)
tensed at mind.
d) Timid behavior/shy
A Cooperative (Positive Behaviour)
- Usually seen in a overprotective child at
a) Cooperative Behaviour
the first visit
Child is cooperative, relaxed with minimal
- Is shy but cooperative
apprehension.
 SECTION 4 : PSYCHOLOGICAL DEVELOPMENT AND BEHAVIOUR MANAGEMENT I CSI

e) Whining type: Complaining type of behaviour

allows for treatment but complains through­
out the procedure.
f) Stoic behavior: Seen in physically abused chil­
dren. They are cooperative and passively ac­
cept all treatment without any facial expres­
sion.

Factors which affect child’s behaviour in the dental

office: (Table 4.7)

I. UNDER THE CONTROL OF THE DENTIST

Fig. 4.2 Developing rapport with the child patient.
1. Dental clinic:
■ Dental office should be warm and simulate a
are piWerable for younger children. Children
homely environment Healthy communication
should not be kept waiting for too long in the
with the child should be^established. A pleas­
waiting area because they tend to become rest­
ant environment helps the children to be relieved
less.
of anxiety about the dental situation (Fig. 4.2).
■ No long appointments are given to children
■ The operating environment should be made
because of a trend towards deterioration of
colorfuljand lively with posters. TV-and
behavior towards the end of the treatment pe­
\ridepgames and a separate waiting room for
riod.
the children is necessary and this should con­
« Preparatioiiof theehild to the dental clinics
tain toys, for all age groups, story books and
can be done by use oftelephone/letter/pani-
comics.
phlets. This decreases the anxiety of die child.
• It should have a separate exit and an entry
door. Dental auxiliary should be kind to the
2. Effect of dentist’s activity and attitudes
' children and should greet them with a smile.
The dentist should form a good impression on die
■ Appointment time should always be short, i.e.
child. He/she should avoid jerky, and quick move-
less than 30-min. Early morning appo^mtriiehts

Table 4.7: Factors which affect child’s behaviour in the dental office

Under the control of Out of control of the dentist Under the control of die parents
the dentist

Effect of dental office Growth and development Home environment

environ nyent.
Effect of dentist’s activity Nutritional factors Family development and peer
and attitudes. influence
Dentist’s attire Past dental experiences Maternal behavior
Presence/absence of Genetics
parents in the operatory
Presence of an older School environment Socio­
sibling economic status.
Œ0> I TEXTBOOK OF PEDODONTICS

mcnts and should be fluent in his words and d Empathy and support: Empathy is the capacity
actions. to understand and to experience the feelings
of another without losing one’s own objectiv­
Jenks (1964) has described six categories of ac­ ity. Dentists should noFbe totally engrossed
tivities by which the dentist can foster or enhance in the technical aspect of therapy. They must
cooperation in children. They are: have the sensitivity and capacity to respond
a. Data gathering and observation to the child’s feelings. He/she can achieve
b. Structuring this by the following examples:
c. Extefnalization - permitting the child to express their feel­
d. Empathyand support ings without rejection
e. Flexible authority - communicating to the child that their
f Educationandtraining reactions are understood
- comforting the child when it is needed
a. Data gathering and observation - encouraging children when they show
This involves collecting the type of informa­ acceptable behavior
tion about a childandhis parents that can be - listening to the child’s comments when
obtained by a formal or informal office inter­ they wish to talk.
view or by a written questionnaire. Observa­
tion includes noting the behavior of the child e. Flexible authority: This includes compromises
as he steps into the dental office during his­ made by the dentist to meet the needs of the
tory taking and while the dental procedure is particular patient.
being carried out.
£ Education and training: The dentist should im­
b< Structuring: Refers to establishing certain plement a program which both educates chil-
guidelines of behavior set by the dentist and dren and their parents as to what constitutes
his team to the child so that the child knows good dental health and which stimulates them
what to expect and how to react. For example to make the behavioral changed necessary to
the dentist explains to the child in a language achieve these goals.
that he understands, the importance of the den­
tal treatmehtahd~its purpose. He also pre­ 3. Effect of dentist’s attire: If a chi Id has previously
pares the child for each phase of the treatment experienced a stressful situation which includes
in advance. the presence of someone in white attire such as a
physician, the mere presence of a white clothed
c Extern alization : It is a process by which the individual would be sufficient to evoke a nega­
child’s attention isjocussed away from the tive behavior.
sensa^tions„jS5Q£iated wiHrihedental treat­
ment. There are two components of externa li- 4. Presence or absence of parents in the operators:
zation: This depends on the behavior of the child, parent
- distraction and dentist. Mother’s presence isessential for a
- involvement preschool child, handicappedchild etc. An older
The objective is to interest and involve the child does not require mother’s presence because
child but at the same time not to let him into of emotional independence of these children as
verbal or motor discharges which might inter­ they grow older. Dentists are usually comfort­
fere with the necessary procedure. able and relaxed when parents are in the recep­
tion room.
 SECTION 4 : PSYCHOLOGICAL DEVELOPMENT AND BEHAVIOUR MANAGEMENT |

5. Presence of an older sibling: An older sibling tive behavior. Therefore the emotional quality of
serves as a role model in a dental situation. This past visits rather than the number of visits is sig­
again depends on the age of the patient. Presence nificant.
3f an older sibling has:
■ little effect on behavior of a 3 year old patient 4. Genetics
i no effect in case of 5 year old patients « Genetics plays a very important role in psy­
■ most noticeable effect among 4 year olds chological development.
■ This genetic influence is again modified tty the
OUT OF CONTROL OF THE DENTIST environment i e.; there should be a constant
interaction between genetic programme ofthe
L Growth and development child and environment for the psychological
■ If therelslideficlenc}' in physical growth and development of the child.
development or congenital malforh^tions, e.g.
cleft lip, as awareness^ of the deformity in- 5. School environment
creases it leads to psychological trauma due 50% of the child’s development is affected by
to rejection by the society. school and thejetMim^5()%by the home envi­
■ Mental retardation, epilepsy, cerebral palsy etc. ronment. In the school, teachers and peers help
make the child mentally handica] .Here, the to influence the behavior of the younger children.
child cannot react to the requirements of the Also, seniors become role models to the juniors.
mother and the expectations_of the society.
Hence, there is a failure of cognitive develop­ 6. Socio-economic status
ment and therefore variations in the behavior ■ High socio-economic status child may develop
are encountered. normally because the family can provide all
■ Also, a venr young child reacts very differ­ the necessary requirements to aid in a normal
ently and the same response may be trans­ psy chologic development. On the other hand,
formed to a positive behavior, as the child this child may also become spoilt if he always
grovvsolde£^TIiusthcintellectual age of 3 gets what he wants..
years seems to be that point in developmental ■ A low socio-economic status - child develops
progress that signifies a maturational readi­ resentment and is tensed as the child gets lit­
ness to accept dental treatment. tle attention and is often neglected. It also can
directly affect the child’s attitude towards the
L Nutritional factors value of dental health.
■ Studies have shown that an increased intake
of sugarcausesan irritable behavior“ III. UNDER THE CONTROL OFTHE PARENTS
■ Hypogiy^nja causes a criminal behavior
■ Skipping breakfast leads to an impaired per­ 1. Home environment:
formance ■ The home is the first school where a child
■ Nutritional deficiency also affects the mile­ learns to behave. All the home individuals
stones of biological and cognitive develop­ influence the child’s behavio£ but none so
ment much as the mother, e.g. in case of a broken
home, the child may feel insecure, inferior,
>. Past medical and dental experiences apathic and depressed. Mother child relation-
Any past unpleasant dental experience, prior hos­ ship has been described as one-tailed. «
pitalization, surgicaHntervention, sickness, etc., ■ Postnatal behavior of the child d^»^ ^
are associated with a high degree of uncoopera­ the prenatal emotional status tlte
 «ED I TEXTBOOK OF PEDODONTICS

2. Family development and peer influences: Maternal influences on personality development

■ Position of the child, status of the child in the Parental characteristics are viewed as unilateral in­
family, parental attitudes can influence the fluences on the developing child and is described as
child’s behavior. Over indulgence by parents, one tailed’. Most of the relevant mother-child rela-
can lead to a spoilt behavior in the child^who “ tionship fall into 2 broad category
may show sudden outbursts and temper tan­ a. Autonomy vs. control
trums. b. Hostility vs love
■ Internal family conflicts affect children’s
behavior. The child can sense disharmony in Mothers who allowed enough autonomy, and who
the family and this can emotionally fnistrate expressed affection had children who were friendly,
the child. and cooperative. Punitive mothers and those who
ignored their children did not have sons who exhib­
Sibling relationship influences child behavior ited these positive behavioral features.
as follows:
Maternal attitude and child’s behavior
Older sibling
Mother’s Child’s behavior
I behavior
Sabotage younger child's Sibling Overprotective Shy, submissive, anxious
adaptiveness Rivalry dominant
Over indulgent Aggressive, demanding, display
of temper tantrums
Misbehavior by the child in
the dental office Under Usually well behaved, but may
affectionate be unable to cooperate, shy,
may cry easily
The younger child always tries to follow the model t
of the older sibling and family members thus show­ Rejecting Aggressive, overactive, disobedient
ing the same behavior of siblings.
Authoritarian Evasive and dawdling

3. Maternal behavior:
1. Overprotective mother
■ Maternal influence on the children’s
■ There is usually a close relationship between
physical and emotional development begins
the mother and the child: both physical & emo­
even before birth.
tional interdependence from birth to 4 years.
■ Somatic development of the foetus depends
« Exaggeration of this love and affection leads
on the nutritional status of the mother.
to overprotection, which is harmful to the nor­
■ Neurohormonal system of mother transfers
mal psychological development of the child;
emotion tp the foetus.
overprotection is seen in children whose moth­
■ Postnatal behavior of the child is linked to pre­
ers are ox er indulgent or dominating. They give
natal emotional status of the expectant mother,
everything to the child so that the child is to­
e.g. Emotional stress during pregnancy can
tally dependent.
lead to ail excessively active and irritable in­
fant.
Causes of oyerprotection:
■ Agents such as and
keratogenic/totipotentdrugsaffect the child’s a. Mothers who have conceived a child after a
long time.
development if coiisumed durin^thepregna^. )
 SECTION 4 : PSYCHOLOGICAL DEVELOPMENT AND BEHAVIOUR MANAGEMENT |

b. Only child. Features of the child:

c. Sick child/handicapped child. The child appears to be well behaved and well
d. Financial reasonsfetc adjusted. They are shy and it is difficult to estab­
lish a good rapport, and may be uncooperative to
Features of auoverprotection and dominance in dental treatment However, through affection and
child love the child may be made to respond.
■ The overprotected child is not permitted to use
his own initiativeorniakedecisions forTiim- Causes for under affection
self. a) Unwanted child
■ The mother takes active part in his social ac­ b) Childbirth was not anticipated
tivities. The child does not leam to cope with c) Hampers the mother’s career and ambitions
the problems and anxieties of life. d) Unhappy mother because of absent father due
■ The child is submissive, shy, ajixious and fears to death, divorce etc. Lack of attention
new situations, lacks in self-confidence. These e) Emotional problems
children may be co-operative but it may be dif­
ficult to create a good rapport with the child. Rejecting mother
They are polite, obedient, disciplined. This may be in the form of physical violence or
verbal ridicule
Management
■ Create self-confidence in the child Neglect manifests as:
■ Familiarize the child with the clinic, and the a) Physical punishment, violence, especially in
dentist’s auxiliaries the uneducated mothers. Battered baby syn­
■ Tell-show-do technique drome.
b) Refusal to spend time with the child
Z. Overp rotective - overindulgent mother c) Refusal to spend money on the child
Features of the child: d) Neglect child’s health
■ The child is aggressive, demanding, display e) Emotional and physical neglect
temper tantrums, if their wishes are not met.
These children expect constant attention and Features of the child
services. a) Ол ег reactive, revoltmg. aggressive, disobe­
■ They are used to getting their way at home dient -
They are obstinate, stubborn, spoilt. These b) Tries to gain attention of others by showing
children will try to dominate over the dentist overt behaviors
and demanding. They demonstrate angiy out­ c) These children are constantly criticized,
burst if their demands are not met with. These nagged, tortured with displays of displeasure.
children are well behaved and well adjusted d) Lack of self-esteem
but the dentist will be unable to establish a e) They are most difficult to deal in the clinic be­
good rapport with the child. cause outwardly they are well behaved and
adjusted but are emotionally insecure.
J. Under affectionate mother
Here, the child is devoid of love and care. Under Management
affection varies from mild detachment to neglect a) Develop confidence in the child by shoeing
and this may begin during pregnancy or later in love and care.
childhood. b) Meet their demands as soon as possibly
 I TEXTBOOK OF PEDODONTICS

5. Authoritarian mother Behaviour modification: is defined as the attempt to

The mother is very authoritarian and has^otcgr- alter human behaviour and emotion in a beneficial
tain norms forlhe child to follow. This may vary way and in accordance with the laws of learning.
from physical abuse to verbal ridicule.
Behaviourmanagement cobejJ^^
Features of the child: ■ Non pharmacological (Psychological Approach)
a) Submission withresentment and later evasion ■ JPh^n^btowfl’" S
b) Evasive, dawdling child, obeys commands slowly
and with delay. Non-phannacological methods of behaviour manage­
c) Parents are not supportive to the child and rather ment
criticize them. Therefore, these children are often 1. Communication
afraid of dentist and resist dental treatment. 2. Behaviour shaping (modification)
d) The child shows a heightened avoidance gradi­ a) Desensitization
ent and seeks to evade or delay the response. b) Modelling
c) Contingencymanagenient
Effects of maternal anxiety 3. Behaviour management
a) Attitudes and experiences of one’s family in rela­ a) Audio analgesia-
tion to dentistry seem to be the most important b) Bibfeed back
factor in determining how an individual will react c) Voice control
to dentistry. d) Hypnosis-
b) People who come to thé dentist conditioned to e) Humor-
respond with tension and fear do so chiefly be­ f) Coping.
cause of the way dentistry is presented to them g) Relaxation
in their homes. h) Implosion therapy \
c) The mother’s reaction to dental treatment has a i) Aversive conditioning
profound influence on the child’s attitude towards
dentistry. Highly anxious mothers may have their Pharmacological method of behaviour management
children displaying negative and uncooperative 1. Pre-medication
behaviors. a) Sedatives ahff hypnotics
b) Anti-anxiety drugs
BEHAVIOUR MANAGEMENT c) Antihistamines
2. Conscious sedation
Definitions 3. General anesthesia

Behaviour management: is defined as the means by Communicative management

which thedcntal health team effectiveiv aiidjefîi- ■ Communicative management is universally used
ciently performs dental treatment and thereby instills in pediatric dentistry with both the co-operative
a positive dental attitude (Wright 1975). and uncooperative child (Chambers 1976).
■ It comprises the most fundamental form of be­
Behaviour shaping: is the procedure which slowly haviour management in that it is the basis for es­
develops behavior by reinforcing a successive ap­ tablishing a relationship with the child which may
proximation of the desired behaviour untiTtHe de- allow a successful completion of dental proce­
sired behaviour comes into being. dures and at the same time, may help the child
develop positive attitudes towards dental care.
 SECTION 4 : PSYCHOLOGICAL DEVELOPMENT AND BEHAVIOUR MANAGEMENT | <!TO

■ It is the means by which the dentist gets his point ■ Sitting and speaking at the eye level allows for a
across, making himself understood by the use of friendlier atmosphere.
words or expressions. One should always try to ■ Communication is a multisensory process, which
establish communication from the first entry into includes a transmitter, the spoken word is the me­
the reception area. dium and the pediatric patient is the reiver;

Types of communication: Use of euphemisms: Euphemisms are substitute

a) Verbal communication is by speech words, which can be used in the presence of chil­
a) Nonverbal (multisensory communication) is by: dren.
- Body language
- Smiling Choice of words, which is used by the dentist or
- Eye contact staff influence the emotional status of the child.
- Expression of feelings without speaking Therefore the use of euphemism7reframing is very
- Showing concern important while addressing to the child.
- By touching the child ■ Anaesthetic solution is referred as water to put
- Giving him a pat the teeth to sleep.
- Giving a hug Cariesls7elg®das a tooth bug
:) Both using verbal and non-verbal. Rubberdam as a raincoat
■ Radiograph as tooth picture
How to communicate?
■ Communication should be comfortable and re- Reframing: It is defined as taking a situation out­
Jææd. side the frame that up to that moment contained the
i Language that is chosen should contain words individual in différait conditions, and visualize
that express pleasantness, friendship and con­ (reframe) it in a xwy acceptable to the person in­
cern. Verbal effects are delineated through selec­ volved and with this reframing, such that both the
tion of words and/or sounds, tone of voice and original threat and the threatened situation can be
voice infection (Korch 1972). safely abandoned <Beiyai Hill Peretz 1999).
1 ^rt>al communication is best for younger chil-
dren more than 3 years of age. Voice that is used The dental office/reception/waitingarea is a medium
, shoulcTbeconstant and gentle. Tone of voice of communication, which sends messages to the pa­
can express empathy and firmness. Content of tients. A friendly a
the conversation should be such that from the the child can be made Swi fortable with the environ­
very beginning the dentist should make the child ment. In younger children, nonverbal communica­
feel that we are his well wishers. The conversa­ tion is more important.
tion should include asking the child’s name, age,
class and background Behaviour shaping
i The patient always prefers to be addressed by ■ It involves the use of selected reinforces that
his name. being learned will hopefully change a child’s
i Compliment him about his appearance. Ask ques- behavior from an inappropriate to an appropriate
tions about his class,fris likes/dislikes. Commu­ form. This is based on the “stimulus-response”
nication should be from a single source, either theory. For example when a child enters the re-
between the dentist and the child or the child and ception room and associates this with a previous
the dental assistant to avoid confusion. The child dental experience which was unpleasant, the
is very sensitive to expression changes. child’s’ internal responses would be fear and
ety while the external response would be crying.
 <EE>"I TEXTBOOK OF PEDODONTICS

■ This is a step-by-step procedure to make the child come the many small dental related anxieties
involved in dental therapy. When shaping the of any chi ld.
behavior the dentist is teaching a child to be­
have. These children needloTbe communicative Indications
and cooperative to absorb information that may a) Firstvigit '
be complex to them. Children cannot always grasp b) Subsequent visits when i ntroducing new den­
the overall procedure with a single explanation. tal procedure
Therefore it is necessary to divide the explana­ c) Fearful child
tion for the procedure and consequently have to d) Apprehensive child because of information
be led through the procedure slowly; it is neces­ received from parents/peers
sary to riiake all explanations at the child’s level
of understanding by an appropriate use of eu­ TSD technique is applied as follows:
phemisms. a) The dentist using the language that the child
can understand and tell the patient what is to
Behaviour modification involves three techniques. be done, it is presented slowly and repeatedly.
b) The dentist demonstrates the procedure to the
1. Desensitization child using a mrfdel or himself and is done
«“Joseph Wolpe (T975) used to remove fears and slowly.
tension in children who have had previous un­ c) The dentist proceeds to do the dental proce­
pleasant dental experience or negative dure exactly as described.
behavior.
« Desensitization is accomplished byjeaching This is effective in children more than 3 years of
the child a competing response such as relaxa.- age.
%

tion and then introducing progressively more

threatening stimuli. 2. Modeling (Fig. 4.3b)
■ It is ah effective method for reducing a mala­ Introduced by Bandura (1969) developed from so­
daptive behavior. cial-learning principle procedure involves allow­
• Systemic desensitization is effective because ing a patienttoobserve one or more individuals
the patient learns to substitute an appropriate (models) w ho demonstrate a positive behavior in
or adaptive emotional response (relaxation) for a particular situation; Therefore the patient will
an inappropriate or maladaptive response - frequently’ imitiate the models behavior when placed
anxiety. in a similar situation. Modeling can be done by:
aJJLive~models - siblings, parents of child etc.
Method popularly used now-a-days for modifying bTFilmed models
the behavior by desensitization in children is: c) Posters
Tell ShowDotechnique (TSP) (Fig. 4.3a) . d) AudioyisuaLaids
>^Addleslon 1959, introduced the concept of Tell,
Show, Do. Learning through modeling is effective when:
■ Tell and^show every step and instrument and a) Observer is in a state of arousal.
explain what is going to be done. b) When the model lias relatively more status and
■ Continuously and in grades from the least fear prestige.
promoting object or procedure and move in c) When there are positive consequences asso­
higher grades to more fearful objects. ciated with models behavior.
■ By having verbal (tell) and nonverbal (show ■ Modeling technique seems to improve the
and do) interactions, available, one can over- behavior of apprehensive children who
 SECTION 4 : PSYCHOLOGICAL DEVELOPMENT AND BEHAVIOUR MANAGEMENT |

Fig. 4.3a Behaviour modification by Fig. 4.3b Behaviour modification by Modelling

Tell Show Do Technique

Fig. 4.4 Involving the child in Fig. 4.5 Hand over mouth technique
watching his favourite program on for aversive conditioning
TV. fixed on ceiling at eye level
(which also serves as a distraction
technique)
 CEE) I TEXTBOOK OF PEDODONTICS

have had no previous dental experience ■ Behaviour management methods in pediatric den­
(Klarman R1980). tistry are directed towards the goals of communi­
■ An important advantage of live modeling cation and education. The relationship between
is that no additional equipment; personnel the dentist and the child is built through a dy­
or alterations in the dental routine are namic process of dialogue, facial expression, and
required. voice tone; all methods of delivering a message.
The goals of behaviour management are to
3. Contingency management
achieve good dental health in the child and to
It is a method of modifying the behavior of chil-
help develop the child’s positive attitude towards
drenby presentation or withdrawal of reinforcers.
dental health.
These reinforcers can be:
■ Behaviour management is thus not an applica­
a) Positive reinforcer: is one whose contingent
tion of individual techniques created to deal with
presentation increases the frequency of
the child, but rather a comprehensive methodol­
behavior (Hemy W Fields 1984).
ogy meant to develop a relationship between the
b) Negative reinforcer: is one whose contingent
patient and the doctor which ultimately builds
withdrawalincreases the frequency of behavior
trust and allays fears and anxieties.
(Stokes and Kenndy 1980). Negative reinforcer
is usually a termination of an aversive stimu­
Child can be managed by the following methods:
lus e.g.: withdrawal of the mother.
1. Audio analgesia: or" white noise” is a method of
Types of reinforcements can be reducing pain. This technique consists of pro­
a) Social: for e.g. praise, positive facial expres- viding a sound stimulus of such intensify that
j sion, physical contact by shaking hand, hold- the patient finds it difficult to attend to anything
| ing hand, and patting shoulder or back. else (Gardner, Licklider, 1959). Auditory stimulus
| b) Material: may be given in the form of toys, such as pleasant music has been used to reduce
games. Sweets are not given - as reward since stress and also reduce the reaction to pain.
it causes caries. 2. Biofeed back: involves the use of certain instru-
c) Activity reinforcers: Involving the child in nientstodetect certain physiological processes
some activity like watching a TV show/special associated with fear (Buonomono, 1979).
programmes with him. For the benefit of con­ For example if blood pressure is high the instru­
tingency management-social reinforcers are the ment gives stimulation and the subject is taught
most effective. to control the signals, therefore it is useful in anxi­
ety and stress related disorders. Electroencepha­
Behaviour management logram, electromyography can also be used in
• Behaviour management should go hand in hand bio-feed back.
with the hand piece skills and knowledge of den­ 3. Humor: helps to elevate the mood of the child,
tal materials for the successful treatment of chil­ which helps the child to relax. Functions of humor :
dren. Disruptive behaviour can interfere signifi­ a) Social: forming and maintaining a relationship
cantly with providing quality dental care, result­ b) Emotional: Anxiety relief in the child, parent
ing in increased delivery time and risk of injury to and doctor.
the child. Surveys of clinicians have found that c) Informative: Transmits essential information in
dentists consider the uncooperative child to be a non-threatening way.
among the most troublesome problems in clinical d) Motivation: It increases the interest and in­
practice. Recent findings suggest that nearly one volvement of the child.
in four children (22%) seen by pediatric dentists e) Cognitive: distraction from fearful stimuli
may present marked management problems. (Fig. 4.4).
 SECTION 4 : PSYCHOLOGICAL DEVELOPMENT AND BEHAVIOUR MANAGEMENT |

4. Coping: It is the mechanism by which the child 6. Relaxation This technique is used to reduce
copes up with the dental treatment.(It is defined stress and is based on the principle of elimination
aisTliTcognitive and behavioral efforts made by of aiixietyRdaxation involves a series of basic
an ^dividual to master, tolerate or reduce stress­ exercises, which may take several months to learn,
fill situations (Lazaue 1980). Patients under stress and which require the patient to practise at home
prefer to draw comfort or reassurance from an for at least 15 min per (fay.
authority figure. Thus establishing a close or
trusting relationship with the doctor or nurse. 7. Hypnosis: Hypnosis is an altered state of con­
sciousness characterized by a heightened sug­
Coping effects may be of two types gestibility to produce desirable behavioraTand
a) Behavioural: are physical and-veibal activities physiological changes. Hypnosis is one of the
in which the child engages to overcome a most effective nonpharmacologic therapies that
stressful situation. can be used with children for a number of differ­
b) Cognitive: The child may be silent and think­ ent procedures (Romanson, 1981). When used in
ing in his mind to keep calm. Cognitive coping dentistry, it can be termed as hypnodontics
strategies can enable the children to: (Richardson 1980) or psychosomatic or sugges­
■ Maintain realistic perspective on the events tion therapy. Greatest benefit of hypnosis is to
at hand (reality-oriented working) reduce anxiety and pain.
■ Perceive the situation as less threatening
(cognitive reappraisal) 8. Implosion therapy: Sudden flooding with a bar-
■ Calms and reassures themselves that rage of stimuli which have affected him adversely
everything will be all right (emotion regu­ and the child lias no other choice but to face the
lating cognitions) (Sandra L Cuny (1988). stimuli until a negative response disappears. Im­
plosion therapy mainly comprises of HOME, voice
Signal system: This method is followed in our
control and physical restraints.
clinic wherein as a part of coping, when it hurts,
we ask the child to raisejusjiand as suggested
9. Aversive conditioning
byMusslemann 1991.
Child who displays a negativebehavior and does
The normal coping mechanism utilized by den­ not respond to moderate behavior modification
tists to reduce pain and tension are friendliness, technique falls into the category5 *7 of Frankel’s de­
support and reassurance. finitive negative behavior. Aversive conditioning
can be a safe and effective method of managing
5. Voice control extremely negative behavior. Those dentists who
■ It is the modification of intensity and pitch of contemplate using it should obtain parental con­
one’s own voice in an attempt to dominate the sent prior to its use (Patricia P Hagan 1984). Two
interaction between the dentist and the child. common methods used in the clinical practice are
■ Used in conjunction with some form of physi­ HOME and physical restraint:
cal restraints and hand-over-mouth exercise.
(HOME) is considered as acceptable by the A HOME (Hand over mouth exercise)
parents for nearly all-dental procedures (Henry The behavior modification method of aversive
and Marilyn 1984). conditioning is also known as HOME. Introduced
« Change in tone from gentbLiafirm is effective by Evangeline Jordan 1920 (Fig. 4.5)
in gaining the child’s attention and reminding
him that the dentist is an authority figure to be The purpose of HOME is to gain
obeyed: a child so that communication canbe
 <EF> | TEXTBOOK OF PEDODONTICS

Indications: HO MAR (airway restricted)

■ A healthy child who can understand but who ■ The advantagc behind airway restriction is that
exhibits defiance and hysterical behavior dur­ the child will be quiet so as to breathe and the
ing treatment. screaming will decrease so that the doctor can
■ 3.-6.ycaxsjOld^r proceed.
• A child who can understand simple .verbal com- ■ Together witkTumdoyer mouth nostrils arc
pinched for 15 sec.
■ Children displaying uncontrollable behavior ■ Bela nger 1993, believed that airway restrict ion
was the critical element and it should be
Contraindications avoided.
■ Child under 3 years of age
B. Physical restraints: Last resort for handling un­
■ Handicapped cluld/iinniature child, frightened
cooperative patients or handicapped patients.
child
Restraints are usually needed for children who
■« Physical,jnental and emotional handicap
are hypermotive. st ubborn or defiant (Kelly 1976).
The child is seated in the mother’s lap and one of
Factors to be considered before applying HOME
the mothers hand is placed on child’s forehead
technique
while the other hand isglaced on both thc child’s
« HOME technique should not be used as a rou­
wrists. Physical restraints involve restriction of
tine procedure for the man'a^^iffpf the child.
movement of the child’s head, hands, feets or
« Inform’The’parents about the procedure.
body. Itcan be:
« Consent of the parents is very important.
■ active - restraints performed by the dentist,
I « Pediatric dentists should be aware of the
slalf or pa rentwithout the aid of a restraining
| changing laws that govern inform consent
device.
1 (Hagan 1984, Nash 1988, Scott 1991).
I « passive - with the aid of restraining device
i
J Technique: After determining the child’s
I behavior, the dentist firmly places his hand over^ Types of restraint:
a) For body - Pedi wrap 1
| the child’s mouth and behavioral expectations are
-— ^Papoose board
I calmly expfaineddoseto the child’s ear. When
- Sheets
J the child’s verbal outburst is completely stopped
I and the child indicates liis willingness to co-op- - Beanbag with straps
I erate, the dentist removes his hand. Once the - Towel and tapes
b) For extremities -Velcro straps
J child co-operates, he should be complimented for
- Posey straps
( being quiet and praised for^good^ehayiorTlt
- Towel and tape
j ^-^shouid be noted that the child’s airway js not
c) For the head - Head positioner
restricted while performing the technique and the
- Forearm body support
whole procedure should not last for more than
d) Mouth
20-30 sec.
-Mouthblocks
Several variations of HOME -Banded tongue blades
■ Hand over mouth with the airway unrestricted -Mouth props are used at the time of local
« Handover mouth and the nose and the airway anesthesia to prevent child from closing
restricted his mouth. Mouth props can also be used for:
• Towel held over the mouth only - Physical/mental handicapped child.
■ Dry towel held over thenose and mouth - Young child who cannot keep the
■ Wet towel held over the nose and mouth mouth open for a long time.
 SECTION 4 : PSYCHOLOGICAL DEVELOPMENT AND BEHAVIOUR MANAGEMENT | <!%>

- Child becoming extremely fatigued 2. What are the factors that influence the child’s
because of long appointments and behaviour in the dental office?
J frequently closes his mouth. 3. What is timid behaviour?
4. What is Frankel s behaviour rating?
c) Others - Straps arc attached to dental unit to 5: Wliat is the behaviour of a neglected child?
restrain a child at the chest w aist and 6. What are the causes of overprotection?
, legs. It is used mainly to control the 7. What is contingency management?
* activity of mentally or physically 8. Differentiate between behaviour management and
handicapped patients. behaviour modification,?
- Sheets: are also used to restrict 9. What is desensitization?
patient’s movements. This type of 10. What is Tell Show Do approach?
restraint does not secure the child to 11. What is audio analgesia / white noise?
the dental chair unless an additional 12. Wliat is aversive conditioning?
sheet is used to tie around the 13. Wliat is HOME technique?
patient and the chair. 14. What is stimulus-response theory?
- Papoose board/Pedi wrap 15. What is hypnodontics?
16. What is voice control technique?
Self-Assessment
1. Défi ne behavioural science?
 4.4 Pharmacologic Means of Patient
Management
Kevin Allen (late), Stephen S

The performance of painless procedures for the child protective reflexes, including inability to respond
is one of the key factors in establishing a good rap­ purposefully to a verbal command.
port. To this effect the use of pharmacologic means
has made dental treatment acceptable to a large 3. General anesthesia - a controlled state of uncon­
extent. These procedures can be carried out in the sciousness, accompanied by partial or complete
normal circumstances with the help of behavior
loss of protective reflexes, including inability to
shaping techniques.
maintain an airway independently and respond
purposefully to physical stimulation or verbal
In cases of disruptive behaviour, the use of behavior
management techniques can also be used. Unfortu­ command.
nately in some cases, it may not be possible either
due to the patient lacking cooperation or the sys­ 4. Ambulatory, outpatient or day care anesthesia
temic background of the patient demands that phar­ refers to the delivery of anesthetic care in which
macological means be used. The use of sedation, patients are discharged home on the day of treat­
relative analgesia or general anesthesia may be war­ ment.
ranted in these cases, depending on the compliance
of the patient and the procedures required. SEDATION

Terminologies
The use of sedation is advocated in children lacking
cooperation for the short duration procedures. The
American Dental Association [1993] has defined as:
1. Conscious sedation - a minimally depressed level use of sedative agents can also be done in cases
of consciousness, that retains the patient's where premedication is required as in cases of gen­
ability to maintain an airway independently and eral anesthesia. This serves the purpose of making
respond appropriately to physical stimulation and the treatment more acceptable and less anxiety prone.
verbal command. The various routes of commonly used sedatives have
been given in table 4.8
2. Deep sedation - a controlled state of depressed
consciousness, accompanied by a partial loss of
 SECTION 4 : PSYCHOLOGICAL DEVELOPMENT AND BEHAVIOUR MANAGEMENT | <E9

Table 4.8: Sedation [Routes and Agents]

Routes of administration Indications and benefits Limitations and risks

1. Inhalation: [Nitrous ■ Can be used for mild to ■ Agent has weak potency
oxide] moderate.levels, of anxiety ■ It can be used to decrease
■ Analgesia for brief, comfortable the anxiety levels, but not in
procedures children with severe behavior
■ Rapid onset and early problems
elimination and recovery ■ Also cannot be used in
■ The duration of action can be claustrophobic patients,
easily controlled respiratory tract infections.

IL Oral [Several drugs ■ Can be used for preoperative “ ■ Delayed onset of action .
are used] sedation- coupled with unpredicatable
« Used for all levels of anxiety absorption
■ Better acceptability and ease of. ■ Depends on patient
administration compliance
■ The incidence of ARD is less ■ Difficulty in dertermining
drug dosage
■ Trained personnel
proficient in management
of unconscious patient
required

A Hydroxyzine ■ Mild sedative along with ■ Better used in combination

[Vistaril] antiemetic and anticholinergic with other agents
[25 mg/5cc] action
■ Potentiates narcotic and CNS
depressants

B. Promethazine ■ Same as above ■ For mild levels of anxiety only

[Phenergan] ■ Better used in combination
[12.5 mg/5cc,
2.5 mg/5cc] ♦

Ç. Chloral hydrate « For all levels of anxiety ■ Not recommended in

[Noctec] ■ Long working time children below 6 years of age
[500 mg/5cc] ■ Believed to have *a wide range ■ Agitation common in the latent
of safety period and as effects
dissipate
« No analgesia
■ Maximum dose not to exceed
1500 mg

D. Meperidine ■ Best used in combination for ■ Poor oral absorption

[Demerol] 1. Brief procedures with ■ Contraindicated in children with
[50 mg/5cc] promethazine or hydroxyzine COPD, Hypothyroid or liver
2. Longer procedures with dysfunction
chloral hydrate
confd.
 I TEXTBOOK OF PEDODONTICS

Routes of administration Indications and benefits Limitations and risks

E. Diazepam [Valium] ■ Safe agent for mild to moderate ■ Multiple doses required to
[5 mg/5cc elixir, anxiety particularly in children achieve sedation
2, 5, 10, 15 - mg with cerebral palsy, mental ■ Not effective in severe anxiety
tablets] retardation when used alone
■ Children less than 6 years of age
■ Oral absorption equally good as
parenteral

F. Triazolam [Halcion] ■ In addition has anticonvujgant ■ Safety guidelines not fully

0.125, 0.25 mg tablets] activity established
■ Good oral absorption

G. Chorpromazine ■ Used in combination [Lytic ■ Unpredicatable and less

[Thorazine] cocktail] with meperidine or studied
[10 mg/mlsyrup, 10, promethazine
25, 50, 100, 200 ■ Useful in severe behavioural
mg tablets] problems

III. Intramuscular ■ Rapid onset of aciton ■ Injection required and will not
■ More reliable with little patient be liked by children
compliance ■ May cause injury during
administration
■ Limited control over
reversibility

1. Ketamine ■ Dissociative anesthesia where ■ Safety of oral use not yet

[Ketalar] a cataleptic state can be induced established
[10 and 50 mg/ml] ■ Potent analgesic
■ Potential for oral use

2. Midazolam ■ Possesses hypnotic, ■ Little data for effective dose

[Versed] anticonvulsant and muscle in pediatric context
[1 and 5 mg/ml] relaxant properties as well as ■ Used mainly for short
being antegrade amnesic and procedures.
anxiolytic
■ Greater potency as compared to
diazepam
■ Rapid onset of action

IV. Intravenous ■ Most rapid onset of action « Requires extensive armament­

[commonly used is ■ Permits titration and is easily arium, training [specially in
Midazolam] reversible pediatric cases due to anatomic
■ Maintains a line for emergency and behavioural considerations]
drugs ■ Precautions to be taken in
■ feest for invasive procedures Of significant hepatic or thyroid
short duration disease.

■ Rectal, submucosal or subcutaneous are rarely used.

 SECTION 4 : PSYCHOLOGICAL DEVELOPMENT AND BEHAVIOUR MANAGEMENT |

Fig. 4.6a Quantiflex for relative Fig. 4.6 b Quantiftex for relative
analgesia. analgesia.

CONCIOUS SEDATION [RELATIVE’ANALGESIA] 2. Patient should be conscious, respond to verbal

stimuli.
As a dentist, one must decide for oneself, what rep­ 3. Patient should be co-operative.
resents acceptable behaviour. The judicious use of 4. All protective reflexes intact.
conscious sedation has its place in dentistry, but it 5. Vital signs stable and normal.
can also be abused. Conscious sedation is useful 6. Child’s pain threshold should be increased.
if long procedures are advocated for a nervous and 7. Amnesia should occur.
apprehensive child. But it does not approach the
problem of teaching the child to accept the dental Indications
situation as an experience that he or she must meet
■ Patients who cannot cooperate or understand for
several times^a year for the rest of his or her life.
definitive treatment ~
Thus it should be used in conjunction with the
« Patient lacking cooperation because of lade of
psychologic means of behaviour management. What
psychological or emotional maturity
really happens in relative analgesia is that the pa­
a Patients with dental care requirements but are fear­
tients threshold to pain, cold, warmth aid light touch
ful and anxious
is raised. Thus, although the special senses may be
partly obtunded and a sensation numbness is de­
Contra-indications
scribed,superficial and deep reflexes remain active
and the sensorium remains clear (Fig. 4.6a, b). Chronic obstructive pulmonary disorder [COPD],
pregnancy, myasthenia, epilepsy, obesity, bleed­
Objectives ing disorders.
Uncooperative patients, unwilling, unaccompanied
Benett [1978] has stated the objectives to be: Dental difficulties prolonged surgery, iris Tire» uate
1. The patients mood should be altered. personnel
 I TEXTBOOK OF PEDODONTICS

Nitrous oxidé - O,X mixture for conscious sedation Stages of anesthesia and conscious; sedation

This is the most widely used form of conscious se­ The stages of anesthesia have been described by
dation using inhalation of the gases. several authors but the same may not always be
■ Roberts in 1990 has constructed a triad of ele­ possible to delineate during the procedure. How­
ments in relative analgesia (Inhalational) O2/N2O ever during conscious sedation it is important to
gas mixtures (low to moderate as per the patient) . monitor the stages, since the contact with the
• The three elements of importance stated were: patient should be maintained at all times.
1. The administration of low to moderate con­
centrations of nitrous-oxide, carefully titrated Plane 1 - moderate sedation and analgesia
to the patients need.
2. The patient is simultaneously subjected to a ■ Achieved with concentrations of 5 -25% N2O (95 -
steady flow of reassuring and semi-hypnotic 75%).
suggestion. ■ As the patient inhales, reassure that the symp­
3. The use of equipment, such that it is not toms may not be felt. When the symptoms are
possible toadminister 100% nitrous oxide ac­ felt, specially in children the instructions have
cidentally or deliberately. to be adapted to the terminology understood.
Simultaneously, it is also important to use sug­
Pharmacology ofNf) gestion. For example, it important to connote a
floating, light feeling.
a. The patient at rest has tidal volume of 6-8 liters. ■ patient may sense dizziness.
With anxiety this increases. Thus it is necessary ■ Patient may feel tingling in the fingers, toes,
to establish flow rate as per the patients tidal cheeks, tongue, back head or chest.
volume. ■ Marked sense of relaxation, the pain threshold is
raised. \
Capacity of the lungs
■ Diminution of fear and anxiety occurs.
R at e/m inute Tidal volume Average tidal ■ Hearing, vision also impaired but pupils are
volume/minute normal and contract when a light is shown.
■ Perioral musculature is also relaxed.
Adults 12-16/m 500 cc 7 liters
Plane II- dissociation sedation and analgesia.
Child 20-24/m 200-250CC 5 liters

Infant 25-30/m 100-175cc 3 liters ■ Concentrations of25-45%.

■ May or may not experience symptoms.
b. Nitrous oxide is carried in a simple solution in the ■ Psychological symptoms such as dissociation or
body and does not enter any chemical combina­ detachment are felt. A euphoric state, similar to
tion i.e. its solubility in blood is extremely low. alcoholic intoxication (the laughing gas parties).
Thus free state is high and a rapid equilibrium ■ The patient is suffused by a warm wave and may
between alveolar and arterial tension takes place, experience a slight humming or buzzing in the
and the onset as well as elimination occurs in a ear, with a ‘floaty’ feeling.
few minutes. ■ Reduction in blink rate.
■ Patient has pleasant dreams and has a level of
c. It is a weak GA gas and cannot produce full gen­ psychosedation with a leg, hand sliding off the
eral anesthesia on its own. But it is an excellent chair.
analgesic.
 SECTION 4 : PSYCHOLOGICAL DEVELOPMENT AND |EHAVIOUR MANAGEMENT |

■ Patient is conscious and responds to questions, Plane-IV: many develop beyond 65-85%
with however a considerable mental effort in­ Light anesthesia - contact with patient lost.
volved in thinking.
NITROUS OXIDE HAZARDS
Plane-Ill: Total Anesthesia (Analgesia)
Several hazards have been reported such as :
■ Achieved with 45-65% concentrations - ■ Forthe Patient
■ Analgesia is complete. Patients may undergo 1. If enclosed spaces - contraindicated such as
extraction procedure. pneumothorax.
■ Marked amnesia develops. 2. Upper Respiratory Tract Infection,
■ Zone between analgesia and light anesthesia. 3. Respective depression where respiration is on
■ Federmesser has subdivided this into 3 planes. CO2 drive, as O2 increase will diminish this drive
a Lightest plane - state where a kaleidoscope e.g. Bleomycin therapy -pulmonary fibrosis.
of images and thoughts are present 4. Pregnancy as spontaneous abortions may
b. Somnolent state- where contact is still main­ occur.
tained. If deeper planes are readied, nasal air 5. Diffusion hypoxia, which can be avoided by
removed and the patient is asked to breathe keeping the patient on 100% oxygen.
ambient air. He/she will return to lighter plane
in 15-20 seconds, or reduce to 10-15% N2O if ■ Patients/personnel
slower regression is desired. The open mouth 1. DNA synthesis affected - Vitamin B12 oxida­
sign, where the patient has the ability to re­ tion may be suppressed even with brief expo­
spond by keeping his mouth open by himself. sures (continuous inhalation of N2) of at least
Thus never use mouth props, as this may not 6 hours.
enable to assess this sign.
2. Altered Hematopoesis, pernicious Anaemia.
c. Deepest plane - the patient carries put only Thus the procedure of concious sedation has
the simplest of commands only after repeated to be carried out with the maximum precau-
several times.

Table 4.9: Differences between Concious Sedation and General Anesthesia

♦
Concious Sedation General Anesthesia

« At several visits the procedure may ■ Generally a single sitting, once in a

be performed < lifetime procedure
« Patient is cooperative, but anxious and « Patient is uncooperative
fearful
■ Generally no extensive investigations are ■ At least basic investigations are a
required. No premedication is required must. Premedication is also required
either.
■ Patient is conscious and contract is ■ Ventilation is required
maintained
■ Airway is maintained
■ No mortality ■ 99% success rate reported
■ Recuperation period is 1-2 minutes ■ Time consuming procedure
■ NPO not required
« Patient feels he is in control of the ■ NPO strict
situation ■ Patient cannot control the situation
 <M>> | TEXTBOOK OF PEDODONT1CS

lions. The use of scavenging systems have ■ Patients wherein local anesthesia is not effective
been advocated to reduce or eliminate nitrous or the patient is allergic to it.
oxide. ■ Patients who have sustained extensive orofacial
trauma.
Differences between concious sedation and gen­
■ Fearfiil, uncooperative, anxious patient with no
eral anaesthesia are given in table 4.9
expectation that behaviour will improve.
GENERAL ANESTHÉSIA ■ Patients with dental needs who would other­
wise receive comprehensive dental care eg: rural
Certain conditions or situations exist where the man­
areas.
agement of the patient is difficult or impossible with
the psychological means alone. These patients gen­
Chairside general anesthesia [day care, office or
erally as a last resort and as a single sitting proce­
ambulatory anesthesia]
dure may be managed by means of general anesthesia
(Fig. 4.7)
■ In the practice of pediatric dentistry, generally
ASA I or ASA II patients can be taken up for
indications for General Anaesthesia
chairside general anesthesia, where in the proce­
■ Patients with certain physical, mental or medi­ dure may be taken up on an OPD basis, and pa­
cally compromising condition tient discharged the same day. However, depend­
ing on the recover»7 from anesthesia, the patients
may sometimes have to make an overnight stay.
■ Our experience suggests that the three common
reasons for the use of general anesthesia are
handicapped or mentally retarded children, un­
cooperative child, and inability to come for fre­
quent visits. ,
Reasons for administration of GA are given in
'

table 4.10 t
»♦•
« **
* » í**
’

PREANESTHETIC EVALUATION AND PROCEDURES

The American Association of Pediatric Dentistry

Fig. 4.7 Dental procedure under chair side [ 1985] has laid down the following guidelines for the
general anaesthesia documentation to be done prior to treatment.

Table 4.10: Reasons for administation of GA

Group No. Reasons Percentage

1 45 Handicapped/medically compromised 39.14 %

2 27 Uncooperative/lacking cooperative ability 23.48 %

3 43 Coming from far/inability for repeated visits 37'40 %

Tharian and Tandon (1995)
 SECTION 4 : PSYCHOLOGICAL DEVELOPMENT AND BEHAVIOUR MANAGEMENT |

Instructions to parents Cardiovascular systems

The practitioner should provide verbal and written 1. Oxygen consumption is higher in a child than the
instructions to the parents. It should include expla­ adult, resulting in higher metabolic rate. Thus
nation of potential/anticipated postoperative behav­ when apnea develops, hypoxemia develops more
iour and limitation of activities along with dietary rapidly.
precautions. 24-hour contact number should be pro­
vided. 2. Rather than stroke volume, cardiac output in the
child depends more on heart rate. Thus bradycar­
Preoperative health assessment dia is a much more serious sign.

It should be done within 2 weeks prior to the proce­ Renal

dure, to be reviewed at the time of treatment. It should
include: The Glomerular Filteration Rate [GFR] is less in chil­
dren. Thus the fluid electrolyte balance is delicately
i. Health history : a review of the medical informa­ maintained. For this purpose the various kidney dis­
tion available should be performed. The patient orders are to be ruled out.
should be evaluated for
■ Histories of allergies/allergic reactions. Bleeding and other disorders
■ Current medications, including dose, time,
route and site of administration. Are to be ruled out to prevent any complications,
■ Diseases, disorders or abnormalities. GIT system for the refluxing and regurgitation phe­
« Previous hospitalization. nomena, Endocrine and metabolic disorders to pre­
■ Family history is also important and may act vent exacerbation of the sa me.
as pointers.
SPECIAL CONDITIONS
it Review of systems: the respiratory and cardio­
vascular systems are very important. The visuali­ 1. Diabetes and NPO considerations.
zation of larynx is important for laryngoscopy and
thus the Malampati classification is used for pre­ 1. Attention deficit and hyperactivity disorder
dicting the larynx visible on the basis of how much [ADHD] Generally occurring in age 7 to 9 years,
the tongue and soft palate can be seen. when diagnosed may present with difficult *pre
operative period. Also medications methyl
PEDIATRIC CONSIDERATIONS phenidate and clonidine may have interaction.

Respiratory systems 2. Mental retardation - biggest obstacle is history

as they are placed in care of someone other than
Pediatric airways are smaller than adult airways and family
shaped differently. The trachea is shorter and the
narrowest part lies below vocal cords. Also the 3. Down x syndrome - macroglossia and the airway
tongue is relatively enlarged and posterior displace­ management is a problem.
ment of the tongue may cause complete airway ob­
struction (also enlarged tonsil tissue). Lower airway 4. Cerebral palsy ~ Stoetling and Durdorf [1993]
is more complaint and supported by less cartilage. have reported that such patients have a propen­
Thus airway obstruction is easier. sity for gastroesophageal reflux and poor laryn-
 lifîfrl | TEXTBOOK OF PEDODONTICS

geal and pharyngeal reflexes. Thus they are more Emergency

prone to aspiration. Also hypothermia may be a
problem. E -Emergency operation - any of the above class
operated as an emergency (e.g.II E would indicate an
5. Dentinogenesis imperfecta - loose teeth cause ASA II patient being taken up as an-emergency
concern during intubation. Besides, hyperther­ procedure)
mia may also be present.
Vital signs - pulse and BP to be recorded. Normal
Risk assessment paediatric vital signs are given in table 4.11

Laboratory testing - as mostly surgical procedures

In 1963 American Society of Anesthesiologists
are performed, the blood and urine picture is essen­
[ASA]. Classification given is:-
tial.
Class I : No organic, physiologic, biochemical or
Child’s physician - name and address of the child’s
psychiatric disturbance. The pathology
physician
for which operation is to be performed is
localized and is not a systemic
Rationale for sedation - briefly state the reason
disturbance.
for anesthesia.
Class II : Mild to moderate systemic disturbance
caused either by condition itself or by
Informed consent - written consent to be obtained.
other pathophysiological processes.
ClassIII / Severe systemic disturbance, even
Medications and instructions [Doctors orders]
though it may not be possible to define
the degree of disability with finality. a To parents
Class IV: Severe life threatening, not always ■ NPO instructions must be clearly written on
correctable by the operative procedure. the order sheet. The most common reason
Class V : Moribund patient who has little chance that a patient is disqualified for a scheduled
of survival but is submitted in despera­ anaesthetic is that they have not complied
tion. with the pre-operative nothing per oralinstruc­
Class VI : Brain dead. tions.

Table 4.11 : Normal paediatric vital signs

Age Heart Rate Blood Pressure Respiratory Rate Tidal Volume

3 years 101 + 15 " 100/67 + 25/23 24 + 6 112

5 years 90+10 94/55 •+RM» 14/9 23 + 5 270

r 1
12 years 70 + 17 109/58 + 16/9 19 + 5 480

Adult 77 + 5 122/75 + 30/20 12 + 3 575

 SECTION 4 : PSYCHOLOGICAL DEVELOPMENT AND BEHAVIOUR MANAGEMENT |

The goal of pre-operative fasting is to de- attention. Some sedatives specially the bar­
| crease gastric acid volume and minimize the biturates and the opiods have the disadvan­
pneumonitis that may result in the event the tage of causing nausea and vomiting. Also it
\ patient aspirates gastric contents. (Latham is contraindicated in patients with renal im­
1999) NPO after midnight for 6-8 hours pre­ pairment and hepatic impairment.
operative (solids) while clear liquids may be
j taken in healthy patients 2-3 hours pre-opera- 3. Anti-emetic - they are indicated only if patient
tive. is highly prone to vomiting or sedatives have
been added in the premedication. Commonly
h To assistant used is Hydroxyzine (Vistaril) or Meta-
Premedication with a systemic background clopromide. Also useful in reducing anxiety
■ Patients with Subacute Bacterial Endocarditis and tension in younger children.
- antibiotic prophylaxis is needed.
■ Patients with abscess - antibiotic therapy Guidelines for premedication [Steward, 1983]

Premedication in a normal child 1. Infants under 1 year

The purpose of premedicating a child is: Atropine ().02mg/kg - i. v. at anesthesia.
i m., 30 minutes before
Objectives 2. Healthy children 1-3 years of age
1. To block unwanted autonomic reflexes. Atropine 0.02mgZkg - i.v. at anesthesia
2. To prevent excessive secretions. i.m., 30 minutes before
3. To produce sedation and allay anxiety. 3. Healthy children over 3 years of age
4. To facilitate induction of anesthesia and to « Optimal psychological management.
.f supplement and reduce the amount of the same « If indicated add 4mg/kg diazepam suspension.
I to be administered. ■ Atropine 0.02mg/kg - i.v. at anesthesia
There is considerable deba te on the use of pre­ i.m., 30 minutes before
medication in outpatients. However, a judi­
cious use of the same is recommended. Other conditions

Drugs used Certain other conditions exist where sedation may

L Anticholinergics - Drug used most commonly be beneficial are: 4Mb.

is atropine. In recent times, Glycopyrrolate

[O.Olmg/kg IV] has also been found to be ■ Congestive Heart Disease
very effective. The central effects are negligi­ They benefit from sedation as to minimize oxy
*
ble with greater drying effect as well as less gen consumption and demand on Cardiovascular
tachycardia than atropine. System during induction

2. Sedatives - These may be required in certain ■ Intracranial vascular malformations

cases where the patient may be apprehensive Sedation to prevent dangerous hypertension
about the procedure. Benzodiazepines and prior to or during anesthesia.
Barbiturates have been commonly used for the
same. Davis [1988] has stated that chloral hy- ■ Mental retardation
drate and Meperidine are the most commonly Difficulty in induction of anesthesia. It. is also
used oral sedative agents. In recent times helpful to allow parents to accompany during
Midazolam has also received considerable induction.
 <ïîE> I TEXTBOOK OF PEDODONTICS

PROCEDURE
■ C onnecto mask adapter
■ S uction
Methods of administration : General Anesthesia can
be administered by using following types of circuits:
h Quick re-examination as children may develop
■ Open Method - where no rebreathing and nores-
URTI or other infections overnight.
ervoir is present. _ ,
■ Semi Open - has à reservoir but no breathing.
c. Knowledge of the agents being used for the
■ Semi closed - reservoir and partial rebreathing.
various stages of anesthesia. Briefly they care
■ Closed - reservoir and complete rebreathing.
described in table 4.12
Pre-Induction Consideration
Protection
a Preparing Equipment - The anesthetist has to
check the equipment available. A brief check Eye and corneal abrasions are prevented by closing
list includes using the nemonic STATICS : the eyes-with artificial tears and by also winding the
» S cope[laryngoscope] gauge over them. The mask should not be allowed
■ T ube to creep up above the bridge of the nose.
■ A irway
■ T ape to fix the tube
■ I ntroducer stilet

Table 4.12: Commonly used parenteral anaesthetic agents

*
Drug family Representative Benefical Adverse effects \ Clinical uses
agents effects

OPOIDS ■ Morphine ■ Sedation ■ Respiratory ■ Sedation

■ Fentanyl ■ Analgesia depression ■ General
■ Alfentanil ■ Euphoria ■ Nausea anaesthesia
« Sufentanil « Vomiting ■ Severe pain
■ Remifentanil ■ Gastroparesis managment

BENZO
DI AZEPI NES ■ Diazepam ■ Sedation ■ Respiratory ■ Sedation
■ Midazolam « Anxiolysis depression
■ Triazolam ■ Amnesia

BARBITUR­ ■ Methohexital ■ Loss of ■ Respiratory ■ Induction of

ATES » Thiopental consciousness depression general
■ Cardiovascular anaesthesia
depression

DISOPROPY ■ Propofol ■ Sedation ■ Respiratory ■ Sedation

LPHENOL ■ Loss of depression ■ General
consciousness ■ Cardiovascular anaesthesia
■ Rapid recovery depression
 SECTION 4 : PSYCHOLOGICAL DEVELOPMENT AND BEHAVIOUR MANAGEMENT Î

x Intravenous induction a Divinyl Ether - was used for induction by open

drop method. If used for more than 30 minutes
« This is the preferred route for the induction of
causes severe liver toxicity. Thus not used.
anesthesia in adult patients. The maintenance
h Diethyl ether - Guedal *s stages are seen. Slow
of anesthesia is, however not: preferred with
induction, irritating to the respiratory mu­
these agents.
cosa, increased incidence of nausea and vom­
■ The agent most commonly used is thiopenthl
iting - explosive. It has the advantage that there
sodium. The advantage is a rapid onset of ac­
is little CVS or respiratory7 depression. It also
tion and also recovery time.
maintains blood pressure.
■ EMLA cream, a powerful topical agent is to
c. Halogenated Hydrocarbons as a group show
be applied for comfortable securing of the IV
following features:
line.
1. Progressive reduction in the BP as
■ The preoxygenation concept, is that the pa­
anesthesia (feepens.
tient is to be kept on 100% oxygen 2-5 minutes
2. Moderate to marked respiratory7 depression.
before induction. In absence of
3. Produce cardiac arrythmias. due to
preoxygenation, during induction, the blood
sensitization of the heart to endogenous
oxygen saturation is seen to drop to levels of
catecholamines.
.60% to 70% on induction with thiopental in
4. Hepatotoxicity.
healthy patients breathing room air.
■ A few ml of Thiopental sodium (2.5%) is in­
Generally combined with nitrous oxide provides
jected as a test dose.
excellent anesthesia and little nausea or vomiting is
■ 5% thiopental sodium injected rapidly is used,
encountered.
but may lead to apnea. It is suggested that
2.5% every 15 seconds upto 0.5g (in avg.
Masks for induction
male) with 0.2 to 0.25mg in children is given.
■ Too rapid induction can produce hiccuping
a Shape of mask-for the children, induction is
and involuntaiy muscle movement.
generally carried out by the use of inhalatipn.
■ Rarely epileptiform conclusions may occur.
The shape of mask is modified to make it ac­
« It is inadvisable to administer thiopental as the
ceptable to the children. E.g. balloon mask, Mickey
principle agent for operations lasting more than
mouse with a wide open mouth.
1 hour or that more than 1g be given to a pa­
tient.
h Scented masks - the use of scented masks to
Absolute contraindications for the use of thio­ disguise the odours of the inhalation agents in­
pental are: cludes addition of drops of fruit extract on the
■ Presence of respiratory obstruction. mask (Fig 4.8a).
■ Cardio vascular instability, shock.
■ Severe asthma or bronchospastic disease. « Also vapourizing volatile fruit flavours into the
■ Porphyria. anaesthetic gas mixtures is acceptable.

b. Maintenance of anesthesia [Inhalation] Controlled ventilation and Assisted

The maintenance of general anaesthesia is gen­ ventilation
erally by inhalation general anesthetics.
They can be classified as During the procedure, the anesthesiologist may
1. \61atile exert control over a patients breathing by two well
2. Gaseous. defined methods.
 I TEXTBOOK OF PEDODONTICS

When conditions are judged to be proper, the exist­

ence of the continuing neuro muscular block should
be determined by diagnostic tests. Neostigmine, in
a dose of 3()mg/kg is the most commonly used drug
for reversal.

Fluid electrolyte balance

The fluid electrolyte balance is maintained during

the procedure with an i.v. saline infusion, which is
continued even after the procedure is over.

Fig. 4.8a Different coloured fragnant nose tips Postoperative period

especially for children to give relative analgesia.
■. Often it is essential to comfort the parents and
assure them that everything is normal. The
procedures performed should be explained to
the patient.
■i The patient is to be started off with clear fluids at
least 3 hours after the procedure is over. The
importance lies in the fact that the first fluid
administered may sometimes be associated
with vomiting. This is generally prevented by
adding anti emetics like metaclopromide into
the saline which is infused, over a period. Clear
fluids are then followed by milk and soft diet [
also taking into consideration the extraction sites].
■ The presence of any bleeding front the oral cav­
ity, extra oral swelling should be checked for.
Fig. 4.8b Dr. Kevin Alien demonstrating relative
■ The patient can be started off with analgesics if
analgesia on child patient
pain is present. If required antibiotics can also be
judiciously used.
■ Controlled ventilation- manual or mechanical ven­ ■ The child should be evaluated for the various
tilation in which the frequency of breathing is systems such as the cardiovascular function,
determined by the ventilator according to pre­ whether the patient can independently main-
setcycling pattern without initiation by the pa­ tain the airway which can be assessed by means
tient. of various arousal and protective reflexes. The
• Assisted ventilation - where the patient initiates recovery of the patient should be such that it is
inspiration and establishes frequency of breath­ aS close to the preoperative level as possible. This
applies particularly in children with cerebral palsy
ing.
or mental retardation where the responses ex­
pected from a normal child cannot be elicited
Reversal even preoperatively. -
Before attempting drug reversal, a satisfactory ■ The child should be monitored constantly and
physiologic state and ‘adequate recovery from the should not be allowed to play in the ward as, the
effects of anaesthetic agents must prevail. patient may be disoriented for some time to come.
 SECTION 4 : PSYCHOLOGICAL DEVELOPMENT AND BEHAVIOUR MANAGEMENT i € 6

The parents should be advised not to leave the 2. What are the objectives ofrelative analgesia?
child unattended even for the next day. 3. What are the stages of anesthesia?
■ Any instructions regarding the restorative pro­ 4. What are the drugs used for premedication?
cedures performed should be given. The patient 5. What are the pediatric considerations for *general
may be recalled for a check up after 3 months for anesthesia?
review. 6. Enumerate the indications for general anesthesia.
7. What are the absolute contraindications for the
Self-Assessment use of thiopented sodium?

I. Define conscious sedation, deep sedation and

general anesthesia?

i
 4.5 Ephebodonties - Dentistry for Adolescents

GoelR

Introduction Adolescence represents an extremely important time

in the dental care of the child patient. Prevention of
Ephebos is the Greek noun referring to a youth en­ dental diseases is certainly one bf the pivotal con­
tering manhood and from it is derived the word cerns of the dentist who cares for adolescents. Ado­
ephebodonties, which encompasses total dentistry lescence marks a time in which the role of the parent
for the individual undergoing the transition from in the child’s dental home care needs to be mini­
childhood to adulthood, ie., the period of life known mized, and the responsibility of the adolescent for
as adolescence. managing his/her own oral health program must be
emphasized. The dentist must play a role in educat­
J The word “adolescence” is derived from the Latin ing and motivating such patients, for not only in
| “adolescere”, which is composed of the Latin words caries problem but also periodontal disease and its
i “ad” or to, plus “oleve”, to grow, or “olere” to nour- unfortunate implications.
i ish. This chapter is an attempt to highlight the various
i dental problems occurring in this group, ’and their
I It is an in between age in our society and needs to be management since the dentist needs to be aware of
j understood as something independent of either child- the different characteristics of the adolescent as they
I hood/adulthood. It is a time of enormous transition relate to age.
I and is certainly not of short duration. Hence, the
J term teenager ( 13-19 years) has become synonymous Common dental problems observed
J with the term adolescence in our society. 1. High caries attack rate
2. Pulp size
L Definition 3. Partially erupted teeth which affect;
a) Placement of rubber dam
Ephebodontics/adolescent dentistry is the science b) Placement and retention of rubber dam clamps
of dentistry which deals with the children who are in c) Taking impressions
the process of growing up from childhood to man­ d) Placement of matrix bands
hood or womenhood. e) Design of retainers
4. Gingival and periodontal problems
Medically adolescence can be considered as the pe­ 5. Congenitally missing teeth
riod beginning with the appearance of the second­ 6. Motivation for prevention
ary sex characters and terminating with the cessa- 7. Traumatically injured teeth
l tion of somatic growth. 8. Rapid changes in occlusion following removal of
teeth
 SECTION 4 : PSYCHOLOGICAL DEVELOPMENT AND BEHAVIOUR MANAGEMENT I

9. Gingival recession ■ The brow area becomes larger as a result of

10. Esthetic results pnuematization of tlie frontal sinuses and ap­
11. Social behavior position of the glabella.
12. High cost in cases of long standing dental ne- ■ By puberty, the sinuses are usually fully de-
although they may continue to en­
large.
Subtle changes observed ■ There is an average increase in the palatal vault
of approximately 10 urn frombirth through ado­
A. Physical changes lescence, but simultaneously tlie palate moves
downwards, as a result of appositional growth.
Body ■ The growth of the jaws continues during this
Puberty is tlie landmark in physical development period. This growth may be sufficient to de­
when an individual becomes capable of sexual velop room for the third molars. In many cases,
reproduction. The advent of puberty is paralleled the growth is inadequate and these molars
by the development of genital tissue and sec­ become impacted.
ondary sexual characteristics, such as, tlie devel­ ■ Mandibular growth has taken place at the
opment of hair in the area of the genitals. condyles in the same mode as interstitial carti­
The following changes are seen in the body of an lage growth. Such growth imparts an increase
adolescent in tlie vertical height of the ramus ofthe man­
■ It is a time when there is a increase in mass of dible, and it also becomes more upright.
tlie muscles, a redistribution of body fat, and ■ The whole face is a great deal longer vertically
an increase in the rate of skeletal growth. and more sloping as a result of many changes
■ There is a growth spurt assqciated with the ■ The adult facial skeleton is literally twice as
time of life. large as that of the newborn but that the brain
■ Since males have a longer pre-growth spurt differs in size by only 50%.
maturation period, the total height of males • By completion of adolescence, the 27 bones
generally exceeds the height of females. (15 single and 8 pairs, excludingtlie hyoid and
■ The earlier growth spurt of females also ac­ . ear bones) tliM originally made up the skull
counts for a period of time when mean height have become 22 bones (06 single and 8 pairs
of a group of young female adolescents may excluding the hyoid and ear bones) and are so
exceed the mean height of the males. closely adapted that the skull can be consid­
■ It is important to realize also that in females ered as a single bone.
menarche serves as a signal that * growth is
ending, but for males there is no such marker. B. Dental changes

Craniofacial (Head and Neck) ■ All tlie permanent teeth generally will have
During adolescence, subtle changes take place erupted by age 12, except possibly the four
in skeletal growth ofthe face and skull to give the second molars, which may erupt as late as age
individual tlie final adult appearance. 13, and the thud molars, which usually erupt
« In adolescence the nose and tlie chin become between the ages of 17 and 21.
more prominent, the face increases in height ■ Except for the third molars the dentist should
and and becomes prognathic. be concerned about any unerupted permanent
■ The convex profile in tlie lip region of children tooth after age 13 and should examine the area
tends to be reduced by these growth changes. in question radiographically
 <FZî> | TEXTBOOK OF PEDODONTICS

■ The roots of all the teeth are considered to E Social changes

have been completed by-ageU6, except for
those of the third molars, which could achieve Peers are very important social agents in large,
completion as late as 25 years. technological societies, in which children of thé
same age group are often kept together. The rela­
C Cognitive changes tionships and dependencies upon parents starts
to decline and the importance of peers escalates.
The adolescent continues his or her cognitive The adolescent finds it difficult to share secrets,
development and by the middle to late adoles­ thoughts and fantasies with his/her parents and
cence is capable of extremely sophisticated intel­ takes a close friend as his confidant. In such
lectual tasks. High ability at abstract thinking cases, the peer is a valuable and useful audience.
allows the adolescent to deal with complex and At the same time an adolescent may tty drugs,
difficult vocational and educational challenges. participate in criminal acts, or defy authority7, to
avoid rejection or ridicule from the peers.
Formal operational thinking and the ability to store
information in the memory after perceiving it are Another important social change in the adoles­
the hallmarks of the maturation of cognitive abil­ cent is an increase in the size and range of ac­
ity of the adolescents. The new information avail­ quaintances. Children younger tend to limit their
able to the adolescent, along with more sophisti­ friends to those in their neighbourhood, school
cated ways of analyzing this information, often and perhaps church. Adolescents can, on the
makes him/her appear to be a rebel, a complainer, other hand, have individual friends, belong to a
and an accuser. clique of friends and can. identify7 with larger
groups such as a football team. An adolescent’s
The thoughts of adolescents are both introspec­ ability to sustain relationships with ail 3 groups
tive, analytical and also egocentric. This dwell­ is indicative of good social skills .and that the
ing upon one’s self makes an individual overly socialization process is going well.
self-conscious. Clothes, car, hairstyle, music
tastes and identity with certain people or groups The adolescent who gets along well with his/her
probably reflects the adolescent’s involvement peer group seems to relate successfully with
in self consciousness. adults. Those who do not get peer acceptance
seem to have more problems with adults and grow
D. Emotional changes up to have a variety of social and emotional diffi­
culties.
The very rapid dramatic changes that happen to
adolescents can be paralleled with many emo­ The psychology of adolescence
tional circumstances.. The self confidence and
personal identity of the adolescent may be com­ As a psychosocial phase extending over a number
promised if his/her feelings about body image are of years, adolescence is a developmental phenom­
wrong. The following issues are seen to have the enon unique to man.
possibility of misinterpretation and anxiety for this
age group. Personal Identity: The crucial problem of adoles­
a) being attractive or unattractive cence
b) being loved/unloved
c) being strong/weak The adolescent is faced with a major developmental
d) being masçuline/feminine task of achieving a stable personal identity, which
 SECTION 4 : PSYCHOLOGICAL DEVELOPMENT AND BEHAVIOUR MANAGEMENT I

will provide him with orienting concepts of what sort he says he will do. He is orderly and persistent m
of person he is, what his strengths and limitations his work. He is very self-critical, sets high stand­
are, and how he can anticipate others response to ards for himself, sometimes doubts that he can
him. This requires the youngster to relinquish his achieve his goals, but drives ahead until he ac­
self-image and the role of childhood while not yet complishes what he lias set out to do. He is strong-
being to fully embrace the role of an adult. The ado­ willed and may be somewhat stubborn. Uc is said
lescent may need to give up and sometimes to ac­ to have a ‘strong’ personality.
tively rebel against his dependent, submissive rela­
tionship to his parents if he is to establish a healthy 2. Self adaptive person
personal identity of his own. This may give rise to an The self-directed adolescent is in sharp contrast
emotional disorder rather specific to adolescence, to the second type of definitely healthy, adjusted
termed acute identity confusion. If mutual interac­ personality; the “adaptive person”. The adaptive
tion between the parents and the child fails to de­ adolescent is friendly, vivacious, outgoing and,
velop it may give rise to a great confusion on the though he does not strive for it as does the self
part of the youth as to who or what he is, a subjec­ directedyouth, he accepts leadership and respon­
tive feeling of unreality, an acute sense of isolation, sibility naturally and easily. The adaptive person
a loss of drive and sense of purpose, which makes has a well developed sense of personal identity
concentration impossible and disturbs the capacity and is quite aware of his relationship to others;
to appreciate time or to apply himself to practical however, he seems in tune with society and is a
endeavors. Efforts to cope with the stresses of ado­ successfill conformist
lescence and to stave of acute identity confusion
may lead to a type of behavior highly distressing to 3. The submissive person
parents and to the adult society at large - the as­ He is one who continually calibrates and, hence,
sumption of a “negative identity”. insures his sense of identity in terms of the de­
gree to w hich he meets the expectations of au­
Therefore it can be seen that this is a period of life thority and the approval he receives for this. Con­
during which a greater degree of inner turmoil and sequently he feels more secure as a follower,
unpredictability in behavior is considered more nor­ avoids conflicts, does not initiate action, and is
mal than would be so at other times in life. For the apt to be a relative nonentity. Though the sub­
greatest number of adolescents the stresses of this ♦ missive person may be docile and uncritical of an
period are coupled with vitality and exuberance which authority he accepts, he is not submissive to eve­
makes life an exhilarating experience. ryone; he may have ^strongly developed sense
of duty1*7 and may vigorously resist demands that
Typical personality types: The adolescents can be run counter to his principles. Nevertheless he
divided into the following personalities does not have a strong sense of his own identity.

1. The “self-directed” youth 4. The “defiant person”

They have a very well developed sense of self This is an adolescent who is definitely unsuc­
and display those aspects of a strong personal­ cessful in establishing a true sense of his own
ity such as leadership and achievement, provid­ identity and is defensive, counter-attacking
ing a very different picture from the sociable, gre­ against a frustrating world by assuming a nega­
garious teenager The self-directed person enjoys tive identity. “The defiant person is openly hos­
a very good reputation, especially for responsi­ tile to society. He shows his hostility by doing
bility and honesty. He is known as a conscien­ poor school work, refusing to conform to social
tious person, who can be counted on to do what expectations. Because he has been neglected or
 I TEXTBOOK OF PEDODONTICS

mistreated by society he bears a never-ending seem important to be alert to particular attitudes

grudge which prevents him from making any con­ of the adolescent toward the teeth and the mouth
structive adjustment to his age mates, to his fam­ and the part these play in the young person’s
ily, to school, or to a job. He is a definitely malad­ emerging body image. These attitudes may well
justed individual. determine the adolescent’s degree of cooperation
in necessary dental treatment and in carrying out
5. The “unad justed person” good oral hygienE
He shares with the defiant person an inability to
master the tasks required to establish a stable Time and industry diffusion
sense of identity. However, the unadjusted per­
son is not so openly hostile and attacking of so­ ■ Perhaps the most difficult task confronting many
ciety and is not apt to assume a negative identity, adolescents concerns the need of the youth to
though he is much more in danger of suffering give up the child-like dependence or identifica­
acute identity confusion. He is an anxious, inse­ tion with the parents and to replace this with an
cure, unhappy youth in need of help. identification with his peers. For a number of
young people this engenders a painful feeling of
Emotional disturbances common to adoles­ isolation and deprivation, and when the parents
cents: Disturbance in body image resist this separation because of their own emo­
tional needs, there may be the added distress of
■ Whatever may be the personality of the adoles­ conflict and antagonism between the parents and
cent, he must confront certain developmental the child.
tasks. Among these the revision of the body
image and the accommodation to primary sexual ■ The parents view this aimless, desultory
impulses and secondary sexual characteristics is behaviour as “lazy” and they become angered
of major importance. and dismayed as school work declines and home
chores are neglected. It is often when school
■ The changes in the body which are so evident to grades are perilously close to failure that the help
others are also the source of great concern and of the psychologist is sought.
interest to the young person. Short stature in
boys, tallness and big bones in girls, failure in the ■ It falls to the psychologist to convince the par­
maturation of identifiable secondary sexual char­ ents and the teachers that the young person is
acteristics, all may cause alarm and defensive bel­ not malingering when he complains that he can­
ligerence or withdrawal within the young person. not concentrate. He literally cannot concentrate,
Obesity and angular build can make a girl doubt he cannot marshal his resources, and he cannot
her femininity, while chubbiness or lack of mus­ engender the energy and drive necessary for ef­
cular development can dismay a youth as to his fective action unti l he finds himself and gets his
developing manhood. bearings as a person with his own destiny in life.
The efforts of the parents to motivate him through
« Attitudes toward changing body image can have outside pressure and to expect him to exert him­
a profound effect upon the adolescent’s care of self to gain their approval as he did during child­
his body. These distorted attitudes toward the hood only increases his inability to come to grips
body grade into actual psychosomatic disorders. with his problems.

■ For the dentist, who is responsible for the care of

the teeth and the mouth of the adolescent, it would
 SECTION 4 : PSYCHOLOGICAL DEVELOPMENT AND BEHAVIOUR MANAGEMENT |

Negative identity veys the attitude to the adolescent that “any­

thing goes”.
■ For the adolescent to embrace a negative identity
constitutes a maladaptive solution to his prob­ ■ Unspoken competition between the parent and
lems. In certain circumstances, however, it ap­ the child evoked by the youth’f increasing physi­
pears the only avenue open to him to escape the cal stature and independence may stimulate anxi­
acute identity contusion. When the demands and ety concerning loss of vigor and approaching age
the expectations for achievements placed on the for the parent.
adolescent are so great he feels that he can never
measure up to them, he may be forced into a nega­ ■ Studies of adolescents who have been most suc­
tive identity. A young person may also be forced cessful in mastering the stresses of this period
into assuming a negative identity as a protective indicate that the parent-child relationship is gen­
measure when one of the parents insists on be­ erally one of mutual respect and trust in which
ing so much a part of his life that he is literally each one allows the other to live his own life with­
suffocated in his efforts to establish his own in­ out efforts at coercion or manipulation.
dividuality7.
The three sub-stages of adolescence
Peer group influences: It is in his peer group that
the adolescent finds a base of acceptance and secu­ Sub-stage Characteristics
rity from which to solidify his changing body image
Early Casting off of childhood role and
and independence from the parents. To “belong” to
adolescence emergence into adolescence
a group and to develop a language, mode of dress,
Middle Participation in teenage subculture
and behavior uniquely their own, which clearly sets
adolescence and peer group identity
them off from adults, provides the adolescents with
Late Emergence of adult behavior
a temporary refuge with others of their own kind for
adolescence
making a transition from childhood to adulthood.

Special considerations during assessment

Parents influences: There may be no other time in
their child’s life which is as personally anxiety invok­
1. Rapid, unpredictable, and irregular skeletal and
ing and frustrating to the parent as is adolescence
dental growth.
and in certain instances it can lead to severe emo­
2 The environmental challenges, with obstacles and
tional disorder in a parent. The successful mastering
pitfalls. Drugs, smoking, sexually transmitted dis­
of the tasks of adolesceiioe requires a collaboration
eases, peer pressure, acne, more competitive edu­
between the adolescent and the parent in which the
cation, career decisions, alcohol, family pressure
parent provides the image of a mature adult provid­
make up for some of the challenges facing to­
ing guidance and ultimate authority while allowing
day’s adolescent Dental professionals see trauma,
the young person increasing independence in ques­
oral manifestations of sexual activity, hormonal
tioning, revising, and finally establishing his own
gingivitis, smokeless tobacco induced hyperkera­
beliefs and values.
tosis, non compliance to dental recommendations,
and drug related behaviors.
■ Dictatorial, overbearing parents who allow little
3. Learning to cope, make decisions, and become
freedom and independence to their adolescent
independent. Adolescence has always been atime
offspring can anticipate troublé;. Equally perni­
to make decisions, seek independence from fami-
cious, however, is the submissive parent who
lieS; deal with sexuality, and choose a career. The
cannot cope with adult responsibilities and con­
 I TEXTBOOK OF.PEDODONTICS

Table 4.13: Examination possible clinical findings in examination of the adolescent

Structure Finding Comment

Extra-oral evaluation . Acne Adolescent may be taking
Skin antibiotics
Intra-oral evaluation Generalized erythema Effect of smoking, sexually
Mucosa transmitted disease
1t
Buccal mucosa Erythema hyperkeratosis Use of smokeless tobacco |
i
Tongue Coating, odor Smoking, poor hygiene fungal i
overgrowth from medication
Breath Acetone, alcohol Excessive dieting, alcohol abuse,
metabolic disorders (eg. Diabetes)
Gingiva Inflammation Hormonal change
Pregnancy tumor Use of oral contraceptive
Pregnancy
Teeth Erosion Bulimia
Wear facets TMJ disorders, bruxtsum
Excessive stains Tobacco use
Discoloration j Existing pulpal pathosis from
trauma

dentist often sees this turmoil in poor oral hy­ 2. Rampant caries: Clinicians have noted that in ram­
giene compliance or refusal of treatment. The pant caries (more often in adolescent female) per­
missed appointment is just of many ways to say sonality problem manifestations can be varied,
“I am too involved in my search for self, my chang­ with a girl cry ing silently or not saying a word
ingvalues, and handling my environment to worry during the appointment. In some *
cases, treat­
about my teeth”. ment appointments can degenerate as the child
whimpers and finally loses composure. Time and
Behavioural assessment engagement in conversation are often the most
successful behavioral management keys in deal­
1. Sexual abuse: The young adolescent female or ing with these adolescents. Dramatic changes in
male who has been sexually abused with oral pen­ behavior occurs with the dentist’s verbal rein­
etration may exhibit reluctance in accepting den­ forcement of improved hygiene and provision of
tal care from a dentist of the same sex as the per­ even temporary esthetic anterior restorations that
petrator. Aids in uncovering this situation are a allow the patient to smile and experience a more
good history of previous compliance, behavioral positive self-image.
cues such as depression, and overt refusal of care
when oral contacts is made. Nonetheless, confir- 3. Extreme anxiety The behavioral management of
mation is difficult, since the abuse may be un­ the child who exhibits extreme anxiety at the
known to the parent or parents. It maybe the limit thought of dental treatment can be achieved by
of the dentist’s role to recommend counseling for desensitization by psychological intervention.
a child to uncover reasons for refusal of care with Tools available to the dentist include non-inva-
the idea that intervention may uncover the cause. sive therapies at first, reinforcement of positive
 SECTION 4 : PSYCHOLOGICAL DEVELOPMENT AND BEHAVIOUR MANAGEMENT |

accomplishments, positive peer interaction, and 4. Adolescents are preoccupied with health matters
involvement with a psychologist. The poorly in general and appearance in particular. Use these
managed or unmanaged adolescent phobic may concerns as mechanisms for motivating the type
become the adult dental phobic. of behavior conducive to enhancing rapport and
improving oral health.
4. Anorexia nervosa;The treatment of the child with
an eating disorder can be difficult Experience 5. Frequently, adolescents regress to childlike
indicates that these patients, mostly females, will behavior in the dental office. This is a defense
develop dependency on a male authority figure. mechanism to what is perceived as a traumatic or
They will also require a dentist’s full attention unpleasant experience. Since this age group is
during office visits and, unless counseled, will particularly sensitive to being treated as a child,
demand time outside scheduled appointments. the dentist should adapt his treatment approach
appropriately. Be extremely careful not to cause
5. Illicit drug use: Manifestations of drug inges­ the patient obvious embarrassment.
tion can be varied from a slight mental dissocia­
tion or drifting to outright verbal aberrations or 6. Adolescents tend, to worry about many circum­
stances; conditions in the home, parents, school,
extreme changes in personality.
social injustice, peer relationships, and world af­
fairs constitute major concerns. Dentists should
Common adolescent behaviour problems
encourage conversation on these matters to a
and suggested solutions
reasonable extent. Allow the patient to do most
of the talking.
1. The adolescent is basically insecure and is often
unable to cope with many situations; eg dental
7. Generally, a larger amount of food is consumed
setting. There maybe weeping, crying, laughter,
over a 24 hour period during adolescence than at
squirming, and stoic silence all during a single
any other time in the life cycle. This circumstance
office visit and without an apparent reason. Be
provides the dentist with an opportunity3 *7 to moti­
kind and understanding, it will be highly appreci­ vate patients toward adequate nutritional intake
ated. and proper dietary practices from the perspec­
tives of obesity and oral health. Both of these
2. Adolescents have varied interests; determine health conditions are vital concerns of adoles­
what these are, and encourage discussion on cents. Maximize their potential in the dental set­
these issues. However, join the discussion ac­ tings.
tively only if you are familiar with the topic; if
not, let the adolescent talk and inform you. Be The role of the dentist
intelligent - considerable rapport with the patient
can be gained through discussion when handled ■ The pedodontist should have a knowledge ofthe
properly. crucial psychosocial tasks to be mastered that
will provide a framework for understanding the
3. Adolescents tend to reject adult authority; how­ problems facing the young person. The dentist,
ever, they are generally responsive to empathetic acts as a parent surrogate and will take on certain
guidance, because they are somewhat afraid of aspects of the parent for the adolescent, as do
the very independence they desire. Be firm but the physician, teacher, and minister. However,
kind; display authority7 in clinical matters, but do precisely because he is not the parent, the
not be authoritarian.
 I TEXTBOOK OF PEDODONTICS

dentist is afforded an opportunity to offer a mean­ 3. Belanger GK, Ti|liss TSI: Behavior management
ingful adult relationship to the adolescent. techniques in predoctoral and post doctoral
« The dentist must perceive his young patient as a pediatric dentistry programs. J. of Dental'Educa-
unique individual deserving respect and capable tion. 57,232-238,1993.
of independent action. 4. Carah WL et al: The dentist-patient relationship:
• h is important not to involve the parents unnec­ perceived dentist behavior that reduce patient
essarily in thé adolescent's treatment to the point anxiety and increase satisfaction. JADA, 116,72-
that he is excluded from all participation. 76,1988.
« He should be given as much responsibility as 5. Chapman HR, Kirby-tumer N. C. Dental fear in chil­
possible for making his own appointments, for dren a proposed model, BDJ 187,408-412,1999.
discussing the nature of his treatment, and for 6. Collins V J : Principles of anesthesiology, general
carrying out, on his own, necessary prophylactic and regional anesthesia. Vol. 1 *3 ed.Lea & Febiger
and remedial procedures. , Philadelphia, 1993.
« Educating the adolescent regarding the impor­ 7. Corah N. L, Gale E. N., Illig S. J. Assessment of a
tance of various procedures and the necessity of dental anxiety scale, J Am Dent Assoc, 97:816-
adopting good oral hygiene practices serve as a 819,1978
significant aid in the success of treatment. 8. Gale. E. N. Fears of the Dental Situation. J Dent
Res, 51(4): 964-966,1972
Self-Assessment 9. Guthrie A. Separation Anxiety: an overview. Ped
Dent, 19(7):486-489,1997
L Define ephebodontics. 10. Higgins S.M ; Anesthesia for periodontal sur­
2. What are the commonly occurring dental prob­ gery. Dental clinics of North America, 43 [2], 263-
lems seen in these individuals? 287,1999.
3. When does the calcification of third molar com­ 11. Kuhn BR, Allen KD: Expanding child behavior
plete? management technology in Pediatric dentistry, a
4. What do you understand by a "defiant adoles­ behavioral science perspective, Pediatric Den­
cent”? tistry: 16, 13-17,1994. t
5. What are the characteristics of a self directed 12. KunbergG. Hwang P.C. Children 's dental fear pic­
adolescent? ture test (CDFP). A projection test for the assess­
6. What is the identity confusion faced by the ado­ ment of child dental fear. J of dent Child. 89-96,
lescent? 1994.
7. What is the role of the dentist in managing the 13. Lawrence SM et al: Parental attitudes toward
adolescent? behavior management techniques used in
pediatric dentistry. Pediatric Dentistry. 13, 151-
Further Suggested Reading For Section -4 155,1991.
14. Milgram P et al :Origin of childhood dental fear,
1. American Academy of Pediatric Dentistry : Guide­ Behav. Res. Ther 33,313-319,1995
lines for the elective use of conscious sedation 15. Parkin S. F. The assessment of two dental anxiety
and general anesthesia in pediatric patients rating scales for children. J Dent Child, 269-272,
Pediatric Dentistry 7[4] 334-337,1985. 1988
2. Ayer WA et al: Overcoming dental fear: Strate­ 16. Peretz B, Gluck GM,: Reforming - re appraising an
gies for its prevention and Management. JADA, old behavioral technique. The J. of Clinical
107,18-27,1983. Pediatric Dentistry. 23,103-105,1999.
 SECTION 4 : PSYCHOLOGICAL DEVELOPMENT AND BEHAVIOUR MANAGEMENT | CT»

17. Quality assurance criteria for pediatric dentistry: 24. Ten Berge M, Hoogstraten J, Veerkamp J. S. J,
Behavior Management, American Academy of Prins P. J. M. The Dental Subscale of the Chil­
Pediatric Dentistry7 95, Ref. Manual, 1998-99 dren’s fear Survey Schedule : a factor analytic
18. Roberts G J: Inhalation Sedation [Relative Anal­ study in the Netherlands, Community Dent Oral
gesia ] with oxygen/Nitrous oxide gas mixtures: 2, Epidem, 26:340-3,1998
Practical techniques. Dental update; 17 [5], 190- 25. Troutman K: Behavioral management ofthe men­
196,1990. tally retarded. DCNA, 21,62-636,1977.
19. Rousset C., Lambin M., Manas E The ethological 26. Veerkamp J. S. J et al: Dental treatment for fearful
method as a means for evaluating stress in chil­ children using nitrous oxide. The parent’s point
dren two to three years of age during * of view ASDC J dent Child, 59,115-119,1992.
dentalexamination. J Dent Child ,99-106,1997 27. Wein Stein P: The effect of dentist’s behaviors
20. Saxen M.A; Wilson S; Paravecchio R: Anesthesia on fear related behavior in children. JADA, 104,
for Pediatric Dentistry7. Dental Clinics.of North 32-38,1982.
America.43[2] 231-245,1999. 28. Weiner A. A., SheehanD. V. Differentiating Anxi­
21. Scott D. S., Hirschman R. Psychological aspects ety - Panic Disorders From Psychologic Dental
of dental anxiety7 in adults, J Am Dent Assoc, Anxiety, DCNA, 32(4):823-840,1988
104:27-31,1982 29. Weinstein P: Dentist’s responses to fear and non
22. Sokel DJ, Sokel S, Sokel CK: A review of non fear related behaviours in children, JADA, 104,38-
intensive therapies used to deal with anxiety and 40,1982.
pain in the dental office. JADA, 110,217-222,1985.
23. Steward D J Anticholinergic premedication for
infants and children. Can. Anesth-Soc-J, 30(4],
325-8,1983.
 SECTION - 5

Dental Caries in Early

Childhood.
5.1 Introduction
Tandon S

Dental caries is the most prevalent chronic disease esthetic problem it poses. Systemic complications,
affecting the human race. In many ways it can be such as Subacute Bacterial Endocarditis have also
considered a disease of modem times as the occur­ been documented to be associated with dental car­
rence of caries seems to be much higher in the last ies. The masticatory apparatus may also be affected
few generations. It is said that once it occurs-the leading to difficulty in mastication and deglutition.
scars persist throughout life evenlhough the lesion
is treated. Therefore it is mandatory for the clinician to under­
stand the magnitude of this problem and the risk
factors in the community to plan suitable preventive
measures. This chapter is an attempt to highlight the
current concept of caries, to enable the student to
detectit at an early stage with its underlying causa­
tive factors in an individual and to implement timely,
effective health care services.
§
Definition

The word ‘CARIES’ is derived from the Latin word

meaning ‘rot’ or‘decay’. It is also akin to the Greek
word ‘ker’ for‘death’.
■ Ostrom[19^hasdefinedft^
Fig. 5.1Upper dentition showing extensive caries
in a 314 years old child/ or dentin dissolution that is caused by microbial
action at the tooth surface and is mediated by
There are practically no geographic areas in the world
physiochemical flow of water dissolved ions.
whose inhabitants do not exhibit some evidence of
■ Hume [1993] states that caries is essentially a pro­
dental caries. It affects persons of both sexes, in all
gressive loss by acid dissolution of the apatite
races, all socioeconomic strata and in every age group,
[mineral] component ofthe enamel then the den­
though some people may be more prone to it than
tin, or of the cementum then dentin.
others. Though it may be argued that the disease is
notjifeth^
interpretation of the carious process
are far reaching. The cost involved in treating the
disease in terms of manpower and the hours spent is
■ The histopathologist may define caries in terms of
enormous. Also, the excruciating pain experienced
the stages of the lesion viewed microscopically.
by the patient can affect the patient as much as the
 SECTION 5 : DENTAL CARIES IN EARLY CHILDHOOD |

■ The chemist describes the process in terms of the ■ Occult caries:

interrelationship between pH, mineral flux, and Occult or hidden caries is used to describe
solubility at the tooth-saliva interface. such lesion, which is hot clinically diagnosed
■ The microbiologist on the other hand defines car­ but detected, only on radiographs. The nature
ies in terms of the inter-actions involving oral bac­ of these lesions, their etiology and reasons as
teria and the dental tissues. to why they have eluded early clinical diagno­
■ Thus on a more broad basis, dental caries is a sis are still unclear. The prevalence of occult
multifactorial disease, which is the result of inter­ caries has been reported to range from 0.8% in
action between the tooth [host] and the environ­ premolars in 14-15 years to as high as 50% in
ment around it including the bacteria, saliva and 20 years olds (Seow 2000). It is believed that
diet of an individual. bite wing and OPG radiographs along with
other noninvasive adjuncts like fiber optic tran­
Classification sillumination (FOTI), laser luminescence, elec­
trical resistance method (ERM) are used for
Dental caries may be classified on the basis of three diagnosing these occlusal lesions.
factors:
These lesions are’not associated with micro­
A. Based on anatomic site organisms different to those found in other
■ Occlusal (pit and fissure) carious lesions. These carious lesions seem to
■ Smooth surface caries (proximal and cervical car­ increase with increasing age. Occult lesions
ies), which can be classified under crown caries. are usually seen with low caries rate which is
■ Root caries is seen in older age groups. The pre­ suggestive of increase fluoride exposure. It is
disposing factor for the occurrence appears to be believed that increase fluoride exposure en­
the recession of the gingival margin. (Table 5.1) courages remineralization and slows down
progress of the caries in the pitand fissure
B. Based on the severity enamel while the cavitation continues in dentin,
and the lesions becomes maskedby a relatively
■ Incipient caries
intact enamel surface. These hidden lesions
The early caries lesion, best seen on the
are called as fluoride bombs or iltioride
smooth surfaces of teeth, is visible as a4 white ♦
syndrome. Recently it is seen that occult car­
spot’. Histologically the lesion has an appar­
ies may have its origin as pre-emptive defects
entlyintact surface layer overlying subsurface
which are detectable only with the use of ra­
demineralization. Significantly many such le­
diographs.
sions can undergo remineralization and thus
the lesion per se is not an indication for re­
■ Cavitation
storative treatment.
Once it reaches the dentinoenamel junction,
■ These white spot lesions may be confused ini­ the caries process has the potential to spread
tially with white developmental defects of to the pulp along the dentinal tubules and also
enamel formation, which can be differentiated spread in a lateral direction. Thus some amount
------ by their position [away fromthe gingivM mar­ of seiisitivifymaybe associated with thistyfe
gin], their shape [unrelated to plaque accumu­ of lesion. This may generally be accompanied
*
»it»:

lation] and their symmetry [they usually af­ by cavitation and can be detected by the ra­
fect the contralateral tooth] . Also on wetting, diograph.
the caries lesion disappears while the devel­
opmental defect persists.
 [ TEXTBOOK OF PEDODONTICS

C Based on progression D. Based on chronology

It has been stated that over a lifetime, caries inci­
■ Arrested caries dence i.e. the number of new lesions occurring in
With the shift in the oral conditions, even ad­ a year, shows three peaks-at the ages 4-8,11-19
vanced lesions may become arrested. Arrested and 55-65 years.
caries involving dentin shows a marked brown
pigmentation and induration of the lesion [ the Early childhood caries
so called ‘eburnation ofdentin’]. « Early childhood caries would include two vari­
ants: Nursing caries and rampant caries. The
■ Recurrent/secondary caries difference primarily exists in involvement of
Recurrent caries is that occurring immediately the teeth [ mandibular incisors] in the carious
next to a restoration. It may be the result of process in rampant caries as opposed to nurs­
poor adaptation of a restoration, which allows ing caries.
for a marginal leakage , or it may be due to ■ Linear enamel caries (odontoclasia) is seen to
inadequate extension of the restoration. In ad­ occur in the region of the neonatal line of the
dition, caries may remain if there has not been maxillary anterior primaiy teeth. The line, which
complete excavation of the original lesion, represents a metabolic defect due to the trauma
which later may appear as a residual or recur­ of birth, may predispose to caries, leading to
rent caries. gross destruction of the labial surfaces of the
teeth.
■ Radiation caries
Radiotherapy is frequently associated with Teenage caries (adolescent caries)
xerostomia due to decreased salivary secre­ ■ This type of caries is a variant of rampant car­
tion. This and other causes of decreased sali­ ies where the teeth generally considered im­
vary secretion may lead to a rampant form of mune to decay are involved. The caries is also
caries, indicating the significance of saliva in described to be of a rapidly burrowing type,
preventing caries. with a small enamel opening. The presence of

Table 5.1: Root caries based on the extent of lesion

Grade 1 (initial) Grade 2 (shallow) Grade 3 (cavitation) Grade 4 (pulpal)

a. Surface texture: a. Surface texture: a. Surface texture: a. Deeply penetrating

soft, can be soft, irregular, soft, can be penet­ lesion with pulpal or
penetrated with rough, can be rated by dental root canal involvement
a dental explorer penetrated with explorer. b. Pigmentation:
b. No surface defect a dental explorer. b. Penetrating lesion, variable, brown to
c. Pigmentation: b. Surface defect cavitation present dark brown.
variable, light tan (less than 0.50 (greater than 0.50
to brown mm in depth) mm in depth) no
c. Pigmentation: pulp involvement.
variable, tan to c. Pigmentation:
dark brown variable, light brown
to dark brown
Billings (1986)
 SECTION' 5 : DENTAL CARIES IN EARLY CHILDHOOD |

a large pulp chamber adds to the woes, caus­ with the availabilty of refined carbohydrates has
ing early pulp involvement. influenced the diet to an extent that caries be­
came highly prevalent. In fact, it is interesting to
Adult caries
note that Nearchos, Alexander the great’s admi­
■ With the recession of the gingiva and some­
ral found in the Indus valley a rare and costly
times decreased salivary function due to atro­
Indian salt' that tastes like honey. Thus sugar
phy, at the age of55-60 years, the third peak of
preparation spread from India to Persia and Ara­
caries is observed. Root caries and cervical
bia, presently known as the dental arch criminal.
caries are more commonly found in this group

Present status
EPIDEMIOLOGY OF DENTAL CARIES

The global epidemiology of caries can be seen to

■ To a great extent dental caries is a disease accom­
exhibit three distinct patterns.
panying advances in civilization. Its appearance
however can be traced back to the ancient times 1. In the first group there is still scarcity of develop­
where the disease has been found in the skulls of ment and the infrastructure is relatively poor. The
human beings adopting the practice of agricul­ mortality rate is quite high. The areas included in
ture. Thus caries has been found in the ape-man this type of a population would be rural China,
and hominid type as well. A carious lesion has Africa, South America and underdeveloped Asian
also been described in the Pithecanthropus, the countries. In this state of affairs, the availability
Java man. The occasional occurrence of caries in of dental care is almost non-existent and the car­
the Neanderthal skulls has also been reported. ies experience is higher in the cities than in the
rural areas.
■ The so called process of modernization has a tell­
ing effect on the incidence of caries. The settling 2. It is found that in newly industrialized or the de­
down of populations in the urban areas coupled veloping countries there is evidence of increas-

SALIVA
"7 PLAQUE - Changes in
properties
DIET CONTROL
-Improved -Bitterhome
care rate
FLUORIDE Nutrition - Buffer
- Decreased - Batter materials
- In water capacity
amount of professional - Fissure
- Toothpaste - Immunoglob­
sugar care sealants
- Varnish Gels ulin content
- Decreased - Chemical
control - Agglutinins
in school frequency volume
of sugar - Antibiotics
- Antimicrobial changes in
additives microflora

Fig. 5.2 Reasons tor decline

 I TEXTBOOK OF PEDODONTICS

Table 5.2: Prevalence of dental cariés in children

Country Age Year DMF Decayed Missing Filled

Argentina 12 1961 4.5 3.2 1.0 0.3

1985 3.2 2.0 0.2 1.0

Australia 12 1954-55 0.3 4.8 1.1 3.4

1981 2.9

Bangladesh 12 1979 3.0 3.0 0.1 0.0

1984 1.5 1.4 0.1 0.0

Brazil 12 1965 7,2 5.6 0.5 0.0

1980 7.3 4.7 0.8 .0.8

Canada 12 1966-70 11.1 3.2 1.0 1.0

1984 3.3 0.5 0.5 1.6

China 12 1965 0.1

1985 0.4 0.4 0.0 0.0

Ethiopia 12 1983 0.7 0.7

** ♦
1985 0.4

India 12 1965 2.4 2.3 0.1 * 0.0

1982 3.2

Kenya 12 1973 1.7 1.4 0.3 0.0

1985 0.2 .0.2

Nepal 12 1983-84 0.2 ..... 0.2............. 0.9 0.0

1986 0.5 0.5 0.0 0.0

South Africa 12 1978-79 3.6 2.5 1.0 0.0

1982 3.2 1.9 0.7 0.6

Sri Lanka 12 1978 2.1

1983 1.9 1.7 0.1 0.1

(Annual Statistics Mond 1987)

 SECTION 5 : DENTAL CARIES IN EARLY CHILDHOOD |

Table 5.3: Prevalence of dental caries in India

Author Year Age Place Prevalence of
caries (%)

Shourie K L 1941 7-13 India 55.50

Kokil et al 1951 * Gujarat 68.7
Shegal I960 4-18 Bombay 90
Shiek 1960 5-19 Bombay 30.9
Antia et al 1962 5-16 Bombay 2.57 (DMFT)
Dutta 1965 - Calcutta 43.9
Tewari • 1977 6-16 Chandigarh 72.35
Mishra et al 1979 5-16 Behrampur 60.4
Sarkar 1979 6-16 Calcutta 99
Dhar et al 1979 - Hazratbal 30.62
Nagaraja Rao 1980 5-15 Udupi 1.7 (DMF)
Kapoor 1980 - ——————— 49.1
Singh et al 1981 5-13 Patna 50.3
Saimbi et al 1983 - Lucknow 60.4
Chopra et al 1983 6-14 Bombay 63.27 .
Vaish 1983 - Orissa 48.60
Gauba 1986 ___ 7r.17_____ Punjab 87.5
Navin and 1986 W Manipal 82
Tandon 5-6 71.11
15-16 67.11
Jawadekar et al 1989 i 12 Sirur 52.4
Borle et al 1990 4-20 Wardha 6.9
Gangawar et al 1990 5-14 Lucknow 38.3
Tandon & Paul 1992 6-11 Manipal 90.66
Gaikwad et al 1993 5-15 57.89 (Boys)
45.2 (Girls)
Damle 1994 12-16 * Bombay 78.83
Ramësh et al 1995 6-10 Nashik 64.0
Singh et al 1997 12-16 Haryana 78-83
Gopinath et al 1999 3-12 Thiruvallur 59.1
A

Table 5.4: Prevalence in preschool children

Author Year Place Prevalence

Navin & Tandon 1986 5 years Manipal 71.11%

Virjee et al 1987 4-5 years 65.0%
Ibrahim A 1992 3-5 years 50%
Sethi & Tandon 1996 24-60 months Udupi 65.5%
(19.44% Nursing caries)
(3.96% Rampant caries)
 CED | TEXTBOOK OF PEDODONT1CS

ing rate of caries in the children and the adults as One of the earliest studies in epidemiology in dental
well. These populous nations areJaced with con­ caries in India was carried out by Day et al [1940].
sumerism and urbanization coupled with in­ They examined 750 subjects from Lahore in the age
creased consumption of refined carbohydrates. group of 5 -18 years & reported that the caries preva­
The dental care available is concentrated in the lence was 94.04 %. Other studies, which have been
urban areas and is involved more in CurafiveWhd reported, are given in table.
palliative services with the problems of the masses
still unaddressed. This pattern may be observed The first National oral health survey was planned in
in countries such as Taiwan, India, Chile, Uganda 1984 by Indian Dental Association with the commit­
and Thialand. ment to achieve WHO goals in our country. Region
wise distribution was found as:
3. The third pattern is found in the developed coun­ ■ In Northern states, an increase was noted at the
tries where the availability of dental services cou­ age of 5-6 years except for Punjab, where fluoride
pled with a more preventive and maintenance tooth pastes and preventive programs may have
approach has lead to a decrease in the DMFT brought about the decline. In the permanent
scores and greater number of retained teeth. dentition (15 years), however, the caries seems to
have declined.
Suggested reasons for decline in caries are ■ In Eastern states, the urban areas (Calcutta) have
given in Fig. 5.2 shown incline in both deciduous and permanent
dentition.
PREVALENCE OF DENTAL CARIES IN CHILDREN ■ In Southern states, an incline in dental caries was
(Table 5.2) noted in both primary and permanent dentition.
A declining trend was. noted at Manipal
■ The DMFT figures were found to decline remark­ (Karnataka) again probably due to well organized
ably at age 12 in most industrialized countries. school health programs.
■ It was found that the countries, which fell in the ■ In urban areas of Western region (Bombay)
DMFT range of 1.8 - 3.0, were Hong - Kong, Thai­ though slight decrease was noted^ it is well above
land; USA, Australia, Singapore, Nigeria, & the the WHO goal. §
United Kingdom. Similarly, in the range of 3.3 -4.8
they found New Zealand, France, Sweden, Neth­ PREVALENCE IN PRESCHOOL CHILDREN
erlands, Ireland, Finland, Norway & Denmark. Very few studies are conducted in pre-schools of
« Wall [1984] reported that nationally Australia was our country. (Table 5.4)
observed to be rapidly approaching the WHO
target figure of 3 DMFT in the 12 yr. age groiip Self-Assessment
[Common Wealth Department of Health, 1982 ]
1. Define dental caries.
PREVALENCE OF DENTAL CARIES IN INDIA 2. What is odontoclasia or linear enamel caries ?
3. What is incipient caries? How do you clinically
Dental caries in our country (Table 5.3) is consist­ differentiate between incipient caries and enamel
ently increasing in prevalence and severity especially hypoplasia ?
in children. Today according to a number of investi­ 4. What are recurrent and arrested caries?
gators, 70-80% are suffering from this disease. The 5. What are the reasons for caries decline in devel­
average number of decayed, missing and filled teeth oping countries ?
at the age of 15-16 years is about 4 in rural and 5 in 6. What is the trend of caries in India ?
urban areas. Because these studies have recorded 7. What is the average number of decayed, missing
point prevalence using no uniform criteria, cross and filled teeth in rural India ?
comparison of these studies has been difficult.
 5.2 Caries Risk Factors

Tandon S, Vanka A

ETIOLOGY OF DENTAL CARIES: at this stage and thus the role of microorganisms
was not highlighted.
Early theories

■ The legend of the -worm Parasitic (septic) theory

Several early references to the decay process in?> The role of microorganisms in the process of den­
elude the ‘Legend of the worm’ where th$ tal decay was substantiated by Leeuwenhoek
Marshes created the worm, an equivalent of which who found ‘animalcules’ from the scrapings of
were also found in the Japanese and Chinese lit­ his teeth even after maintaining meticulous oral
erature. This theory also found acceptance in In­ hygiene. But the mechanism as to why and how
dia and Egypt and several remedies were directed they cause the destruction of the tooth was not
towards the 'worms’ such as fumigation, acupunc­ clear.
ture etc.
I Miller 'schemico parasitic theory
ENDOGENOUS THEORIES (acidogenic theory)
Miller, the best known of the early investigators
■ Humoral theory of dental caries, published extensively on the re­
The four humors that were thought to maintain sults of studies on caries in 18 89. He summarized
the body health included ‘blood, phlegm, blackbile *
** his theory as follows.
and yellow bile’. All diseases including dental “Dental decay is a chemico parasitic process con­
caries were attributed to the imbalance between sisting of 2 stages, the decalcification of enamel,
these factors. which results in its tptal destruction & the decal­
cification of dentin, as a preliminary stage, fol­
* Vital theory lowed by desolution of softened residue. The acid
Hie tooth was thought to be the source and ori­ which affects this primary decalcification is de­
gin of the disorder in that the process started rived from the fermentation of starches & sugar
from the tooth within. lodged in the retaining centers of the teeth”.
The significance of Miller’s observation is that
EXOGENOUS THEORIES he assigned an essential role to 3 factors in the
caries process:
■ Chemical (acid) theory 1. the oral microorganisms in acid production &
The developments in the field of chemistry en­ proteolysis
couraged the investigators to propose the role of 2. the carbohydrate substrate,
inorganic acids causing the decay process. Fer- 3. the acid which causes dissolution of tooth
mpntatinn wac fhniiaht fn bp n nnn-vifal nrnrpcc •_____1 _
 <ETîï I TEXTBOOK OF PEDODONTICS

This theoiy has been accepted by the majority of complexing compounds produced by bacteria
investigators in a form essentially unchanged cause further tooth disintegration. Saliva is an
since its inception. abundant source of inorganic phosphate for bac­
terial utilization. Hence it is highly improbable that
« Proteolytic theory depletion of phosphate in the plaque by oral mi­
The presence of pigmentation in the carious proc­ crobial metabolism results in phosphate with­
ess combined with the fact that abundant organic drawal from enamel.
material is present on the tooth surface led
Gottlieb[1947] to propose this theory; This states ■ Burch & Jackson hypothesis:
that the organic pathways are invaded first and Based on the Burch’s theory of ‘auto-aggressive
destroyed by proteolytic action. theory of the cause of growth, disease and ag­
ing’, Jackson and Burch [1970] suggest that genes
« Proteolysis - chelation theory [partly inherited and partly as a result of muta­
The proteolysis - chelation theory of dental car­ tions] determine whether or not a site on the tooth
ies, as proposed by Schatz et al [ 1955], states that is at risk. An abnormal mitotic control protein has
the bacterial attack on enamel, initiated by been proposed that causes disorders of the
keratinolytic microorganisms, results in a break­ odontoblasts as a random event that lead to
down of the protein & other organic components changes in the resistance of the enamel to acid
of the enamel, chiefly " keratin'4. This results in attack.
the formation of sùbstances, which may form
soluble chelates with the mineralized component CURRENT CONCEPT
of the tooth and thereby decalcify the enamel at a
Caries is perceived to be a prolonged imbalance in
neutral or even alkaline pH.
the oral cavity such that factors favouring deminer­
alization overwhelm factors that favour
OTHER THEORIES OF CARIES ETIOLOGY
remineralization or healing of tissues. Therefore, to
• Sulfatase theory: understand the caries process, it is^necessary to
Pincus [1950] advanced the sulfatase theory, probe the reaction process that occurs at the sur­
whereby bacterial sulfatase hydrolyzes the “mu- face.
coitin sulfate” of enamel and the “chondrotin
■ Demineralization
sulfate” of dentin producing sulfuric acid that in
The mineral content of tooth surface is hydrmtyá-
term causes decalcification of dentinal tissues.
patite 4Ca{₽O4 }¿ { OH }2] which is in equilibrium
The concentration of sulfated polysaccharides
and neutral environment saturated with calcium
in enamel is very small and not readily accessible
and phosphate. It is reactive to hydrogen ions at
as a substrate for enzymatic degradation. This is
the critical pH of 5.5 and below. H+ ions react
a highly unlikely hypothesis for the degradation
with the phosphate group in the aqueous envi­
of tooth enamel.
ronment immediately adjacent to the crystal sur­
• Complexing & phosphorylating theory: face with the conversion of phosphate to
[Lura, 1967] hypophosphate by addition of hydrogen ions be­
According to this theoiy, the high bacterial utiliza­ ing buffered at the same time. The hypophosphate
tion of phosphate in the plaque causes a local is not able to contribute to the normal hydroxya­
disturbance in the phosphate equilibrium in the patite equilibrium because it contains phosphate
plaque & the tooth enamel resulting in a loss of not hypophosphate. Thus the hydroxyapatite
inorganic phosphate from tooth enamel. Soluble crystal dissolves and the process is termed dem­
calcium - ineralization.
 SECTION' 5 : DENTAL CARIES IN EARLY CHILDHOOD |

■ Remineralization PRIMARY MECHANISM OF CARIES FORMATION

The demineralization can be reversed if the pH is
neutral and there are sufficient calcium and phos­ In simple terms the caries process can be explained
phate ions in the immediate environment. Either as:
apatite dissolution can reach neutrality by buff­
ering or the calcium and phosphate ions in saliva CARIOGENIC SUITABLE
can inhibit the process of dissolution through BACTERIAL + LOCAL — ORGANIC
the common ion effect. This enables rebuilding PLAQUE SUBSTRATE ACIDS
of partly dissolved apatite crystals and is termed
remineralization. ORGANIC TOOTH
DEMINERALIZATION-REMINERALIZATION CYCLE ACIDS + MINERAL — LOSS OF
[McIntyre et al, 1998] [IN PLAQUE] ENAMEL

Critical pH DEMINERALIZED BACTERIAL

TOOTH + PROTEOLYTIC — CAVITATION
6.8 6.0 5.5 5.0 4.5 4.0 3.5 (DENTIN) ENZYMES

Hydrogen ions Demineralization: FA and HA

reacts with HA dissolves, dissolve 1. THE TOOTH
phosphate ions FA forms in The three aspects of the tooth to be-considered
in saliva and presence of are,
plaque fluoride
If H
* ions
- Composition
Remineralization exhausted or - Morphologic characteristics
FA reforms neutralized and - Position
all ions retained.

6.8 6.0 5.5 5.0 4.5 4.0 3.5 > a Composition

The enamel composition varies according to
the inorganic content as well as the crystal
HA - Hydroxyapatitie FA - Fluorapatite
configuration and size, \fcrious trace elements
Primary factors responsible for dental caries: are also present in the enamel, notably fluo­
ride and carbonate.
■ Caries is truly a multifactorial disease. Interaction ■ It is seen that the surface is more resistant
between 3 primary factors is essential for the to caries than the subsurface enamel. It has
initiation & progression of caries; [Keys, 1960] also been observed that the surface enamel
is highly mineralized and tends to accumu­
1. a susceptible host tissue, the tooth ; late more quantities of fluoride, zinc, lead
2. microflora with a cariogenic potential; and iron than the subsurface layer. The sur­
3. a suitable local substrate to meet the require­ face contains less carbonate, less water and
ments of the pathodontic flora. has more organic material than the subsur­
face layer.
■ Caries Tetralogy (Newbrun 1982) includes a fourth
factor, time to the still existing concept of Keyes, ■ The fluoride content of enamel & (fentin
depicting the significance of changes taking place from sound teeth was found to be 410ppm
over a period (Fig. 5.3, 5.4). and 873 ppm respectively; but only 139 ppm
and 223 ppm respectively in carious teeth.
 I TEXTBOOK OF PEDODONTICS

Fig. 5.3 Primary risk factors in caries.

TOOTH PH
Fluorides flora
Morphology Strep, mutans
Nutrition (Substrate)
Trace Elements Oral Hygiene
Carbonate Level Fluoride in Plaque
TOOTH FLORA
co
CARIES

SUBSTRATE

SUBSTRATE
Oral Clearance
SALIVA
Oral Hygiene.
Detergency of Food
Frequency of Eating
Carbohydrate (type, concentration)

Fig. 5.4 Secondary risk factors in caries (Neubrun 1982).

 SECTION 5 : DENTAL CARIES IN EARLY CHILDHOOD |

h The morphology of the tooth ■ Other microorganisms like Lactobacillus

The presence of enamel hypoplasia has been acidophillus, Lactobacillus cassi, Actinomy­
seen to predispose the tooth to the develop­ ces and certain species of Streptococcus san­
ment of dental caries & that the more severely guis also have the ability to produce caries,
the tooth is affected, the more extensive will biit their caries activity is not comparable to
be the caries. A type of caries has been de­ that of Streptococcus mutans.
scribed to occur in the cases of Linear Enamel ■ All the microorganisms produce extracellular
Hypoplasia [LEH]. polysaccharide from either glucose or sucrose
■ Presence of deep, narrow occlusal fissures ■ The number of lactobacillus increases only
or buccal or lingual pits predisposes to after caries lesion has developed.
caries. Such fissures tend to trap food, % ■ Microorganisms capable of destroying dentin
bacteria and debris, and since defects are must not only possess the ability to produce
especially common in the base of fissures, acid, and to survive in aciduric conditions, but
caries may rapidly develop in these areas. also be able to break down the protein struc­
ture of the dentin.
c. Position
' Teeth which are malaligned, out of position,
Window of Infectivity
rotated or otherwise not normally situated may
be difficult to cleanse & tend to favor the ac­ Carfield (1993) monitored oral cavity levels from
cumulation of food & debris. This in a sus­ birth upto 5 years. He noted the initial acquisition
ceptible person, would be sufficient to cause mutans S. and designated the time period as ‘win­
caries. Besides, certain teeth and in each tooth, dow of infectivity’. As the teeth' (primary teeth)
erupt in to the oral cavity they provide a virgin
certain surfaces are seen to be more suscepti­
habitate which enable MS to colonize the oral cav­
ble to the occurrence of caries.
ity avoiding competition with other indigenous bac­
2. ESSENTIALITY OF ORAL BACTERIA teria. Thus in the window period in deciduous teeth
There is now enough convincing evidence that the MS is established by 7-24 months of age and
caries is an infectious disease. The carious lesion may have difficulty in establishing later because it
develops as a result of a change in the ecosystem would need to compete with other indigenous bac­
at the tooth surface and one of the essential fac­ teria.
tors responsible for this change is the shift in thé Krass etal (1967) Edrman et al (1975) reported 2-6
microbial community. A sterile oral cavity of the yrs of age the child is less susceptible to acquiring
newly born child withiii a few hours ofbirth starts MS. The ‘Second Window Infectivity’ is present in
getting invaded by a good number of bacteria permanent dentition between 6-12 years of age
notably the species Streptococcus, Neisseria, (Klock and Kroske (1977). 90% of teenager have
Actinomyces, Veillenella and Lactobacillus. They MS colonization while others found only 3% of
colonize the oral environment These bacteria must adults (mothers).
be able to stick to the receptor sites in the mouth
Davey and Rogers (1984) reported that children ac­
including the teeth, tongue, cheek, or find refuge
quire additional strain of MS as they get older and
in the places such as interdental areas, where they new teeth emerge but remain undetected since they
can resist the flow of saliva to develop a carious are present in low numbers.
lesion. Various studies have proved that:
■ Streptococcus mutans is the important patho­ 3. THE ESSENTIALITY OFORALSUBSTRATE
gen in initiation of caries and takes about 5-6 The presence of readily fermentable carbohy­
years to penetrate the enamel of 2.7mm thick­ drates has been thought to be responsible for
ness in a human tooth.
 I TEXTBOOK OF PEDODONTICS

this loss of caries immunity. The cariogenicity of more effective in its buffering action than
a dietary carbohydrate varies with the frequency unstimulated saliva.
of ingestion, physical form, chemical composi­ ■ The critical pH at which demineralization starts
tion, route of administration & presence of other is about 5.2 to 5.5, depending on the calcium
food constituents. and phosphate concentrations of the mixed
saliva.
Essential cariogenic factors regarding the diet ■ The tooth that erupts into the oral cavity is
■ The frequency of consumption of sugar-con- not fully matured. After erupting into the oral
taining food is directly proportional to the car­ cavity, it undergoes a process of ‘post-erup­
ies experience tive maturation’. This makes the tooth less
■ The frequency of in between meal snacks of prone to caries as compared to the immature
candies, cookies, chewing gum or carbonated tooth. Though the exact mechanism is not fully
beverages play an important role in increasing understood, saliva has been thought to play a
the caries rate. key role in this process.
■ Frequent ingestion of sucrose even with a rela­ ■ Although saliva does bring about the deposi­
tively low concentration of 1.25 % wall cause a tion of calcium phosphate, it does not have
drop in pH to between 4 and 5. unlimited potential. The calcium and phos­
« A significant correlation exists between a high phate in the saliva exist in two forms:
sugar concentration in saliva with a prolonged ultrafilterable and non-ultrafilterable. The
clearance time and caries activity. ultrafilterable form has the potential to come
■ Retentive, sticky, sweet foods with a little de­ out of the solution and thus it may precipitate.
tergent or self cleaning properties may be po­ On the other hand, the non-ultrafilterable form
tentially highly cariogenic. is bound to salivary proteins that prevent its
« Monosaccharides & disaccharides are more precipitation. These proteins consisting of
harmful as they are easily fermentable than statherin and proline rich protiens.also inhibit
polysaccharides. hydroxyapatite formation by blocking crystal
growth of calcium phosphate. §
4. ENVIRONMENT
Important mechanisms of salivary factors related
■ The integrity of the enamel environment is to­ to dental caries are given in table 5.5
tally dependent on the composition and chemi­
cal behavior of the surrounding fluids, con­ PLAQUE
sisting of saliva and/or the plaque fluid.
■ More important in the carious process is the
Saliva plaque tooth interface
• Under normal physiological conditions, the ■ The mechanism of carbohydrate degradation to
saliva is supersaturated in terms of calcium and form acids in the oral cavity by bacterial action
phosphorous with respect to the enamel sur­
occurs through enzymatic breakdown of sugar.
face. This prevents the hydroxyapatite from
■ The mere presence of acid in the oral cavity is of
dissolving in the oral environment as long as
far less significance than the localization of acid
the pH of the environment is maintained.
« A pH drop, initially is countered by the buffer­ upon the tooth surface. Dental plaque acts as a
ing action of the saliva due to the bicarbo­ reservoir for holding acids at a given point for
nates and the phosphates. Stimulated saliva, relatively long periods.
with a higher bicarbonate content is said to be
 SECTION 5 : DENTAL CARIES IN EARLY CHILDHOOD |

Table 5.5: Important mechanisms of salivary factors related to dental caries

Salivary Effects on Effects on Effects on Role in

Factors Mineralization Bacteria Bacterial raising saliva or
Aggregation or Plaque pH
¿Adherence

Buffering factors Main buffer in saliva

HCO, Releases NH3
Urea Releases NH,■w
Agrinine-rich
proteins

Antibacterial Binds to iron, also

factors inhibits indepen­
Lactoferrin dently of iron

Lysozyme Hydrolyzes cell wall May promote

polysaccharides clearance
through
aggregation

Peroxidase Produces OSCN,

inhibits glycolysis

Secretory IgA Neutralizes toxins Binds to bacterial

and enzymes surface, prevents
adherence

Alpha amylase Produces glucose Indirectly

and maltose produces glucans

Factors
affecting
mineralization

Histatins Bind to hydro­ Some inhibition

xyapatite aid in of mutans
supersaturation streptococci
of saliva ♦

Proline-rich Bind to hydro­ Bind to oral

proteins xyapatite aid in bacteria-promote
supersaturaticn adherence in
of saliva
i some cases >

Cystatins Bind to hydro­

xyapatite aid in
supersaturation of
saliva

Statherin Bind to hydro­ Bind to oral

xyapatite aid in bacteria-promote
supersaturation adherence in
of saliva some cases

Mucins Provide physical Aggregation and

and chemical clearance of oral
barrier in enamel bacteria (MG2)
pellicle
 <FF> | TEXTBOOK.OF PEDODONTICS

■ Factors in plaque that may be responsible for the ■ Chronic administration of syrups sweetened with
initiation of caries aré: sucrose in children, leads to an increased inci­
dence of caries in their deciduous as well as per­
a. The ability of the plaque to buffer the pH manent dentition.
changes caused by a carbohydrate exposure.
Otherfoods
This is also related to the rate of and diffusion
or concentration of the lactic acid produced in
■ Several investigators have suggested that pre­
the plaque. natal deficiencies of protein, minerals and vita­
b. The quantitative and qualitative changes in , mins predispose the infant to subsequent devel­
the plaque microflora. Thus the presence of opment of caries.
streptococcus mutans, in higher levels [ cari-
ogenic] as compared to more benign microor­ The vitamin content of diet
ganisms [Actinomyces, Veilonella] will deter­
mine the predisposition to caries. ■ A high incidence of caries was observed in the
enamel hypoplasia developed due to vitamin de­
OTHER FACTORS CAUSING CARIES ficiency'.
Infants with rampant caries who had no history
Heredity of using a nursing bottle were found to be strongly
associated with vitamin deficiency.
■ The racial tendency for high caries or low caries
incidence appears to follow hereditary patterns. Protein
■ Black children exhibited less dental caries than a
I comparable group of white children. ■ Protein deficiency during dental development
• A high DMF father & a high DMF mother are leads to a delay in eruption & a greater suscepti­
j seen to produce an offspring with a high DMF bility to caries.
J rate. ■ Protein has also been seen to protect against dem­
| ■ A greater resemblance between identical twins ineralization of enamel.
| than between fraternal twins with respect to car-
f ies incidence is also noted. Trace elements

Systemic conditions Trace elements like selenium, cadmium, lead, manga­

nese and barium have been found to increase the
■ The presence of a systemic disease or abnormal­ caries experience.
ity may directly or indirectly [ as a side effect of
treatment] affect the incidence of dental caries. CARIES RISK ASSESSMENT
Xerostomia caused due to a variety of factors
such as due to drugs, irradiation of the glands Dental caries is a biosocial disease that can be pre­
and diabetes mellitus can cause an increase in vented if certain risk factors could be identified in
the incidence of dental caries. Similarly, other dis- susceptible individuals or community The risk
> eases such as cystic fibrosis and phenylketonu­ groups or individuals for the purpose of caries con­
ria, which require a specific diet regimes and life trol are presented in Table 5.6
A styles may also affect the caries incidence.
 SECTION'5 : DENTAL CARIES IN EARLY CHILDHOOD |

Table 5.6: High and low risk child groups for the purpose of caries control

HIGH RISK CHILD LOW RISK CfflLD

Social History
Low socioeconomic status Middle class/upper class
High caries in siblings Low caries in siblings
Poor dental awareness Conscious of dental health
Motivation level low Motivation level high

Medical History
Handicapped (poor manual control). No medical problem, handicap or
Medical conditions predisposing to salivary deficiency with normal birth.
xerostomia.
Long term cariogenic medicines
(syrups).
Traumatic delivery.

Dietary Habits
Frequent sugar intake (solid exposure Sugar intake in limits.
>3, liquid exposure >5).
Refined carbohydrate intake. Less
Pacifier habits/prolonged breast No such history.
feeding.

Fluoride
Fluoride deficient. Optimum water fluoride level.
No fluoride supplements, toothpaste - Fluoride supplements (if required
indicated) toothpaste used.

Oral Hygiene
i
Poor oral hygiene with excessive Oral hygiene fair. 9
plaque accumulation.

Saliva
Low buffering capacity. High buffering capacity.
Streptococcus mutans count (more Streptococcus mutans count
than 105) less than 105
Lactobacillus count (CFU) less than Lactobacillus count (CFU) less than
10,000/ml saliva 1000/ml saliva
 CEE) I TEXTBOOK OF PEDODONTICS

Caries susceptibility and activity ■ The commonly used Dentocult test was devel­
oped by Larmas [1975]. It consists of running
Caries susceptibility refers to the number of new le­ undiluted saliva over a dip slide coated with a
sions that may develop in an individual over a period slightly modified Rogosa agar and the growth is
of time while caries activity suggests the number of compared with a standard illustration. Correlation
lesions that an individual has at the time of record­ of 65-90 % have been found between counts of
ing (new and old). lactobacilli and caries experience. In this test, a
count of more than 10,000 colony forming unit
The caries susceptibility varies in different individu­ permli.eC.F.U./ml of saliva is considered high,
als, in an individual in different teeth and also on the whereas a count of less than 1000 C.F.U./ml is
different surfaces of each tooth. The susceptibility considered low.
of the teeth and surfaces in descending order is given
below. ■ Indications for the use of Dentocult-LB count.
a. For pre-selection of patients for yearly or half
Primary teeth: Second molar, First molar, Canine, yearly check-ups in communities.
Lateral, Central. b. It is an important educational aid for motiva­
tion and dietary counseling among patients.
Permanent teeth: First molars, Second molars, Up­ For this it is important to show the results to
per second bicuspids, Upper first bicuspids and lower the patients and explain what they mean.
second bicuspids, Upper central and lateral, Upper c. Control of the efficacy of dietary counseling.
cuspids and lower first bicuspids, lower central and d. Sometimes a high, steady lactobacillus count
lateral incisors and lower cuspids. indicates medically compromised patients. For
example, diabetes mellitus predisposes the
Surfaces in primary teeth: Occlusal, molar inteiproxi- subject to lactobacillus growth.
mal area, incisor interproximal areas. e. An unchanged DentociSt-LB value is a con­
traindication for expensive bridges, oral im­
Caries activity tests plants or orthodontic treatment The test may
be considered an insurance for the dentist
Tests based on the estimation of the micro-organism aga inst accusations of malpractice.
numbers have been developed and these have been
related to the caries activity. These tests aid the cli­ Counts of Streptococci mutans
nician in educating the patients regarding his or her
caries activity and thereby help in motivating them ■ Numbers of mutans streptococci have been as­
in good oral hygiene practices. sessed in samples of plaque and saliva. The pres­
ence of streptococcus mutans in the oral cavity
Counts of lactobacilli is an indicator of the cariogenic infection. One
diagnostic problem is the fact that caries is not a
Counts of lactobacilli represent one of the earliest specific infection. Thus there are many people
and most widely used tests of caries activity. It was with mutans infection in their oral cavity without
observed in the 1920’s that high numbers of lactoba­ any signs of a caries attack, while abundant car­
cilli were found in subjects with abundant carious ies lesions occur in patients without mutans in­
lesions, and it was consequently believed that lacto­ fection. Thus the diagnostic value of mutans is
bacilli are the causes of caries. only Relative.
 SECTION 5 : DENTAL CARIES IN EARLY CHILDHOOD |

■ The Streptococcus /tnutans tests are useful for ■ A pie circle diagram is divided into 5 sectors, in ’
the following purposes: the foiling colours.
a. For the preselection of patients fór dental ex­ 1. Green? Shows an estimation of the‘ chance to
amination. Like the lactobacilli test it is not avoid caries’
accurate enough for the final diagnosis. 2. Dark Blue: ‘ Diet’ is based on a combination of
b. For the demonstration of cariogenic infection. diet contents and diet frequency.
c. For the evaluation of the effectiveness of any 3. Red: ‘ Bacteria’ is based on a combination of
mouthrinse medication, providing an objective amount of plaque and mutans streptococci.
measure for the treatment. 4. Light Blue sector: ‘Susceptibility ‘ is based on
d. For didactic purposes in health education' a combination of fluoride program, saliva se­
e. For diagnosing mutans bearing parents in a cretion and saliva buffer capacity.
family before eruption of the child’s decidu­ 5. Yellow sector: ‘Circumstances ‘is based on a
ous teeth. combination of past caries experience and re­
lated diseases.
■ The commercially available systems are:
1. MSBB method[Matsukubo et al{ 1981}, Showa Self-Assessment
Yakuhin Co. Ltd. Tokyo, Japan]
2. Caries Screen SM [ Jordan et al {1987} Apo 1. What is caries tetralogy ?
Diagnostics, Toronto, Canada] 2. Which are the micro-organisms that are respon­
3. Strip mutans test [ Jenssén andBratthal {1989}, sible for the initiation and progression of caries ?
Orion diagnostica Espoo, Finland] 3. Which are the secondary factors of caries ?
All three are based on the fact that bacitracin 4. What is the concept of critical pH ?.
inhibits the growth of all other oral strepto­ 5. What is cariogram?
cocci except mutans on the mitis salivaris me­ 6. How will you differentiate between high and low
dium risk caries based on the streptococcus mutans
count.?
CARIOGRAM 7. List out the theories on the etiology of dental
caries.
« Recently, a new method of illustrating the inter­ 8. Which are the most susceptible and least sus­
action of factors contributing to the development ceptible teeth affected by caries ?
of caries has been introduced by Bratthall et al
[1999] called‘CARIOGRAM’.
 5.3 Early Diagnosis of Caries

Tandon S, Vanka A if

Traditionally caries has been diagnosed by the means ■ Slides have been used to gather information about
bf visual examination, tactile sensations and by use caries. With the use of slides, the pictures of the
of Radiographs. However, with the emphasis being posterior teeth tell us more about discolourations,
on prevention in the true sense, i.e primary preven­ decalcifications and translucencies than can be
tion, it is not just enough to be able to diagnose the discerned by oral examination.
relatively late lesion, as by the above methods. The
methods for the detection of caries can be used ei­ • The use of temporary elective tooth separation
ther clinically i.e. in vivo or they can be used purely as a diagnostic aid in general practice has been
for research purposes i.e. in vitro. Though the meth­ stated in both deciduous and permanent denti­
ods used for research can sometimes be applied clini­ tion with more lesions being revealed with the
cally as well, the quantification of the demineraliza­ separator technique than with clinical examina­
tion requires a histological section of the tooth and tion alone (Fig. 5.5).
thus may not be viable clinically.
Tactile examination £

METHODS OF CARIES DETECTION

« The explorer and the floss to certain extent have
Various methods used for caries detection are
been used for the tactile examination of the tooth.
mentioned in Table 5.7
The explorer can be of different varieties such as:
1. Right angle probe [No. 6]
Visual examination
2. Back action probe [No. 17]
The Visual examination of caries encompasses the 3. Shepherds crook [No.23]
use of criteria such as detection of white spot, 4. Cow horn with curved ends [no.2]
discolouration and frank cavitation: Visual examina­
tion on its own and without aids can be quite unreli­ « Over the years the teachings of the use of ex­
able. plorer have been:

1924 Black “Passing the explorer into pits —,

Aids in the Visual diagnosis of caries
noting whether or not there is any
softening, and whether the instru­
• A magnification loupe may be used as an aid in
ment catches or enters at any point”
the process ofvisual examination. The loupes are
comfortable to wear, relatively inexpensive after
1956 Simon “Recognize change or marginal
an initial breaking in period and freely available in
changes around a previously placed
various magnifications from various opticians.
restoration. This can be accomplished
with a mirror and explorer"
 SECTION 5 : DENTAL CARIES IN EARLY CHILDHOOD |

1982 Gilmore "Susceptible site can be entered by 1. &iape of the fissure

the use of a small sharp explorer or if 2. ^^rpness of the explorer
enamel is rough, decalcified or opens 3. Force of application
to the dentin”. 4. Path of explorer placement
1985 Marzouk "Sharp explorer - pressing this tip
into pits and fissures will cause it to Radiographs
penetrate the enamel and /or dentinal
caries cone, making a definitive diagno­ Conventional
sis of caries".
1985 Sturde- “Defects are best detected when an ■ Though conventional radiographs [Bitewing and
vant explorer provides tug back or resist­ ЮРА] are most frequently used for the detection
ance to removal". of caries, they are associated with drawbacks that
it presents a 2-D image of an object, may cause
The use of explorer condemned because overlapping of the teeth due to faulty angulation
, more so with the useof bisecting technique and
■ Sharp probe tips can cause physical damage to may also miss the initial lesion.
small lesions with intact surfaces. The validity of
the same has been shown to be poor. Advances
« Probing may lead to fracture and cavitation in the
incipient lesion. Normal dental examinations with A. Digital Radiography' either with Charge coupled
an explorer may spread the organism in the mouth. device technology or Storage phosphor screen
■ Mechanical binding of the explorer in the fissure technology has been used and is said to have
may be due to non-carious reasons, leading to added advantages such as:
the feeling of catch. This may depend on factors ■ Less image resolution.
such as:

Table 5.7: Methods of caries detection

In vivo In vitro
• •

1. Visual examination ■ Single tooth measurements ........................ -v-p-r;;.. ■ T

■■ '■ ■ i
■'•••• ■ ...............
2. Tactile examination 1. Chemical analysis
3. Radiographs-Conventional, Digital 2. Cross sectional microhardness testing
and Xeroradiography ♦ 3. Polarized light rpicroscopy
4. Fiber optic transillumination. 4. Traditional transverse microradiography
5. Optical methods - Fluorescence, light (TMR) f

scattering 5. Microprobe analysis ?

6. Electronic resistance measurements

7. Ultrasonics ■ Methods for sequential measurements
8. Dyes on tooth slabs
1. Iodine absorbitometry
2. Longitudinal microradiogrpahy : 1

3. Light scattering
4. Surface microhardness
II
<l№> I TEXTBOOK OF PEDODONTICS

Fig. 5.5 Use of separators for detection of Fig- 5.6a Proximal caries in anterior teeth not
proximal caries. clearly seen by visual examinaiton.

Fig. 5.6b Caries disclosed by using

fibre optic transillumination on
the same teeth.

Fig. 5.7 Detecting initial caries with Fig. 5.8 Electronic conductance
diagnodent. measurement for caries detection.
 SECTION 5 : DENTAL CARIES IN EARLY CHILDHOOD | (ED

■ Less radiation required to be greyer in this range than the blue fluores­
■ The image detector is generally larger. cence obtained in the ultraviolet excitation.
■ Detector life-span is unknown.
■ The image is immediately available ■ Recently it lias been found that when illuminated
■ Hard copy image is less diagnostic with argohlaser light, the carious tissue has a
■ Image can be electronically transferred. clinical appearance of a dark, fiery, orange-red
■ Image may be enhanced. colour and is easily differentiated from sound
tooth structure. Decalcified areas appear as a dull,
B. Xeroradiography has also been used with the ad­ opaque, orange colour.
vantages of less radiation and edge enhancement
along with its wide latitude of exposure. ■ DIAGNOdent: A new method of caries detection
is the DIAGNOdent [patented by Kn\fo,1999]
Fiber optic transillumination (FOTI) which is based on the principle of fluorescence.
This system has a range of -9 to 99 with [-9J being
The principle of transillumination is that there is a the value where the tooth is the healthiest The
different index of light transmission for decayed and advantage lies in the early, precavitation stage of
sound tooth. Since tooth decay has a lower index of caries detection. It is also useful in determining the
light transmission than the sound tooth structure, an amount of carious involvement [decalcification]
area of decay shows up as a darkened shadow that in different areas of the same tooth (Fig.5.7)
follows the decay along the path of dentinal tubules.
■ The use of FOTI has been proved to be effective, Electronic resistance measurements
specially when used in the anterior region (Fig.
5.6a, b). The usage in the posterior region is as­ ■ The low conductance of the tooth is primarily
sociated with some difficulty. It has been thus caused by the enamel At locations where the
advocated as an adjunct to visual and radio­ pore volume of the enamel is larger, the electrical
graphic methods. Dyes have also been used for conductance increases considerably. Since the
the enhancement of visualization. conductanceof the tooth and the resistance are
inversely proportional, the increased conduct­
Fluorescence ance or decreased resistance are indicative ofthe
presence of hypo and/or demineralization. The
« The use of fluorescence for the detection of car­ increased pore volume is due to the formatiopof
ies dates back 1929, when Benedict observed that microscopic cavities, which are filled with saliva
normal teeth fluoresce under ultraviolet illumina­ to form conductive pathways for electrical trans­
tion and suggested that this fluorescence might mission (Fig. 5.8).
be useful in the determination of dental caries
when monochromatic light is used at350,410and « When a potential of less than one volt is applied,
530nm on carious and non-carious teeth. In the the resistance of above 600 OOOohms indicates
* carious lesions the emission spectra shifts to more that the tooth is caries free. A resistance below’
than 540nm, or the red range of the electromag­ 250000 ohms indicates that caries involving the
netic spectrum. The largest difference between dentin is present.
the carious and noncarious spectra is found at
600iun. They stated that when the enamel is illu­ ■ Recently, site specific and surface specific meas­
minated with light in the blue-green range the ob­ urements have been found to be useful in the
servable fluorescence occurs in the green-yellow detection of caries in the precavitation stage as
range. They also stated that this difference seems well.
 I TEXTBOOK OF PEDODONTICS

Ultrasonics Though the use of dyes for the detection of cari­

ous dentin is used in the removal of the same,
Ultrasonics is the use of sound waves for detection concern has been expressed that the use of dyes
and this offers considerable potential as a diagnos­ is associated with excessive removal of the dentin.
tic instrument.
■ With the use of this instrumentation, sonic ve­ ■ The use of the dye is based on the fact that in­
locity and specific acoustic impedance can be de­ creased porosity -through tlie development of
termined for the dentin and enamel as well as for capillary like microvoids -is the earliest change in
the soft tissue and bone. the carious lesion. Very fluid solutions, that can
strongly wet the enamel can be used to deposit a
■ The velocity of sound on the enamel surfaces fluorescent material in these pores.
has been found to be Vs= 3,143 121 m/s. Compar­
ing with a radiographic and visual inspection, it ■ Other methods such as Micro-air abrasion, Infra­
has been found that white spot lesions with no red camera, Tuned aperture computed tomogra­
radiolucencies or radiolucencies confined to the phy have also been developed for the detection
enamel produced no detectable or weak surface of caries.
echoes. All sites with visible cavitation and
dentinal radiolucencies produced echoes with a Self Assessment
substantially higher amplitude.
1. What are clinical methods of diagnosing caries ?
Dyes 2. What are caries detector dyes ?
3. What is caries activity and caries susceptibility ?
■ Various dyes have been used in the detection of 4. List out the newer methods of caries detection.
enamel caries [Calcein,Zyglo ZL-22],and dentin 5. What are the reasons the Use of the explorer has
caries [Fuschin,Acid redsystem,9-Aminoacridine]. been condemned ?
 5.4 Nursing Caries and Rampant Caries

Tandon S

Nursing caries is an unique pattern of dental caries ■ Nursing bottle can effectively block the salivary
in very young children due to prolonged and im­ access to the tooth surfaces, thereby increasing
proper feeding habits. Even as the first primary tooth the cariogenicity of the oral flora.
starts erupting, the oral environment can be condu­
cive to the initiation of demineralization. Inspite of 1. Pathogenic microorganism
the fact that dental caries is diminishing in our youth
there are still a large number of children with ad­ ■ Streptococcus mutans is the principle organism
vanced multiple carious lesions, victims of parental which colonizes the tooth after it erupts into the
ignorance of nursing caries which is a distinct clini­ oralcavity.
cal entity. Hence this chapter is aimed to review this « It is transmitted to the infant’s mouth primarily
important clinical problem in depth to enable the stu­ through mother.
dents to extend the best possible care to the infants ■ It is considereclmore virulent because of the fol­
and toddler. lowing reasons:
a. It colonizes the teeth
Terminologies and definitions are given in Table b. It produces large amount of acid
5.8 c. It produces large amount of extra cellular
polysaccharides which favor plaque formation.
Classification of early childhood caries are given
■ It is seen that a child’s infection is nine times
in Table 5.9 ♦ greater when maternal salivary count of S.mutans
Prevalence of Nursing Caries are given in Table is greater than 100,000 colony forming units per
5.10 ni
< ■ S.mutans is more commonly evident in rapid and
Etiologic agents in nursing caries smooth surface caries and less common in pit and
fissure caries.
• Bovine milk, milk formulas and human breast milk
have all been implicated in nursing caries because
2 SubMrate (Fermentable carbohydrate)
of their lactose contents. Additional sweeteners
Carbohydrates are utilized by microorganisms to
in the form ofjuices, honey dipped pacifier can
form dextrans which
also cause this type of caries.
a. adhere organisms to tooth surface
■ The basic mechanism of demineralization (Caries
b. cause organic acid to demineralize the tooth
initiation) is the same and the caries tetralogy is
the key in the whole process of nursing caries as
In infants and toddler, the main sources of
all the four variables, pathogenic microorganisms,
substrates, host factor (tooth) and time are es­ fermentable carbohydrate are:
sential in causing demineralization.
 I TEXTBOOK OF PEDODONTICS

Table 5.8: Terminologies, and definitions

Terminologies Author and Year Definition

Nursing Caries Winter et al, 1966 An unique pattern of dental decay in young
children duerto prolonged nursing habit.

Nursing Bottle Mouth Kroll et al, 1967 A syndrome characterized by-a severe
caries pattern beginning with the maxillary
anterior teeth in a healthy bottle fed infant
or toddler.

Nursing Bottle Syndrome Shelton et al, 1977 A devastating condition that may render
Bottle-Propping Carres young children dentally c.rippled.
Labial Caries
Comforter Caries

Night Bottle Syndrome Dilley et al, 1980 A unique pattern of dental caries in young
Baby Bottle Caries, children.
Nursing Mouth

Baby Bottle Mouth Groll, 1984 A very destructive carious process which
Nursing Mouth Decay can affect infants and toddlers.

Nursing Bottle Caries Tsamtsouris, 1986 Caries caused by a prolonged use of a bottle
filled with any liquid other than the water.

Baby Bottle Tooth Mim Kelly et al, 1987 A caries caused by bottle feeding only not
Decay by breast feeding.

Milk Bottle Syndrome Ripa, 1988 A specific form of rampant decay of the
■ Infancy Caries primary teeth of infants.
■ Soother Caries
■ Circular Caries

Tooth Cleaning Neglect Moss, 1996 Baby bottle decay is renamed to shift the
emphasis away from the bottle to the need
for cleaning.

RIECDD (Rampant infant Horowitz, 1998 It does define the age group affected by the
and early childhood disease and the usual rapidity of its
dental decay) development

Early Childhood Caries Davies, 1998 A complex disease involving maxillary

primary incisors within a month after
eruption and spread rapidly to involve
other primary teeth.
 SECTION 5 : DENTAL CARIES IN EARLY CHILDHOOD |

Table 5.9: Classification of early childhood caries

Type IECC ■ Carious lesions involving the nwlars and incisors.

(Mild to moderate) ■ Seen in 2 to 5 years. 1
■ Cause is usually a combinaron of cariogenic semisolid
or solid food and lack of oral hygiene.
■ Number of affected teeth usually increases as the cariogenic
challenge persists.

Type II ECC « Labio-lingual carious lesion affecting the maxillary incisors

(Moderate to with or without molar caries, depending on age.
severe) ■ Seen soon after the first tooth erupts.
■ Unaffected mandibular incisors.
■ Cause is usually inappropriate use of feeding bottle or at
will breast feeding or combination of both, poor oral hygiene.
■ Unless controlled it may proceed to an advanced stage.

Type III ECC ■ Carious lesions involve almost all the teeth, including
(Severe) mandibular incisors.
■ Usually seen in 3 to 5 years of age.
■ Cause is a combination of factors and a poor oral hygiene.
« Rampant in nature and involves immune tooth surfaces.

Table 5.10: Prevalence of Nursing Caries

Country Year of publication Prevalence percentage

England 1967-1982 3.1 to 12.0 %

United States 1976-1987 1.0 to 53.1 %

*

Canada 1982 3.2 %

Australia 1985 5.4 %

South Africa 1978 to 1981 3.1 to 12.2%

Indonesia 1979 48.0 %

India (Manipal) 1996 65.5 %

 I TEXTBOOK OF PEDODONTICS

Fig. 5.9 The central incisors are affected

quickly while the parents are still waiting for
the eruption of lateral incisors.

Fig. 5.10 Mandibular (occlusal view): The teeth

Fig. 5.11 Maxilla (occlusal view): The maxillary
are affected in accordance with eruption
incisors simply fractured. The first and
pattern, but the mandibular incisors
second molars are seriously
remain intact.
affected.
 SECTION 5 : DENTAL CARIES IN EARLY CHILDHOOD |

■ Bovine milk or milk formulas

■ Human milk (breast feeding at will or on demand)
■ Fruit juices and other sweet liquids
■ Sweet syrups like vitamin preparations
■ Pacifiers dipped in honey or sugar solution
■ Chocolates or other sweets

3. Host

■ Teeth act as the host for the micro-organisms

■ Hypomineralisation or hypoplasia of the teeth
increases the susceptibility of the child to caries
■ Thin enamel in the primary teeth is one of the Fig. 5.12 Nursing caries affecting cervical third
reasons for early spread of lesions of the upper anterior teeth.
■ Developmental grooves also may act as the plaque
retentive areas a. Maxillary central incisors: Facial, lingual, mesial
and distal surfaces.
4. Time b. Maxillary lateral incisors: Facial, lingual, mesial
and distal surfaces
Jt is an important factor that determines caries c. Maxillary first molars: Facial, lingual and occlu­
activity. More the time child sleeps with the bot­ sal, prominent surfaces.
tle in the mouth, the higher is the risk of caries. d. Maxillary canine and second molars: Facial, lin­
This is because the salivary flow and the swal­ gual and proximal surfaces.
lowing reflex decrease, thus providing more time e. Mandibular molars: At later stage
for the accumulation of carbohydrates in the
mouth which are acted upon by microorganisms ■ Mandibular anterior teeth are usually spared be­
to produce acid leading to caries. cause of:
a. Protection by thetongue
5. Other predisposing factors b. Cleansing action of saliva due to presence of
the orifice ofthe duct of the sublingualglands
■ Over indulgence of parents veiy close to lower incisors.
■ Crowded homes
■ Child who has less sleep Progression of the lesion
■ Malnutrition ♦ • Initially, a demineralized dull, white area is seen
■ Recently, it has been seen that salivary gland along the gum line on the labial aspect of maxil­
function is impaired by iron deficiency and ex­ lary incisors, which is undetected by the parents.
cess of lead exposure, which makes the oral envi­
■ These white lesions become cavities which in­
ronment more caries susceptible.
volves the neck of the tooth in a ring like lesion.
■ Low birth-weight infants (less than 2500 g)
■ Finally, the whole crown of the incisors is de­
stroyed leaving behind brown black root stumps.
CLINICAL FEATURES
■ This unique pattern and unequal severity of the
The intra-oral decay pattern of nursing caries is char­ lesions is due to three factors:
acteristic and pathognomonic of the conditions. It - Chronology of primary tooth eruption
affects the primary teeth in the following sequence - Duration of deleterious habits of feeding
of involvement (Fig. 5.12): - Muscular pattern ofthe infants sucking
 €S3 I TEXTBOOK OF PEDODONTICS

Implications nocturnal bottles, demand the breast feeding,

pacifiers dipped in sweetening agents.
■ The child who has nursing caries has an in­ ■ The parents should be asked to try weaning the
creased risk of developing caries even in the per­ child from using the bottle as a pacifier while in
manent dentition. bed.
■ The child with caries is also susceptible to other ■ In case of considerable emotional dependence
health hazards. on the bottle, suggest the use of plain or fluori­
■ The treatment of nursing caries may prove to be dated water.
financial burden for some parents. ■ The parents should be instructed to clean the
child’s teeth after even7 feed.
Management ■ Parents are advised to maintain a diet record of
the child for one week which include the time,
Aims amount of food given to the child, the type of
■ Management of existing emergency food and the number of sugar exposures.
■ Arrest and control of the carious process
■ 1 nstitut ion of preventive procedures Second visit
« Restoration and rehabilitation
It should be scheduled one week after the first visit.
Factors affecting management
■ Analysis of diet chart and explanation of the dis­
■ Extent of the lesion
ease process of the child’s teeth should be un­
■ Age of the patient
dertaken by a simple equation.
■ Behavioral problems of the child due to young
■ Isolate the sugar factors from the diet chart and
age of the child
control sugar exposure by intelligent use.
■ Reassess the restoration and redo if needed.
Treatment proper
■ Caries activity tests can be started and repeated
It can be divided into three visits.
at monthly intervals to monitor the success of
treatment.
First visit
This phase of treatment constitutes treatment of the Third and subsequent visits
lesion, identification of the cause for counseling of
■ Restoring all grossly decayed teeth
the parent. ■ Endodontic treatment
■ All lesions should be excavated and restored
« In case of unrestorable teeth extractions can be
■ Indirect pulp capping or pulp therapy proc dures
done followed by spade maintenance.
can be evaluated by further investigation.
■ Crowns can be given for grossly decayed or en-
« I f t he abscess i s present it can be treated through
dodontically treated teeth.
drainage ■ Review and recall after every 3 months
■ X-rays are advised to assess the condition of the
succedaneous teeth.
Prevention
■ Collection of saliva for determining the salivary
flow and viscosity. ■ The main strategies for the prevention of nursing
« Also, the application of fluoride topically caries should be to create awareness and alert
prospective parents and new parents about the
Parent counseling condition and its causes.
« The parent should be questioned about the child’s ■ Information on nursing caries can be distributeä
feeding habits, specially regarding the use of to new parents through obstetricians or
 SECTION 5 : DENTAL CARIES IN EARLY CHILDHOOD I

Table 5.11: Nursing Caries Vs Rampant Caries

'■n"........ ^9 ................ "■■■ ...........
Nursing Caries Rampant Caries

■ Specific form of rampant caries. ■ Acute, widespread caries with early

pulpal involvement of teeth which are
usually immune to decay. (Fig. 5.13)

Age of occurrence
■ Seen in infants and toddlers. ■ Seen at all ages, including adolescence.

Dentition involved
« Affects the primary dentition. ■ Affects the primary and permanent
t
dentition.

Characteristic features
■ A specific pattern of involvement is seen. ■ Surfaces considered immunie to decay are .
The maxillary incisors followed by the involved. Thus, mandibular incisors ?re
molars are involved. affected.
■ Significantly, the mandibular incisors are ■ Rapid appearance of new lesions and not
not involved. just years of chronic decay due to neglect

Etiology
« Several factors, primarily related to ■ More multifactorial with all the essential
improper feeding practices such as: factors involved and not just feeding
- Bottle feeding before sleep. practices.
- Pacifiers dipped in honey/other ■ Frequent snacks, excessive sticky refined
sweeteners. carbohydrate intake. .
- Prolonged at will, breast feeding. ■ Decreased salivary flow.
« Genetic background.

Treatment
■ If detected in early stages, can be « With presence of multiple pulp exposures
managed by topical fluoride applications would generally require pulp therapy.
and education. ♦ • Long term, treatment may be requited when
■ Directed toward maintenance of teeth till permanent dentition is involved.
the transition occurs.

Prevention
■ At the young age as the child is in ■ Dental Health Education at a mass level
constant contact with the mother, involves people at all ages.
education of prospective and new
mothers is desired specifically.
 03 I TEXTBOOK10F PEDODONTICS

gynecologist, pediatricians, paramedical staff, 3. What are the stages of nursing caries?
health workers and maternal and child health care 4. List out file key differences between nursing and
centers. rampant caries.
■ Sealing of all caries free pits and fissures 5. What are the pre disposing factors of nursing
■ Professional fluoride programs cari^?; ...
■ Use of antimicrobial therapy topically .
■ Supervised home care should be taught Further Suggested Reading For Section - 5
■ Systemic fluoride program if there is sub optimal
fluoride concentration in drinking water. 1. Al Ghanim NA, Adenubi JO, Wyne AH, Khan
■ Parents should be educated NB. Caries prediction model in pre-school chil­
- how and when to feed the child during the dren in Riyadh, Saudi Arabia. Int J Pediatr Dent;
earliest stages of the child 8:115-22.1998.
- when and how to introduce solid foods 2. Alder M E: Intraoral digital radiography. Year­
- breast feeding should be encouraged as hu­ book of dentistry 105-96-18-2:478-480,1996.
man breast milk is highly adapted to the hu­
3. Arnold L V: The radiographic detection of initial
man infant and is almost a complete source of carious lesions on the proximal surfaces of teeth.
all required nutrients. Part 1. The influence ofexposure conditions. Oral
■ Broadly based committees at governmental level Surg Oral Med Oral Pathol.64:221-231,1987.
to address the i ssue of caries and the risk factors
4. Bab I A; Feuerstien O; Gazit D: Ultrasonic detec­
in young children and how to recognize early signs
tor ofapproximal caries. Caries Res 31:322,1997.
of the condition and promote early intervention.
5. Billings R J: Restoration of carious lesions of the
root. Gerodontology.5 :43-49[1986] cited in
Nursing Caries Vs Rampant Caries are given in Newbum Ernest: Problems in caries diagnosis.
Table 5.11 IntDent J.43:133-142,1993.
Choksi Soli K: Detecting approximal dental car­
ies with transillumination: A clinical evaluation.
J Am Dent Assoc. 125:1098-1102,1994.
Dowd. F J : Saliva and dental caries. DCNA
43(4),579-598,1999.
Ekstrand K V ; Qvist A ; Thylstrup O : Light
microscope study of the effect of probing in oc­
clusal surfaces. Caries Res. 21:368-374,1987.
FusayamaT; Terachima S: Differentiation of two
layers of carious dentin by staining . J Dent
Res.51:866,1972.
Huysmans J M ; Verdonschot E H ; Rondel P :
Fig. 5.13 Rampant caries affecting teeth not Electrical conductance and electrode area on
usually prone to decay. sound smooth enamel in extracted teeth. Caries
Res 29:88-93,1995.
Self-Assessment 11. Lopex J: Xeroradiograpy in dentistry. J Am Dent
Assoc 92[1]: 106-110,1976.
1. Define Rampant caries. 12. Mitropoulos C: A comparison of fiber optic tran­
2. What are the other terminologies of nursing sillumination with bitewing radiographs. Br Dent
caries? J.159[l]: 21-23,1985.
 SECTION 5 : DENTAL CARIES IN EARLY CHILDHOOD | Œ)

13. Mouyen Francis; Benz Cristoph ;Sonnabend E 15. Tinanoff LW. Introduction to the Early Child­
et.al: Presentation and physical evaluation of Ra­ hood Caries Conference: initial description and
dio Visio Graphy Oral Surg Oral Med Oral Päthol. current understanding. Community Dent Oral
68:238-42,1989. Epidemiol;26:Suppl 1:5-7,1998
14. Reisine S, Douglass JM. Psychosocial and 16. Wyne AH. Early childhood caries; nomenclature
behavioral issues in early childhoodjarifö. Com­ and case definition, Community Dent Oral
munity Dent Oral Epidemior.26:SuppI 1:3244.1998 Epidemiol;27:^3-5,1999.
 SECTION - 6

Preventive Approach to
Caries Control
6.1 Infants Oral Health Care
Tandon S

introduction preventive measures in its truest formi.e. 'primor­

dial’ or 'primary’ prevention. Time and again, meas­
The preventive and treatment protocol would be ures initiated before the onset of the disease have
guided by the risk group of the individual as out­ proven to be effective.
lined in the Table 6.1.
Why infant oral health care?
The caries preventive program needs an individual­
ized approach which can and should be started right ■ Oral mucosa is the first in the human body where
fromfhe prenatal period through infancy to adoles­ microorganisms are seen to be established soon
cence and even further. It thus includes measures after the birth within 6 to 8 hours in an infant who
such as: may be considered as a child who'has not yet
reached the age of one year. §
« infants oral health care
• parent counseling, diet counseling L Oral cavity of the infant is invaded by a variety of
• fluoride programs microorganisms but most of them are transient.
• pit and fissure sealants and Streptococcus is found to be consistently present
■ other methods on the horizon. within few hours after birth,

INFANT ORAL HEALTH CARE 2. The eruption of teeth is an event that brings about
a qualitative and quantitative change in the
While the industrialized countries may claim of a re­ microflora. The colonization of the 'Pioneer Bac­
duction in the caries incidence, developing coun­ teria’ is a special process, which then gives a
tries such as India still face an uphill task, as the substrate to attach the 'Secondary Invaders’.
caries incidence is still on the increase (not with­ Oral health care measures at this stage prevents
standing the goals of WHO). In an attempt to strike the colonization by the secondary and generally
at the root of the problem, Infant Oral Health Care is more pathogenic microorganisms.
an invaluable foundation step. While assessment as
to the risk of the infant developing oral diseases in 1. Infectious diseases of the oral t avity: It has been
later life, may not be entirely accurate, a general policy proven that streptococcus mutans, a primary
will go a long way in reducing the incidence of the causative factor in the initiation of caries, is trans­
same. What better timing exists, than to initiate the mitted from the mother to the infant. These gather
 SECTION 6 : PREVENTIVE APPROACH TO CARIES CONTROL | WÜ

Table 6.1: Modalities of treatment based on risk assessment

HIGH RISK GROUP LOW RISK GROUP

Professional Home Care professional Home

Therapy Therapy Care
.... / .. .....
« Oral prophylaxis ■ Supervised home care ■ Annual ■ Fluoride
■ Complete rehabilitation (use of disclosing agents topical dentifrice
of all carious lesions. for patient motivation) application (if not in use)
■ Antimicrobial therapy ■ Home fluoride application ■ Regular recall
(chlorhexidine gel) « Sustained release of for 6 months.
« Pit and fissure sealants fluoride tablets. ■ Dental health
(specially in young ■ Self gel applications education
permanent teeth) ■ Fluoride dentifrice (if not
■ Topical fluoride in use, above 4 years)
appliations (preferably ■ Salivary substitutes (in
varnish) case of xerostomia)
« Diet modification ■ Chewing gum with
■ Dental health education anticariogenic properties.
A more frequent recall
and review program
(every 3 months)

a foothold in the mouth immediately after the erup­ 4. Child abuse and Neglect may also be detected.
tion of teeth.
5. Handicapped children, cleft lip, palate cases'and
With a weaning of the diet and adoption of a cari-
other such children requiring special attention,
ogenic diet, caries may develop in the oral cavity
may do so right frontbirth.
and cause severe and rapid destruction of the
hard tissues if left unchecked. The diet, particu­
6. Problems of speech, language would require early
larly drinks with low pH, has the potential to cause
detection.
erosion.

Nursing bottle caries has been found to be preva­ To all these problems, the traditional approach has
lent in the population due to faulty feeding prac­ been to treat the effects of the disease. By delineat­
tices by the mothers. ing an infant oral health policy, one may not have to
encounter the disease process or its effects.
2. Traumatic injuries: With lack of motor coordina­
tion, trauma to the developing primary dentition, Thus Nowak (1997) has stated that “the goal of the
may also occur. first oral supervision visit is to assess the risk for
dental disease, initiate a preventive program, pro­
3. Habits: Such as thumb sucking usually have their vide anticipating guidance and decide on the perio-
inception at this age and may persist to cause dicity of subsequent visits”.
 I TEXTBOOK OF PEDODONTICS

How to proceed for infant oral health care? This in turn brings us to the queries of the par­
ents as to when do the teeth erupt. The age at
As in the evaluation of any case, a proper history which teeth erupt varies greatly between children
coupled with a vigilant assessment including knowl­ and a difference of 6-12 months can be consid-
edge of what is normal and what is not at this age is ered normal.
essential.
Age Teeth erupted
L History: A detailed history involving the prena­ 6-10 months Bottom front teeth then top front
tal, birth and post natal periodsis necessary. De­ or side bottom front teeth
mographic details of the parents including the
socioeconomic status need to be evaluated. 9-13 months Top front teeth
Grindefford (1995) has stated that one of the fac­ 13-19 months First molars, then canines,
tors which is a significant predictor of early car­ then second molar
ies development is socio-demographic factors
(importantly, the mother’s education). 2 14 - 3 years All the teeth

2. Examination: A deQtjst should not be blinded by Since the parent encounters eruption of teeth for
the necessity to do a dental examination only. ‘ A the first time, the signs of teething should be made
general assessment would provide an insight to aware to the parent. Various home remedies may
systemic problems, if any. Once satisfied that the be traditionally carried out in these circumstances,
j infant is in apparently normal health, a thorough such as rubbing honey over the gums. Such prac­
I oral examination is warranted. tices predisposing to caries should be strictly dis­
■
couraged. Symptomatic treatment such as teeth­
| 3. Risk assessment is carried out by noting down ing toys or hard sugar free rusks are however
| various factors. These include dietary factors, acceptable.
| amount of the plaque present on the teeth present
| and feeding practices. This should be followed b. Feeding practices: From nutritional point of view,
by customization of a preventive protocol, rather breast milk has several systemic and immunologic
than generalization. advantages over proprietary formulas. Thus the
j -e: : importance of breast feeding cannot be over em­
4. Any therapy, restorative procedure or prophy- phasized.
lactic measures needed should be instituted. However, on the flip side, prolonged and at will
. breast feeding, beyond the stipulated weaning
1 Role
....... - of dentist time of the child, specially throughout the night
$ ■■ ■:

and sometimes throughout the day, has been as­

I-The dentist is a valuable source of information, on a
sociated with nursing caries;
i one to one basis or in small gatherings. On a larger
; scale, the dental association can be involved in teach-
Breast feeding Vs Bottle feeding is given in
Jfling the masses. Table 6.2
< The timing of first visit - The dentist is well placed
to decide as to when the child should visit the
Importance of weaning
H dental operatory. With the benefits of a compre­
hensive preventive program well documented, the Weaning is a process of expanding the diet to in­
first dental visit should be within the first six clude foods and drinks other than breast milk or milk
I months ofthe eruption ofthe first primary tooth. formulae.
 SECTION 6 : PREVENTIVE APPROACH TO CARIES CONTROL |
i s

Table 6.2: Breast feeding Vs Bottle feeding £

Breast Feed ing Bottle Feeding

Functions:
■ It stimulates the muscles around the ■ Muscles don’t have to work hard, hence
mouth and tongue activity for normal normal growth of the teeth and jaws may
growth of the teeth and jaws get affected
■ Breast feeding allows milk flow on ■ Milk flows from the bottle in a continuous
demand flow thus does not allow muscles to work.
■ It allows gravity working correctly oh ■ Bottle feeding while lying on their back
the muscles involved in swallowing keeps the tongue in a unnatural forward
position to keep from drowning

Nutrition:
a Milk is more nutritious as it is a complete a It may not provide, complete nutrition as
source of all required nutrients some children are not able to digest it
a Easily digestable easily because of the nature of its fat
a Higher percentage of lactoalbumin rich in a Percentage is less
sulfur containing amino acids a Do not have sufficient amount
a Higher percentage of certain vitamins like
vitamin C and D are present

Immunologic
a Colostrum rich in certain antibodies like a It lacks this natural defence against
IgA and contains maternal macrophages infection
which protect the child against infections

Others'
■ Colostrum may contain a gut control factor a Does not contain colostrum
and stimulate growth of Gl tract a No control on overfeeding and gain more
a Infant controls own intake and reduces weight during the first year of life, which
possibility of feeding is not desirable
a Reduced risks of the ear and respiratory • a More common
infections a Incidence is high
a Decreased incidence of deleterious habits

■ Weaning brings about the introduction of a more nursing caries. In this respect, the sugars taken
sophisticated diet and includes infant foods as before sleep, when little saliva deansing a nis
well. It is suggested that vegetables be intro­ present, should be assessed and highlighted to.
duced before fruits so that the infant develops a the parents. A simple schematic representation,
habit to accept the vegetables, while the sweeter of the carious process, with the acid production
fruits are naturally welcomed. destroying the teeth should be explained.

Some important tips on Bottle feeding

Bottle feeding: Often, parents who are too busy
to deal with the crying child, try to quieten the Parents should be instructed to:
child by using the bottle containing milk or other ■ Provide more attention to the child
sweetened drinks as a pacifier. This, when given ■ Remove the bottle immediately after feeding
frequently to the child before and during sleep ■ Substitute the milk or non-sweetened juices with
nloin wofpr
 I 'TEXTBOOK OF PEDODONTICS

■ Encourage your baby to stay in upright position where the child develops sufficient neuro muscular
with a bottle control to brush his/her teeth.
■ Use a bottle with a nipple that has a small hole to
enable the infant to work with his muscles activ­ iii. Pacifiers: Several disadvantages have been
ity to get the milk from bottle (Fig. 6.1) found with the use of pacifiers (Fig. 6.2a,b) such
■ Introduce a cup to drink as soon as possible as:
« Bottle feeding be allowed atintervals ■ those dipped in honey or sugars can cause
• It should not be used as a pacifier increased caries
w Give water after feeding with the bottle and clean ■ malocclusion
the mouth soon after feeding
■ unhygienic conditions leading to infections
and GIT disorders
This cleaning activity should be preferably performed
after every meal or at least once in a day. Besides the
D. Anticipateiw guidance
maintenance of good oral hygiene at this age, this
routine also goes a long way in establishing a prac­
Nowak (1995) describes anticipatory guidance as a
tice to be followed in the years to come.
proactive, developmentally based counseling tech­
nique that focuses on the needs of a child at each
The parents should be advised to thus take care of
stage of life.
the gum pads and teeth as they erupt, till the time

Edwall's physiologic Edward’s functional

pacifier. nursing nipple.

Fig. 6.2a

Nuk sugar Primary pacifier Secondary pacifier

(cross sectional view)
Fig. 6.2b
Fig. 6.1 Difference betweenNuk sugar and
Conventional Nipple.
 SECTION 6 : PREVENTIVE APPROACH TO CARIES CONTROL | FIFl

What it effectively means is that one should not get for positionBg and tooth cleaning should be dem­
disheartened, for many times a patient may lack co­ onstrated.
operation at this young age. Providing an insight
i Gum pads: The cleaning of gum pads can be
into the development of a child will involve the par­
started as early as within the first week of birth.
ent, with a much more focussed strategy. Also, at
every stage it is essential that the dentist takes into Cleaning infants mouth (Fig. 6.3a, 3b)
consideration the various milestones of dental de­
The parents can be instructed to:
velopment. Such anticipatory guidance can make the
« Lay the baby down with his/her head in your
parents more at ease during childhood dental visit,
lap and feet pointing away
these pointers are also essentials inpreventing many
« Open the baby’s mouth and slide the forefin­
of the possible dental problems children would oth­
ger inside along the cheek and press down on
erwise often face.
the back side lower gum pad.
■ Take a small gauze (2” x 2”) between thumb
E Oral hygiene practices
and forefinger and wipe vigorously over the
ridge of the baby’s top and bottom jaws.
Many parents would not be even aware of the fact
■ Nowadays specially designed for infants tooth
that oral hygiene practices can be essential at this
brushes, finger cots and wipes are available,
age.
which can also be used.
« Use adequate pressure just to remove the film
A thorough intra oral examination may reveal the
that covers the child’s gum pad.
plaque on the tooth surfaces and food debris as well.
■ Clean at least every day twice after morning
In such cases and in all other cases as well if the
and last feed in the night.
child has been brought early, the proper technique
■ Spend at least two to three minutes in cleaning.

Fig. 6.3a Upper gum pad in infant Fig. 6.3b Lower gum pad in infant
being cleaned with wet gauze being cleaned with wet gauze.
 Q© I TEXTBOOK OF PEDODONTICS

ii. Teeth: The positioning of the infant, depending ■ Weaning foods free of, or low in non-milk extrin­
on whether one or both the parents are involved sic sugars be recommended to the mothers.
in the procedure should be first demonstrated and
then supervised by the dentist. ■ Depending on the amount of fluoride present in
community water, and the requirements of the
While performing these procedures care should child, a fluoride supplementafiofiprogram can be
be taken that the child is supported at all finies instituted.
and the movements are slow and careful, so as to
not cause any injury and address the problem in ■ Pediatrician should be made aware of the dentist
that light, not just keep reinforcing a particular population in Iris vicinity for the purpose of refer­
set of instructions. ral. This in cases of large multi-specialty centers
is easily done, but in smaller places with dental
Role of pediatricians centers spread over a larger area may be difficult.

■ The pediatricians or prima ry care physicians treat Role of other personnel

infants and monitor the growth and development
of children. They are thus usually the first health Nurses, midwives do not always manage the care of
care providers and can act to evaluate their oral the neonate beyond the first few weeks of life, but
health status. they can be assets in providing guidance and refer­
ral if anticipated at the time of the newborn screen­
« In this respect, they can be the forebearers in ing. They can provide information about immuniza­
providing information to the parents as they are tion, accident prevention and dental health.
more often in contact with the child and parents. ■ The need for commencement of tooth brushing
The dentist should establish a contact with or cleaning with gauze as soon as the first tooth
pediatrician and formulate a policy regarding den­ erupts can be emphasized through prenatal
tal health for the infant. classes by the gynecologist or obstetrician.
■ Neonatalogists can also play a significant role by
« Following topics needed to be discussed advising and counseling the parents regarding
- Tooth eruption any congenital defect, such as cleft lip and pal­
- Preventive oral hygiene ate, regarding the dental and the overall health
- Orofacial development aspect of the child.
- Fluoridation ■ Importance of breast feeding can be emphasized
- Diet * by these medical personnel.
■ Mothers can be informed about the transmission
• Johnson (1997) has also discussed the interac­ of antibiotics via breast milk and their effect of
tion with the pediatrician at the time of weaning. dental health.
When the child is 10 months old, the assertive­ ■ Importance of the mother’s own oral hygiene is
ness of the child may make the parents to give in equally important as poor oral health of the mother
by giving a sleep time bottle. A solution sug­ can affect the health of the fetus and the new­
gested is the gradual dilution of the liquid. Thus born. Poor maternal periodontal health has been
1 week 1/3 bottle water found to increase the potential for pre-mature low
2nd week 2/3 bottle water birth weight of babies. High caries level in the
3rd week only water mother can result in an equally high level in the
child.
 SECTION 6 : PREVENTIVE APPROACH TO CARIES CONTROL 1 6D

Guidelines to parents Clean thrums and later teeth with a cloth or soft
brush after every meal or before sleep.
Children are our most precious resource. Their opti­ Parents should brush or clean their baby’s gums/
mal oral health should be provided not only on a teeth everyday till the child is old enough to man­
therapeutic but also on a preventive basis early in age himself.
life itself. Parents should be educated at the earliest 12. Contact the dentist immediately if there is any
possible time by not only the dentist but also the accident or trauma to the baby 's teeth.
general practitioner in order for to provide them a 13. Parents should know about the benefits of fluo­
disease free environment. ride and its proper use such as that used in infant
formulas and dentifrices.
1. The parents should bring their child for his/her 14. Half- yearly visit to the dentist should be routine.
first dental visit early, at least by the time the baby
is 6 months of age. Self-Assessment
2. Breast feed the baby but do not indulge at will.
3. Avoid frequent use of the bottle with sugared 1. What are the reasons for starting oral health care
milk or drinks as this can lead to nursing bottle in the infants?
caries. Instead, give the child more attention. 2. What do you understand by the colonization of
4. Do not put the child to bed with the bottle or at pioneer bacteria?
the breast but take the bottle away immediately 3. When does the oral cavity get invaded with the
after feeding. microorganism?
5. Dilute the milk gradually in the bottle and end 4. What is ‘anticipatory guidance’?
with plain water. 5. What is the role of the pediatrician in infant’s oral
6. Feeding should be supervised at all times. health care?
7. Start the child on semi-solid foods by 5-6 months 6. List out the differences between breast and bot­
and reduce the use of bottle or breast feeding. tle feeding?
8. Do not use pacifiers or dummies dipped in honey 7. How are the gum pads of the infant cleaned?
or other sugar items. 8. Summarize the various measures involved in im­
9. Avoid extended use of sugared medicines such parting oral health care to infants?
as syrups.
 6.2 Parent Counselling
Tandon S

When we consider the tremendous backlog of unmet ■ Obtaining the cooperation of a child patient, es­
dental needs and ever-increasing demand for care, it tablishing a good rapport with the child and also
becomes obvious that dental disease, can not be using effective techniques of behavior manage­
controlled by treatment alone. It can be managed ment
only through prevention, especially in children. ■ Educating the parents about various dental prob­
Health education is thus basic to prevention. lems and diseases and their sequelae and how
they can be prevented with accurate preventive
Parents serve as role models and children are influ­ measures if recognized earlier.
enced early in life by their varying opinions. In the
dental setting the cooperation of the child is directly IFWE ARETO HAVE A GOOD CHILD PATIENT WE MUST
related to the opinion and anxieties of the maternal FIRST EDUCATE THE PARENTS. A DENTIST WHO FAILS
figure. Thus to change the children’s dental behavior TO DO SO IS NOT USING EVERY MEANS AVAILABLE TO
effectively, dental health educators and professional HIM IN MANAGEMENT OF THE CHILD.
need to target the mothers and educate them to be­
come models of proper dental health practices. INSTRUCTIONS TO THE PARENT
«
Definition Inform the parents:
■ Not to voice their own personal fears in front of
Parent counselling can be defined as educating the the child.
parents regarding the child’s oral health status, opti­ ■ Never to use dentistry as a threat of punishment.
mal health care and informing them about the pre­ ■ To familiarize their child to dentistry by taking the
vention of potential dental diseases child to the dentist. This helps in making the
child accustomed to the dental office and to get
Purpose acquainted to the dentist.
■ About the home environment and importance of
The purpose of parent counselling in pediatric den­ moderate parental attitudes in building well-ad­
tistry involves: justed children. Regular dental care helps in pre­
• Discussion of emotional problems of children, serving the teeth and also in formation of good
particularly in relation to dental treatment. dental patients.
■ To offer the dentist an insight into parental influ­ ■ Never to shame, scold or ridicule the child to over­
ences which may produce unnecessary anxieties. come the fear of dental treatment.
■ Knowing about the attitude of parents towards ■ Not to promise the child what the dentist is or not
behaviour management techniques used during going to do.
dental treatment of children.
 SECTION 6 : PREVENTIVE ^PpRdACH TO CARIES CONTROL |

■ Not to bribe their child to go to the dentist. Why are the p rimary teeth important?
■ To convey to the child in a casual manner that
they have been invited to visit the dentist. a Primary teeth act like the foundation stone for
■ To commit the child to dentist’s care in the office permanent teeth.
and should not enter the treatment room unless ■ They maintain proper space for the permanent
requested by the dentist. ---- teeth to occupy.
s Occasional display of courage by the parent’s in ■ These teeth help in normal growth ofjaw height
dental matters will build courage in the child. and give shape to the face, just like in older indi­
viduals whose face looks completely collapsed
EDUCATION OF PARENTS IN VARIOUS ASPECTS when they take out their denture.
OF DENTISTRY ■ Teeth provide a sense of self worth by contribut­
ing to one’s appearance.
Preventing dental diseasefrom conception to 8 Primary teeth certainly help in the first step of
3 years of age: grinding of food, once the infants start eating
solid food.
a A large number of children experience a dental
disease before 3 years of age. Nursing caries is Preventing dental diseasefrom 3 to 6 years ofage
particularly a devastating form of caries frequently
seen in this age group. Thus, it is important to Children in this age group frequently exhibit gingivi­
educate the parents so they can make appropri­ tis and may experience rampant decay. The rampant
ate decisions regarding the management oftheir decay is often a sequelae to nursing caries initiated
infants and toddlers oral health. during the first 3 years of life or extensive caries may
develop as a result of eating patterns initiated after
PARENTS EDUCATION GUIDELINES FOR INFANTS weaning.
AND TODDLERS are given in Table 6.3
1. Diet: Pa rents are educated about the role of diet
Prenatal counseling: Parents should be educated and their ill-effect on initiation of caries.
regarding: 8 - The frequency of exposure is the most impor*.
nil ­
tant factor in development of dental caries.
a. Dental development of their child. ■ The rate at which sugar is cleared from the oral
b. The dental disease process. cavity is also the important factor in the cari-
c. Appropriate feeding practices emphasizing the ogenic potential of a food. The sticky reten­
hazards of improper bottle and breast-feeding. 4 tive items such as chocolates, toffees have
d. Oral hygiene measures appropriate for infants and
toddlers.
e. Expectant parents can also be told regarding the • When the exposures are too frequent or the
mother’s health during pregnancy and the poten- sugar is retained too long, the net result is dis­
tiat detrimental effects that poor health and un­ solution of tooth structure and formation of a
healthy habits may have on their child’s dental cariouslesion.
development. * Food items that can be recommended as rela-
f. Also in pregnancy the food need increases to
meet the special physiological changes in the milk, sugarlessgum, and raw vegetables. Items
body to support the growth of the foetus and to be particularly avoided include sugared gum,
facilitate normal labour.
tfFÏÏÏ I TEXTBOOK OF PEDODONTICS

Table 6.3: Parent's education guidelines for infants and toddlers

Content area Dentist’s action

Oral development
Gum padg.to^ompletion of primary Discuss the patterns of eruption.
dentition. Discuss the myths about unhygienic habits
practised during teething.
Educate the parents about teething facts.
Discuss oral stimulator.
Establishment of occlusion. Discuss the importance of primary teeth.
Discuss bruxism and its ills.
Fluorides
Importance of topical and systemic Recommendation against topical fluoride use
fluorides. till 3 yrs. of age.
Assess the fluoride status.
Discuss the fluoride supplements if needed.
Professional application of fluoride begins at the
age of 3 yrs. when swallowing can be controlled.
Oral hygiene/health
Care of gum pads. Clean the gum pads with a soft clean cloth after
each feeding.
Mouth cleaning techniques Instruct the parents about the use of a soft brush and
pea size toothpaste.
Brushing technique taught to the parents.
Periodicity of dental visit. Educate the parents about the importance and need
of periodic dental visits. \
Habits
Non-nutritional sucking. Review pacifier use and safety and hygiene issues.
Pacifier use.
Thumb-sucking. Discuss the ill effects of thumb sucking to the
dentofacial structures.

Nutrition and diet

Baby bottle tooth decay pattern. Discuss the proper feeding practices & use of the bottle.
Importance of diet. Role the child’s food plays in his growth and
developement.
Discuss how frequent sugar intake results in initiation
of caries.
Injury and prevention
Oral trauma Immediate referral to the dentist as an injury to, the
teeth of young child can have serious and long-term
consequences.
Home child proofing Use of baby walker when infant begins to learn to walk.
Use of car seat or the child should be in mother’s lap.
Child should not be left alone for a long time.
Discuss the electric cord & safety measures to be taken.
(Also see Chapter on Infant Health Care)
 . I
SECTION 6 : PREVENTIVE APPROACH TO CARIES CONTROL |

■ The most important dietary advice is to limit

the number of carbohydrate exposures per day Prevention ofdental diseasefrom 6 to 12
rather than to limit the total amount of carbo­ years ofage:
hydrate consumed.
Eruption of the first permanent molar at about the
(Also see chapter on Diet Counselling).
age of 6yrs. is a milestone requiring preventive ac­
tion. Parents are educated about the importance of
2. Oral hygiene
the first permanent molar. They are told how the vari­
■ The 3 to 6 year olds require parental assist­
ous preventive measures taken at this stage can pre­
ance to achieve effective plaque removal.
vent the progression of caries.
■ Parents should be instructed to brush for the
child at least once a day, and to clean between
L Sealants
any teeth that are in contact with each other
« The most effective aid for preventing pit and
with dental floss. Bedtime is the ideal time to
fissure decay is professionally applied seal­
establish this routine because the salivary flow
ants. Most children benefit from the applica­
rate slows during sleep. Thus natural protec­
tion of sealants to their permanent molars
tive mechanisms are reduced.
whichallows them to maintain a caries free den­
■ Additionalbrushingsmaybeperformedbythe
tition into adulthood.
child unaided.

2. Diet
3. Fluorides
« Children of school age are developing some
■ Fluoride consumption should be investigated
autonomy in eating habits. They often make
and supplemented if appropriate.
their own food choices at school and may pur­
■ The use of fluoride containing toothpaste
chase snack items. Parents are instructed to
(once daily) should be carefully monitored.
monitor the dietary practices, especially for
Parents should be instructed to dispense only
children who experience smooth surface decay
a pea-sized amount for their child. The child
should brush under the supervision of the
3. Fluorides
parent so that they can monitor to ensure ex­
■ As the child develops control over swallow­
pectoration. Other times the child can brush
ing, topical fluorides canbe safely used and at
with non-fluoridated toothpaste.
this age they begin to assume an important
■ Professional application of high concentration
role in prevention.
fluoride gels is usually begun at the age of
■ Regular use of toothpaste(twice-daily fluori­
3yrs. when swallowing can be controlled.
dated toothpaste) is recommended for its abra­
sive action in removal of the plaque as well as
4. Professional dental care
fluoride exposure. By the age of 6yrs. most
« The parents are educated that in small primary
patients are capable of expectorating but par­
teeth, caries progresses at a high rate. Also,
ents should monitor it.
because of rapid developmental changes, the
timings of the visits can be critical for initiat­ 4. Oral hygiene
ing preventive measures. « Parents need to remain active in supervising
■ Semiannual dental visits should begin at the the home care practices of 6 -12 year old.
age of 3yrs. and continue throughout child­ ■ During this age span a transition can be made
hood and adolescence. from care provided by the parent to supervised
self-care.
 I TEXTBOOK OF PEDODONTICS

« By the age of 10 most children are capable of the dentition. It is usually associated with poor
fine motor coordination necessary for adequate oral hygiene practices and a high frequency of
tooth brushing and begin to assume responsi­ sugar consumption.
bility for daily flossing. Parents should con­ ■ Progress of lesions can be hdted^ith an ap­
tinue to monitor brushing and flossing fre­ propriate diet control and an aggressive topi­
quency and adequacy. cal fluoride therapy.

5. Habits: 3. Fluorides
« Education about any oral habits if it is present. ■ Systemic fluorides are no longer of benefit af­
■ Also educate the parents about transitional ter the last permanent tooth erupts at about
changes in the developing dentition and the age of 13yrs.,except for patients who have func­
importance of primary and permanent denti­ tional third molars.
tion. ■ Topical fluorides are the most effective pre­
ventive measure for the patients who experi­
Prevention of dental disease in the adolescent: ence smooth surface caries.
■ Use of fluoride containing dentifrices regu-
■ Prevention of dental caries continues to be an larly( thrice daily) provides an economical and
oral health priority during adolescence and pre­ effective fluoride source.
vention of periodontal disease becomes a special
concern. This is a very unique age group. At the 4. Orthodontics:
stage of adolescence the main processes utilized ■ Many patients undergo orthodontic treatment
are: during adolescence. These patients are at a
a. Rejection of many parental values. high risk for both gingivitis and the resultant
b. The beginning of independent struggle and gingival hyperplasia ánd for dental caries
c. The testing out types of behavioral around and under the appliance or braces.
experimentations. ■ Topical fluoride therapy is indicated to pre­
vent decay.
Parents are educated that they should tackle the child ■ A thorough removal of the plaque from the
at this stage very diplomatically. The child should be gingival areas should be performed to prevent
given enough emotional support from the family and gingivitis and periodontitis.
his various habits should be monitored by the par­
ents. The parents should have a friendly approach. 5. Smokeless tobacco
1. Oral hygiene ■ Peer pressure and advertising exert pressure
■ The adolescent patient possesses the fine on children and adolescent to establish a habit
motor skills necessary for adequate tooth that may result in addiction and ultimately in­
brushing and flossing, but problems in com­ duce oral cancer.
pliance are likely to be encountered. ■ Evidence of tobacco use, such as shreds of
■ For periodontal health it is necessary to re­ tobacco present in the oral cavity or localized
move the plaque from all areas of the tooth hyperkeratosis should be a signal to initiate
that contact the gingiva. Dental floss can be efforts to motivate the patients to discontinue
used to effectively remove the interproximal the habit.
plaque. ■ Parents should be instructed/counselled not
2. Diet to nag or punish the adolescent as it might
■ In patients with a high caries rate, rampant den­ further entrench the habit.
tal decay may result in an extensive damage to
 SECTION 6 : PREVENTIVE APPROACH TO CARIES CONTROL | GPEb

Parents should assess why the adolescent got ries the prognosis worsens. The unfavorable con­
the habit? sequences are more likely to occur with delay in
a) Is it because of peer pressure/influence? treatment of the injury.
b) Is it because of home environment? • However, the best approach is to take active meas­
c) Is it because of bad company? ures to prevent injuries.
d) How long he has been using tobacco? ■ Most injuries to the primary teeth occur within
toddlers 12 to 30 months of age. For measures to
■ The dentist being an authority in clinical matters be taken to prevent the injury in this age group
along with parents support should start the refer chapter on Infant Oral Health Care.
counselling. ■ Another major cause of dental injuries in children
is falls during play. Children who engage in con­
The adolescents are preoccupied with health matter tact sports are at the greatest risk of dental inju­
in general and appearance in particular. This concern ries. Athletic mouth protectors(mouth guards) sig­
can be used as a mechanism for motivation to dis­ nificantly reduce dental injuries.
continue the habit.
In order to achieve maximum effective results, pre­
Preventing dental injuries: ventive efforts should be initiated early in the life of
the child. Althoughmost children experience dental
An injury to the teeth of a young child can have disease, a mouth free of caries and periodontal dis­
serious and long-term consequences that may lead ease is a potentially attainable goal for all children
to discoloration, malformation and even the loss of when they use currently available techniques.
teeth. Such consequences can have a considerable
emotional impact on the children. Self-Assessment
■ If during the trauma to the orofacial structure
1. Define parent counselling?
tooth is avulsed, the parents should be instructed
2. What is the purpose of parent counselling ?
to keep the avulsed tooth under the tongue of
3. What are the topics which need to be discussed
child or to store the tooth in milk or saline. The
with the parents?
survival of replanted avulsed tooth will be en­
4. What is the significance of prenatal counselling?
hanced if avulsed tooth is stored in some media *
5. Who influences more an adolescent to develop
prior to replantation.
the habit of smokeless tobacco ?
■ Parents are advised to immediately contact the
dentist, as in nearly all situations of dental inju­
 6.3 Diet Counselling
’•i

Tandon S

Introduction Diet: referred to as food and drink regularly

consumed. (Oxford Dental Dictionary)
It has become increasingly evident that dietary ■ Total oral intake of a substance that provides nour­
counselling is the most neglected of all preventive ishment and energy.(Nizel 1989)
measures suggested by the researchers in terms of
daily diet on the level of health as well as the suscep­ Balanced diet: one which contains varieties of foods
tibility to a wide variety of diseases including oral in such quantities and proportion that the need for
cavity. The dental practitioner is faced with a wide energy, amino acids, vitamins, fats, carbohydrates
variety of patients and the clinician must accept each and other nutrients is adequately met for maintain­
individual as he or she is, and be prepared to adapt ing health, vitality and general well-being and also
his or her technique to the specific needs of that makes provision for a short duration of leanness.
individual. At times the clinician must teach the pa­ (Chauliac 1984)
tient about diet, health and cause and prevention of
disease. Successful diet counselling depends on the HOW OUR FOOD AFFECTS HEALTH? *

ability of the clinician to make the patient see the

problem clearly and thereby work upon the solution. The food that we eat affects our body in 2 way

Definiton Systemic effect: depends on their content of nutri­

ents and includes the influence of such nutrients on
Nutrition: The sum processes concerned in the general health, growth and development, cell renewal,
growth, maintenance and repair of living body as a ability of the tissues to repair and resistance to dis­
whole or its constituent parts. (Oxford Dental Dic­ ease.
tionary)
« Science of food and its relationships to health. It Local effect: consists of what food can do to the
is concerned primarily with the part played by the tissues or their environment because of their mere
nutrients in body growth, development and presence in such an environment. In dentistry, most
maintenance. (WHO 1971) local effects result from the interaction between food
residues and oral bacteria, which leads to plaque for­
Food: Any substance which when taken into the body mation. The metabolites from the plaque bacteria have
of an organ may be used either to supply energy or effects on the soft and hard oral tissues.
to build a tissue. (Oxford Dental Dictionary)
■ Anything that is eaten, drunk or absorbed for CLASSES OF NUTRIENTS
maintenance of life, growth and repair of the The classes of nutrients necessary for the growth of
tissues.(Nizel 1989). the child are:
 SECTION 6 : PREVENTIVE APPROAClfï^ARIES CONTROL | <

i Energy providing carbohydrates and lipids. and retentive sucrose containing foods are more
i Tissue building protein. cariogenic than sugar containing foods that are
i Regulator vitamins and minerals liquid and non-retentive.
i Water comprising 55 to 65% of the total body ■ The frequency and time of ingestion of foods are
weight also important. The sucrose containing food be­
comes more dangerous if it is eaten more fre­
3ASIC FOOD GROUPS (Table 6.4, 5,6) quently. Food eaten at meals produces less car­
ies than the same eaten between meals does.
/arious nutrients play an important role in growth ■ In decreasing order of cariogenidty, the food are
md development. However, terms like protein, cal- grouped as:
ium, riboflavin (Vit. B2), etc. have little meaning to - Adherent, sucrose-containing foods eaten fre­
he layman and must be translated into the languages quently between meals.
>f foods. Eg. The mother should be asked to buy - Adherent, sucrose-containing foods eaten
nilk, which contains carbohydrates, proteins, cal- duringmeals.
:ium and riboflavin. - Non-retentive(liquid)sucrose-containing bev­
i The basic five food groups are called foundation erages consumed frequently between meals.
foods. Consuming these foods in the quantity - Non-retentive(liquid)sucrose-containing
recommended will provide from 75 to 100%ofthe foods consumed during meals
recommended dietary allowances (RDA). The five
food groups are, however, low in calories and for PROPOSED DIET COUNSELLING PROGRAM
this reason additional food are recommended, e.g.
fats and oils such as butter,vegetable oil,sugars. Objectives of diet counselling program for the den­
tal office comprise:
)IET AND DENTAL CARIES ■ The correction of diet imbalances that could ef­
fect the patient’s general health and sometimes is
The patients diet and dental caries activity are also reflected in his oral health.
related. From the dietetic view point,dental car­ ■ The modification of dietary habits, particularly
ies is widely accepted as being caused by the the ingestion of sucrose containing foods in
ingestion of fermentable carbohydrates, particu­ forms, amounts and circumstances that promote
larly sucrose. caries formation.
i Fermentable carbohydrates and more specifically
sucrose are rarely eaten as such. They are eaten The proposed program is based on a step by step
as components of foods that contain other ingre­ progression through:
dients and have different texhires ■ Interview, where diet diary forms are introduced
i The cariogenic potential of foods containing su­ with a brief discussion of the purpose of diet
crose depends on many variables such as the
ability to: ■ A 24 hour diet record is prepared to get an idea of
- Be retained by teeth. food the child is consuming.
- Form acids. ■ A six days diet diary is advised to be prepared by
- Dissolve enamel. the patient
- Neutralize or buffer acids. ■ Complete records of six days diet diary are
i Certain characteristics of sucrose containing analyzed regarding the balanced and unbalanced
foods or conditions surrounding their consump­ diet.
tion are more important in terms of cariogenidty ■ Isolating the sugar factors.
€35 I TEXTBOOK OF PEDODONTICS

Table 6.4: Food groups with proteins and calories per serving

Food Amount in In terms of Grams/Servings In standard

group grams servings (approx.) cup Protein Calories
(approx.) (grams) (approx.)

Cereals
Cereals 370 gm 4 90 gm 1/3 cup 10 gm 325
Pulses 70 gm 2 35 gm 1/3 cup 6 gm 128

Vegetable
Green leafy
vegetables 125 gm 2 60 gm 6 bundles 4 gm 25

Other
vegetables 75 gm 2 35 gm 2.0 gm 24

Roots and
Tubers 75 gm 2 35 gm 0.5 gm 40 (rava)

Fruits
Fruits 40 gm 1 40 gm 0.3 gm 34
I

Milk
Milk & milk 4
product 200 ml 2 100 ml 14 cup 3.2 gm 63

Meat
Meat, fish 30 gm 1 30 gm 4.0 gm 62
and egg 30 gm 4.0 gm 52
small
50 gm 6.2 gm 87
large

Others
Fats/oils 40 gm 3 tbsp 5 gm 1 tabs 48
Sugar 40 gm 3 tbsp 5 gm 1 tabs 20

One preet cup: Rice - 250gm

Wheat flour - 150 gm
Rava - 150gm
Pufees - 220 gm
Ragi flour - 150 gm
 SECTION 6 : PREVENTIVE APPROACH TO CARIES CONTROL | FFH

Table 6.5: Daily food plan for different age groups

Daily food Toddler Pre-school School Adolescent Adult Pregnant

plan S - gms S - gms S - gms S - gms S - gms Women
S - gms
Cereals
Cereals 2 1/3 - 90 2 - 200 3-250 4-350 5 1/3 - 475 414.-400
Pulses 1 14 - 35 2-60 2-70 2-70 2 ’/4 - 80 2-70
Vegetable
Green leafy
vegetables 14-60 14 - 40 1/4-75 - 2 14-150 2 - 120 214 - 150
Other
vegetables 14-30 1-40 2-70 2-75 5-175 5-175
roots and
Tubers
Fruits
Fruits 1-30 1-40 1-50 2-75 1-30 1-35
Milk
Milk & milk 1 14 - 150ml 2 14 - 250ml 2 - 200ml •2 - 200ml 2 - 200ml 3 14 - 325
product
Meat
Meat & fish 1r30 1-30 1-30 1-30 1-30
Egg 1-50 1-30 1 - 30 1 - 30
Others
Fats/oils 4 tsp - 20 5 tsp - 25 • 2 tsp-30 7 tsp - 35 234 tsp - 40 7 tsp - 35
Sugar 4 tsp - 20 2 tsp-30 . 2 tsp - 30 2 tsp - 30 214 tsp - 40 2 tsp - 30
S - Servings
Gms - grams
tsp - tea spoon

i
Table 6.6: Daily caloric & protein for different age groups

Toddler Preschool School Adolescent Adult Pregnant

Women

fÿlloriç 1200 - 1500 1500 1800 2500 2800 2800

require­
ment

№- 18 -20 gms 22 gms 33 gms 50 gms 55 gms 100 gms

^■•^^ein
redire-
\ihpnt
 €EE> i TEXTBOOK OF PEDODONTICS

■ Educating the patients in the role of sugar in the ■ To adolescents group, direct communication and
decay process. diet counselling should be performed.
■ The consumption of acceptable substitutes in­
stead of more cariogenic foods. DIETARY COUNSELLING
■ The recognition of practical limitations to imme­
First appointment: Before counsellinga child or his
diate success.
mother, determine what the child is eating. In a 15 to
« Provision of continous positive reinforcement.
20 minutes appointment the diet diary forms are in­
troduced with a brief discussion of the purpose of
Where should the counselling take place?
diet counseling such as, explain to the patient
■ That we are looking for possible dietary causes
counselling as well as most patient education should
of the caries problem of the patient. So that we
take place in a consultation type of room/office, not
can reduce the risk of future caries by dietary
in the dental operator?. Distractions and anxiety pro­
means.
ducing instruments may break down communication
■ What beneficial outcome could be available for
between the patient and the counsellor in the dental
him in better oral health and appearance and pos­
operatory.
sibly improved health in general.

Who shold give counselling?

Here it is important:
■ Not to be judgmental about the patient’s re­
The counsellor should possess dental and nutrition
sponses as otherwise he may tend to present his
knowledge as a result of professional education and
best side.
J training. These best-qualified professionals are:
■ Not to emphasize the role of sucrose-containing
| ■ Dentist
foods before the diet diary is completed, for oth­
j « Dental hygienist
erwise the patient may tend to present an ideal
| ■ Nutritionist
I rather than real diet.
■ The patient should not be patronised or lectured.
|
If
Who should receive counselling?
I

DIET DIARY (Table 6.7a)

j ■ Ideally all children brought to dental care need to
| be counselled.
■ Please record every food item consumed solid,
| • The child under the age of 6yrs. is almost com­
liquid, during 6 consecutive days. Record food
pletely dependent upon the parent usually the
consumed at mealtime, between meals, at soda
mother for his or her food supply and subsequent
fountain or while watching a movie, picture or
food habit development. Therefore the dentist
television. Also record candies, chewing gum,
must counsel the mother in an effort to prepare
cough drops or syrups.
her for an important role as an educator and model.
■ Elementary school child: as the cliild matures and ■ The approximate amount in household measures
develops more control over food selection, more
such as 1 cup,2 table spoon(T),l tea spoon(t).
efforts can be directed in educating him with the
parent as the observer.
■ The kind of food and how it was prepared, such
■ Counselling should be at an elementary level and
as baked chicken raw apple, cooked cereal, etc.
should not exceed 45 minutes. Several sessions
of 20 minutes may be preferable to one long ses­
« Additions to food in cooking or at the table: but­
sion.
ter, sugar, cream, etc.
 SECTION 6 : PREVENTIVE APPROACH TO CARIES CONTROL J

Table 6.7a: Diet diary of the patient for a week

Patient’s Name:

Day Breakfast Lunch Dinner Between meals

Amount Food . Amount Food Amount Food Amount Food

1.
2.
3.
4.
5.
6.

List of foods containing sugar (Table 6.7b) ISOLATE THE SUGAR FACTORS

Foods containing sugar in solution. ■ The patient should be aided in identification of

Soft drinks, soda pop,powdered drink mixes, those foods which are likely to cause oral dis­
fruit drinks. eases; the time when they are most harmful and
Sweetened condensed milk, syrups. also those which are most nutritious and least
Sweetened sauces such as chocolate,
cariogenic (Table 6.7b)
butterscotch.
Chocolate milk,hot chocolate, cocoa.
■ The interviewer and the patient together code the
Milk shakes, malts.
record by any two different colours, for eg. red
Solid retentivefoods containing sugar. Xs for harmful choices and time and by blue Xs
Cakes, doughnuts, cookies, candy bars, for good choices and meal pattern.
brownies, chocolates.
Pastries, pudding, muffins, sweet rolls, pies. ■ Taking this as a game can motivate the child. He
Sugar-containing cereals, sugar-coated gum. is asked to count the number of red Xs which are
Dried fruits such as raisins, dates, apricots. * harmful for his teeth Next, ask the child which Xs
Fruit cooked in sugar. marked food he can eliminate. Have him write them
fcecream, jams jellies, marmalades. in appropriate spaces in his workbook. Tell him
Sugar-containing chewing gum, caramels,
that he should be able to reduce number of red
bftihdns.
Xs when he comes next. When the child comes
Hariliaridy, mints, lollipops, jellybeans.
Fro^lB^honey. with a reduced number of red Xs, he should be
Cough drops,syrups. praised for his effort (Table 6.8).

* In addition to these foods, some medicines such

as cough syrups,antacids (both liquid and tab­
lets) contain variable amounts of sucrose.
 | TEXTBOOK OF PEDODONTICS

Table 6.8: Sample recording

First day: Patient’s name: Age: Form of food

Time Sugars in solution During

meals 1
7.30 am Breakfast 3idly-X
1 glass milk (2t Between
.sugar added) - X meals 1

10.30 am Snack 3 cookies - X At bed

1 coke (small time 1
glass) - X
Solid retentive food During
12.30 pm Lunch 2 chapaties - X containing sugar meals 1
1 cup vegetables —X
1 cup rice - X Between
1 doughnut sugar meals 4
coated - X
At bed
1.30 pm Snack 1 pastry (small) - X time 1
1 cream filled cup
cake - X

6.00 pm Snack 1 candy bar

(large) - X

7.30 pm Dinner 2 chapaties - X y

1 cup vegetable -- X
1 cup dhal - X

9.00 pm Snack 1 cup caramel - X

1 glass chocolate
mild - X
‘X’ Total No. of exposures - 9

■ The cariogenic potential of a patient’s diet is which enamel decalcification can occur for an aver­
evaluated by determining the total number of ex­ age of 20 minutes after the introduction of sucrose
posures to sucrose-containing foods during 6 into the mouth).
consecutive days.
■ Exposure is defined as eating the food at one time EDUCATE THE PATIENT IN THE ROLE OF SUGAR IN
and is not related to the amount of food sucrose DECAY PROCESS
ingested.
■ The plaque that forms in the teeth every day con­
tains bacteria(germs).These bacteria change the
Grand total, time of exposure to acid = (total expo­
sugar present in food into acids.
sure X 20 minutes)
(This time is based on Stephan’s curve that the pH of SUGAR (in food) + PLAQUE / BACTERIA (germs) =
the plaque drops and remains below a critical level at TOOTH +ACID = DECAY
 SECTION 6 : PREVENTIVE APPROACH TO CARIES CONTROL |

The grand total of time of exposure to acid is used The list of substitutes should be formed by the
here, to give the patient a roughidea of the risk that joint efforts of the demist and the patient. The
his diet is imposing on his teeth. dentist should propose substitutes and also
ask what substitutes the patient will be willing to
DETERMINE THE ADEQUACY OF DIET accept.
It is not fair to cut down all the sugar from the
■ Determine the number of servings of food in each child diet. Intelligent use of sugar must be there
of the basic five food groups and compare this and that is:
with the recommended number of servings. (Re­ - Use sugared food during meal time and
fer Table 6.4, 5, 6) - Food consumption followed by appropriate
oral hygiene measures.
List of substitutes (Table 6.9) ■ Sometimes a compromise may benecessaiy. It is
better to go from a very cariogenic to a less cari-
Peanuts, walnuts,peacans.almonds,other types ogenic than to obtain nothing.
of nuts.
Popcorn, corn chips, potato chips, whole wheat RECALL VISITS
biscuits, unsweetened,dry cereals.
Cold cuts of meats (unsweetened). ■ During the next months at regular intervals, die
Cubes of cheese. dentist should evaluate the patient’s progress and
Pizza, toasts. provide psychological reinforcement.
Fresh fruits, salads. ■ Evaluations are made by means of:
Vegetables such as carrot slices, celery sticks, - The patient’s comments.
cucumber slices. • New diet diaries.
Baked potatoes, fried potatoes. - Susceptibility tests such as snyder tests and
Hamburgers, hot dogs. • Clinicaljudgement
Unsweetened fruit juices, freshly squeezed ■ Reinforcement is provided by praising the pa­
fruit juices. tient’s efforts. Point out the improvements made
Sugarless chewing gum. in the diet as well as in the test results and the
Sandwiches. absence of new caries lesions.
■ Emphasis should be placed on making the pa­
Katz and other researchers in 1981, suggested • tient folly aware of the benefits derived from the
that nuts and cheese tend to diminish the pH in program and that the benefits are the product of
plaque after the ingestion of acetic foods orthose the patient’s own efforts.
containing sugar.
PATIENTS WITH HIGH CARIES ACTIVITY DIET
BUBEST SUBSTITUTES FOR FOOD ITEMS For such a patient counseling should be part of pre­
ventive procedure and it should include:
■ Immediate removal of all carious tissue and place­
summary of exposures to fermentable car- ment of ZnOE (temporary) restorations.
? determine the dietary changes that are ■ Topical fluoride applications.
g ^^^^^Wed for better dental health.
« Plaque control instructions
t substitutes should be reasonable, which are ■ Home use of fluoride containing dentifrices and
acceptable to the dentists in terms of lesser mouth rinses.
cariogenicity as well as to the patient as far as
tasteand preferences are concerned. Food guide for children is illustrated in Fig. 6.4
 I TEXTBOOK OF PEDODONTICS

S - Servings
Fig. 6.4 Food guide for children.

Self-Assessment

1 Define food, nutrition, diet and balanced diet.

2 Which are the basic food groups ? Give their Rec­
ommended dietary allowances in children.
3 Prepare a diet chart such that the sugar expo­
sures can be highlighted ?
4 What are the steps in conducting diet counseling
for a high risk caries child ?
 6.4 Pit and Fissure Sealants

Bali RK, Batía R, Tandon S

Introduction and characteristically form a triangular or cone

shaped lesion with its apex at the outer surface
The high susceptibility of pit and fissures to caries and its base towards DEJ. Pit and fissures pro­
presents a major dental problem and provides the duces greater cavitation than the proximal smooth
rationale for caries control of these areas. While oc­ surface caries.
clusal surfaces represent approximately 10% of the
enamel surface at risk, they account for almost 50% With this understanding of the onset of occlusal
of the caries in human dentition. caries, the eradication of pit and fissures would
eliminate them as caries opportunity sites thus pre­
Caries of Pit and Fissure venting the disease.

n The caries process, particularly in the first and HISTORY

second molars, usually starts soon after eruption.
It is usually rapid and can often result in loss of Milestones of pit and fissure sealant
the tooth. The very presence of pits and fissure Methods aimed at eliminating pit and fissure have
may be the single most important factor in deter­ been tried since the early 1920’s.
mining the presence of caries in these sites.
Hyatt(1923) Proposed technique called prophylactic
■ However at the turn of century, Black (1897) noted ------- — ~ odontotomy. This technique Consisted of"
that pit and fissure don’t cause caries process. tilling the fissures with silver or copper
They instead provide a sanctuary to those agents, oxy-phosphate cement as soon as the
which cause caries. They permit the entrance of teeth eri$ted Ihto the oral cavity. Later
when they are fully erupted, preparing a
microorganisms and food into this sheltered,
small occlusal cavity and filling it with
warm, moist, richly provided incubator and the * amalgam.
dental plaque can be expected to form here.
Bodecker ProposetHechnique called fissure eradi-
■ In a caries susceptible person, when carbohy­ ~(1929) cation. This technique involved mechani-
drates in food comes in contact with the plaque, T^aTeradication of fissures in order to
acidogemc bacteria in the plaque create acid. This transform deep, retentive fissures into
acid damages the enamel walls of the pit and fis­ cleansable areas.

sures and caries results. The enamel in the bot­ Bunocore Advocated the filling of pit and fissure
tom of the pit and fissures may be very thin, so ~ with bonded resin. He observed that
after treatment of the enamel with a con­
that early dentin involvement frequently occurs.
centrated phosphoric add solution (85%)
■ In occlusal pit and fissures the form of caries le­ for 30 seconds, attachment of acrylic
sion is different from that of smooth surface le­ resin to the tooth surface is greatly
sion. Caries follows the direction of enamel rods increased.
 taUb I TEXTBOOK OF PEDODONTICS

Mid1960’s First materials used experimentally as

■ The shallow, wide V and U shaped fissures tend
sealants were based on cynoacrylates
but they were never marketed.
to be self-cleansing.and somewhat caries resist­
ant.
Bowen Reported BIS-GMA material development
■ Deep, narrow I shaped fissures are quite con­
(1965) The basis of BIS-GMA resin is the reac­
tion product of bisphenol A and glycidyI- stricted and resemble a bottleneck. They have a
methacrylate. narrow slit like opening with a larger base as it
extends towards the dentino enamel junction.
BIS-GMA is the base resin to most of the current These caries susceptible, I shaped fissures may
commercial sealants. Urethane dimethacrylate and also have a number of different branches.
other dimethacrylates resins are also used in the seal­ ■ Similarly, K shaped fissures are also very suscep­
ant materials. tible to caries.
■ Usually non-invasive technique is recommended
Definitions for U and V shaped fissures and invasive tech­
nique for I and K type fissures.
Pit:^ItJs defined as a small pinpoint depression lo-„
cated at the junction of de\?elo.piiicntahgroeves'Of at PIT AND FISSURE SEALANTS
terminals of those grooves. The central pit describes
a landmark in the central fossae of the molars where Fissure sealants are defined whereby pits and fis­
developmental grooves join (Ash, 1993). sures that occur principally on the occlusal surfaces
of the molar and premolar teeth are occluded by ap­
Fissure: It is defined as deep clefts between adjoin- plication of fluid materials, which are then polymer­
ing cusps.^They provide areas for retention of caries ized. Currently used methods are based on the prin­
producing agents. These defects occur on occlusal ciple that the adhesion of acrylic and composite resin
surfaces of the molars and premolars, with tortuous to enamel is greatly increased if surfaces are first
configurations that are difficult to assess from the etched withan acid. The acids used are oftwo main
surfaces. These areas are impossible to keep clean types: those that polymerize after mixing two compo­
and highly susceptible to advancement of the cari­ nents and those that polymerize only after exposure
ous lesion. (Orbans, 1990) to an appropriate light source.

MORPHOLOGY OF FISSURES Effectiveness of sealants

For sealant to be effective, first of all it must be re­
Pits and fissures are enamel faults, narrow shafts or tained. Whether or not a sealant is retained is de­
cracks of some length whose blind ends are directed pendant upon the:
more or less towards the dentino-enamel junction. 1. Technique of application.
These differ from grooves that are shallow linear de­ 2. The type of sealant material.
pressions formed tty the perfect joining of the differ­ 3. The morphology of the tooth surface to which it
ent lobes. is applied.

Nango (1960) in a study of crown sections described Classification of Pit and Fissure Sealants
four principal types of fissures, based on the alpha­
betical description of shape. Mitchell and Gordon (1990) stated that the sealants
V type can be differentiated in the following ways:
Utype
I type 1. Polymerization methods
Ktype a Self activation (mixing two components)
 SECTION 6 : PREVENTIVE APPROACH TO CARIES CONTROL I

b. Uglg^Uvamii:-------- 6-7 years of age for the first permanent molar.

| light
11-13 years of age for th^second permanent molars
- Second generation: Self cure
and the premolars.
Hl - Third generation: Visible light
•Ilf - Fourth generation: Fluoride releasing
■ The approach that considers only selected pa­
tients for sealants has been discussed by
SIlMS Resin systems
Simonsen in 1983. He recommended triaging pa­
BIS-GMA—...' _ „.
tients into thrje groups:
||t ■ Urethane acn late
Group 1: Caries-free patients judged at no risk
to decay.
Vt^ii^tilted and unfilled
Group 2: Patients judged to be at moderate risk
to decay.
Group 3: Patients with rampant caries at a high
-,-^iear sealants have been shown to have bet-
risk to decay
H ter flow characteristics than tinted or opaque,
Sealing of teeth in group 2 patients is done, but
Bljl ' but this can be an advantage or disadvantage
not in group 1 and 3.
depending on the position of the tooth to be
sealed. Although the retention rates of the two
« Most realistic approach for deciding which crite­
types are similar, colored sealants are more
ria should be used in selecting patients for seal­
easily appreciated by the patient and moni­
ant application is to judge clinically. Clinical judge­
tored by the dentist at subsequent recalls.
ment is done to select the teeth that are most
■ The sealant is applied in a viscous liquid state
likely to decay based on:
that enters the micropores, which have been
1. Age
enlarged through acid conditioning. Then the
2. Oral hygiene
resin hardens because of either a self-harden­
3. Familial mid individual history of dental caries
ing catalyst or application of a light source.
4. Fluoride environment and history
The extensions of the hardened resin that have
5. Dietary habits
penetrated and filled the pores are called tags.
6. Tooth tyrpe and morphology
Requisites of an efficient sealant as (Brauer, 1978):
Indications
1. A viscosity allowing penetration into deep and
narrow fissures even in the maxillary teeth. Clinical judgement is the decidingfactor in the place­
X Adequate working time. ment of sealants.
3 i cure. * ■ Newly erupted both primary molars and perma­
«M» and prolonged adhesion to the enamel. nent bicuspids ami molars with complete reces­
5 tow sorption and solubility. -— sion of pericoronal operculum and with open and/
or sticky grooves and fissures.
uiiiauu ■ Stained pits and fissures with minimum decalcifi­
IllfW/fCariostatic action. cation or opacification and no softness at the base
of fissures.
l^^rañges for sealant application ■ The tooth in question should have erupted less
than 4 years ago.
T^iyearsofagefor the primary molar sealant appli­
cation.
 I TEXTBOOK OF PEDODONTICS

Fig. 6.5 Clinical guidelines for application of fissure sealants (Fig. 6.6a, b, c)

Patient’s selection
■ Child with extensive caries in primary teeth:
- Seal all the first permanent molars.
■ Children with special needs. For eg.
- Medically compromised.
- Mentally or physically handicapped.
- From a disadvantaged social background.

Tooth selection Do not seal if:

■ Child with occlusal caries on one of the first Pit and fissure have
permanent molar. remained caries-free
- Seal the remaining sound first permanent for 4 yrs. or longer.
molars.
■ Occlusal caries affecting one or more first The tooth can not be
permanent molars isolated.
- Need to seal the second permanent molar
as soon as they have erupted sufficiently. Caries on proximal
■ Tooth should be sealed within 2 yrs. of eruption. surface of tooth.

I
Doubt about the integrity of an occlusal surface
on clinical examination.

I I

Take bite wing radiograph

I
I I I_______
If no sign of dentin Early dentin Extensive caries discovered on
involvement involvement suspected investigation

I I I
Seal the surface as Investigate the fissures Standard dental restoration
preventive measures using small burs should be inserted

Recall: Evaluate sealed Place a minimal composite

teeth for sealant integrity restoration incorporating a
and retention and caries fissure sealant to protect the
progression. rest of the occlusal surface.
 SECTION 6 : PREVENTIVE APPROACH TO CARIES CONTROL I &&

Fig. 6.6a Occlusal fissure of the first molar tooth is

suspect because the patient has recently established a caries rate.

Fig. 6.6b Preparing the enamel surface for

fissure sealant.

Fig. 6.6c The same patient showing fissure seal about

2 year after placement.
 I TEXTBOOK OF PEDODONTICS

Contraindications

« Individual with no previous caries experience and

well coalesced pit and fissures. Monitor if the
individual and the teeth are not at risk.
• Radiographic or clinical evidence of caries on the
proximal surface of the tooth should not be
sealed.
« Wide and self-cleansable pit and fissures.
» Tooth that can not be isolated or partially erupted
tooth.
» Pit and fissures that have remained carious free
for 4 years or longer. Fig. 6.7a S.E.M. picture of a freshly etched enamel
showing a typical porous surface pattern.
TECHNIQUE OF APPLICATION

1. Cleaning: the surface of the tooth selected for Adhesive or resin

sealant placement should be cleaned first with a
shiny of pumice and water. It is important that
neither a prophy paste nor a paste containing
fluoride be usedrns they will compromise the acid
etching procedure and therefore the sealant’s ef­
Conditioned surface
fectiveness.
Adhesive or resin
2. Washing and drying: immediately following clean­ Original
ing, the tooth is washed with water and air-dried. surface*

3. Etching: occlusal surface is then etched with a

30-50% solution of phosphoric acid liquid or gel
for 60 seconds (Fig. 6.7a, b) •Non-conditioned surface
« Etching produces microscopic porosities in the
Fig. 6.7b Microstructure of enamel.
enamel. The resin extends into these micro­
scopic porosities and forms tags which attach
it firmly to the tooth surface. 4. Washing and drying: following etching, the tooth
surface is washed with water for 30 seconds to
**■ With different etch times, no quantitative dif­ remove all the etchant, then air-dried. A property
ferences in the surface morphology of ena mel etched tooth surface has a dull frosted appearance.
are observed. (Tandonet. al.. 1989). This shows ■ After etching the tooth the surface should re­
that the retentive character of the etched sur­ main dry and free of any moisture contamina­
face is similar for different etch times. Thus, a tion until the resin is applied and cured. The
short etch time of 15 sec. is satisfactoiy for tooth can usually be kept diy with cotton rolls
primary enamel and is also sufficient to pro­ and suction. If not, then a rubber dam must be
duce the required etch pattern for the strong used.
binding of sealants. ■ If the surface becomes contaminated, it must
be re-etched for an additional 10 seconds.
 SECTION 6 : PREVENTIVE APPROACH TO CARIES CONTROL | fEEi

5. Application of material: care must be taken when If it is necessary, that the sealant material should be
applying the material to avoid incorporating air added at this time.
bubbles
Sealants have been shown to be safe, efficient and
effective methods of preventing pit and fissure car­
6. Curing: material is cured according to the manu­
ies ami as such should be used by all dental person­
facturer’s directions. Once the material has been
nel for prevention of ravages of dental caries.
ftilly cured, it is carefully examined with an ex­
plorer to make certain that
■ all pits and fissures are covered. Self-Assessment .
■ all excessive material has been removed.
1 Define pits and fissures.w
■ material is firmly adherent to the enamel surface.
2 Classify the pits and fissures seen in the tooth.
3 What considerations should be considered be­
7. Recall: along with other forms of dental care, the
fore the application of the sealants?
sealants should be thoroughly checked at sub­
4 Briefly describe the procedure of application of
sequent recall appointments to ensure:
the sealant.
« it is still firmly adherent, and
■ no sealant material has been lost (Fig. 6.5c).
 6*5 Fluorides

Tandon S

The Fluoride element is the most electronegative el­ rine. Since then numerous studies have confirmed it
ement, which never exists in free state in nature but as an essential micronutrient for the optimum forma­
combined chemically with other elements as fluoride tion of the crystalline structure in mineralized tissues
compound. It has not only notable chemical quali­ such as bone and teeth. The crystalline structure of
ties but also physiological properties of great impor­ the enamel formed under the influence of fluoride
tance for human health and well being. Its selective becomes morphologically and chemically better
effect on the hard tissues of the body attributes sig­ suited to withstand the odontolytic microorganisms.
nificantly to prevention and control of dental caries.
Fluorine word is derived from the Russian word “flor” The milestone studies are discussed in Table 6.10
which comes from “floris” meaning destruction in
Greek and from Latin word fluor” means to flow since MECHANISM OF ACTION (Fig. 6.8b)
it was used as a flux. Fluoride apparently is ubiqui­
tous in its distribution and is the 13th among the Fluoride’s role in decreasing theprevalence of caries
trace elements in order of abundance in the earth’s has been well accepted for many years. However, the
crust. It is a highly reactive anion with an atomic beliefs about fluoride have changed. It is now deter­
weight of 19 and atomic number of 9. Fluoride is mined that the presence of fluoride in and on enamel
widely distributed in the biosphere; is present in the surface is the key to the effectiveness of fluoride.
lithosphere, hydrosphere, atmosphere and in all liv­ Fluoride is incorporated through out the tooth crown
ing organisms. It enters into the atmosphere by vol­ formation during development. To understand the
canic action and entrainment of the soil and water cariostatic effect of fluoride it is necessary to know
vapours due to the action of the wind. It returns to the enamel structure and the process of deminerali­
the earth by deposition as dust or in rain, snow and zation.
fog. It comes to the hydrosphere by leaching from
the soil and minerals in to the ground. Enamel structure: Enamel consists of apatite like crys­
tals, which are primarily carbonate ions. These crys­
Fluoride in the environment is depicted in Fig. 6.8a tals are arranged in rod like structures, having hy­
droxyl ions, which run parallel to the long axis. There
History
are numerous atomic scale structural imperfections
The history of fluoride is more than hundred years within the enamel crystals, as well as the spaces be­
old. The first hint of possible connection of fluoride tween the rods. These structural imperfections, as
and dental health was given by Sir James Crichton- well as inclusions such as carbonates and magne­
Browne in 1892. He suggested the probable cause of sium within in the enamel crystals increase the acid
dental caries as a change in bread, which did not solubility of the crystals. Since carbonate accounts
have bran or husky part of wheat containing fluo­ for five percent of human enamel it is often
 SECTION 6 : PREVENTIVE APPROACH TO CARIES CONTROL |

Fig 6 8a Fluoride in the environment

I
r I -3
In Lithosphere In Bioshphere In Hydrosphere In Atmosphere

t t t t
Rocks Minerals Plants (2 - 20 mg/g) Ground water Ambient air
(> 50) (0Ä6 mg/m3)

t I t t
Earth, Crust Leafy vegetables Lake water Through technology
(300 ppm) (11 -26 mg) (150 mg/kg) (0.05 - 1.8 micrograms/

t t f m3) à
1
Soil Animal Feed Sea water Ground lofty
(500 ppm) (15 -18 mg) mountains

t I
Volcano Rain water

Table 6.10: Milestones studies of fluoride

Year and Investigation Discovery or Report

1901, Dr. Frederick ■ Permanent stains present on the teeth of the local inhabitant of
McKay Colorado Spring, U.S.A., known as ‘Colorado Stains’ noticed.
■ Stains characterised by minute white flecks, yellow or brown spots
scattered all over the surface of the tooth were termed as mottled
enamel (most obviously and unmistakably defective enamel).
1902, Dr. J. M. Eager ■ Described similar stains seen on the teeth of certain Italian emigrants
embarking at Naples as “denti di chiaie”.
1916, Dr. Green « Supported McKay work with histologic evidence reporting it as an “an
Vardmin Black endemic imperfection of the enamel of the teeth”
4
1918, Dr. O. E. Martin « Britton in 1898 had changed its water supply from shallow well to a
Dr. F. McKay deep drilled artesian well. All those who had passed through child
hood before the change of water had normal teeth and who grown
after this had mottled enamel. Thus, it was concluded that some
mysterious
* element in water was present.
1925, Dr. F. McKay ■ Change of wgter supply from spring water of the Great salt lake of
Oakley, Idaho city showed no brown stains in children who were born
after change of the water supply.
1928, Dr. McKay ■ Similar observation found in Bauxite where changed water supply (in
Dr. Gromer Kempt 1909) from a shallow well to foot well resulted in children with badly
stained teeth. They found that no mottling occurred in the people who
grew upon Bauxite water prior to 1909.
coM.
 I TEXTBOOK OF PEDODONTICS

Year and Investigation Discovery or Report

1931, Mr. H. V. Churchill ■ A spectrographic analysis of Bauxite city water showed the presence
of fluoride at the level of 13.7 ppm.

1933, Dr. H. Trendley ■ Shoe Leather Survey conducted in 97 localities with the help of ques­
Dean tionnaire with the aim to find out minimal thresh hold of fluoride, the
level at which it began to blemish the teeth.
1939, Dean and McKay ■ Came out with the most conclusive and direct proof that fluoride in
domestic water is primary cause of human mottled enamel (dental
fluorosis)

1939, Dr. H. Trendly ■ Hypothesis showing the inverse relationship between endemic dental
Dean fluorosis and dental caries emerged with survey of four Illinois cities.

Table 6.11 : Caries inhibitory effect through water fluoridation

1944 - 1959 > GRAND RAPIDS-MUSKEGON STUDY (water fluoridation) Grand

Francis Arnold, Rapids as experimental town and sodium fluoride was added to
Philip Jay and water at 1 ppm and Muskegon as control.
John Knutson ■ First crucial step proved caries reduction from 12.48 to 6.22 DMF
indicating that previously observed inverse relationship of fluoride in
water and dental caries was a cause and effect relationship.
1945 - 1955 ■ NEWBURGH-KINGSTON STUDY - 10-year study.
David et al. Newburgh children showed caries decline from 23.5 to 13.9% after
water fluoridation.
1967 (1946-1960) ■ EVANSTON-OAK PARK STUDY-14-year study.
Dr. J. R. Blayney, Fluoridation in Evanston showed a 40% reduction of caries.
T N. Hill,
S. O. Zimmerman
1951 Hutton et al. ■ CANADIAN STUDY (Brantford, Sarnia and Stratford)
1965 Brown and Stratford with a naturally present 1.3 ppm fluoride in water was auxiliary
Poplove control. After 17 years of fluoridation, Brantford showed a 50% reduc­
tion in caries.
Fluoride inhibits smooth surface caries
1961, Backer Dirks ■ DUTCH STUDY (Tiel-Culemborg)
et al. Tiel was fluoridated at the level of 1.1 ppm. Culemborg with 0.10 ppm
served as a control. 13 years study showed 88% reduction in smooth
surface caries and 43% in pit and fissure caries.
1965, Ludwig • NEW ZEALAND STUDY
Study carried out in Hastings from 1954 to 1964 showed a DMF
decline from 5.48 to 2.46 with reduction of approximal caries by 69%
and occlusal caries by 49%.
1969, World Health ■ Recommended first time 1 ppm fluoride in drinking water for a practica­
Organization ble and effective public health measure.
 SECTION 6 : PREVENTIVE APPROACH TO CARIES CONTROL |

referred to as carbonate apatite. Enamel is the hard­

est body tissue and contains 85% of mineral by vol­
ume. The remaining 15% consists of water, protein
and lipids in spaces between the enamel crystals and
the rods. These act as diffusion channels fbr fluo­
ride, minerals and acids.
The action of fluoride^n the enamel surface can be

divided into the following:

■ Fluoride incorporation in enamel

Incorporation of fluoride into enamel throughout
development is not a principal mechanism of
cariostatic effect. It is believed that pre-eruptive
exposure to fluoride may produce teeth more re­
sistant to caries by making pits and fissures shal­
lower. but post eruptive exposure of fluoride too
has a significant role in it.

■ Pre-eruptive incorporation
Fluoride gets incorporated in the fluid filled sac,
which surrounds the developing tooth. It then
enters the developing enameL Highest concen­
tration of fluoride is seen in enamel crown located
at or near the tooth surface.

■ Post-eruptive incorporation
Fluoride continues to enter the enamel surface,
causing crystals to change from predominantly
A An apatite crystal.
carbonated apatite and hydroxyapatite to fluora­
B. Relationship between hydroxyl and patite (FAP) and fluorhydroxyapatite (FHAP)
calcium ions. cry stals. These fluoride rich crystals are less acid
C. Fluoride lends stability to hydroxyl column soluble than the original enamel apatite.
and apatite lattice.
■ Remineralization of acid dissolved enamel
Minerals of tooth enamel are continuously in ex­
Open circles: Calcium
change with the minerals of saliva and thus the
balance is maintained. This equilibrium can get
Grey circles: Oxygen
disturbed with the organic acids produced by the
Black circles: Hydrogen
metabolism of fermentable carbohydrates by the
microorganisms. This leads to a drop in pH of the
Fig. 6.8b Mechanism of action of fluoride
(Ekstrand 1988) plaque on the enamel surface and in the
sub-surface. Minerals, particularly calcium and
phosphate leave the dissolved enamel in their
 I TEXTBOOK OF PEDODONTICS

ionic form and enter the plaque fluid. This proc­ enamel, near the incisal edge and steeply decreases
ess is called as “demineralization”. This gets re­ towards the more recently formed cervical region.
versed with the factors like fluoride and is termed Thus in younger children enamel is much more sus­
“remineralization”. The surface and sub-surface ceptible to demineralization around the neck of the
of the enamel absorb and hold minerals and fluo­ tooth. This can be inhibited with the topical applica­
ride, which are present in the plaque fluid and tion of fluoride. In older children the concentration
enhance the regrowth of the partially dissolved of fluoride is inverted. The active role of fluoride in
crystals. Fluoride’s ability to facilitate the the caries process, thus, recommends that the clini­
remineralization process is presently believed to cian should follow the rationale for semiannual fluo­
be more significant than its inhibition of deminer­ ride application which is rested on the following two
alization. The regrowth by fluoride incorporation basic premises:
chemically forms new crystals that are larger and ■ Increase the fluoride content in enamel to as high
more acid resistant and contain a higher concen­ as possible in a short time.
tration of fluoride. This explains why the “white ■ Prevent the formation ofcalcium fluoride and other
spot” i.e. incipient lesions which have been ar­ fluoride precipitates that are more soluble than
rested or healed due to fluoride application are fluoridated hydroxyapatite.
considerably less reactive to further acid chal­
lenge than the adjacent unaffected enamel. Effect of fluoride during pH - cycling:

White spot (Incipient caries) In the oral environment there is a continual cycling
of pH change resulting from acid challenge and neu-
The high concentration of minerals and fluoride at tralizationby saliva. Itis believed that fluoride present
in oral fluid can range from undetectable to 20ppm,
the surface layer of the enamel and the loss of miner­
depending on the individual cs recent exposure to
als diffract light, creating an opacity that appears
fluoride. When this fluoride containing enamel crys­
clinically as a white spot. Although the white spot is
tals get embodied in pellicle on the enamel surface,
generally recognized as the first clinical evidence of
its ability to resist transfer of minerals out of enamel
developing caries, the caries initiates much earlier. In
is improved. This hypothesis demonstrates the sub­
the presence of fluoride the spot becomes smooth
tle but critical interaction between saliva, enamel and
and shiny, but in the absence of fluoride it appears
fluoride.Fluoride inhibits plaque formation
rough and chalky. The surface of the white spot
should not be probed too hard, though it appears
Plaque is a reservoir for fluoride and approximately
intact because it is mineral deficient and weak layers
2% of the fluoride in plaque is present as a free ion. It
may break and form cavitation. Therefore, this intact
was seen that fluoride can not cross the cell wall and
incipient lesion should be treated with topical fluo­
the membrane in ionized forms, but can rapidly travel
ride and allowed to remineralize.
through the cell wall and into cariogenic bacteria in
the form ofhydroxyfluoride (HF). Hydrogen and fluo­
INHIBITING DEMINERALIZATION
ride ions combine as the bacteria produce acid dur­
ing the metabolism of fermentable carbohydrates.
It is believed that demineralization is slowed down Hence, the acid helps in the fall of pH and a portion
with the continuous exposure of fluoride and a of the fluoride ion in the plaque fluid then combines
stronger acid challenge is required to demineralize with hydrogen ions and rapidly diffuses in the cell
the enamel crystals. As discussed in incorporation effectively drawing more HF from the outside, and
ef fluoride into enamel structure, it is seen that a so on.
maximum fluoride concentration is in first formed
 SECTION 6 : PREVENTIVE APPROACH TO CARIES CONTROL | 00

5. In a clinical trial of 6 - 1 lyrs olds low fluoride

H+ +F- containing (289ppm) dentifrices have shown to
have similar effect on primary and permanent (fen­
Bacterial ceil tition in reducing the caries increment of high fluo­
ride (900ppm) dentifrice (Tandon and Paul 1996)
pH 7 H+ +F- HF 6. Teeth irradiated switched Nd-YAG laser at
50mJ followed by fltwide application have shown
pH 4 H+ +F- HF maximum resistance to the artificially induced
caries. (Altai and Tandon 1996)
Once inside the bacterial cell, HF dissociates again,
acidifying the cell and releasing fluoride ions, which FLUORIDE METABOLOSM
interfere with essential enzyme (enolase) activity,
thereby inhibiting bacterial metabolism and inhibit­ Source of fluoride
ing plaque formation against the progression of den­ The principal source of human fluoride ingestion is
tal caries. water.
■ It is present in nearly all ground water, though
Role of low7 fluoride in oral environment concentration in water supply is very small
■ It is also derived from plants, marine animals and
Brown and Coworker (1996) predicted that low con­ even dust particles
centration of fluoride could enhance remineralization. ■ Fluoride content varies in different types of food,
Since fluoride ion is most effective at enamel saliva like
interface it is believed that it is beneficialto provide a. Certain types of fishes, dried mackerel and
a continuous supply of fluoride ions at that inter­ dried salmon contain a large amount of fluo­
face. It provides and maintains caries inactive state. ride i.e. 84.5 ppm
The study conducted in pedodontic department of b. Potatoes give 6.4 ppm
Manipal with a low fluoride level showed the follow­ c. Tea contains an average of 97 ppm
ing results:
L 0.4% APF provide equally effective protection in GENERAL SURVEY OF DIETARY ITEMS FOR FLUO­
enamel against acid attack in a vitro study as that RIDE CONTENT: (Tandon & Thomas 1989) Theav-
of 1.23%APF (Tandon and Tissy 1988) erage fluoride content in the commonly consumed
2. The lower concentration of 0.4mg NaF in a sus­ dietary items are given in Table 6.12,13,14.
tained release tablets has shown no difference
with that of a high concentration of200mg NaF in THE CHEMISTRY OF FLUORIDE
reducing dental caries (Shyama and Tandon, 1991)
3. Fluoride dentifrices containing lbw concentration Chemically fluoride is so violently reactive that it
of 175ppm NaF is found to increase the rarely or never occurs in nature^s elemental fluo­
microhardness of the enamel. This takes place rine. Its atomic weight is 19.0 and it exists chemically
slowly and steadily as compared to high concen­ in the form of fluorides, chiefly as:
tration of 300, 700 and lOOOppm, respectively ■ Fluorspar (CaF2)
(Tandon et al 1992) ■ Fluorapatite (Ca10(PO4)6F2)
4. A continuous uptake of low fluoride of 289ppm ■ Cryolite (Na^AlF^)
toothpaste by the enamel was seen and a signifi­
cant difference was observed in 12 weeks as com­
Berndt and Stearns (1972) viewed that, the
pared to the high concentration (900ppm) of fluo­ crystallographic unit cell for apatite contains 10
ride in dentifrices/ Sandra and Tandon 1994) calcium, 6 phosphate and 2 fluoride ions. The ionic
 | TEXTBOOK OF PEDODONTICS

Table 6.12: Average fluoride content of commonly used cold beverages

Name/brand of drink Fluoride content in ppm Fluoride content in 200 ml

Thums up 0.233 46
Frooti (mango, orange, 0.165 - 0.202 33-40
appy)
Orange juice 0.100 20
Sugar cane juice 0.085 17
Tender coconut water 0.083 17
Butter milk 0.108 22

Table 6.13: Average fluoride content of commonly used hot beverages

Fluoride content in ppm Approx,

Quantity of fluoride
Brand of tea coffee Coffee/tea Coffee/tea content in 1
and coffee powder/tea without milk with milk cup of coffee/
, used leaves used and sugar and sugar tea (200 ml)
with milk &
sugar (micro >
gms)

Local coffee
(Panduranga) 1 tsp 0.192 0.174 34

Commercial
coffee 1 tsp 0.175 - 0.185 0.164-0.171 32 - 34
(Nescafe
& Bru)

Local-Kelagur
CTC tea 1 tsp 1.710 1.54 200
leaves

Commercial
tea (Brooke
Bond, Lipton 1 tsp 1.00 - 1.19 0.928 - 1.11 190 - 222
green label,
Taj Mahal)
 SECTION 6 : PREVENTIVE APPROACH TO CARIES CONTROL | @3)

Table 6.14: Average fluoride content of commonly used food items

Items Dry wt of substance Fluoride (ppm) in Fluoride in 100gm

(gms) dry wt of substance sample (micrograms)
M__
Cereals group
1
Raw rice 9.00 0.42 38
Wheat 8.90 0.53 47
Rava (sogee) 8.80 0.51 45
Jowar (millet) 8.90 0.64 57
Ragi 9.10 0.79 72
Corn flour 9.00 1.52 137

Pulses group
Black gram dhal 9.20 1.17 107
Sambar dhal 9.20 0.89 82
Green gram flour 8.60 0.77 67
Green peas 8.90 0.72 64

Roots and tubers

Onion 2.70 1.34 36
Potato 2.80 1.55
Carrot 1.50 3.04
Beetroot 0.70 1.59
Ra'dish 0.75 1.83
Ginger 4.20 0.91

Vegetables group
Beans 2.50 2.38 ' 59
Tomato 1.80 1.56 28
Brinjal (local) 2.70 2.21 60
Cucumber 1.40 0.98 14
Ladies finger 1.03 • 0.86 9
Green chillies 1.30 1.14 15
Pumpkin 1.10 0.54 6

Leafy vegetables
Cabbage 2.10 2.14 45
Spinach 1.50 3.84 58
Coriander leaves 1.50 2.40 36
contd.
 I TEXTBOOK OF PEDODONTICS

Items Dry wt of substance Fluoride (ppm) in Fluoride in 100gm

(gms) dry wt. of substance sample (micrograms)

Fruits
Orange 0.86 ^1.03 9
Pineapple 1.40 1.03 14
Green grapes 1.04 0.55 6
Banana 2.46 0.39 10
Apple 1.30 0.32 4
Guava 1.70 0.43 7

Animal foods
Chicken 4.60 0.92 42
Whole egg 4.10 4.62 189
Pork 3.80 1.17 45
Mutton 2.20 1.80 40

Sea foods
Fresh water fish 2.10 0.58 12
Dried sea fish 8.20 165.44 135.70

Miscellaneous
Coconut 2.60 0.86 22
Common salt 9.30 1.52 M42
Jaggery 8.00 0.73 58
Sugar 9.60 0.43 41 i
Tamarind 075 0.75 54

structure of apatite readily permits the substitution ■ A third and very rare route of absorption is
of other ions of the same charge. Since the calcium, through the skin. It may occur when hydrogen
phosphate or fluoride are approximately of the same fluoride is applied to the skin. However, the re­
size, when substitutes exists, they maintain the size sulting bum is more serious than the fluoride ab­
of the unit cell. sorbed.
■ It is believed that soluble fluoride in drinking water
ABSORPTION OF FLUORIDE would be absorbed nearly completely regardless
of fluoride in the water supply. The absorption of
• It is readily absorbed into the body. Absorption fluoride from food depends on thé solubility of
occurs mainly in the stomach, is passive in na­ inorganic fluorides in the diet and its calcium con­
ture and no active transport mechanism is in­ tent. If calcium or aluminum compounds are
volved. added, fluorine absorption is reduced.
■ It can also occur from the lungs by inhalation of
fluoride dust and gases.
 SECTION 6 : PREVENTIVE APPROACH TO CARIES CONTROL |

EXCRETION OF FLUORIDE ■ The ions present in the crystal surface might mi­
grate slowly into vacant spaces in the crystal in­
Fluoride is excreted in urine, lost through sweat and terior during recrystallization.
excreted in feaces. It occurs in traces in milk, saliva,
hair, and tears. The principal route of fluoride excre­ Fluoride in bone t
tion is via the urine and urinary fluoride level is re­
garded as one of the best indices of fluoride intake. Fluoride ions are able to enter the hydroxyapatite
The very rapid rate of excretion is one of the most lattice. The fluoride concentration in living human
protective factors in severe poisoning. bone builds up slowly with age. The distribution of
fluoride within bone is not uniform. It is the highest
Spencer et al. (1978) reported that the kidney is the in the areas of most active growth.
main pathway of fluoride excretion with an average
fluoride intake of 3.9mg/day. Urinary fluoride is 30 Fluoride in enamel and dentin
percent of fluoride intake in renal patients and 50 to
60 percent in normal person. The faecal fluoride is Fluoride uptake in dental tissues also increases with
low. The antacid aluminum hydroxide is commonly age and with increasing concentration in water. It is
used to decrease the serum phosphorus level and considerably lower in the enamel and the dentin than
inhibits the internal absorption of fluoride. that found in the bone of the same individual. After
the tooth has folly formed, fluoride is chiefly incor­
STORAGE OF FLUORIDE porated at tissue surface. The highest fluoride in den­
tin is found adjacent to odontoblastic layer. Mahajan
Fluoride is stored in the hard tissue of the body. The
and Sidnu (1981) found less resorption of the roots
extent of fluoride uptake in different parts of the skel­
of the teeth that are treated with fluoride.
eton and dentition depends upon the amount in­
gested and absorbed, the duration of fluoride expo­
Fluoride in blood
sure and the type, region and metabolic activity of
the tissue concerned.
Approxiriiately three-quarters of the total blood fluo­
ride is in plasma and one-quarter in red blood cells.
UPTAKE OF FLUORIDE IN BODY TISSUE
The regulation of plasma fluoride concentration is
It slightly alters the chemical composition of bone due to a large volume of extracellular body fluid,
and teeth minerals. The carbonate and citrate con­ which dilutes absorbed fluoride by deposition of fluo­
tents are lowered and magnesium level remains un­ ride in the skeleton and by excretion in urine.
changed
Fluoride in plaque
Three-stage mechanism takes place for the entry of
the ion into the apatite lattice as follows: Dental plaque is the main storage source in the oral
■ Fluoride ion exchange with one of the ion or po­ cavity. Its concentration in plaque is many times
larized molecules present in the loosely integrated higher than in saliva, especially gingival crevicular
shell. fluid where it is 10 to 20% more than plasma concen­
■ Second stage involves the exchange of fluoride tration of fluoride.
in the hydration shell with anion group at the
surface of apatite crystal. Ionic exchange occurs Fluoride in placenta andfoetus
between fluoride ion and hydroxyl and bicarbo­
nate groups and also fluoride ions already present Evidence concerning the extent of placental transfer
in the crystals. in human has been conflicting. Higher fluoride values
 f&ifo i TEXTBOOK OF PEDODONTICS

are present in maternal blood and the placenta tissue COMMUNITY WATER FLUORIDATION
of pregnant women living in the areas, where drinking
water contains Ippm than those of non-fluoridated area. ■ Community water fluoridation in the process of
adjusting the amount of fluoride in a community
Fluoride in saliva water supply to an optimum level for the preven­
tion of dental caries.
ft is seen that fluoride from ingested food, water and ■ The effect of fluoride in drinking water on dental
supplements returns to the mouth in saliva in suffi­ caries has been the subject of research com- /
cient quantities. Most children have oral fluid fluo­ menced decades before. Studies have shown that
ride levels ranging from 0.01 to 0. Ippm, with the av­ the adjustment of fluoride concentration in drink­
erage concentration falling in the range of 0.02 to ing water to the optimal level of Ippm is associ­
0.03ppm. A recent study concluded that a difference ated with a marked decrease in dental caries. The
of only 0.02ppm of fluoride in oral fluid might indi­ world health organization recognized these facts
cate why one child is caries active while another is by its resolutions in 1969 and 1975, in which it is
caries resistant. stated that water fluoridation application should
be the corner stone of national health policies for
MODE OF FLUORIDE ADMINISTRATION (Fig. 6.9) prevention of caries.
■ The recommended daily dosage of fluoride for
SYSTEMIC FLUORIDE children above 3 years of age is Img. This can be
obtained by drinking one liter of water with a con­
Fluoride after the ingestion can get absorbed and centration of Ippm fluoride ion. Since the amount
incorporated into developing enamel and can ben­ of water consumed will vary with temperature,
efit teeth before eruption. It also benefits the teeth the fluoride ion concentration considered opti­
after their eruption, when it returns to mouth in sa­ mal for a particular locality is predicted upon the
liva and gingival exudate. average of the maximum dally temperature.

Fig. 6.9 : Mode of fluoride administration

Fluoride Administration

Systemic Topical
”3
■ Dietary fluoride Water fluoridation Professional Self
■ Salt fluoride School water fluoridation application application
■ Fluoride in sugar Milk fluoridation — fluoride solution
— varnish
• Dietary fluoride — fluoride drops — foam
supplements — fluoride drops with vitamins *— gels
— fluoride tablets/lozenges
— fluoride tablets with vitamins
— fluoride sustained release
— fluoride devices
i— fluoride rinse fluoride solution
 SECTION 6 : PREVENTIVE APPROACH TO CARIES CONTROL |

Fluoride compounds in community water RECOMMENDED LEVEL OF FLUORIDE IN WATER

(WHO 1971)
Sodium fluoride was the first compound used in a
controlled fluoridation program. Owing largely to its ■ Concentration 0.7 to I .^pm
low cost, sodium silico fluoride replaced sodium fluo­
ride as the chemical most often used to fluoridate Depending upon a community mean maximum daily
water. There has been an increased use,fof temperature:
hydrofluorsilicic acids as the fluoride ion source. ■ Cold climate 1.2ppm
■ Summer season or temperate climate 0.7ppm
BENEFITS OF WATER FLUORIDATION
CALCULATION OF OPTIMUM LEVEL OF FLUORIDE
Cariostatic effects of water fluoridation ill children
are not limited to permanent dentition but also ex­ ppm fluoride=0.34 IE
tended to primary dentition as well. E=0.38 + 0.0062 X temp, in °F
■ This method is preferred since some tooth sur­ (E is estimated water intake)
faces receive greater protection against caries
than other. For example smooth surfaces of teeth, RECENT RECOMMENDATIONS (WH01994)
especially proximal surface, derive maximum pro­
tection than do pit and fissures on the occlusal In view of the increased concern about the toxic ef­
surface. fect of fluoride through systemic ingestion, espe­
« Water fluoridation have both pre-eruptive and cially about opacities of developing dentition, WHO
post-eruptive effects lias recommended optimum level of fluoride in drink­
■ Fluoridated drinking water not only acts systemi- ing water as: 0.5 to 1.0 ppm.
cally during tooth formation to make dental
enamel more resistant to dental decay, but also Table 6.15 Percentage caries reduction with differ­
lias topical effect through the release in saliva ent methods
after ingestion.
« Fluoride in saliva through the systemic mode re­ Method of fluoride Average %
mains elevated for an extended period, provides administration reduction of caries
protection against demineralization, and facilitates
remineralization. ■ Community water
■ It changes the morphology of occlusal surfaces, fluoridation 50-60%
by making pit and fissures more shallow and self­ ■ Salt water fluoridation 40%
cleansing.
■ Dietary supplements 50-85%
■ Fluoridation of community water is the least ex­
pensive and most effective way to provide fldo- ■ Fluoride dentifrices 20-30%
ride to a large group of people. « Professional applied
■ If there is a question regarding the fluoride con­ topical fluoride 30-40%
centration, which is not an additive but is natu­
rally present to some degree in water, the local ■ Self applied topical
authority of health can test samples and can pro­ application 20-50%
vide accurate information.
! ■ Beverages bottled in fluoridated areas or other SCHOOL WATER FLUORIDATION
such products may pass on the beneficial effects ■ School water fluoridation is the adjustment of the
i to fluoride deficient/deprived population. This is fluoride concentration of a school’s water supply
( termed ‘Diffusion’ or cHalo’ effect. for caries prevention.
 | TEXTBOOK OF PEDODONTICS

■ After observing the beneficial effects of commu­ calendar year. They also allow7 supplementation to
nity water fluoridation, an alternative method for begin at birth, so that maximum protection can be
supplying systemic fluoride for children was de­ afforded to both primary and permanent teeth.
cided. School water was fluoridated to provide
maximum cariostatic effect in developing teeth. Dietary fluoride supplements are administered in the
Since children spend only 6 to 8 hours in school, following forms:
concentration of fluoride 4 to 6 times more than 1) Fluoridated milk
2) Fluoridated salt
that designated for community water, was recom­
mended. For instance, in Elk lake, Pennsylvania 3) Fluoride in sugar
4) Fluoride in citrus beverages
the school water supply wa s fluoridated at 5ppm
5) Fluoride drops
and in five years there was a reduction of 28.6%
6) Fluoride drops with vitamins
seen in caries. After 10 years of school water fluori­
7) Fluoride tablets/lozenges
dation, the children who attend school continu­
8) Fluoride tablets with vitamin
ously had 39 percent less decayed, missing and
9) Fluoride oral rinse supplements
filled teeth than did their counter parts. Similarly
several hundred of rural schools in the United Fluoridated milk
States and few schools in Brazil and Thailand prac­ Milk fluoridation is suggested as an alternative to
tice school water fluoridation. water fluoridation for caries prevention, Jolan
Banoczy et al. (1984) undertook a longitudinal study
Advantages and disadvantages to see the effect of milk consumption in 3 to 9 years
■ Results of several school water fluoridation pro­ old children with homogenous living condition. Chil­
grams indicate that it can be an effective public dren were given 200ml milk daily, fluoridated with
health measure to reduce dental caries in commu­ 0.4mg of fluoride for preschoolers (3 to 5 years old) ;
nities where fluoridation of water supply is not and 0.75mg fbr schoolers (6 to 9 years old) for 300 i
possible. days in a year. Caries increment was seen consider­
• This method has some disadvantages also. Most ably less in the second year and the third year com­
of children are 5 to 6 years old upon starting pared to the first year.
school; at this age their dental development pre­ «
cludes the fluoride from school water fluorida­ Disadvantages
tion and will not provide pre-eruptive contact to Although most of the studies have shown evidence
the primary teeth. It allows only limited pre-erup- of protection from caries, milk is not an ideal vehicle
tive protective benefits to the primary teeth. for fluoride delivery because of the following reasons:
■ Another disadvantage is intermittent fluoride ex­ ■ It provides only a limited exposure to children, as
posure of children. Most children who attend consumption of milk tends to decline with in­
school for 5 to 6 hours are actually in school less crease in age.
than 180 days during a year and do not receive ■ Absorption is slow as compared to water fluori­
complete effect of fluoride. dation.

DIETARY FLUORIDE SUPPLEMENTATIONS Fluoridated salt

The addition of fluoride to table salt is a feasible way
Though a school based program assures that par­ to deliver systemic fluoride, particularly in countries
ticipating children are regularly receiving their fluo­ that lack a widespread municipal water system. Fluori­
ride supplements, the time of exposure to the devel­ dated salt has been sold in Switzerland for many
oping dentition is not at the maximum level. In com­ years. France and a few countries in Western Hemi­
munity water fluoridation they receive an advantage sphere have introduced salt fluoridation in recent
of being able to administer the fluoride for the entire
years. Wespi (1961) first promoted the use of table
 SECTION 6 : PREVENTIVE APPROACH TO CARIES CONTROL |

Table 6.16: Recommended dietary fluoride supplements (Revised schedule, 1999).

Age in years Concentration of fluoride in drinkj|^ water in ppm

< 0.3 ppm 0.3 to 0.6 ppm > 0.6 ppm
Birth to 6 months None None None
6 months to 3 years 0.25 mg/day None None
3 to 6 years 0.50 mg/day None None
6 to 16 years 1.00 mg/day None None

salt as a vehicle for fluoride in the mid 1940s. Initially S.mutans count compared to the control group.
supplementation was 90mgF/kg of salt. Recently it (Tandon 1994, unpublished data)
has been recommended in the range of 200 to 250
mgF/kg salt. Commonly used salts are potassium fluo­ Disadvantages
ride (250 mg/kg) and sodium fluoride (225 mg/kg). All
over the world only five countris (Belgium, France, It is believed that the marketing of cariologically harm­
Germany, Spain and Switzerland) have specific poli­ less fluoridated sucrose products would increase the
cies of use of salt fluoridation. A sixth, Hungaiy, is general consumption of sucrose and thus will pro­
presently contemplating a recommendation (Banting mote a nutritional imbalance. Further more, one type
1999). of fluoridated sugary product may not reach all those
needing the fluoride supplements.
Advantages and disadvantages

Fluoride in citrus beverages

Salt fluoridation holds a great promise for under­
developed countries and countries like India where
Citrus beverages may also be considered as a poten­
water fluoridation is not feasible due to a limited cen­
tial vehicle for the administration of fluoride as di­
tral water supply and not accessible to a majority of
etary supplements. (Galon et al. 1983)
the community. Salt is the vehicle, which is not ex­
pensive and is used almost in all the houses. Fluo­
Prescribed fluoride supplements. [Tablets, drops, vi­
ride supplied in salt is usually ingested with meals
tamins etc.]
hence absorption is relatively slow.
4
Fluoride supplements are prescribed by the practi­
Fluoride in sugar
tioner for children living in areas with a suboptimal
■ Several studies have shown that adding fluoride level of fluoride in the drinking water. Recently, the
to sugar and sugar products has potential to re­ recommendations of American Academy of Pediatric
duce the cariogenic effect of sugar or fermentable Dentistry [AAPD] and the American Academy of
carbohydrates among population groups, espe­ Pediatrics [AAP] have been revised by qualified
cially where it is impractical to use other fluoride health care providers as given in Table 6.16
vehicles. 42% reduction in caries was observed
in a 3 year clinical trial. (Luoma et al. 1979) Precautions to be considered
■ In Manipal department of pedodontics too, a clini­
cal trial conducted with fluoridated sugar rinse in ■ Before prescribing a fluoride supplement for a
children has shown a high potential in control­ child, a physician or dentist should know the
ling caries risk factors like salivary pH and child’s ace.
 <%%> I TEXTBOOK OF PEDODONTICS

■ The concentration of fluoride in the child’s deeply into enamel. These ions tend to provide only
‘primary source” of drinking water. local protection.
Generally infants are given fluoride drops with or
without vitamins, which are directly placed in the PROFESSIONAL APPLICATION
mouth or added as foods. Fluoride tablets are geh-~
erally prescribed after a child has a full comple­ When fluoride is applied to an enamel surface it dif­
ment of the primaiy teeth. The effectiveness of fuses inward by way of the less dense inter prismatic
fluoride drops or tablets is neither enhanced nor spaces to a depth related to its concentration, the
reduced by adding vitamins. However, there may treatment time, pH and the type of fluoride agent Fluo­
be increased compliance as a separate route is ride agent should not be swallowed while applied.
avoided when fluoride is prescribed in vitamins.
Procedure to be followed:
Prenatal fluoride supplements To reduce the likelihood of ingestion of fluoride dur­
ing a professionally applied topical application, the
Prior to 1966, fluoride was prescribed in prenatal sup­ following procedures should be kept in mind.
plements for potential caries prevention in teeth « Seat the patient in an up right position
where development begins in intrauterine life and at « Use trays with absorptive liners
birflt There was a belief that fluoride would cross ■ Limit the amount of the agent, for example during
the placental barrier and get acquired by the devel­ gel application, the gel is placed in the tray to no
oping teeth sufficiently to provide caries protection. more than 2 5 ml (one-half of a teaspoon)
; Legros et al [1983] reported that prenatal fluoride ■ Use suction during and after treatment
| protect the teeth by: ■ Have the patient expectorate thoroughly after the
| a. By affecting the morphology of teeth, promoting trays are removed.
the formation of smooth teeth with shallow
grooves and fissures. Commonly used agents in clinics for topical
i b. Enamel shows less depth of etching and is com- applications are discussed in Tables 6.17-18,
j posed of more densely placed enamel rods with 19*
| more mineralized apatite crystals and with a slightly
| better crystallinity. ?
f c. Recently, another school of thought is that di-
, etary fluoride supplements to pregnant women
can not be recommended because there is no con­
clusive evidence that it reduces dental caries in
the teeth of their offspring.

Fluorideoral rinse supplements

Fluoride oral rinse supplements provide both a sys­
temic and topical effect. The patient swishes the so­
lution producing a topical effect, and then swallows
the solution, providing a later systemic effect.

TOPICAL APPLICATIONS (Fig. 6.10)

Fig. 6.10 Various topical fluoride products.
Topical fluorides are directly applied to the erupted
teefli. Fluoride ions in such agents do not penetrate
 SECTION 6 : PREVENTIVE APPROACH TO CARIES CONTROL |

Table 6.17: Commonly us-ed-fluoride agents in clinics

_____________________ SOLUTION__________ g________

Amount 2% NaF (9,040 ppm) pH-7 8% SnF2 (19,360 ppm)

Method of * To prepare 2% Na F, dissolve * ‘O’ No. gelatin capsules are priorly

preparation 20 gms of NaF powder in 1 liter of filled with 0.8 gm, powdered SNF2
distilled water in a plastic bottle. and are stored in airtight plastic
* NaF should always be stored in containers.
plastic bottles. If. stored in glass *. To prepare 8% SNF2, content of one
containers, the *F of the solution can capsule is dissolved in 10ml of
react with the silica of glass forming distilled water in a plastic container
SiF2 reducing the-availability and then shaken.
of free active fluoride * SnF2 solution is to be prepared just
for anticaries action. before each application.
Technique of Knutson and Feldman technique Muhler (1957) technique.
application (1948) * Do a thorough prophylaxis.
* Clean and polish the teeth in only * Isolate a quadrant with cotton rolls
the first of four applications. arid dry the teeth.
* Isolate the upper and opposing * Apply the freshly prepared 8% SNF2
lower quadrant with cotton rolls. continuously to the teeth with cotton,
* Dry the teeth thoroughly. applicators.
* Apply the 2% NaF with cotton rolls * Reapply the solution to the tooth
applicators and allow it to dry on every 15-30 sec. So that the teeth
the teeth for about 4 minutes. are kept moist with the solution for
* NaF is applied once because once 4 minutes.
a layer of CaF2 (dorhinant product * Instruct the patient not to eat, drink
of reaction) gets formed it interferes or rinse for 30 minutes. This, helps
with further diffusion of F to react in prolonging the availability of F
with hydroxyapatitie. This is called to react with the tooth surfaces.
choking off phenomenon. ✓
* Instruct the patient to avoid eating,
drinking for 30 minutes.
,No. of * Second, third and fourth applicat- * Once per year.
application ions are done at weekly Interval.
per year * Application is recommended at 3,
*7, 11 and 13 years.
Advantages * Chemically stable * The rapid penetration of tin and
* Acceptable taste because of fluoride within 30 seconds.
neutral pH. * Highly insoluble tin-fluoro
* Non-irritating to the gingiva. phosphate complex forms on
* Does not discolor the teeth. enamel surface that is more
* Cheap and inexpensive. resistant to decay than enamel.
contd.
 I TEXTBOOK OF PEDODONTICS

Amount 2% NaF (9,040 ppm) pH-7 8% SNF2 (19,360 ppm)

Disadvantages * Patient has to make four visits to * Unstable in aqueous solutions and
the dentist within a relatively short should be prepared fresh for each
time. patient.
* Its naturally low pH (2.1 to 2.3) is
rather astringent and the solution
has a metallic taste.
* It may cause gingival irritation,
particularly to the dehydrated and
diseased gingival tissue.
* Produce discoloration of the teeth
particularly in hypocalcified areas.
* Causes staining on the margins of
restoration.

Mechanism of aciton: NaF

Ca10 (PO4)6 (OH)2 + 20 F —± 10 CaF2 + 6PO4~ + 2OH

CaF2 + 2Ca5 (PO4)3 OH 2Ca5 (PO4)3 F + Ca (OH)2

Mechanism of action: SnF2

Low concentration:
H Ca5 (PO4)3 OH + 2SnF —> 2CaF2 + Sn2 (OH)PO4 + Ca3 (PO4)2
;£
j

High concentration. V
5 Ca. (POX OH + 16SnF, —► CaF, + 2Sn,F.PO. + Sn7(OH)PO„ + 4CaF,(SnR),'
f
5 ' 4'3 2 2 3 3 4 2' '4 2' 3'2 e
I 2Ca5(PO4)3 OH + CaF2 —► 2Ca5(PO4)3F + Ca (OH)2

Table 6.18:

SOLUTION GEL
Amount 1.23% F APF (12,300 ppm) pH - 3.0 23% F APF (12,300 ppm) pH - 4 - 5

Method of * To prepare APF solution dissolve * To prepare $ gel, a gelling agent

preparation 20 gms of NaF in 1 liter of 0.1 M methylcellulose or hydroxyethyl
phosphoric acid. cellulose is to be added to the
* To this add 50% hydro fluoride solution and the pH is adjusted
acid to adjust the pH at 3.0 and *F between 4-5.
concentration at 1.23%.
contd.
 SECTION 6 : PREVENTIVE APPROACH TO CARIES CONTROL |

SOLUTION
. __________ A____________________________

Technique of Brudevold technique (1963) * Do a thorough prophylaxis and dry

applicaton * Do a thorough prophylaxis and the teeth.
isolate a quadrant with cotton rolls. * Fill the U/L tray with APF gel.
* APF solution is continuously and * Insert the U/L trays simultaneously
repeatedly applied with cotton into the mouth and have the patient
applicators. bite down tightly for 4 minutes.
* Keep the teeth moist for 4 minutes. * Thixotropic gel displays a high
* Pass the floss through each viscosity at low shear rates and a
interproximal embrasure to very tow viscosity at higher shear
ensure wetting of these surfaces. rates. The clinical importance of
* Repeat the procedure for this is that the gel thins out under
remaining quadrant. biting forces and more easily
* Instruct the patient not to eat, drink penetrates between the teeth.
or rinse for 30 minutes. Conversely, when it is not under
stress it remains in the tray and
does not tend to run down the
patient’s throat.
* Instruct the patient not to eat, drink
or rinse for 30 minutes.
No^ of applica­ * Semiannual * Semiannual
tion per year
Advantages * Fluoride uptake following the * Acceptable by the child due to
applicaton of APF solution is ^flavoured taste.
greatly accelerated whereas that * Easy to apply as with gel fluoride
following NaF is much slower. comes in constant contact with
50% more effective than NaF. teeth so re-appxlication is not
* APF solution is cheap, can be required.
prepared easily. * Can be self-applied.
* It is stable with a long shelf-life, * Thixotropic property.
when stored in an opaque plastic. * Caries reduction more than when
bottle. i compared to APF solution.
Disadvantages * Teeth must be kept wet with the * Can cause irritation to inflammed
solution for 4 minutes. gingival tissue and to the open
* APF solution is acidic, sour and carious lesion thus, it should be
bitter in taste so necessitates the applied only after restoration of all
use of suction. carious teeth.

Mechanism of action: APF

J?ja5 (PO4)3OH + 4H+ 5Ca++ + 3HPO4" + H2O (dehydration and shrinkage)

Ca++ + HPO4~ Ca.HPO4.2H2O (DCPD)

\ z (hydrolysis) (Di calcium phosphate dihydrate) (Intermediate product)

1 SCaklPO 9H n * r- --------r o /Dfi \ C a OUDH - X TU+X OU n

 | TEXTBOOK OF PEDODONTICS

Table 6.19:

VARNISH
* FOAM

Amount Bifuoride 12 (2.71% NaF, 2.92% CaF2) 0.92% F (9200 ppm) pH - 4.5

Method of * Commercially available * Commercially available

preparation (discovered by Schmidt in 1964) z
Technique of * Do the thorough prophylaxis and
application dry the teeth (do not use cotton for
isolation as varnish is sticky and
tend to stick to cotton)
* Drop the varnish onto the brush
or foam pellet.
* Paint the varnish thinly first on
the lower arch (as saliva collects
more rapidly on it) and then on
upper arch starting from the
proximal surfaces. Layers, which
are too thick, separate too easily
* Instruct the patient:
a. Not to rinse or drink anything
at ail for that day.
b. Not to eat solid for that day.
c. Take liquid and semisolids
f
till next morning.
d. Not to brush that day. f
No. of applica­ Semiannual application Semiannual application
tions per year
Advantages * Forms a watertight protective film * It is less dense than gel and is able
insulating against thermal and to flow better, allowing a free movement
chemical influences. of the fluoride ion on the tooth
* With correct application and proper surface and interproximal areas.
mouth hygiene varnish remains * Total density by weight is less than
in place for several days. During gel application. This reduces the
this time fluorides act on the risk of ingestion and systemic
treated surface. toxicity of fluoride.
. Disadvantages * Patient compliance is required. * Retention on to the tooth surface
is less as no polymers are added.

* Other varnish preparation: Duraphat (Germany), Fluorprotector (Lichenstein), Fluoritop (India)

Mechanism of action: Varnish

10Ca5(PO4)3OH + 10F- 6Ca5(PO4)3F + 2CaF2 + 6Ca3(PO4)2 + 10OH
2Ca5(PO4)3OH + CaF2 2Ca5(PO4)3F + Ca (OH)2
 SECTION 6 : PREVENTIVE APPROACH TO CARIES CONTROL I

Otherfluoride applications (by the professional) ■ Fluoride containing varnish and sealants were
considered of potential value in Pedodontic
1. Fluoride impregnated prophylaxis paste and cup practice. A poly^ethane based material con­
The temperature of enamel surface is raised dur­ taining 10% sodium monofluorophosphate
ing a prophylaxis because of the friction between commercially available as “Expoxylite 9070” has
the prophylaxis cup and the tooth. High tempera­ shown 36.6% less carious surface on first per­
ture enhances the uptake from fluoride contain­ manent molar.
ing prophylaxis paste or solutions (Putt et al 1978). ■ Glass ionomers are the recent innovation which
It is therefore reasoned that if a fluoride impreg­ seem to dominate the other materials because
nated prophylaxis cup or paste are developed, of their fluoride leaching property.
fluoride would be released under optional condi­
tions. Laboratory evidence have also confirmed SELF APPLIED TOPICAL APPLICATIONS
that prophylaxis cup made from a blend of ther­
moplastic resins and impregnated with sodium Fluoride Dentifrices
fluoride and stannous fluoride will increase the
fluoride content of enamel. When fluoride con­ Fluoride containing tooth pastes now account for
taining prophylaxis pastes are used, the effects approximately 85% ofdentifrices market in the world,
were generally found to be similar whether a con­ especially in the USA. The Council on Dental Thera­
ventional or fluoride impregnated prophylaxis cup peutics of the American Dental Association currently
was used (Stookey and Statiman, 1976) recognises few caries preventive dentifrices with
ADA seal acceptance. They all contain between 1,000
2. Iontophoresis and 1,500 ppm fluoride formulated from either so­
It is based on a theory that small electric current dium fluoride or sodium mono-fluorphosphate and
will help to drive fluoride ion further into the none contains stannous fluoride.
dental enamel, producing the desired effect, re­
duced enamel solubility, increased fluorapatite for­ Advantages
mation, reduced dentine sensitivity and even steri­ /
lization of root canals. Because fluoride dentifrices usually are used regu­
larly two or three times a day, they provide a frequent
3. Dental materials containing fluoride source of fluoride in low concentration that can in­
Several studies were conducted to see the hibit demineralization and enhance remineralization.
cariostatic effect of dental materials containing
fluoride and a highly significantly fluoride up­ Availability
take by enamel was recorded that was placed in
contact with the materials. Fluoride dentifrices are available and recommended
■ Carboxylate cements are now used more ex­ for the people of all ages whether they live in fluori­
tensively for cementation of crowns and or­ dated or non-fluoridated areas.
thodontic bands.
■ Fluoride in amalgams have also been tried. Precautions to be considered
Jerman (1970) added 1.5% of stannous fluo­
ride to silver amalgam alloy and noted that the ■ Preschool age children should be supervised
enamel surface placed in contact with this al­ while brushing to avoid ingestion of excessive
loy showed a significant reduction in enamel amount of paste.
acid solubility. ■ Only a dab or pea- size amount ofdentifnoeshould
be used by six years of age or below.
 Îflîïïl | TEXTBOOK OF PEDODONTICS

■ A ribbon of dentifrice that covers the bristles of mal surfaces receive the benefit of additional fluo­
an adult-sized toothbrush contains about one ride dental flossing, this may increase its value as a
gram of dentifrice. Swallowing the amount of fluo­ caries preventive aid.
ride which is present in this toothpaste should be
avoided. Gillings (1973) utilizing sodium fluoride and stannous
■ At least one brushing with fluoride tooth paste fluoride successfully developed and patented sev­
should be done just before bed time, placing fluo­ eral formulas of fluoride of fluoridated dental floss.
ride in the mouth prior to a period of low salivary Because of the unknown sample size and the lack of
flow thus prolonging fluoride availability (Table clinical size and date, no definitive conclusions about
6.20) this cariostatic effect could be made.

Table 6.20 Use of fluoride tooth pastes Fluoride rinses

Child age Recommendations for use of fluori­ Fluoride mouth rinses for school based health
u
'I
de tooth paste programs or in home are currently popular as a
:F
simple way to expose teeth to fluoride frequently.
h
Below 4 Fluoride tooth paste is not recomm­
The early trial with neutral sodium fluoride, acidu­
years ended
-s-
lated phosphate fluoride and stannous fluoride rinse
' 1 4 to 6 Brushing once daily with fluoridated proved to reduce caries by 20 to 50 percent.
■’
G ■?
•A À
years toothpaste and other two times with
; ; J
a non-fluoridated toothpaste. Amount of Fluoride in Self Applied Fluoride
• A
Rinses are given in Table 6.21
j£ ÿ
■ $
6 to 12 Brushing twice, daily with fluoridated
kj
years toothpaste and once with a non­ z.

Usually non-prescribed fluoride mouth rinses con­

fluoridated toothpaste.
■ ■ t
n
tain 0.05% NaF (about 225 ppm). They should be
Above Brushing three times with fluoride swished vigorously once a day for bne minute and
£
12 years toothpaste. expectorated. Prescription fluoride rinses generally
contain 0.2%. NaF (about 900 ppm). They are de­
signed to be used under supervision, once a week
fluoride Impregnated Dental Floss
for one minute.
Dental floss is an essential part in the plaque control
intheinterproximal enamel surface. Iftheinteiproxi-

Table 6.21 : Amount of fluoride in self applied fluoride rinses

Program Agent Frequency Fluoride Volume used Amont of

Concentration fluoride

Home 0.05% NaF Daily 0.023% 10 ml 2.3 mg

0.044% APF Daily 0.02% 10 ml 2.0 mg
0.01% Snf2 Daily 0.024% 10 ml 2.4 mg
School 0.2% Naf Weekly 0.09% 10 ml 9.0 mg
 SECTION 6 : PREVENTIVE APPROACH TO CARIES CONTROL |

Precautions to be considered:Children under five 70kg or about 1.0 to X0 gm sodium fluoride for a
years and some handicapped children may swallow child of 15 kg. Amount less than this, however, can
the rinse rather than spit it, hence mouth rinses are cause:
not recommended for them. ■ Nausea
■ Writing
Sustained release fluoride » Diffuse abdominal pain
■ Diarrhoea
Constant exposure of teeth to low levels of fluoride ■ Excess salivation
has been found to be more effective in reducing car­ ■ Thirst
ies by remineralization of incipient carious lesions. ■ Muscle tremors
The objective of sustained release fluoride is to pro­
vide a regular release of fluoride slowly intra-orally Treatment
fora longer period.
■ Vomiting should be induced with a syrup of ipeac
or digital or mechanical by stimulation of tongue
A number ofdental materials containing fluoride have
or throat.
been develop as cements, acrylics and resin while
a Subsequent effects should be made to decrease
intra-oral devices used are copolymer membrane
the absorption offluoride by administering fluo-
beads and glass pellets. (Refer appendix 14b, c)
ride binding liquids like warm water, Calcium hy­
droxide liquid, antacid containing aluminum or
FLUORIDE TOXICITY
magnesium hydroxide or milk.
a The affected individual should be hospitalized
Accumulated evidence from numerous studies shows
and stomach should be thoroughly washed with
that the prolonged use of fluoride at recommended
additional lime water
levels does not produce harmful physiological ef­
a At the sigp of a muscle tremor calcium gluconate
fects in human. Dental fluorosis which has been
should be administered intravenously, along with
found to be true in individuals consuming drinking
saline to prevent a shock
water containing upto 8-0 ppm fluoride, about eight
times the recommended amount. In India many of the
Chronic toxicity
states have been identified with some circumscribed
areas of high fluoride level and are marked as en­ Chronic toxicity is due to a long term ingestion of a
demic fluoride belts (Fig. 6.11). These areas are hav­ smaller amount of fluoride which usually effect the
ing ground water with more than 4.00 ppm. * hard tissue and kidney.

Dental fluorosis occurs in human being consuming Table 6.22 Chronic toxicity effects of excessive fluo­
water containing 2.0 mg/lit or more of fluoride par­ ride ingestion
ticularly during first eight year of life. Skeletal
fluorosis can occur if water contains more than 4 Effect Dosage Duration
ppm fluoride and is consumed regularly.
Dental 2 time optimal Until 5 years
fluorosis (Excluding third
Acute Toxicity molars)
Skeletal 10-25 mg/day 10-20 years.
Ingestion of an acute fatal dose of fluoride is very
fluorosis
rare. The amount of 35 to 70 mgF/kg body, weight of
soluble fluoride is to be lethal. This is equivalent to 5 Kidney 5-10 mg/day 6-12 months
a
Fig. 6.11
 SECTION 6 : PREVENTIVE APPROACH TO CARIES CONTROL |

Table 6.23a Lethal and safe dosages of fluoride Methods

for a 70kg adult
* f
To reduce the fluoride concentration to less than
■ Certainly Lethal Dose (CLD) 5-10 gm NaF 1 mg/L, which is suitable for health in drinking water,
or depends on the materials and methods used.
32- 64 mg F/kg Defluoridation methods using organic or inorganic
substances nowdays are available.
■ Safely Tolerated Dose (STD) = % CLD
1.25-2.5 gm NaF 1. Adsorption and ion exchange method
or. Some substances adsorb fluoride ion by the sur­
8-16 mg F/kg face, arid it canbxchange its negative ions such
as OH
* group for fluoride ions. Thus the concen­
Table 6.23b CLD’s & STD’s of fluoride of selected tration of fluoride in water decreases. This proc­
ages* ess depends on suitable conditions like pH, tem­
perature, flow rate, grain size of the material. Some
Age Weight (lbs)° CLD (mg) STD (mg) of the commonly used materials are:
22 320 80 Activated Alumina (Al? O3), Fluidized Activated
2
4 29 422 1Ô6 Alumina, Activated Bauxite (Hydrate of A1 (OH)3),
6 37 538 135 Zeolite (NaO2. A12O3), n SiO3x H2O, Tricalcium
8 45 655 164 phosphate (Ca 3(P04)2orTCP), Superphosphate
10 53 771 193 (COHPOj-bCaSOJ,Activated bone char (Ca10
12 64 931 233 (PO4)8 OH2).Magnesite(MgOO3)
14 83 1,206 301
1,338 334 ^Activated Carbon, Palan Carbon, Charcoal, Clay
16 92
18 95 1,382 346 and Soil, Bricks.

* 3rd percentile of the normal age-specific weight distri­ 2. Precipita/ion Method

bution. In a high pH condition, co^recipitatipn of sev­
eral elements in water with fluoride ions forms
Table 6.24 Common signs and symptoms of fluoride salts. Sometimes, it may cause
acute fluoride toxicity* flocculation if the substance used is Aluminium
ions. Thus, the fluoride concentration in water
Low dosages High dosages decreases. A well known substance of this group
■ Nausea ■ Convulsions is Alum, which is used in water supply systems
■ Vomiting ■ Cardiac arrhythmias and water treatment. These substances include:
■ Hypersalivation ■ Comatose Alum(KAl(SO4)2.12H.O), AlumandJimgfCaO)
• Abdominal pain Lime Softening (Ca (OH)2), Calcium chloride (Ca
■ Diarrhea CI?)
3. Methods based on membrane separation
* Stanley and Herschel (1984)
In the industrialized world 'reverse osmosis* pipc-
ess is well known. All elements in water get <|L
DEFLUORIDATION
minishedafter filtration. This method is claimed
to be the best water purification process avail­
Defluoridation is a scientific means to improve the
able. This method seems to be expensive for de­
quality of water with high fluoride concentration by
veloping countries as 30% of raw water is lost in
adjusting the optimum level in drinking water
the process.
 I TEXTBOOK OF PEDODONTICS

INDIAN TECHNOLOGY FOR DEFLUORIDATION ■ The chemicals are same as those used in a
muncipal urban water supply.
Nalgonda Technique ■ It is cost effective.
■ Designs are flexible to use at different location.
This technique first developed in India in 1975, is the ■ Defluoridation meets with standard laid down by
most simplest, the least expensive and the easiest to. the Bureau of Indian Standard (fluoride content
operate of all the other methods of defluoridation. less than Img/L).

Using Lime and Alum Combined Nalgonda and Calcined Magnesite

technique
National Environmental Engineering Research Insti­
tute (NEERI), Nagpur has been involved in In Tanzania the calcined magnesite technique and
defluoridation research since 1960 s. One of their Nalgonda technique both were introduced as a flow
work which could be successfully transferred from system of a pilot plant for experiments in 1985 and
laboratory to the field and implemented in Nalgonda completed in 1990. In this plant the Nalgonda tech­
Technique. The first community plant for removal of nique was passed through a filter bed consisting of
fluoride from drinking water was constructed in the calcined magnesite granules. Fluoride was absorbed
district of Nalgonda in Andhra Pradesh., in the town by the calcined magnesite granules thus further re­
of Kathri, thus the name of the technology. ducing fluoride concentration. However, there was a
rise in pH over 10.0 and the treatment water needed
Procedure adjustment before being drunk. This method is found
impractical for rural regions as calcined magnesite
Raw water is mixed with adequate lime and alum. The needs to be regenerated.
amount of lime depends on the alkalinity of the raw
water. If the raw water has adequate alkalinity, the Prasanti technology
i
lime addition is not required. Alum solution, is added
after theaddition of lime, stirred gently for 10 min­ In Indian villages this method of utilizing Activated
utes and the flocs formed are allowed to settle. This Alumina is found to be most popular and cost effec­
process of floc formation, and setting requires an tive material for defluoridation. It originated as a re­
hour. ~~ sult of research carried out by the Bio-Science, De­
partment of Satya Sai University for Higher Learning
Domestic use in Prasant Nilayam, Anathapur District, Andhra
Pradesh, at which 25 community defluoridation plant
In rural areas this method is advised for domestic were constructed, each serving 200-400 people in
use of defluoridation of drinking water as required. location and have been functioning since 1998. Be­
The advice is given to mix water with lime and ahimiru sides the community plants, approximately 500 do­
a closed big vessel and leave it overnight so that mestic defluoridation filters are being used by peo­
next morning the clean supernatant is decanted for ple living in endemic area.
use and is safé for tansumption
Other materials tried in India
Advantages of Nalgonda Technology
■ Fish bone charcoal
■ This method can be used both at domestic and Researches of the University of Roorkee suggested
community levels. practical application of Fish bone charcoal as a
« Operations are possible manually. comparatively cheaper and mix effective materials.
 SECTION 6 : PREVENTIVE APPROACH TO CARIES CONTROL |

■ Drumstick plant (Moringa Cleifera) 13. What is anti-enzymatic action of topical fluorides?
Was also, used as an alternative to defluoridate 14. How fluoride renders the enamel more resistant
drinking water as it is easily accessible (could be to acid dissolution through systemic action?
seen in the house hold of rural and Urban) and it 15. How does fluoride bring about remineralization
has been widely used tb reduce water turbidity of incipient caries?
because of its excellent coagulating and clarify­ 16. Name the modes of administration of fluorides?
ing properties. The defluoridation efficiency of 17. Who introduced topical application of NaF in
the seeds of drumstick could possibly be due to dentistry ?
calcium and magnesium levels in the plants. 18. What is the technique of application of 2% NaF
called as ?
■ Askali - extract mycetial biomass 19. How much of fluoride solution is required for topi­
Researchers from Osmania University, cal application of full mouth?
Hyderabad, have demonstrated the ability of this 20. What is the choking-off effect?
- material from Aspergillus riger to bind fluoride 21. What is the method of preparation of 2% NaF
from fluoride containing water but the mechanism solution?
is still not clear. 22. What is fittydent?
23. Instructions to be given after NaF application ?
■ Clay Minerals 24. What is the technique of application of stannous
Two fluoride sorption Clay materials : fluoride called as?
montmoslloniteKSF, Kaolin and a Silty Clay Sedi­ 25. What are byproducts released after SnF applica­
ment Series (used in making pottery) were tried tion?
for defluoridation. 26. Which is the byproduct that makes the tooth
stronger to acid dissolution?
■ Tricalcium Phosphate (TCP) 27. What is the frequency of 8% SnF application ?
The TCP may be able to produce a complex chemi­ 28. What is APF and what is the technique of appli­
cal reacting mechanism in defluoridation which cation called as?
needs energy. 29. What is the difference between APF gel and APF
solution?
Self-Assessment 30. WhatisDCPD?
31. What do you mean by thixotropic property?
1. What is fluoride? 32. What are the commonly used fluoride varnishes?
2. What are Colorado stains? 33. What are the composition ofcommonly used fluo­
3. What do you mean by the term mottling ? ride varnishes?
4. Who are Mckay and Martin ? 34. What are the technique of application ofduraphat,
5. What are the causes of mottling? * fluorprotector and Bifluoride -12 ?
6. WhowasDr. H.V Churchill? 35. What are the advantages of fluoride varnish?
7. Who conducted the shoe leather survey and 36. Name some fluoride mouth rinses.
where it was done? 37. Name the fluoride containing dentifrice in the
8. Who is called the father of fluorides in dentistry? Indian market?
9. What was the recommendation for fluoride in 38. What is tiie a
drinking water for its caries prevention? dentifrice?
10. What are the sources of fluorides? 39. What is the mechanism of action of sodium
11. What is the plasma half-life of fluoride? monofluorophosphate?
12. List out the systemic and topical actions of fluo­ 40. List the recommendations for use of fluoridated
rides tooth paste in children.
 €03 I TEXTBOOK OF PEDODONTICS

41. Define fluoridation and defluoridation. 51. What are fluoride tablets?
42. When was the water fluoridation started and in 52. Name some commercially available fluoride tablets?
which cities? 53. What is the daily dose of fluoride tablets?
43. Name the milestone studies in water fluoridation 54. What are the two types of fluoride toxicity?
44. What is the optimum level of fluoride in water? 55. What are the clinical features of fluoride toxicity?
45. What are the types of water fluoridation? 56. What are GLD and STD for fluorides?
46. What are the endemic fluoride areas in India? 57. What are the emergency treatments for acute fluo­
47. Why is water fluoridation is not effective in India? ride toxicity ?
48. Who introduced milk and salt fluoridation ? 58. Name the defluoridation methods.
49. Why salt fluoridation is a viable method of sys­ 59. What are anion and cation exchange resins?
temic fluoride ingestion? 60. What is the Nalgonda technique?
50. What are fluoride drops?
 6.6 Methods on the Horizon

Tandon S

A lot of research has been directed towards efforts 2. Altering surface morphology/Increasing tooth
to develop methods to prevent caries, which have resistance
ranged from simple to highly sophisticated tech­ A so called ‘surface active polymeric agents for
niques. These current approaches are still under trial, surface adhesive binding has been developed
and based on three prong-strategies. by Bowen et al [1995] comprising of application
1. Combating caries inducing micro-organisms in 2 stages for increasing tooth resistance to den­
2. Increasing tooth resistance against acid attack tal decay.
3. Modifying cariogenic diet ingredients ■ Monomer which would have a chemical bond
followed by
« A polymeric top coat which would enhance
1. Antiplaque agents.
durability and esthetics.
The role of plaque in the formation of dental car­
■ Tooth resistance is improved using two steps
ies is well documented. Thus anti bacterial and
procedure by enhancing the fluoride uptake in
anti adherence agents are being tested as a plaque
enamel. This method involves initial applica­
building blockers.
tion of an acidified calcium phoshate solution
■ The enzyme glucosyltranferase [GTE] may be
followed by suitable fluoride solution. Such a
inhibited by the use of analogues of sucrose
two component system can be used as a pro­
interfering with glucan synthesis.
fessional topical application or self applied
■ In the recent times some plant and fungal prod­ mouth rinse or alternately using chewing gum
ucts that alter the adhesion of cell surface of an amorphous calcium phosphate ( ACP)
glucans are also being identified. In this con­ and tooth paste containing fluoride.
text, cheaper modalities that are accessible to
the masses are being tested in the form of in­ 3. Lasers
digenous products. Rajesh et al [1997] tested ■ CO2 lasers can be used to alter the tooth sur­
the efficacy of Mango leaf, Neem leaf and Tea face of enamel and make it less prone to caries.
K extracts and found that all the three products Concern however exists regarding the depth
i were effective in reducing the plaque forma­ control and optimum irradiation conditions.
tion as well as the streptococcus mutans count. Pits and fissures and root surfaces may be the
■ The antibacterial products may have the draw­ areas targeted by the lasers.
back of being rapidly eliminated from the oral
cavity and for this purpose, Controlled Release 4. Benign microorganisms/ Replacement therapy
Devices [CRD] or polymers are being used to • Using the ‘Use a thorn to draw a thorn ‘phi­
increase the substantivity in the oral cavity. losophy, an approach would be to supersede
the cariogenic bacteria by more benign ones.
 | TEXTBOOK OF PEDODONTICS

■ The dominant acid [lactic acid] produced by peutic agents such as urea may be recom­
S. mutans is controlled by a gene which can be mended in high risk caries children.
mutated.
■ Genetic engineering provides a better alterna­ 7. Tooth friendly sweets
tive producing inactivated forms and then clon­ Use of noncariogenic sweeteners have proved to
ing it, for example, a new approach is being be excellent measures in the control of caries. A
used to transfer the genes from bacteria that short term plaque study was undertaken by
naturally produces enzymes such as mutanase Tandon et al (1997) to evaluate effect of lactitol 4-
which degrades the extra-cellular sticky poly­ O (b- Galactosy) -D-glucitol on plaque by incor­
mers involved in plaque adhesion and build porating it as a sweetener in biscuits. Significant
up into bacteria such as streptococcus reduction was found in plaque formation, carbo­
gordoni. hydrate content, increase in calcium, phosphate
■ An attempt to transfer arginine diminase gene, and protein with lactitol when compared with the
which produces base in S sanguis, into S control.
mutans , to counter its acidogenic potential
has been made. 8. Microdentistry
Here treatment begins before conditions arise. It
5. SAP (Self assembling polypeptides) enables the use of a microscope to detect condi­
Preliminary reports have suggested the use of tions invisible to the naked eye. This can again
self assembling polypeptides [Strafford et al 1999] be used as an educational and motivational tool
for augmentating host resistance. These may be by helping the patient observe his own oral con­
useful in promoting enamel remineralization, pre­ ditions. For example, letting the patient see the
sumably as a result of their nucleating potential. microorganisms in the plaque
Following incubation in the mineralizing solution,
large crystal deposits were found within the SAP. 9. Teledentistiy
These protective peptides are used as pacifiers It is the provision of dental care where the patient
for young children to help modify the bacterial and provider are not physically ip the same loca­
flora againt baby bottle caries. These peptides tion. This is a relatively new field of study, which
have also been used in mouth rinses and denti­ can also be used as an adjunct iit providing pre­
frices. ventive home care advices.

6. Chewing gums 10. Indigenous products

« A novel technique involves the use of chew-' Recently a lot of emphasis has been placed on
ing gums after meals in order to counter the the utilization of the rich natural resources present
pH drop that occurs with the intake of sugar. in India. In this context studies have been con­
Various sugar free gums have been tried out, ducted on the use of various products such as
with additions such as xylitol, lactitol and Urea. Mango leaf, Neem and Tea. These have been
■ A clinical trial conducted by Gopinath and found to have antiplaque and anticariogenic po­
Tandon [1996] compared the plaque pH change tential.
in the groups using urea, fluoride and sugars.
The results indicated that the chewing gum CARIES VACCINE
containing urea showed the highest pH fol­
lowed by fluoride and sugar. Thus the study Preventive dentistry has taken long strides in the
concluded that chewing gum containing thera­ direction of eliminating dental diseases. In this
*Wïg SECTION 6 : PREVENTIVE APPROACH TO CARIES CONTROL | €EE)

|ptfae; caries vaccine has generated a good The various routes that have been tried out include:
sm. This modality of treatment can L Oral route t
t the occurrence of caries on a large scale. Systemic route
Active gingivo-salivary route
îtion Active immunization

a suspension of
_^^^fcdor killed micro-organisms administered for Oral route
^^^^^vention, amelioration or treatment of infoc- The oral route of administration has concentrated
J^Ssdiseases’. [Stedman’s dictionary, 1990]. on stimulation of the secretory IgA antibodies
via the common mucosal system [consisting of
S|^|||g'<oicept of a vaccine can be visualized primarily MALT and GALT], which is activated in the spe­
the recognition of mutans streptococci as the cial cells of the intestinal tract.
key microorganisms in the development of caries.
Thus efforts have been directed at preventing its For the colonization of streptococcus mutans in
colonization in the oral cavity oral cavity, the enzyme Glucosyltransferase is of
paramount importance. Thus several studies have
How it works been carried out using it
The basis of a vaccine is that it keeps the patient in a
The disadvantages associated with the oral route
state of readiness such that in case an infection does
of delivery is the rapid breakdown of the protiens
occur, the immune response [i.e. the secondary im­
or peptides. But it also considered safer than the
mune response] which is more rapid and effective
systemic route due to the concern of cross reac­
can be mounted. Thus during the first response, both
tivity to the streptococcal antigens.
B and T lymphocytes form memory cells that later
"remember6 the earlier attack and respond muchbet-
2. Systemicroute
Subcutaneous administration of S.mutans has
been tried out in monkeys and it elicited predomi­
The main immunoglobulin in saliva, as in any other
nantly IgG, IgM and IgA antibodies. These were
secretions in the body, is the secretory IgA. On the
found to enter the oral cavity through the gingival
other hand the IgG is present in very low concentra­
crevicular fluid.
tions. The significance of antibodies in the protec­
tion against dental caries lies in that, the presence of
3. Active gingivo-salivary route.
|levels of antibodies in the gingival fluid has
J^n correlated with low levels of caries. Also the 1" There has been some concern expressed regard­
ing the side effects of using these vaccines with
J^B^hocytes, in caries free subjects, have been found
the other routes, hi order to limit these potential
to possessT lymphocytes with greater potential for
side effects, and to localize the immune response,
W antigenic stimulation with S. mutans than caries
the gingival crevicular fluid has been used as the
route of administration. Apart from the IgG, it
also associated with increased IgA levels.
juries ofadministration.
In general, two schools of research have evolved.
The various modalities tried out were:
One concerned with IgG and systemic vaccination
■ Direct injection oflyzozyme into rabbit gingiva
using a cell wall constituent of S. mutans, while the
which has elicited local antibody forming cell
other with the oral route of vaccination and stimula­
response.
tion of IgA.
 | TEXTBOOK OF PEDODONTICS

■ BrusliingliveS.mutansontotliegingivaofrhe- tively target the cells to where it should reach.

sus monkeys[ which failed to induce antibody These liposomes are closed vesicles with
formation] bilayered phospholipid membrane. The effi­
■ Using smaller molecular weight streptococci cacy using liposomes has been found to in­
antigen, which resulted in better performance, crease two fold in a rat model. In humans in­
probably due to better penetration. creased IgA Antibodies have been found.

4. A dive immunization: ■ Passive immunization

Various new approaches have been tried out in As the name suggests, passive immunization
order to overcome the existing disadvantages. involves passive or external supplementation
of the antibodies. This carries the disadvan­
■ Synthetic peptides: tage of repeated applications as the immunity
Any antigen derived from animals or humans conferred is temporary.
has the potential for hypersensitivity reaction.
The chemically synthesized peptides hold an Several approaches tried out are:
advantage in that this reactivity can be ■ Monoclonal antibodies
avoided. This has also been found enhance Monoclonal antibodies to the S.mutans cell
the immune response. In humans synthetic surface antigen I/II has been investigated. The
peptides elicited both IgG and T-cell prolifera­ topical application in human subjects brought
tive response, and the antibodies were both a marked reduction in the implanted strepto­
anti-peptide and anti-native. coccus mutans. Thus by bypassing the sys­
tem less concern exists about the potential
The synthetic peptides give antibodies not side effects.
only in the gingival crevicular fluid but also in
the saliva. The synthetic peptide used is de­ ■ Bovine milk and whey
rived from the Glucosyl tranferase enzyme. [Pu­ Systemic immunization of cows with a vaccine
rified water soluble and insoluble]. using whole mutans streptococci lead to the
bovine milk and whey containing IgG
■ Coupling with cholera toxin subunits antibodies.This was then added to the diet of
It has been found that coupling of the protein a rat model. The immune whey brought a re­
with nontoxic unit of the cholera toxin was ef­ duction in the caries level.
fective in suppressing the colonization of strep­
tococcus mutans. This approach was tried out This whey was also used in a mouth rinse by
as the cholera toxin effectively binds to the Filler et al[l 991 ]. This resulted in lower per­
lymphoid cells and functions as an excellent centage of streptococcus mutans of plaque .
adjuvant. The intra-oral route of administra-
tionwas tried outfKatz, 1993]. ■ Egg-yolk antibodies
The novel concept of using hen egg-yolk anti­
■ Fusing with salmonella
bodies against the cell associated glucosyl
The avirulent strains of salmonella is an effec­
transferase of S. mutans was introduced by
tive vaccine vector so that fusion using
Hamada [1990]. Vaccines used were formalin-
recombinant techniques have been used.
killed whole cells and cell associated glucosyl
■ Liposomes transferase in the other. Caries reduction has
These have used in the delivery of several, been found with both these treatments.
particularly anticancer, drugs so as to effec­
 SECTION 6 : PREVENTIVE APPROACH TO CARIES CONTROL |

• Transgenic plants 3. Bardsen A; Bjdlvatn K : Risk factors in the de­

Latest in these developments in passive im­ velopment of dental fluorosis. Clin Oral Investig.
munization is the use of trangenic plants to 2,155-60,1998
give the antibodies. They have the advantages 4. Basil G., The cariogenicity of snack food and con­
that: fections, JADA, W. 90,121-132,1975.
- The genetic material can be easily ex­ 5. Bibby B.G., Enamel demineralization by snack
changed. foods, JDR, Vol. 54,881-890,1975.
- It is possible to manipulate the antibody 6. Brambilla E et al: Caries prevention during preg­
structure so that while the specificity of the nancy : Results of a 30-month study. J Am . Dent
antibody is maintained, the constant region Assoc. 129,871-877,1998.
can be modified to adapt to the human con­ 7. British Paedodontic Society: A Policy Document
ditions, thus avoiding cross reactivity. for Fissure Sealants, BDJ, ,42-3,1987.
- Large scale production is possible as it 8 Chad Lee,Teaching parents at WIC clinics to ex­
would be quite cheap. amine their high ride babies,JDC, 347-9,1994.
9. Feigal RJ, Sealants and preventive restorations;
■ An apple a day keeps the tooth doctor away review of effectiveness and clinical changes for
Researchers are working on ways, to inject a improvement. PedDent. 20(2),85-92,1998.
peptide - a fragment of a protein that blocks 10. Gawronsky T.H, Effects of dietary sucrose levels
the bacterium streptococcus mutans which on extracellular polysaccharide metabolism of
causes tooth decay into the fruit so that cavi­ dental plaque, JDR, Vol. 54,881-890,1975.
ties and painful visits to the dentist could be­ 11. Geopfaerd S. J: An infant oral health program: the
come a thing of the past. first 18 months Pediatr. Dent. 9(1):8-12,1987
12. Griffen Ann L. .Preventive oral health care for the
British scientists at Guys Hospital in London infant,child and adolescent,Pediatric Oral Health,
have already isolated a gene and the peptide Oct,1209-1226,1991.
that prevents the bacterium from sticking to 13. Holt RD, Maynihan PJ.: The weaning diet and
the teeth. Professor David James (2000), a plant dental health. Br. Dent. J. 181:254-258,1996
biotechnologist at the Horticulture Research 14. Infant oral health care: Pediatr. Dent. Special Is­
International in Southern England, is trying to sue: Reference Manual 18(6):25,1996-97
find ways to deliver the peptide into the mouth' 15. Jensen M.E.: diet and dental caries, DCNA.43(4),
through apples or strawberries. 615-634,1999.
16. Johnsen K., Siegel M: Resources for improving
Though some difficulties are being faced
* at the oral health of maternal and child populations.
the present, caries vaccine is certainly a very J. Pub. Health Dent 50 Special (6):418-26,1990
vibrant issue. The potential implications are 17. LimebackH., Introduction to the conference. Com­
enormous and should be pursued with the same munity Dent. Oral Epidem, 27,27-30,1999
vigor as before. 18. Long M.H., Hsai L.S.: The role of the CNM in
newborn management J. Nurse, Midwideiy.
Further Suggested Reading For Section - 6 1992,37 (suppl) :8S-17S, 1992
19. Meiers J.C., Management of the questionable
1. Banting D W: International fluoride supplement carious fissure: invasive Vs noninyasive
recommendations . Community Dent. Oral techniques,JADA, W. 108,64-70,1984.
Epidemiol .27,57-61,1999 20. Mitchell L. and Gordon P.H., Fissure sealant- Re­
2. Barcoiiey Linda S.,Parental influence on child pref­ cent development, Dental Update, vol.7,299-301,
erence of a dentist,JDC, March-April, 101-9,1986. 1990.
 | TEXTBOOK OF PEDODONTICS

21. Moore C.E., Pit and fissure sealants; one more 30. Stephen K W et al: Effect of fluoridated salt in­
time, J AD A, Vol.54,729-30,1988. take in infancy: a blind caries and fluorosis study
22. Newbrun E and others. Comparison of dietary in 8th grade Hungarian pupils. Community Dent
habits and dental health of subjects with fruc­ Oral Epidemiol.27,210-215,1999
tose intolerance and control subjects, J AD A, Vol. 31. Tandon S., Kumari R., Udupa S., The effect of
101,619-626, Oct 1980. etch time on the bond strength of a sealant and
23. Nowak A. J., Casamassimo P.S.: Using anticipa­ on etch pattern in primary and permanent enamel,
tor}' guidance to provide early dental interven­ JDC, Vol. 56, 186-90,1989.
tion. J. Am. Dent. Assoc. 126-1156-63,1995 32. Tandon Shobha,Infant oral health care,Kerala
24. Ripa L. W., The current status of pit and fissure dental journal. Vol 20,No. 4,115-122,1997.
sealants, J CanndDent Assn, No. 5,367-77,1985.
33. Tewari A., Gauba K., Goyal A.: Evaluation of the
25. Rock W P ; Sabieha A M: The relationship be­
change in the knowledge of community regard­
tween reported toothpaste usage in infancy and
ing infant dental care subsequent to intervention
fluorosis of permanent incisors . Br. Dent. J .
strategies through existing health monpower in
183,165-170,1997
rural areas of Haryana (India) Ind. Soc. Pedo. Prev.
26. Schneider Howard S.,Parental education leads to
Dent. 12:29-34,1994
preventive dental treatment for patients under age
of 4yrs,JDC, Jan-Feb,33-7,1993. 34. Warren D P ; Chan. J P : Topical fluorides ; effi­
27. Sethi B., Tandon S: Caries pattern in preschool cacy, administration and safety. 45,134-40(1997]
children J.J.D.A. 67:141-145,1996 35. Warren J J; Levy S M: A review of fluoride den­
28. Simon Katz, A diet counseling programme, JADA, tifrice related to dental fluorosis . Ped Dent
Vol. 102,840-845,1981. 21,265-271,1999
29. Slavkin H.G. : First encounters; Transmission of 36. Workshop on guidelines for sealant use: Recom­
infectious oral diseases from mother to child. mendations, Journal of public health dentistry,
J.A.D.A. 128:773-778,1997 Vol.55.No.5,special issue,263-73, 1995.

I
 SECTION - 7

Pediatric Restorative
Dentistry
7.1 Introduction
Mount G J

Introduction On the basis of the recent concept of caries which is

discussed elsewhere it is now apparent that it is pos­
There is no doubt that prevention is better than cure sible to remineralize and heal a carious lesion, to at
and this is never more so than in relation to restora­ least some degree, so complete removal of extensive
tive dentistry for children. The problems multiply rap­ areas of natural tooth structure is no longer required.
idly when a young patient begins to show signs of It addition there are now tooth coloured restorative
active caries and, in view of the small size of the materials which will adhere very effectively to natu­
tooth crowns, it is essential that treatment be under­ ral tooth structure so that mechanical interlocking
taken at the earliest possible moment. The cause and designs for retention are not necessary either. These
progress of the disease is discussed in some detail materials will be discussed in detail in the next sec­
elsewhere in this book so the contents of this chap­ tion and it will become apparent that it is now possi­
ter will be confined mainly to methods of treatment ble to think again about how to deal with active car­
for teeth which have already been damaged by the ies providing that the primary step always is modifi­
disease. cation of the bacterial flora, which is the essential
cause.
In the past, operative procedures were predicted
upon the notion that it was essential to remove all of Deciduous teeth are endowed with the task of per­
the tooth structure that had been demineralised by forming a variety of fonctions such as:
caries on the grounds that it was not possible to heal ■ Help in speech and mastication
it. It was also assumed that there were some parts of ■ Promoting an esthetic appearance
the crown of a tooth which were more susceptible to ■ Maintenance of arch length
caries than others and once a lesion had commenced, ■ Maintaining a healthy oral environment free of
it was essential to remove the entire surface to pre­ pain
vent any recurrence. The end result of these theories
was that a classification of cavities was developed Therefore, in short these functions help in contribut­
to fulfil the requirements and specific cavity designs ing to the health of the child as a whole and a clinty
were dictated based upon rather mechanical con­ cian needs to know the art of restoring and preserv­
cepts. As the restorative materials available at that ing these teeth until their normal exfoliation. Before
time were entirely neutral, showed no biological ac­ going to the procedures concerned with cavity prepa­
tivity and did not adhere to tooth structure, the cavi­ ration and restoration, it is essential to have a thor­
ties designed to accept a restoration were geometric ough knowledge regarding the morphology of pri­
and precise, included mechanical interlocking devices mary teeth as well as the differences between the
and paid little attention to the extent of the actual primary and permanent teeth.
lesion.
 I TEXTBOOK OF PEDODONTICS

Morphologic differences between Primary and Permanent Teeth

The anatomy of the primary teeth resembles in general that of corresponding permanent teeth expect for
special functional adaptations necessitated by the smaller jaw of the child (Table 7.1). There is one major
exception that mandibular first deciduous molar does not resemble any other teeth.

Table 7.1: Morphologic differences between Pimary and Permanent Teeth

' Primary Teeth Permanent Teeth

The Crown:
■ Lighter in colour, bluish white (milky white) ■ Darker in colour, grayish or yellowish white.
also called as milk teeth as its refractive
index is same as milk i.e, 1.
■ Quration of deciduous dentition^ j ■ Duration of permanent dentition:
^6 months to 5 % years. (f 6 years onwards.
■ Number of teeth: 20 ■ Number of teeth: 32
2 incisors, 1 canine., 2 molars 2 incisors, 1 canine, 2 premolars,
(five teeth in each quadrant) 3 molaras (eight teeth in each quadrant)
» ^Smaller in all dimension. Exposed aíéh is « Larger in dimensions.
about one-half that of the permanent teeth.
■ The crowns are wider in their mesjo-distal ■ The crowns of anterior teeth are larger in
dimension in relation to the ceryico- fyjp’ cervico-occlusal dimesnion than the mesio-
occlusal height. This gives a cup^shaged distal. This gives a longer appearance to
appearance to anterior teeth and squat M permanent anterior teeth. %
shaped appearance to molars.
■ Cuspids are slender and tenate be more ■ Cuspids are less conical. *
conical, c&b&t df-
■ The cervical ridges are more pronounced^■ - ■ The cervical ridges are flatter.
especially on the~ buccal aspect of first
primary molar. G < *
d

■ Buccal and lingiial surfaces of molars, ■ There is less convergence of buccal and
especially the first molars, converge towards lingual surface of molars towards occlusal
occlusal surface so that they have^ narrow surface.
occlusal table in a bucco-lingual plane.9W!A y q O'.
■ The occlusal plane is relatively flats» * ? ■ The occlusal'plane has more curved contour/
■ Molars are more bulbous and are sharply They have less constriction of neck,
constricted (bell shaped) cervically.
The enamel is thinner and has a more ■ The enamel is thicker and has a thickness
consistent depth of about 1 mm thickness of about 2-3 mm.
throughout the entire crown.
B^The contact areas between molars are ■ The contact point between permanent molars
broader, flatter, and sjtuated! gingivally. is situated occlusally.
■ The enamel rods at the cervical slppe^J p . The enamel rods are oriented gingivally.
r-j
occlusally from the DEJ. -
■ The supplemental grooves are more. % The supplemental grooves are less'
__________________________________ /,- ________________ c________ Z. 1
contd.
 SECTION 7 : PEDIATRIC RESTORATIVE DENTISTRY |

■ Mammelons absent ■ Mammelons present on incisal edges of newly

(Fig. 7.1a) erupted incisor teeth (Fig. 7.1b). a

Fig. 7.1a Mammelons are absent in~ Fig. 7.1b Mammelons are present on
decidous teeth. newly erupted central incisors.

■ First molar is smaller in dimension than ■ First molar is larger in dimension than second
second molar. molar.
The root: zU4^ '!
V
, ■ TFtle roots are larger and more slender in ■ The roots are shorter and bulbous in
' comparison to crown size. % 7 ! comparison to crown.
■ Furcation is more towards cejvical area so ■ Placement of furcation is apical thus the root
that root trunk is smaller. - 4 7 CA^C trunk is larger.
■ The roots are narrower mesio-distally. ■ The roots are broader mesio-distally.
■ At the cervical region, the roots of the ■ Marked flaring of roots is absent
•
primary molars flare outward and continue : ■' . r^r : <

to flare as they approach the apices to .

r,T 'ty-J '7 ■
accommodate permanent molars. -> %T
■ Undergo physiologic resorption during ■ Physiologic resorption is absent.
shedding of primary teeth.
The pulp: The pulp chamber anatomy in both primary and permanent teeth closely approximates
the surface shape of the crown.
■ Pulp chamber larger in relation to crown * ■ Pulp chamber smaller in relation to crown
, size. /.iW- __ size.
w Pulpal outline follows the DEJ more closely.. Pulpal outline follows DEJ less closely.
I The pulp horns are closer to the outer ''/ ? ■ The pulp horns are comparatively away from
surface. Mesial pulp horn extends to a the outer surface.
closer approximation of surface than does
the distal pulp horns.
High degree of cellularity and vascularity ■z Comparatively less degree of cellularity and
in tissue (at least in stages prior to (■; Vascularity in tissue.
advanced physiologic resorption of roots) f
■ High potential for repair. • Comparatvely less potential for repair.
contd.
 I TEXTBOOK OF PEDODONTICS

■ Comparatively less tooth structure. ■ More tooth structure protecting for repair.
■ Greater thickness of dentin over the pulpal « Comparatively lesser thickness of dentin over
wall at the occlusal fossa of molars. the pulpal wall at the occlusal fossa of molars.
■ Root canals are more ribbon like (Hibbard ■ Root canals are well defined with less
and Ireland 1957). The radicular pulp branching. .
follows a thin, tortuous and branching path.
■ Floor of pulp chamber is porous. Accessory ■ Floor of pulp chamber does not have any
canals in primary pulp chamber floor leads accessory canal.
directly into inter-radicular furcation.
Histolgoic differences
■ Roots have enlarged apical foramens. Thus, ■ Foramens are restricted. Thus reduced blood
the abundant blood supply demonstrates supply favours calcific response and healing by
a more typical inflammatory response. calcific scarring.
■ Incidence of reparative dentin formation ■ Reparative dentin formation is less.
beneath carious lesion is more extensive
and more irregular
■ Pulp nerve fibers pass to the odontoblastic « Pulp nerve fibers terminate mainly among the
area, where they terminate as free nerve odontoblasts and even beyong the predentin.
endings.
■ Density of innervation is less because of ■ Density of innervation is more.
which primary teeth are less sensitive to
operative procedure. Neural tissue is the
first to degenerate when root resorption
begins.
■ Localization of infection and inflammation ■ Infection and inflammation ip pulp is localized.
is poorer in pulp. i

Mineral content t

■ Enamel and dentine are less mineralized ■ Enamel and dentin are more mineralized.
(inorganic content is less).
■ Neonatal lines present (both in enamel ■ Neonatal lines seen only in first permanent
and dentin) molar (as the mineralization takes place at birth)
■ Enamel: bands of Retzius are less common, ■ Bands of Retzius are more common.
this may be partly responsible for. bluish «
white color of enamel.
■ Dentin: dentinal tubules are less regular. ■ Dentinal tubules are more regular.
■ Dentin thickness is half that of permanent ■ Dentin forming cells are functionally acitve
teeth. As a result dentin forming cells are by 700 days.
functionally active by approximately 360 days.
• Interglobular dentin is absent. ■ Interglobular dentin present just beneath the
homogenous and well calcified mantle layer
of dentin.
« Dentin is usually less dense. This difference ■ The dentin is difficult to cut.
can be observed clinically by resistance
offered to the cutting of the bur. The dentin
is cut more easily and also abrades more
rapidly.
contd.
 SECTION 7 : PEDIATRIC RESTORATIVE DENTISTRY |

« Periodontal structure: the cementum is ■ The secondary cementum is present.

very thin and of the primary type. Secondary
cementum is characteristically absent
■ Alveolar atrophy is rare. ■ Alveolar atrophy occurs.
■ Gingivitis (gingival inflammation) is « Gingivitis is common in adult.
generally absent in healthy child. Similarly,
recession is infrequent.

Self-Assessment

1. List out the functions of deciduous teeth?

2. What are the anatomic differences between the
primary and permanent teeth?
3. How does the primary and permanent tooth differ
in terms of localization of infection?
i

7.2 Principles and Concepts of

Cavity Preparation
Mount G J, Tandon S

Various classifications for cavity preparations have Class n lesions

been advocated. The more relevant classification They are found on the proximal surfaces of the bi­
pertaining to primary teeth and young permanent cuspids and molars.
teeth are discussed below.
Class III lesions
A. Black’s classification (Fig. 7.2): Lesions found on the proximal surfaces of anterior
teeth that do not involve or necessitate the removal
of the incisal angle.

Class IV lesions
Lesions found on the proximal surfaces of anterior
teeth that involve the incisal angle.

Class I Class fl Class III Class V lesions

Lesions that are found at the gingiva! third of the
facial and lingual surfaces of the anterior and poste­
rior teeth.

Class VI (Simon’s modification)

Lesions involving cuspal tips and incisal edges of
teeth.
Class IV Class V Class VI
B. Other modifications
Fig. 7.2 Types of cavities

■ Charbeneu’s modification
Class I lesion a. Class II: Cavities on single proximal surface of
Lesions that begin in the structural defects of teeth bicuspids and molars.
such as pits, fissures and defective grooves. b. Class VI: Cavities on both mesial and distal
proximal surfaces of posterior teeth that will
Locations include share a common occlusal isthmus.
■ Occlusal surface of molars and premolars c. Lingual surfaces of upper anterior teeth
■ Occlusal two thirds of buccal and lingual surfaces d. Any other unusually located pit or fissure in­
of molars and volved with decay.
« Lingual surfaces of anterior tooth
 SECTION 7 : PEDIATRIC RESTORATIVE DENTISTRY | ffEl

■ Sturdevant’s classification conservative approach to the preservation of

natural tooth structure. This system is designed
Cavity Feature
to utilize the healing capacity of enamel and
Simple cavity A cavity involving only one
dentin (Table 7.2a).
tooth surface
Compound cavity A cavity involving two sur­
The three sites of carious lesions:
faces of a tooth
Complex cavity A cavity that involves more Site 1 Pits, fissures and enamel defects on occlu­
than two surfaces of a tooth sal surfaces of posterior teeth or other
smooth surfaces.
■ Finn’s modification of Blacks’ cavity prepa­ Site 2 Proximal enamel immediately below areas
ration for primary teeth in contact with adjacent teeth.
Class I: Cavities involving the pits and fissures Site3 The cervical one-third of the crown or,
of the molar teeth and the buccal and following gingival recession, the exposed
lingual pits of all teeth. root.
Class II: Cavities involving proximal surface of
molar teeth with access established The four sizes of carious lesions:
from the occlusal surface.
Class III: Cavities involving proximal surfaces of Size 1 Minimal involvement of dentin just beyond
, anterior teeth which may or may not trea tment by remineralization alone.
involve a labial or a lingual extension. Size 2 Moderate involvement of dentin. Following
Class IV: A restoration of the proximal surface cavity preparation, remaining enamel is
of an anterior tooth which involves the sound, well supported by dentin and not
likely to fail under normal occlusal load. The
restoration of an incisal angle.
remaining tooth structure is sufficiently
Class V: Cavities present on the cervical third
of all teeth, including proximal surface
strong to support the restoration.
Size3 The cavity is enlarged beyond moderate.
where the marginal ridge is not
included in the cavity preparation. The remaining tooth structure is weakened
to the extent that cusps or incisal edges are
C Baume’s classification split, or are likely to fail or left exposed to
a Pit and fissure cavities occlusal or incisal load. The cavity needs to
b. Smooth surface cavities be further enlarged so that the restoration
can be designed to provide support and
D. Classification by Mount and Hume [1998] protection to the remaining tooth structure.
This new system defines the extent and complex­ Size 4 Extensive caries with bulk loss of tooth
ity of a cavity and at the same time encourages a structure has already occurred.

Table 7.2a: Classification by Mount and Hume.

Site Size
Minimal 1 Moderate 2 Enlarged 3 Extensive 4
Pit/fissure 1 1.1 1.2 1.3 1.4
Contact area 2 2.1 2.2 2.3 2.4
Cervical 3 3.1 3.2 3.3 3.4
 I TEXTBOOK OF PEDODONTICS

Principles of ca vity preparation Factors influencing outline form

a. Embrasure area
Conventional concept (Black’s concept) b. Contact with opposing tooth
Dr. G.V. Black has described the concept of “exten­ c. Caries index of the individual: High caries index;
sion for prevention” for cavity preparation. His ba­ more tooth structure is included in the outline
sic idea was to prevent the recurrence of caries by d. Position of the tooth in the arch
placing the margins of restorations along self-cleans­ e. Masticatory forces influencing mesio distal ex­
ing areas. tension
■ Incisors and canines: In these teeth the margins f. Convexity of the tooth
of the proximal cavities are placed beyond the g. Extent of the carious lesion
contact area. h. Proximity of the lesion to other defects in enamel
« Molars and premolars: The contact between the I Esthetic consideration
adjacent tooth is broken. Occlusal step occupies j. Partial edentulism
the entire middle third of the tooth buccolingually k Restorative material to be used
Buccal groove and other sharp grooves are in­ I Existing restorations
cluded in the preparation
■ Gingival third cavities: Cervical margin placed II. Resistance form
subgingivally and the mesiodistal extension It is the shape given to the cavity to enable the tooth
placed in self cleansing areas as well as the restoration to withstand the stresses
of mastication to which it is subjected.
I. Outline form
Features
The locations that the peripheries of the completed
1. Flat pulpal and gingival walls, the formation of
tooth preparation will occupy on tooth surfaces. It
these walls perpendicular to pcclusal forces.
can be:
2. Utilizing box form of cavity preparation
• Internal outline form
3. Cavity prepared in such a way that strong cusp
■ External outline form
and ridge areas remain with adéquat^ dentin sup­
port
Features
4. Rounded internal line angles to avoid stress con­
1. Extend cavity margins to sound tooth structure
centrations.
2. Include all the fissures ’
5. Butt joint between the tooth and restoration
3. Extend outline form to provide sufficient access
6. Removal of unsupported enamel
4. Cavity margins should be placed in self-cleansable
7. 90 degree cavo-surface angle
areas
8. Adequate bulk of the restorative material
5. The pulpal floor and axial wall should have an
9. Adequate depth and width of the cavity
average depth of 0.5 mm into the dentin.
10. Reverse curve in the case of class II cavities, when
6. Margins should be extended to include all defec­
the proximal outline becomes offset
tive enamel
buccolingually.
7. 0.2 - 0.3 mm clearance from the adjacent tooth
11. Gingival cavosuface bevel given in the case of
while preparing the proximal box in class II cavi­
permanent teeth.
ties.
12. The width of the cavity should not be more than
8. Margins of the cavity preparation should not be
l/4th - l/5th the intercuspal distance.
in contact with the opposing tooth.
13. The pulpal floor should be 0.5mm below the
9. If less than 0.5mm of the tooth structure exists
dentino-enamel junction.
between two carious surfaces, then they should
14. The cavity wall should be divergent occlusally at
be joined.
the marginal ridge areas.
 SECTION 7 : PEDIATRIC RESTORATIVE DENTISTRY I

III. Retention form Purpose

ft is comprised of those factors of cavity design that 1. To place the margins on sound tooth structure
prevent the restoration from being displaced. 2. To have smooth walls and rounded angles
3. To facilitate placement and finishing of the re­
Features storative material.
1. Parallel or an inverse taper of 5 degree under the
4. Placement of taper or bevel for the appropriate
triangular ridges of cuspal areas in the case of
restorative material.
class I and class II cavities.
2. Retention cores and grooves as used in class III
VII. Cleansing of the cavity
and Class V cavities.
The operating field should be kept clean and ad­
3. Occlusal dovetail in the case of proximo occlusal
equately isolated by the use of rubberdam, cotton
cavities where only one proximal surface is in­
rolls, and high vacuum evacuation equipment.
volved.
Conditioning of the cavity may be done in certain
4. Pins placed into the dentin
cases like bonding systems for amalgam and com­
5. Acid etching of the ena mel
posite restorations.
6. The proximal box of class II design is divergent
gingivally to contribute to the retention form. Recent Concept
Cavity preparation for operative procedures now no
IV. Convenience form longer adhere to Black’s concept of ‘Extension for
It includes shaping the cavity to facilitate access for prevention’. Increased knowledge of preventive
instrumentation, for condensation, adaptation and methods, advanced techniques, and improved re­
finishing. storative materials render the clinician to follow both
conservative and preventive criteria which can be
Features
met by the present day dentistry based on the princi­
1. Modifications of cavosurface margins for ease of
ple of‘Constriction with Conservation’.
placement of restorative material.
2. Extension of buccal and lingual walls for visibil­ The following principles should be considered while
ity and access to deeper portions of the cavity. ’preparing a cavity according to the recent concept:
3. The proximal lesion can be instrumented from the ■ Cavity designs should be dictated under the site
facial, or lingual embrasures in a tooth with wide, and extent of the lesion and not by any precon­
accessible embrasures and intact marginal ridges. ceived notion of mechanical interlocking patterns.
■ Should not be in expectation of extending the
V. Removal of any remaining infected cavity out to a “caries free” area.
dentin ■ The first choice of a restorative material should
In the case of a small carious lesion, the infected be one that displays some degree of biological
dentin would be completely removed as the abdve activity and will therefore assist in the process of
mentioned principles are achieved. However, when remineralization and healing of remaining tooth
a large carious lesion exists, some amount of infected structure.
dentin still remains inspite of following the above ■ Only that part of the tooth crown that is irretriev­
procedures. In such cases the infected dentin has to ably degenerated and broken down should be
be removed. removed and the remainder even though
demineralized and softened, should be retained
VI. Finishing the enamel walls and remineralized
■ The first function ofthe restoration will be to elimi­
It is the further development of specific cavosurface
nate any surface cavitation that has resulted from
design and degree of smoothness that will bring about
caries because, in the continuing presence of de­
the maximum effectiveness of the restorative mate­
fects on the surface, it will not be possible to
rial being used.
completely control plaque accumulation.
 I TEXTBOOK OF PEDODÓNTICS

Martin et al (2000) have applied the term 'minimal - Repair rather than replacement of defective
intervention’,'minimally invasive’ or 'preservative restorations
dentistry’ to above concept. This approach en­ - Disease control
tails a departure from the traditional surgical
S elf-Assessment
method to the elimination of caries lesion which
is in the inner halt of enamel, at the dentino enamel 1. What are the components of Black’s classifica­
junction, and slightly into dentine but with little tion?
or no cavitation. Minimal intervention is therefore 2. List out the principles of cavity preparation.
based on 'biological’ or ‘therapeutic’ approach 3. Give the newer classification based on site and
with following principles. size.
- Remineralization of early lesions 4. How does the recent concept differ from Black’s
- Reduction in cariogenic bacteria cavity preparation?

Table 7.2b Iatrogenic factors affecting dental pulp

Depth of cavity ■ Increased rate of collagen turn over Minimum 2 mm remaining dentin thickness
preparation ■ Odontoblastic cell damage essential for pulp protection
■ Protein synthesis inhibition

Speed of rotation ■ Low speed result in increased vibrations Speed greater than 1.5 to 2.5 lakh rpm
■ Increased heat generation safest with coolants

Heat generated « Greater than 46° C leads to stasis Avoid heat generation by adequate use
and thrombosis of blood of coolants
■ Greater than 55° C leads to necrosis

Pressure ■ Increased pressure leads to Low speed maximum pressure is less

displacement of odontoblastic nuclei than 4 ounces.
into tubules High speed max. is less than 1 ounces

Dehydration ■ Displacement of cell/nuclei into tubule Avoid excessive drying of cut tdoth
■ Pulpal edema structure *
■ Increased permeability of dentin to irritants i

Nature of cutting ■ Increased heat generated with Use carbide burs with coolants for cavity
instruments abrasives preparations
■ Steel burs produce more heat than carbide

. Size of burs ■ Large size of burs have increased heat Medium/small sized burs preferred
generation.
« Reduced access for coolants
• More loss of tooth structure
Coolants ■ Air spray leads to desiccation of dentin Water spray is preferred as it reduce
(Air spray) heat and washes away debris
Vibrations “REBOUND RESPONSE” Avoid use of low speed which increases
■ Pulpal edema vibrations
• Fibrosis of pulp tissue
■ Changes in ground substances
• Reduction in predentin formation
Pins » Microfractures of dentin Cautious use of pins where indicated
» Undetected pulp exposures
Extensiveness ■ Increases heat generation Avoid cutting excessive tooth structure
Polishing of » Increased heat due to friction Polishing must be done in wet field
restorations
Orthodontic • Interference with apical blood vessels Forces must be limited to less than
treatment leading to disruption of blood supply and 50-70 gms
nutrition to odontoblasts
■ Severe cases-necrosis of pulp
 7.3 Procedures Required for Restoration

Mount G J, Sajida B, Tandon S

1. Isolation A. Fluid absorbents

2. Cavity preparation
3. Placement of matrices The isolation can be achieved by absorption of sali­
4. Material placement vary secretions. These can be used for short periods
when absolute dryness is not required. E.g. examina­
ISOLATION tion, polishing fluoride application.

The oral environment needs to be adequately con­ Various materials that can be used for this purpose
trolled to prevent it from interfering wSth the execu­ are:
tion of any dental procedure. This control is attained ■ Cotton rolls
through isolation. ■ Gauze or throat shields
■ Absorbent paper
Need for isolation in Pedodontics
1. Increased salivation in child patient ‘Cotton rolls (Fig. 7.3) î
2. Excessive tongue movements
3. Short attention span which requires shorter du­
ration of treatment and therefore better isolation
techniques.
4. Decreased danger of aspiration of foreign parti­
cles
5. Convenience to the operator since it improves
visibility
6. Improved properties of restorative material
7. Isolation techniques help in behavior manage­
ment. This especially holds good for use of rub­
berdam.

Various means of isolation

A. Fluid absorbents suction tip
B. Saliva ejectors
C Rubber dam • Cotton rolls are available in different diameters,
D. Use of matrices during restorative procedures cut to variant lengths and have plain or woven
surfaces.
 I TEXTBOOK OF PEDODONTICS

■ These are stabilized and held sublingually with 4. It should not interfere with instrumentation
specific holders or with an anchoring rubber dam 5. It needs to be used with other adjuncts like cot­
clamp. ton rolls and gauze
■ They can be applied without holders, over or lat­
Advantages
eral to salivary glands orifices.
■ It provides an adequate dry field along with the
■ Cotton rolls provide the advantage of slightly
advantage of washed field.
retracting the cheeks aiding invisibility and ac­
■ There is no dehydration of oral tissues
cess.
■ Precious metals sucked can be recovered

Gauze of throat shields Precautions

■ It is used in pieces of 2” x 2" or larger Care should be taken to avoid cross contamination.
■ These are better suited for large areas than cot­ Thus,
ton rolls 1. The saliva ejector should be disinfected after each
■ They are better tolerated by delicate tissues and use.
have less adherence to dry tissues compared to 2. Disposable tips are preferred.
cotton. 3. The child patient is cautioned not to close his
mouth to hold the tip since it may cause backflow
Absorbent paper pads of contaminated solutions into his mouth as a
9 These are of different shapes to fit various loca­ result of pressure changes.
tions in mouth.
■ They are more absorbent than any of the above C. Rubber dam
absorbents.
Rubber dam, which is usually la tex rubber, is one of
B. Saliva ejectors and high volume evacu­ the most effective means of isolating teeth. It was
ating equipment developed by Barnum [1864]. >
t

Saliva ejectors prevent pooling of saliva in the floor Rationale é

of the mouth. High volume evacuating equipment 1. Maintains clean, visible field
removes solid debris along with water unlike the sa­ 2. Patient protection - prevents aspiration of for­
liva ejector. eign bodies.
3. Clinician protection
Types 4. Reduces risk of cross-contamination especially
■ Metallic - are autoclavable and have rubber tip to the root canal system.
to avoid irritating the delicate tissues on the floor 5. Retracts and protects soft tissues
of mouth. 6. Increases efficacy by minimizing patient conver­
9 Plastic - are disposable and inexpensive sation and need for frequent rinsing.
7. Application of medicaments without the fear of
Requirements dilution.
1. The tip should alwaysbe moulded to face back­ 8. Improved properties of restorative materials
wards with a slight upward curvature. 9. Psychological benefit to the patient
2. The floor of the mouth under the tip should be
covered with gauze to prevent injury to soft tis­ Contraindications
sue. 1. A child with upper respiratory tract infection,
3. It should not traumatize the lip or cheek mucosa. congestion of nasal passage or other nasal ob­
struction.
 SECTION 7 : PEDIATRIC RESTORATIVE DENTISTRY | fEEl

2. Presence of some fixed orthodontic appliance Rubber dam has a shiny and a dull surface. The dull
ci 3Arecently erupted tooth that does not retain a surface is kept facing occlusally since it is less re­
flective.
■ ■?Oisnts-with allergy to latex.
S?
* --O'■ ’ Rubber dam frame
■ Plastic frame eg:
HF fie rubber dam should not obstruct patient’s air- Star visi frame
t way and thus should not cover his nose. Nygard - Ostby (Fig. 7.5)
Holes should be prepared in rubber dam for pa- Quick Dam or Handidam frame (has built
Si i^&s with upper respiratory tract obstruction, in plastic frame) (Fig. 7.6)
lii^^^tietits with allergy to latex, latex free rubber ■ Metal frames e.g. Young frame
should be used. Rubber dam napkin can be
used to prevent the latex rubber dam from con­ Rubber dam punch
tacting the patient’s tissues. It aids in punching holes corresponding to teeth
size on the rubber dam sheet.
Armamentarium
1. Rubber dam sheet Lubricants
2. Rubber dam frame Water soluble lubricants are applied in the area of
3. Rubber dam punch punched holes for easier placement of the dam e.g.
4. Rubber dam forceps shaving cream or soap slurry.
5. Waxed dental floss
6. Scissors Clamps: These are made up of shiny or dull stainless
7. Rubber dam napkin steel and consist of a bow and 2 jaws. They aid in
8. Lubricants anchoring the dam to the tooth and in soft tissue
9. Clamps retraction

Rubber dam sheet Types ofclamps (Fig. 7.4)

■ Winged
Rubber dam is available in various thicknesses as ■ Wingless
thin, flat latex sheets. ■ Serrated
■ thin 0.15 mm ■ Clamps with jaws inclined cervically to engage
■ medium 0.20 mm erupting tooth or severely broken down tooth.
» heavy 0.25 mm * ■ Clamps with cndo-illuminator system to illuminate
■ extra-heavy 0.30 mm pulp chamber and canal orifices.
■ special heavy 0.35 mm

It is available as rolls or prefabricated size i.e., 5” x 5“

or 6 ” x 6” while non latex rubber dam is available only
in 6” x6” size.

The dam is manufactured in various colours. Darker

colour offers better visual contrast but the lighter
colour provides the advantage of naturally illuminat­ Winged clamp Wingless clamp
ing tlie operating field and allows easier placement
of film below the dam Fig. 7.4 Types of Clamps
€39 I TEXTBOOK OF PEDODONTICS

Fig. 7.7a Isolation of anterior teeth with Fig. 7.7b Rubber dam is an effective means
rubber dam of isolation

Fig. 7.8 Different techniques of tying dental floss to the clamp.

 SECTION 7 : PEDIATRIC RESTORATIVE DENTISTRY | @8

Common rubber dam clamps for pediatric use a retracts the tissues better than thin type and
1. Partially erupted permanent molar -454A, 8A Ivory b. is easier to place than heavier type
2. Fully erupted permanent molar -14,8 Ivory ■ The dam is then punched.
- F
3. Second primary molar - 26,27, S. S. White, 3 Ivory
4 Firstprimary molar, bicuspid, permanent canine - a. In primary dentition rubber dam is routinely
2,2A Ivory placed over c, d, e (Fig. 7.10)
5. Primary incisors and canine - 0 Ivory

Procedure of rubber dam placement (Fig. 7.7a, 7b)

1. Selection and preparation of the rubber dam.v

2. Decide the tooth to be clamped

3. Select a clamp
4. Introduce the materials to the child
5. Tie a length of floss to the clamp (Fig. 7.8)
6. Place the clamp, rubber dam and frame (Fig. 7.9)

Fig. 7.10 A method of punching holes in

Rubber Dam

For the maxillary arch

The first hole is punched for ‘e’ in the midline of
Fig. 7.9 Placement of Rubber Dam Clamp
rubber dam 1.25” (3.5 cms) from the upper border.
The second hole punched for ‘d’ is one hole
7; Slip a napkin near the rubber dam and spread it
smaller in size, 4 to 5 cm away and at an angle of
over the face.
40 degree vertical towards the dentist
8. Place protective coating of cocoa butter/petrola-
tum/varnish over silicate or GIC restorations to
The third hole for ‘c’ is punched a size smaller
prevent dehydration.
hnd again 4-5 cm from d forming an angle of 40
9 Adapt and slip a saliva ejector tip between the
degree to the vertical.
rubber and napkin on the non-operating side.
For the mandibular arch
Selection and preparation of the rubber dam
Similar procedure is followed for the mandibular
■ Heavy and extra heavy dams are used for restora­
arch with the hole for c punched 1.75” (4.5cm)
tive procedures while medium is considered ideal
from the upppr border in midline.
for endodontic purposes since it
 €30 I TEXTBOOK OF PEDODONTICS

Second hole is punched one hole smaller in size, ■ Mirror and evacuator tip
4-5 mm away at an angle 40 degree to the vertical These help in retraction of oral soft tissues^ spe­
towards the dentist. cially in absence of rubber dam.
■ Mouth prop
Advantages of this method Mouth prop benefits both operator and the pa­
- The dam is centered on thequadrant being tient. They maintain mouth opening during vari­
worked on. ous procedures and prevent muscle fatigue in pa­
- Nasal obstruction is avoided tients.
- Holes can be punched in absence cf the tem­ ■ Drugs
plate Antisialagogues can be used to decrease exces­
sive salivation eg. Atropine.
b. Ready made templates: Local anesthesia is known to decrease pain. This
These can also be used for marking the areas of in addition to the vaso-constrictor in it brings
about a reduction in salivation.
teeth to be punched.

Modifications of Cavity Preparation in Primary

Methods of placement
Teeth
a. The bow of the clamp is positioned through the
hole in the dam and the rubber is placed over the All the principles of cavity preparation of permanent
wings of the clamp. teeth also hold good for the primary teeth. However,
The clamp is stretched and placed on the tooth a few factors have to be taken into consideration
along with dam which is teased under the wings while restoring the primary teeth. These include:
of clamp. The dam is then attached to the frame. ■ The smaller tooth dimension of the deciduous
b. Wingless clamp is placed on the tooth and dam is dentition
stretched over the clamped tooth. « The thin ena mel coveri ng the teeth t
- Tliis allows the clinician to see the area of tooth ■ Broad contact areas
being clamped. ■ Proximity of the pulp chamber to outer tooth sur­
- Variation to this method would be to place the face
rubber dam first followed by clamp and frame. ■ Narrow occlusal table
c. Split dam technique
This is used to isolate anterior teeth without the Class I cavities
use of clamp. This is useful in cases of insuffi­ ■ Due to the narrow occlusal table present the isth­
cient crown structures eg. horizontally fractured mus should not be more than l/3rd the intercuspal
tooth. distance in the case of a small carious lesion.
■ The depth should not be more than 0.5 mm into
Additional isolation Aids the dentin.
■ The pulpal floor should be flat. Any remaining
Moisture control, retraction and access are the main
caries lesion should be removed using round bus.
aims of isolation. Apart from aforementioned tech­
■ Use of preventive resin restoration is advocated
niques other alternatives to provide isolation are:
rather than the conventional cavity preparation
• Retraction cord
which includes all pits and fissures.
It is usually used for cervical lesions when the
use of rubber dam is impractical or inappropriate. Class II cavities
They can be used with non-caustic styptics to « Due to the presence of broad contact areas, the
control sulcular seepage or hemorrhage. gingival floor of the proximal box should be wide
so as to place the margins in self cleansing areas.
 SECTION 7 : PEDIATRIC RESTORATIVE DENTISTRY |

■ The box should however converge occlusally Class III cavity

with the buccal and lingual wall paralleling the ■ When the contact is open, the outline is triangu­
external tooth surface. lar with base towards the gingival aspect of the
■ The walls of the proximal box should meet the cavity
occlusal walls in a straight line to avoid any weak ■ Gingival cavity wall is inclined occlusally to par­
points. allel the enamel rod direction.
■ The walls of proximal shoiiEinot be flared as it ■ Retention pits can be placed at the axiobucco
would lead to unsupported enamel. gingival and axio linguo gingival point angles.
■ The isthmus should have just adequate width that ■ A dovetail may be placed in the middle one third
is it should not exceed 1/3 id the intercuspal width ofthe lingual surface of the tooth. This helps in
in primary molars. gaining access to the carious lesion and in facili­
■ The axiopulpal line angle must be either rounded, tating retention ofthe restoration.
tunneled or grooved for sufficient bulk of the res­
toration. Young permanent first molars
■ The strength of amalgam at the isthmus area can The following special morphological considera­
be increased by an adequate depth of the prepa­ tions should be kept in mind while preparing a
ration. cavity in a young permanent first molar
■ Retention can be improved by a ‘U’ shaped re­ ■ The first permanent molars erupt between the
tention groove along the amelodentinal junction ages of five and six years and, as this is an age
ofthe proximal box. group wherein caries is a common problem, these
■ When the cavity margins exceeded that of an ideal are often the first of the permanent teeth to be­
preparation particularly in the case of a mandibu­ come carious.
lar first primary molar, it is recommended that an ■ The result of various developmental interference
overlay of the distobuccal cusp be prepared. will often result in failure of the enamel to unite
■ The weakened cusp is reduced to the level of the completely and smoothly in the middle of the oc­
pulpal floor of the occlusal preparation. clusal surface and there will be the potential for
Mesiodistally the cusp should not be reduced faults and defects in the occlusal enamel, even
more than l/3rd the crown’s mesiodistal length. before eruption.
■ Since the enamel rods, at the cervical area of the ■ The occl usal surface of any tooth is particularly
tooth, are oriented occlusally the gingival seat susceptible for plaque accumulation within a de-
should not be beveled, rather should follow the fect because of the heavy pressure to which this
enamel rod inclination. surface is subject to during mastication. Such fis­
■ If the depth of the lesion is farther gingivally, the sures can be as far as 1.5 to 2mm deep into the
axial wall should follow the contour of the exter­ enamel and it is possible for them to penetrate
nal surface. This will prevent pulp exposure from right through to dentin.
occurring. « They may range in width from 100 to 500pmand
■ Care should be taken to avoid the mesiobuccal will often be wide at the entry, narrow down to
pulp horn in the case of small first molars. Since less than 200 pm in the middle and then open
the contact with the canine is a point contact, the wider again at the dentin.
proximal box extension and the gingival flare can ■ In many cases the fissures are made up of a series
be minimized. of pits of considerable depths rather than one
■ The proximal box should allow the passage of a n continuous fissure.
explorer tip between its margins and adjacent ■ The result of this convoluted anatomy may be
tooth in all three directions, buccally, gingivally compaction of bacteria laden plaque into the
and lingually. depths of the fissure leading to active deminerali-
 I TEXTBOOK OF PEDODONTICS

zatiort down the walls and into dentin with mini­ ■ Assure diyness and non-contamination of the
mal visible evidence on the.occlusal surface. In operating field.
communities that have systemic fluoridation the ■ Provide shape to the restoration during setting
enamel is often very hard and does not break­ of the restorative material.
down until it is severely undermined. This means ■ Maintain shape during hardening of the restora­
that carie? Jhát has progressed through to the tion.
dentin can progress all the way to pulpal involve­
ment without any visible breakdown on the oc­ Types (Fig. 7.11)
clusal surface.
• The enamel rods within a fissure are not always
as regular in pattern as those elsewhere around
the crown of a tooth. Those at the shoulder
around the entiy to a fissure are often gnarled
and irregular and will not always accept a regular
etch pattern. In the depths of a fissure there may
be a layer of enamel rods lying parallel to the sur­
face rather than at right angles.
■ There is the likelihood of a carious lesion on the
distal of the deciduous second molar extending
some damage on to the mesial of the adjacent
permanent tooth. The carious lesion may become
visible and available for treatment at the time the Fig. 7.11 Different matrices and retainers - on left
deciduous tooth is exfoliated. metallic matrix bands with retainers; on right
celluloid matrix bands
Kinetic Cavity Preparation
Kinetic cavity preparations (KCP), which used fine 1. Matrices for Class I cavity ^compound cavity)
particles'of powder fired at high speed in a control­ ■ Double banded Tofilemire
led manner instead of the traditional high and low
speed drills. Advantages of this technique are that 2. Matrices for Class II
no vibrations or pain sensation, and also no need for ■ SinglebandedTofilemire
anesthesia in most cases. This truly allows us to o « Ivory matrix No. 1
multiple quadrant dentistry so as to decrease the ■ Ivory matrix No. 8
number of patient visits, and better time utilization. ■ Black’s matrices
■ Soldered band or seamless copper band matrix
MATRICES USED FOR RESTORING THE TOOTH ■ Anatomical matrix
■ Auto-matrix
Matricing is the procedure whereby a temporary wall ■ S-shaped matrix band
is created opposite to axial walls, surrounding areas ■ T-shaped matrix band
of tooth structure that were lost during preparation.
3. Matrices for a cavity preparation for amalgam on
Objectives distal of cuspid
The matrix should achieve the following functions: ■ S shaped matrix
• Displace the gingiva and rubber dam away from ■. Tofilemire
the cavity margins. This improves the accessibil­
ity during the restorative procedures.
 SECTION 7 : PEDIATRIC RESTORATIVE DENTISTRY |

4. Matrices for Class III for tooth coloured restora­ Self Assessment
tions
■ Transparent celluloid strips 1. What are the morphological and histological dif­
ferences between deciduous and permanent
5. Matrices for Class IV for tooth coloured restora- teeth?
tions 2. What is the recent concept of cavity preparation
■ Celluloid strips and how does it differ from Black’s concept?
■ Aluminum foil (non-light cure) 3. What is Finn’s classification of cavities?
■ Transparent crown form matrices 4. What are the basic principles in the preparation
■ Anatomic matrix of cavity in primaiy teeth?
■ Modified S shaped band of copper, tin, 5. What is the difference between resistance and
aluminum foil (non-light cure) retention?
6. What are the commonest causes of Class II amal­
6. Matrices for Class V amalgam restorations gam failures in primaiy I molars?
■ Window matrix 7. What are the specific modifications of class II
■ S shaped matrix cavities in primary molar?
8. What should be the width of the isthmus in de­
ciduous teeth?
7 Matrices for Class V tooth coloured restorations
9. Where should be the placement of the gingival
■ Anatomic matrix (non-light cure)
seat in a class II cavily?
■ Aluminum or copper collars (non-light cure)
1(1 What are the different matrices used in
■ Celluloid strips (light cure)
Pedodontics?
11. What is a rubberdam?
X. Sectional matrix with G-rings (retainers) for pos­
12. What is a quickdam?
terior composites (Fig 7.12a. 12b )

Fig. 7.i2a Sectional matrix bands on left with Fig. 7.12b G-rings in place with sectional
retaining G-rings on right matrix
 7.4 Modern Restorative Materials
and Techniques
Mount G J, Hien Ngo, Byrant R W

In view of the limited life span of the deciduous teeth Disadvantage

it is normal to utilize one of the plastic restorative Its physical properties are not sufficient to enable it
materials which are placed directly into the cavity to withstand heavy occlusal loads in large restora­
This will include the first molars because of the diffi­ tions.
culties which will be encountered in trying to place
restorations such as gold inlays or gold foils in a Classification
patient of tender years (Fig. 7.13af b, c) (Fig. 7.14a The following is the accepted classification-
b, c).
Type I-luting
Requirement of an ideal restorative material Cementation of crowns, bridges and
■ Restoration of aesthetics. orthodontic devices
■ Maintenance of the physical strength of the Powder: liquid ratio approximately 1.5.1
crown Radio-opaque \
» Preserving the anatomy of the occlusal surface
and thus preserving the interrelationship with the Type O - restorative
opposing and adjacent teeth. Type II. 1 restorative aesthetic
■ Prevention of further ingress of bacteria or their All types of aesthetic restorations
by-products into the micro space between the Auto- cure or resin modified
restoration and the tooth. Powder: liquid ratio 3:1 or greater
■ Long term adhesion between the restoration and Radiopaque - generally
the tooth to ensure complete isolation. High physical properties
Type II. 2 restorative
GLASSIONOMER Restorations under high occlusal load
Auto- cure or resin modified
This materialwas developed by Wilson et al in the
Powder: liquid ratio 3: l orgreatei
early 1970s. It can be used as a luting cement for
Radioopaque
indirect restorations, a lining under another restora­
Used as a dentin substitute or interim
tive material, or a restoration in its own right.
restoration
Advantages
« It is a tooth coloured material. Type III - lining or base
a It will adhere directly to both enamel and dentin Simple lining under a metallic restoration
through an ion exchange mechanism Powder: liquid ratio 1.5:1 only
• It is biologically active, as it is capable of releas­ Auto cure
ing fluoride, calcium and phosphate ions. Radiopaque
 SECTION 7 : PEDIATRIC RESTORATIVE DENTISTRY |

Fig. 7.13a Occlusal shoulder showing little sign Fig. 7.14a Full mouth rehabilitation - pre­
of demineralization with obvious caries begining treatment showing upper teeth
in the depths of fissures and entering the dentin

Fig. 7.13b S.E.M. picture of similar fissure in Fig. 7.14b Fun mouth rehabilitation - pre­
a molar tooth reveals a small degree of demine­ treatment showing teeth in occlusion
ralization at the base of fissure

Fig. 7.13c Same fissure at higher magnifi­ Fig. 7.14c Full mouth rehabilitation - post­
cation reveals the presence of layer of enamel treatment
which appears to have no rod formation at all
 I TEXTBOOK OF PEDODONTICS

High strength base for lamination technique to be initiated by light of the correct wavelength^
Powder: liquid ratio 3:1 or greater The advantages include early resistance to water
uptake in the newly set cement as well as enhanced
Constituents translucency. The resin utilized in these materials i,s
hydroxyethylmethacrylate (HEMA) and it is incor­
PoWer porated into the liquid in about 15-25% so as to have
The powderw®essentially a calcium fluoroalu­ a powder liquid ratio of about 3:1. setting reaction
minosilicate glass. It is possible to substitute the
calcium with strontium and the percentage of fluo­ Compomer
ride in the formula can also be varied. Phosphate can This is the term developed by the manufacturer with
be added to decrease the melting temperature and a claim to incorporate some of the properties of a
modify the setting characteristics. Fine colloidal sil­ glass ionomer with a composite resin. A compomer
ver can be sintered to the particles and amalgam al­ is a composite resin that uses an ionomer glass which
loy particles can be added to thé mix in an attempt to is the major constituent of a glass ionomer as the
enhance the properties. filler. There is also a small quantity of a dehydrated
polyalkenoic acid incorporated with the filler parti­
Liquid cles.
The liquid is essentially a poly alkenoic acid. The
usual acid is a 40-55% solution of 2:1 polyacrylic or The filler particle is held within an anhydrous resin
itaconic acid copolymer in water or a copolymer of matrix and there is complete absence of water. Hence
maleic acid and poly acrylic acid. The use of copoly­ there can be no ion exchange, acid/ base setting re­
mers improves storage. The inclusion of tartaric acid action and the material initially remains inert. The
will retain the working time so that the mix will be setting reaction is light activated and there can be
clinically workable. no acid base reaction until there has been a degree of
water uptake into the restoration. Following water
Modified glass ionomer cements uptake there will be an ion exchange? between the
glass and the rehydrated polyalkenoic acid followed
“Anhydrous” by a low grade fluoride release, but this will be nei­
In this modification the liquid is delivered in a freeze ther sustained nor at a higher level. Since fluoride
dried form that is then incorporated into the powder. uptake cannot take place a compomer cannot be re­
The liquid to be used is clean water only and this garded as a fluoride reservoir.
may enhance shelflife and facilitate mixing. Another
The most significant difference between the two
alternative is to use a dilute tartaric acid as the liquid
materials is the absence of an ion exchange adhe­
with dehydrated pofyacrylic acid included in the pow­
sion. The adhesive system used with a compomer is
der These alternatives make it possible to use a
based on the acid etch/ min bond system found
polyacrylic acid with higher molecular weight thus
with all composite resins.
improving physical properties.
The term anhydrous is actually a misnomer as it is Finally the percentage filler content is relatively low
not possible for ion transfer to occur, in any material, compared to the hybrid composite resins, both the
in the absence of water. water uptake and the wear factor are relatively high.

Resin modified Setting reaction for glass ionomers (Fig. 7.15a, b)

These are materials which have a small quantity of a
resin into the liquid formula. Less than 1.0% of The setting reaction has been described as an acid
photoinitiators are allowed for the setting reaction base reaction. The surface of all the glass particles is
 SECTION 7 : PEDIATRIC RESTORATIVE DENTISTRY |

Fig. 7.15a A diagrammatic representation of Fig. 7.15b A diagrammatic representation of

the acid/base setting reaction of the glass setting reaction of glass ionomer
ionomer materials as well as ion exchange
union occuring with tooth structure

Fig. 7.16 S.E.M. picture of a glass ionomer Fig. 7.17 S.E.M picture of smear layer left on
restoration adjacent to tooth structure showing the surface of tooth after cavity preparation
presence of relatively large porosities

Fig. 7.18a S.E.M picture showing the surface Fig. 7.18b S.E.M picture showing similar dentin
of dentin following a ten second application of surface following etching with a 37% ortho
a 10% polyacrylic acid phosphoric acid for 15 second
 FETfr | TEXTBOOK OF PEDODONTICS

softened by the polyacrylic acid and both calcium care should be taken to ensure that the materials
and aluminium ions are released through the proton are properly dispensed before mixing.
attack. Calcium ions react first and form calcium
polyacrylate chains followed a little later by a similar Setting reaction of compomer
reaction with the aluminium ions. The calcium poly
acrylate chains are rather fragile and soluble in water There are essentially two^difierent
[WI systems for initi­
and therefore require protection if they are to be re­ ating polymerization in a composite resin. The origi­
tained. The formation of polyacrylate chains will nal materials were all chemically activated however
progress quite rapidly following the initial setting they exhibited an undesirable colour shift. Subse­
reaction. These chains are strong and insoluble in quently a system for light activation was developed
water and form the main body of the restoration. Both and this has proven to be relatively colour stable. It
the calcium and aluminium ions will cross-link as the is also possible to combine the two systems.
reaction progresses and forms a rather porous net­
work. Method of using glass ionomer

A further ion exchange reaction occurs as part of the Hand mixing

setting process where there will be a silica hydrogel Divide the dispensed powder into two equal parts.
formed on the surface of the glass particles. There Gently spread the liquid drop a little over the glass
will be a gradient of ions formed about one third of slab. Roll the first half of the powder into the liquid
the way into the glass to the extent that the glass and incorporate the two together rapidly. This is com­
and the matrix become chemically bound and can be pleted in 10 seconds and the rest of the powder is
regarded as a single mass (Fig. 7.16). brought into the mix. No attempt should be made to
tty and dissolve the powder into the liquid. It is only
Setting reaction of resin modified necessary to wet the surface pf each particle so that
ion release can occur leading to the initiation of the
The setting reaction of resin modified glass ionomers acid/base setting reaction. The final mix should be
is very similar with regards to the acid base reaction completed within 25- 30 seconds.
though at a slightly slower pace. The usual ionomer
salt hydrogel will form along with a poly HEMA ma­ Conditioning the cavity
trix with the possibility of multiple cross linking be­ Following completion of any cavity preparation there
tween the two matrices. The setting reaction of poly will be a smear layer left on the surface of the floor
HEMA matrix will be stimulated by light activation and walls (Fig. 7.17). This will consist of tooth de­
subsequently an oxidation/ reduction reaction will bris, bacterial plaque, pellicle and other debris and if
continue to progress through any remaining left in place may interfere with the development of
unreacted resin chains so that in die long run the the ion exchange adhesion layer. It is therefore nec­
entire restoration will be set. This has been desig­ essary to remove this before placing the restoration.
nated as a “tri cure setting reaction”. ■ For this purpose a 10 % percent poly acrylic acid
is applied and allowed to remain in place for 10
The setting rate depends on the following factors: seconds only (Fig. 7.18a, b). The surface energy
■ Temperature ofthe mixing slab: The lower the tem­ of the cavity walls and floor is modified so that
perature of the mixing slab, the longer the work­ the high surface energy newly mixed cement will
ing time and vise versa. However the temperature adapt better to the low surface energy cavity
should always be above the dew point. walls.
■ Powder liquid ratio. The higher the powder con­ ■ The cavity should be washed thoroughly and
tent the higher the physical properties. However, dried lightly and the cement flowed into place
 SECTION 7 : PEDIATRIC RESTORATIVE DENTIStRY | @9

immediately. Do not over dry the cavity, as the Water balance

glass ionomer is a water based material and may ■ As a water based material, glass ionomer is al­
lose physical properties if dehydrated through a ways susceptible to both water loss and water
lack of water. uptake.
■ It is important to note that conditioning and etch­ ■ All types of glass ionomer will lose wateriftyx-
ing are two different entities. A cavity for restora­ posed to dehydration for longer than a few min­
tion with glass ionomer should always be condi­ utes.
tioned but the enamel margin of the cavity to be ■ The type II. 1 cement remains susceptible to wa­
restored with composite resin must always be ter uptake for at least one hour and up to 24 hours
etched. after placement and if it is not properly protected
it will lose both translucency and physical prop­
erties.
Ion exchange adhesion
■ The most effective method for early protection is
to paint over the newly set restoration a low vis­
One of the greatest hazards in restorative dentistry
cosity, light activated, resin enamel bond immedi­
is microleakage between a restoration and the cavity
ately after removing the matrix. Light activate the
walls or floor. As long as they are present bacteria
bond before releasing the restoration to the envi­
and their toxins will cause a continuing inflammation
ronment. This will ensure stability within the ce­
within the pulp tissue so elimination of micro leakage
ment for the first onerhour during which time the
is essential. The union between glass ionomer and calcium polyacrylate chains can complete their
tooth structure arises as a result of an exchange of formation and the aluminium poly aciylate chains
ions. When the newly mixed cement is adapted to will then become dominant.
either enamel or dentin there will still be a quantity of ■ It must be noted that all glass ionomers may lose
free polyalkenoic acid within the cement. Because of water for periods between two weeks and six
its low pH the acid will attack the tooth surface and months after placement because not all water is
release calcium and phosphate ions which will be . fully bound within that period. The resin-modi­
free to mix with the matrix of the cement Further re­ fied forms of glass ionomer were developed to
lease of ions buffers the reaction and a new material overcome this problem however they also remain
containing ions from both the cement and the tooth susceptible to dehydration for some time after
will begin to form and set at the interface. The new placement so they also should be sealed.
material will be firmly attached to both sides of the
union and will be stronger and more resistant to acid Biocompatibility
attack than either the tooth structure or the cement. • The glass ionomers show a high degree of com­
Some degree ofbond is also developed between glass ♦ patibility with living tissues. The polyalkenoic
ionomer and the collagen fibres of the dentin. This acids used as the Equid are mild adds with a high
arises through either hydrogen bonding or metallic molecular weight and a long complex chain for­
ion bridging between the carboxyl groups on the mation. This makes it difficult fortheacid to per­
poly acid in the cement and the collagen fibres in meate through dentin tubules and even if it do&s
tooth structure. it will not produce a vigorous reaction,
■ Another reason for the relatively high
The strength of this ion enriched material has to be biocompatibility is the presence of free fluoride
properly assessed. Failure of the union will be cohe­ ions within the set cement. Bacteria such as Strep­
sive in either the tooth or the cement rather than tococcus mutans is unable to thrive in the pres­
adhesive at the interface. Therefore.it is important to ence of fluoride so theie will generally be a low
understand the term bond strength in relation to the accumulation of plaque on the surface of a glass
glass ionomers. ionomer.
 I TEXTBOOK OF PEDODONTICS

■ Again in the absence of bacteria the pulp shows Limitations

an ability to recover rapidly and defend itself from ■ Resistance ¿0 fracture is one of the main limita­
inflammation. It is possible to place a glass tions to the use of glass ionomer. It is generally
ionomer directly over a mechanically exposed quite satisfactory for a one surface lesion but a
pulp and expect to find secondary dentin forma­ two surface lesion is always at risk. Resistance to
tion in immediate apposition to the cement. ^TMtfture also depends on the particle size of the
powder and particle size distribution.
Ion release ■ Improvements to enhance strength of glass
ionomer will have to be. of chemical origin or
Glass ionomers show a steady release of flouride through the elimin ation of microporosities.
ions throughout its life span without in any way af­ ■ Resistance to abrasion and wear is a little below
fecting the physical properties of the restoration. The that of composite resin.
fluoride ion remains free of the matrix formation so ■ They also remain susceptible to dehydration
that, immediately following placement, there will be a throughout lifespan so patients with a dry mouth
generous flow that will reduce steadily over the next should not have their teeth restored with glass
month or thereabout. The level will then settle to a ionomer.
steady flow amounting to a level of about 10 ppm in
the ambient saliva. If the ambient level is raised sub­ COMPOSITE RESINS
stantially for brief periods, such as during a topical
fluoride application, then fluoride ions will return to Apart from the glass ionomers, the only other mate­
the restoration. This means that the restoration can rial that has the ability to restore aesthetics and to
be regarded as a fluoride reservoir. develop and maintain adhesion in the oral environ­
ment, is the composite resin. However their ability to
It has also been shown recently that a similar ex­ adhere long term to tooth structure is limited to
change of calcium and phosphate ions can occur in enamel only. %
i
much the same way. Clinical evidence also suggests
that there is a degree of remineralisation under a glass History of composite resins is given in Table
ionomer restoration and it is assumed that the re­ 7.3
lease of all three ions has a positive bearing on this
activity.

Table 7.3: History of composite resins

Late 1930s ■ First mention of the methyl methacrylates.

Kramer and 1949 « Published several papers on a number of materials in this
McLean category.
Buonocore 1954 • Development of a micro mechanical adhesion to enamel
simply by acid etching the enamel for up to one minute
rather than applying a thin coat of a very low viscosity resin.
Bowen 1960s ■ Proved the value of including a variety of fillers.
■ Also modified the resin formula from a relatively simple
methyl methacrylate to a far more complex bisphenol-A
diglycidyl dimethacrylate and the modern concept of 'filled'
or ‘composite resin’ was generated.
 SECTION 7 : PEDIATRIC RESTORATIVE DENTISTRY |

Classification ■ Initiator system to activate the setting mechanism

■ Stabilisers (inhibitors)
Based on filler particle size and size distribution Lutz ■ Pigments (colouring agents)
and Phillips (1983)
^Wptions in composite resins
lypel: macro filled composttowtin Based upon the forgoing information there have been
This type is also known as conventional or tradi­ further variations developed in the composite resin
tional. Because of the relatively large particle size, range based largely upon the filler particles and their
this group exhibits a pattern of unacceptable wear size distribution.
both of itself and of the opposing tooth.
Flowable
Type 2: micro filled composite resin The term flowable has been developed to indicate a
The fillers in this material are amorphous silica parti­ composite resin which is relatively simple to place
cles of 0.04 mm average diameter. With such small into a cavity in contrast to the standard hybrid mate-
filler particles they are translucent and highly aes­
thetic but high filler loading is difficult to achieve. Such a flowable material is manly used in the case of
The wear resistance is low and they cannot sustain a a deciduous tooth. The flowablity of the composite
high filler loading. resin is improved by reducing the filler content

Type 3: hybrid composite resin Packable

These are also known as small particle composites. Another term has been introduced to differentiate a
They contain a combination of macrofiller particles material from a standard hybrid composite resin and
with a proportion of microfiller particles and are prob­ that is the term packable. The difference is achieved
ably the most commonly used composite resins. The by varying the particle size and size distribution
main variation is in the proportion and distribution though the water uptake and the wear factor will re­
ofthe various particle sizes because this will control main standard and acceptable. The main difference
the ability to fill the resin and increase the percent­ will be in the feel of the material when being placed
age loading. into the cavity. The material will be less likely to stick
to the packing instrument and be withdrawn from the
Constituents cavity during placement.

The chemistry and setting reaction of a composite Chemically activated systems

resin is very complex so there are a number of differ­ These materials are marketed as two paste or pow-
ent chemicals and materials incorporated, each with der/liquid systems. One part will contain an initiator,
a specific function and the proportion is likely to benzoyl peroxide, the other part contains a tertiary
vary from one manufacturer to another. aromatic amine accelerator and combination of two
« An organic resin component that forms the ma­ parts will yield free radicals. These radicals initiate
trix e.g. BisGMA polymerisation of the resin.
■ Inorganic filler: These may be
a. Macro fillers with a particle size of about 5-30 Visible light activated systems
mm e.g. glass, quartz, ceramic etc. Single paste, visible light activated composite resin
b. Micro fillers with a particle size of 0.04 mm e.g. systems contain a two component initiator system,
amorphous silica. comprising a dik clone and a tertiary amine. The pho-
■ Coupling agent applied to the particles to unite tosensitive diketone, usually 0.2-0.7%
the filler to the resin silane. camphoroquinone, absorbs the radiant energy of
 *E>I TEXTBOOK OF PEDODONTICS

wavelength approximately 470 mh. At the appropri­ different composite resin is associated with the type
ate stage of excitation, the diketone combine with and amount of monomers and diluents.
the amine to form a complex that breaks down to
release free radicals that then initiate polymerisation The degree of polymerization will also have a bear­
of the resin. « ing so that, if the curing time is reduced by 25% there
will be a 2 fold increase in sorption and a 4 to 6 fold
Other systems increase in solubility. Both the long term durability
Dual activated composites have both a light acti­ of the restoration and its colour stability will be seri­
vated and a chemically activated initiation system ously affected by inadequate polymerization.
and are packaged as two pastes. The light activation Rapid thermal changes may also cause break down
mechanism is used to initiate polymerization and the of the silane coating and in micro filled composites.
chemical activation is relied upon to continue and The bond between the prepolymerized particles and
complete the setting reaction. the matrix is a potential site for hydrolytic failure.

PROPERTIES OF COMPOSITE RESINS Polymerization contraction

The resin matrix in a composite resin is highly sub­
Polymerization ject to a setting contraction whether it is light acti­
The actual chemistry of the setting reaction is rea­ vated or auto cured. The problems and risks are less
sonably complex but is typical of all resin in restoring deciduous teeth because the cavities are
polymerization. In a chemically activated composite relatively small and it is therefore somewhat easier to
resin, the reaction takes place almost uniformly get light activation to penetrate the relatively short
throughout the bulk of the material. In the light acti- distance to the base of the restoration.
vated systems, the depth to which activation will
As the material sets first in proximity to the activator
ccur is dependent on a number of factors. It is im-
light the contraction will be towaMs the light, thus
portant to note that much of the resin not activated
tending to pull the resin away from the cavity walls
initially by the light at the time of curing will remain
and floor. *
unset.
With chemically activated composites the contrac­
In both systems a significant proportion of the meth­
tion develops more slowly and evenly with a ten­
acrylate groups remain unreacted even after some
dency to draw towards the center of the restoration.
hours. The quantity of unreacted methacrylate groups
The polymerization contraction with either material
f will be influenced by the concentration of the differ­
has a substantial impact on adaptation to dentin,
ent monomers. Most of the chemistry of the setting
marginal adaptation and marginal seal. Ina large cav­
reaction and the consequent contraction will take
ity with weakened cusps there is a tendency for cusp
.'|U'Withinthe first few seconds during light acti­
deformation leading to post-restoration sensitivity
vation and the remainder will be complete within two
and even fracture at the base of a cusp.
jj| days.
Wear
> Water sorption andsolubility
Clinical wear of the composite resin remains one of
| Water sorption is higher for micro filled resins and
the main weaknesses in its use as a restoration on
H for hybrid and macrofilled resins. A minimum amount
load bearing surfaces.
* of water sorption is essential to a newly placed com­
posite resin because it will bring^bout a degree of Regardless of the material, clinical wear is associ­
expansion and help to counteract setting reaction. ated with a roughening of the surface of the restora­
\feriation in the water sorption and solubility of tion, due in part to scratching of microfilled compos­
 SECTION 7 : PEDIATRIC RESTORATIVE DENTISTRY |

ites and partly due to loss of particles and frictional Injuvenile enamel there is less mineral and more or­
contact in the case of macro filled composites. The ganic collagen present and therefore the etch pat­
slightly greater resistance to wear of a heavily filled tern is quite different There will be more waterpresent
micro filled composite is consistent with the greater because of the presence of dentin tubules and their
resistance to sliding wear shown by this material. direct access to the pulp and the amount of fluid flow
Therefore it is desirable to use the most heavily filled will only be enhanced following acid etchingbeoause
material available regardless of possible difficulty in it will lead to opening and funneling of the tubules.
clinical handling. In a deciduous tooth even a small cavity will be rela­
tively close to the pulp and therefore there will be a
CLINICAL STEPS (Fig. 7.19a, 19b) greater density of tubules on the floor of the cavity
and a relatively greater fluid flow.
Etching and bonding
An essential prerequisite for the micro-mechanical The goal of a resin dentin bonding agent is to attach
attachment is that the enamel should be etched with composite resin to healthy dentin and to seal the
37% orthophosphoric acid to demineralize the enamel dentin tubules against the entry ofbacteria and their
toadepthof 20 to 30 pm and render it porous. Avery toxins. Hus will avoid post restoration sensitivity
low viscosity unfilled resin is then flowed over the caries and loss of restoration. Bonding to dentin re­
surface and allowed to soak in to the porosities for quires the removal of all demineralized affected den­
about 30 seconds before it is light activated. Com­ tin and this is not always desirable, particularly in a
posite resin is then built over the resin bond. deciduous tooth where there will be little enough
dentin remaining above the pulp and an exposure is
Prerequisites for etching undesirable. It is possible through the use of glass
First, the enamel at the cavity margin must be fully ionomer to remineralize some ofthe dentin and this is
mineralized and soundly based on healthy dentin. the preferred method of sealinga cavity in a decidu­
Also there must be no micro cracks present on the ous tooth.
tooth. The best union will be developed at the ends
of the enamel rods rather than along the long sides Principles to successful resin-dentin bonding
so it is desirable to develop a reasonably long bevel ■ Dentin should be etched to remove smear layer
at the cavo- surface margin. and dentin tubule plugs

Fig. 7.19a Esthetic restoration for localised Fig. 7.19b Teeth* restored esthetically by
enamel hypoplasia veneering
 €ЕЭ I TEXTBOOK OF PEDODONTICS

» Etching should be sufficient to demineralize the curing, the resin will shrink.towards thé tooth struc­
surface layer of both inter and intratubular dentin ture rather than away from it. As it is not possible to
leaving collagen fibres exposed dnd available for excessively light activate any composite resin it is
a mechanical interlock with the resin recommended that the increments be as small as pos­
» The spçgàçe should be thoroughly washed to re­ sible and that the light activator be applied from many
move all remaining etchant positions during build up. However the position and
a The surface should remain wet but not flooded direction of the first application of the light is critical
a Apply a hydrophilic primer containing acetone, to the over-all success of the restoration.
or similar to guide and facilitate penetration of
the resin adhesive around the exposed collagen Depth of cure
fibers. In view7 of the often limited access to the oral envi­
a Finally apply the resin adhesive and cure before ronment in a child patient the depth of cure of a com­
Applying composite resin. posite resin is quite significant. It is imperative that
the activator light be placed within 1-2 mm of the
Delivery and placement surface of the newly placed restoration otherwise
The chemical cure and the dual cure materials will be the depth of cure will be limited.
packaged as a paste/ paste system or a powder/ liq­
uid system. Always follow' the manufacturers’ in­ Failure to light activate the composite resin to the
structions in detail and stay within the time param­ full depth of the restoration has important implica­
eters so as not to go beyond the working time. tions for the success and longevity of the restora­
tion.
Tri ensure complete adaptation to the cavity floor it
is desirable to place the freshly mixed material into Factors to be considered while curing.
the disposable syringe and then tamp the material « The degree of cure will decrease with increasing
into the cavity with a small plastic sponge. depth
■ Increased time of exposure to the light will in­
The light activated materials will always be delivered crease depth of cure. 1
in light proof carpules or syringes which have been ■ The more heavily filled the resin and the larger
loaded under vacuum. This means that they are free the particle size, the greater depth of cure. Micro
of porosity at the time of delivery7. filled resins will cure to a depth of 2-3 mm only
while hybrid resins may cure to a depth of 4-5
Placement must be undertaken with care and atten­ mm
tion to detail with particular reference to the depth of ■ Lighter the shade of the material the greater the
cure available through a curing light. The efficiency depth of cure and the greater the translucency
of the light must be checked periodically to ensure the deeper the cure.
that the lower layers are also cured adequately. ■ Light activator units vary in their light outputs
over time as well as with power fluctuations. The
incremental build up efficiency7 of each unit should be checked fre­
Due to the problems posed by light activation of quently
composite resins, it is essential to be prepared to ■ The tip of the light source should be placed as
undertake incremental build up of any restoration close as possible to the restoration and should
deeper than about 2.0 mm. Incremental placement never be more than 4 mm away.
means placement of the composite in small quanti­ ■ The depth of cure should be measured from the
ties in selected areas of the cavity and then directing face of the activator light.
the light activating unit in such a way that, while
 SECTION 7 : PEDIATRIC RESTORATIVE DENTISTRY |

■ Curing through tooth structure will reduce the

depth of cure to the same extent as if curing
through a composite resin of similar opacity.

Limitations of composite resins

■ Both the resin and the fillers used are anhydrous
and completely inert. However some of the minor
constituents such as HEMA, have been identi­
fied as allergens and pose a potential risk. It has
been shown to be identifiable in the pulp tissue
in certain circumstances and care should be exer­
cised in its use.
■ Any unreacted polymer chains may be an irritant Fig. 7.20 A traditional amalgam restoration tn
to the pulp and lead to post- insertion sensitivity. the distal of deciduous fir&t molar
■ The tissue cells respond less favourably to com­
posite resin than they do to glass ionomer and it biocompatible and it has even suggested that it is
has been postulated that incomplete cure of the carcinogenic. There is no convincing evidence at all
resin is the prime cause of this. for these claims and there has been adequate sup-
port for its continuing use from all the prime scien­
Clinical considerations tific authorities throughout the world.
Clinical placement techniques are probably the most
significant factors in success or failure. Types of dental amalgam alloy
I. a. High copper alloy;
In pediatric dentistry a restoration will not be ex­ Copper content more than 12%
pected to last for more than a few years so a limited b. Low copper alloy;
amount of wear can be tolerated. However a rela­ Copper content less than 6%
tively large setting shrinkage will be undesirable. c. Gallium alloy
Aesthetics and fracture resistance will not be of great
significance but the ability to bond effectively to IL based on particle shape and type
both the enamel and dentin will be relevant. There a Lathe cut; irregularly shaped filings produced
will often be a relatively short concentration span by cutting an ingot of alloy on a lathe.
from the patient as well as limited access to the oral b. Spherical partide; produced by atomisingthe
cavity so simplicity ofplacement techniques will be alloy, whilst still liquid into a stream of inert
important There is often a clear choice between com­
posite resin and glass ionomer and the operator must
be aware of the relevant properties of both so that a III. based on zinc content
logical decision can be made. a. Zinc containing; alloys with more than 0.01%
zinc.
AMALGAM (Fig. 7.20) b. Zinc free; alloys with less than 0.01% zinc

The remaining plastic restorative material of value in IV “y2content”

the restoration of deciduous teeth is amalgam. This Amalgams may be described as y2 containing and
remains the most reliable and inexpensive material of y2 free.
all. There have been a number of scare campaigns
over the recent years suggesting that amalgam is not
 | TEXTBOOK OF PEDODONTICS

Table 7.4: Constituents

Com position of low copper Composition of high copper
amalgam alloys (Weight %) amalgam alloys (Weight %)
■ Silver 68-70% ■ Silver 40-60%
• Tin 26-28% - Tin 27-30%
■ Copper : 2-4% « Copper 13-30%
• Zinc 0-2% ■ Zinc 0-2%
■ Mercury 0-3% ■ Mercury. 0-3%

a. Low copper amalgams contain the Sn-Hg mixed mass is dropped on to the bench from a height
phase which is called the y2 phase to distin­ of approximately 30cm. If the mix is diy and crumbles,
guish it from the y phases of the Ag-Sn and the trituration time should be increased. A well mixed
Ag-Hg alloy systems. amalgam should stay together when dropped on the
b. Within several hours after amalgamation, all bench but should be a little flattened and retain a wet
correctly manipulated high-copper amalgams gloss on the surface. It is better to slightly over tritu­
are y2 - free. rate than to under triturate an amalgam because
greatly extended trituration may reduce plasticity;
Constituents (Table 7.4) shorten working time and increase final contraction.

Amalgams that contain zinc appear to exhibit a lower Condensation

rate of marginal failure'underclinical loading but they This refers to incremental placement of the amalgam
tend to exhibit excessive delayed expansion if con­ into the prepared cavity and compression of each
taminated with moisture during placement. A number increment into the other increments tolform a con­
of elements, such as indium, palladium, and platinum, tinuous homogenous mass that is well adapted to all
may be included in the alloy.in minor quantities. the margins, walls and line angles. It is best carried
out using hand instruments with a smooth flat face
Packability that can deliver reasonable force, per unit area, to
This refers to the resistance offered by the amalgam the amalgam and compress the layers together. Me­
to the forces of condensation used in placing the chanical condensers are available and reduce the need
amalgam. It varies according to the size and propor­ for application of load. However there is an undesir­
tional distribution of lathe- cut or spherical particles. able generation of heat and mercury vapour. Ultra­
Amalgams containing only spherical particles are sonic condensation has been suggested but it is not
relatively easy to pack. recommended because^t allows the release of con­
siderable quantities of mercury vapour into the am­
Trituration bient atmosphere with a consequent risk to the op­
The object of trituratibn is to completely wet the en­ erators.
tire surface of all the alloy particles with the mercury,
to bring about the process known as amalgamation. Placement andfinishing
Amalgamators are made to work at different speeds Following trituration the amalgam should be con­
and the action should be checked periodically The densed into the cavity within four minutes. It can
efficiency can be tested with a trial mix. The freshly then be burnished towards the margins and carved
 SECTION 7 : PEDIATRIC RESTORATIVE DENTISTRY |

to an approximate occlusal form. At a subsequent it to puddle in the comers. It should then be light
appointment any necessary final adjustment can be activated before placing the amalgam so that it
carried out to the occlusal and proximal surfaces. will not be incorporated in the amalgam during
condensation.
Structure ofthe set amalgam
Provided the minimal amount of mercury, commen­ Limitations
surate with complete amalgamation, is incorporated The biocompatibility of amalgam has been the sub­
initially, and then proper condensation techniques ject of extensive investigation, particularly in rela­
are carried out, approximately 35-50%of the final vol­ tion to the presence of mercury. Mercury in dental
ume of the set amalgam will consist of unreacted amalgam may pose threats to the health of patients,
portions of alloy particles, held together by the y to the health of dental care providers and to the en­
phase matrix. vironment.

Moisture contamination Alternative to amalgam

It is essential to keep the amalgam completely free In view of the mercury presented in amalgam a mer­
from moisture contamination during the entire place­ cury free alloy has been suggested. This is gallium.
ment procedures following trituration. The cavity Certain drawbacks ofdental amalgam, noticeably that
must be completely dry and free of gingival seepage of potential mercury poisoning have lead to the
or haemorrhage. Inclusion of water will lead to in­ development of newer materials. One such material
crease in corrosion and tarnish with a reduction of - is gallium alloy, a mercury free metallic substitute to
physical properties. A zinc containing amalgam will silver amalgam. A study was conducted in our de­
develop a delayed expansion. partmentusing gallium alloy as a restorative material
in pediatric patients and it has shown encouraging
Marginal sealing and bonding results.
This means that a newly placed amalgam will be sub­
ject to a degree of microleakage and it is desirable to LINING MATERIALS
take steps to overcome this. There are two alterna­
tives available for this:
1. Copal varnish. This has been used for many years placea fining material on the floor of a cavity prior to
and provides an immediate seal that will last for a placement of the finaliestoration. There have beep a
limited time only. It is recommended that it be number of reasons for their use including sedation
placed in two applications of a very thin coat and of a preexisting pulpal inflammation as well as pre­
the vehicle be allowed to evaporate briefly. vention of further irritationfrom sudden te
2. Resin bond. There has been a move lately to re­ change.
place die copal varnish with an unfilled resin bond
such as those used as an enamel bonding agent The materials used in the past and the reasons for
with composite resin. The theory behind this is their use can be listed as follows-
that the resin bond will develop some degree of
union with enamel and dentin on one side and Zinc phosphate cement: This was used exten
amalgam on the other side and thereby both seal
the margin as well as strengthen the tooth crown strong enough to accept the load imparted to the
and compensate to some degree for the destruc­ dentin by condensation of an amalgam r
tion caused by cavity preparation. A bond with a tion. It was accepted that there was no the
very low viscosity should be used and placed
carefully in a single layer, taking care to not allow
 €E0 I TEXTBOOK OF PEDODONTICS

pulp. Its use was continued for a long time be­ barrier to microleakage of bacteria under a resto­
cause it was expected that an additional layer of ration.
this cement would protect other weaker lining
materials that became popular, from disturbance RECENT MODIFICATIONS IN RESTORATIONS
during condensation of aipalgam. It is regarded
PREVENTIVE RESIN RESTORATION
as out of date at this time.
With the advent of newer restorative materials the
ideology of sealing for prevention of fissure caries
2. Zinc oxide * eugenol
. This became popular be­
rather than ‘the cavity extension for prevention’ came
cause the anti bacterial properties of eugenol were
into practice.
recognised as well as the sedative effectiveness
of zinc oxide. It is used as a temporary sedative
Preventive resin restoration utilizes the invasive and
dressing over a large cavity with an inflamed pulp
non-invasive treatment of borderline or question­
beneath. It is effective because it provides a seal
able caries. The resin placed in the carious areas and
around the periphery of a cavity simply because
adjacent caries susceptible areas, seal them from the
bacteria cannot penetrate past the eugenol. Fast
oral environment and provide a valuable treatment
setting types were developed to allow this to be
alternative to conventional restorations like amalgam.
used alone as a lining but, as it is relatively weak,
it does not offer support for an amalgam restora­
Types of carious surfaces treated
tion placed over the top.
Three types of preventive resin restorations are per­
formed depending upon the carious lesion.
3. Calcium *
.
hydroxide This was introduced as a
1. Group A: Deep pit and fissure susceptible to car­
lining because of its antibacterial properties as
ies.
well as the theory that the excess calcium ions
■ The preparation size is very small
present in the cement would be available to the
■ Unfilled resin or sealant is used to restore the
pulp and would encourage remineralization within
preparations of carious lesions involving
the pulp chamber. The fact that it is very alkaline
round bur of size Vi or less. 1
with a pH 13 ensured the inability of bacteria to
thrive in its presence and this helps to stabilise
2. Group B: Minimal exploratory carious lesion
conditions on the floor of a cavity. If placed too
■ Since the caries can be explored the prepara­
close to the pulp it will cause necrosis of the sub­
tion needs to be extended
jacent soft tissue but, in the absence of bacteria,
■ Preparation size is by size 2 round bur
the pulp is likely to survive beyond the necrotic
■ The restoration requires some filler to the un­
area. It will then lay down a calcific barrier a short
filled resin
distance away and it was this which lead to the
assumption that it was calcium ions from the lin­
3. Group C: Isolated carious lesion
ing which prornoted the repair. It has recently been
■ The caries is very definite and requires con­
shown that calciùni ions do not transfer from the
siderable preparation
lining to the pulp but the conditions developed
■ Larger size bur is used following which a small
by its presence allow the pulp to carry out its
bevel is placed at cavo-surface margin
own repair process.
■ Unfilled resin layer followed by filled compos­
ite is introduced into the preparation
4. Glass ionomer: This is now the material of choice
for lining a cavity because it is an effective barrier Steps of placement:
to temperature change and also provides an ion The steps are the same as for the placement of resin
exchange adhesion that is the most effective restoration.
 SECTION 7 : PEDIATRIC RESTORATIVE DENTISTRY | CTO

Technique Precaution
Placement of preventive resin restoration utilizes prin­ Early loss of preventive resin restorations similar to
ciples of acid etch technique similar to those of seal­ pit and fissure sealant has been attributed to insuffi­
ant placement with the exception of caries removal cient etching. Thus it is very important to maintain
from isolated pits and fissures. excellent isolation from salivary and moisture con­
tamination for the long term success of preventive
Clinical perspective resin restorations.
Preventive resin restoration has shown to improve
the long term health of teeth. A.R. T RESTORATIONS

Materials like glass ionomer cement have been tried The placement of a restoration in a large occlusal
as glass ionomer rest a seaf to incorporate their cavity can be done by means of art technique or
various advantages which are: Atraumatic Restorative Treatment. Once the bacte­
■ Fluoride release benefits and rial involvement is eliminated and further ingress pre­
a True adhesion to enamel and dentin vented it is possible for the tooth structure to heal.
In the past a paste of zinc oxide and eugenol was
However they have inherent disadvantages such as
used to provide the seal and the anti caries activity.
a Technique sensitivity and
Unfortunately it was too weak and subject to water
a Poor wear resistance which makes unsuitable as
uptake and subsequent degeneration. In recent times
restorations in occlusal contact.
it has been realised that glass ionomer will perform
exactly the same way and will also last much longer
Advantages of preventive resin restoration (Fig. 7.21 )
in the oral environment.
1. Minimal cavity preparation required thus prevents
unnecessary removal of healthy tooth structure
History
for retention.
A group in Zimbabwe and another in Thailand be­
2. Seals caries thereby halting the destruction of
gan experimentation to check longevity and effi­
tooth e.g. Teeth with pit and fissure, dens
ciency and their results were so encouraging that
evaginatus.
the system has been adopted by the WHO and is
3. Loss of the restoration and subsequent replace­
being promoted world wide as a useful technique for
ment proves to be less invasive than that for con­
communities that lack regular dental facilities.
ventional restoration like amalgam.

Conventional restqrgtjon leading to Preventive resin restoration with

gross tooth loss minimal tooth loss
Fig. 7.21 Molar life cycle with conventional and PRR.
 CTTÎfr I TEXTBOOK OF PEDODONTICS

Method LAMINATION TECHNIQUES

In this technique there will be only hand instruments There is a very significant relationship between the
available to open and clean the lesion and the re­ composite resins and glass ionomers and the most
storative materials will be hand mixed. A small selec­ important factor isthat they can be successfully com­
tion of hand instruments has been designed to suit bined so that the strength of one can adequately
the system. There is a type of hatchet with multiple compensate for the weakness of the other. Both are
blades to assist in opening through the enamel and acceptably aesthetic but composite resin, with present
provide immediate access to the lesion. There is a techniques, will not bond adequately long term to
group of spoon excavators suitable for cleaning the dentin. This applies particularly in deciduous teeth
walls and it is expected that the floor will be left alone and must be regarded as a significant weakness. On
as far as possible. It is only necessary to clean the the other hand glass ionomer lacks fracture strength
cavity to the extent the walls are clear of the infected to the extent that it is limited in its ability to restore a
layer so that the ion exchange adhesion can be de­ marginal ridge which is under occlusal load. But with
veloped. Aise X’ is a neei^ t0 create sufficient a little care the two materials can be united to the
room for asubstantial thickness of glass ionomer so extent that they make a very useful combination and
that it will withstand occlusal load. The glass ionomer can thus offer sufficient longevity for the average
is provided as a powder and liquid ready for hand restoration of reasonable dimension.
mixing. A conditioner is used prior to the placement
of the cement. At the stage of placement, following The technique for construction of a laminated resto­
cavity preparation an additional drop of liquid is ration involves the use of a fast setting high strength
placed in one corner of the mixing slab and once glass ionomer as a base, or dentin substitute, wili
isolation has been achieved this liquid is picked up allow for the development pf a sound ion exchange
on a wet cotton pellet and placed into the cavity as union between the dentin arid the restoration. Place­
the conditioning agent. It is wiped around the cavity ment of the most wear resistant composite resin over
and then immediately washed out using one or more this will provide an enamel replacement that is aes­
wet cotton pellets. This will remove debris and ex­ thetic and long lasting.
cess polyacrylic acid and prepare the cavity walls for
the ion exchange adhesion. Dry the cavity with fur­ Clinical technique (Fig. 7.22a, b, c)
ther cotton pellets and prepare to mix the cement. Prepare a conservative cavity such that the adhe­
sive materials can support the undermined enamel.
The mix should be thick and it should be placed in Condition the cavity, in preparation for the place­
the cavity and the gloved finger used as a matrix. ment of glass ionomer. For a proximal lesion place a
Thefinger can remain in place until the initial set has short length of mylar strip as a matrix and support it
occurred finis ensuring that the restoration remains gently with a wooden wedge. Place the glass ionomer
dry for that period of time. Cover the cement with and tap it gently into place to ensure good adapta­
varnish to keep the cement free from contamination tion of the cement to the floor of the cavity so that
till final setting takes place. will.be free of porosity Allow the glass ionomer to
set or if a resin modified material is being used, apply
Adjust the occlusion using spoon excavators. This the activator light from different positions for at least
technique has now been in extensive use in develop­ 40 seconds.
ing countries for several years and the success rate
justifies its continuing use. The cavity can then be redesigned as a composite
resin cavity taking into account the relative flexibil-
 SECTION 7 : PEDIATRIC RESTORATIVE DENTISTRY |

Fig. 7.22a Occlusal fissure on lower molar Fig. 7.23a A patient presented with mild
opened conservatively with a very fine tapered symptoms in lower second molar tooth.
diamond bur and conditioned for 10 seconds Illustration shows fissures involved with a
with 10% poly acrylic acid degree of demineralisation

Fig. 7.22b The illustration shows the glass Fig. 7.23b A cavity has been opened to com­
ionomer being painted prior to light plete the exploration of the lesion. The affected
activation dentin on the pulpal floor has not been cleaned
as it is expected to heal

Fig. 7.22c The same patient showing restora­ Fig. 7.23c A cavity conditioned with 10%
tion immediately after light activation polyacrylic acid, an throughly washed and
lightly dried
 €J© | TEXTBOOK OF PEDODONTICS

Fig. 7.23d The centre cavity has been restored Fig. 7.23e The area to be restored with com­
with resin modified glass ionomer built posite resin is etched with 37% ortho-phos­
incrementally and each section light-activated phoric acid for 15 seconds
for 20 seconds

Fig. 7.23f The glass ionomer has been lami­

nated with a hybrid composite in the area that
will bear the heaviest occlusal load

Fig. 7.23g A radiograph of finished restoration Fig. 7.23h Same restoration showing the
comparison with amalgam placed in the first
molar tooth some years ago
 SECTION 7 : PEDIATRIC RESTORATIVE DENTISTRY J

i ty of this material along with its ability to unite with On the other hand the anatomy of the deciduous
the glass ionomer. The cavity must be atleast 2.0 mm tooth suggests that intervention should be under­
deep, all enamel margins should be exposed so that taken early rather than later because of the risk of
the full micromechanical attachment of composite pulpal involvement. At the same time there are con­
resin to enamel is available. If the proximal box is so siderable risks involved in cutting a cavity in certain
deep that there is no enamel at the gingival margin areas, particularly in the proximal surfaces of decidu­
then leave the proximal Moor as glass ionomer only. ous molars in which the mesiobuccal pulp horn is
Having prepared the cavity both the enamel and the often very close to the surface. So the risk/benefit
glass ionomer should be etched with 37% ratio will need to be assessed in may cases before a
orthophosphoric acid for 15 seconds only. Wash the treatment plan is finally formulated.
cavity thoroughly and dry lightly. Now paint the en­
Having decided on the need to prepare a cavity there
tire cavity with a light coat of a resin enamel bond
are at least three alternatives available.
and light activate it. The matrix system can now be
repositioned as required and wedged tightly into Tunnel cavitv
place. The composite resin can now be built incre­ If the cavity is very small aid more than 2.5 mm from
mentally taking care to add no more than 3.0mm in the crest of the marginal ridge, it is possible to de­
depth in any increment. Light activate each incre­ velop a so called tunnel type cavity. This involves
ment for at least 40 seconds and over build a little to approaching the dentin lesion from the occlusal fossa
allow for loss of bulk duringcontouring and polish­ just medial to the marginal ridge using a small ta­
ing. Following final contouring light activate once pered diamond cylinder at intermediate high speed
more for at least 40 seconds to ensure a complete under air water spray. Aim diagonally towards the
cure in depth (Fig. 7.23a, b, c, d, e, f, g, h). lesion and develop a small access cavity. Having
located the lesion upright the same bur and move it
The lamination technique can be utilised for the rein­ cautiously into the marginal ridge and lean it to the
forcement of any material that is regarded as insuffi­ buccal and then to the lingual to develop a triangular
ciently strong for a given situation. entiy tunnel into the carious dentin.

DESIGNING FOR PROXIMAL LESIONS Once the lesion has been identified use a small round
bur at low speed to carefully clean the gingival floor,
Plaque accumulates readily immediately below the the buccal wall and the lingual wall but leave the
contact area between any two teeth, anteriors as well pulpal wall untouched. Hie inner wall of the proximal
as posteriors. In the absence of good plaque control enamel can now be explored carefully for signs of
and regulation of refined carbohydrate intake the pH cavitation. If the wall is intact there is no need to
interproximally will fluctuate frequently to levels well break through to the external surface because the
below pH 5.5 and regular attacks of deminearalisation enamel will most certainly heal in the short term; In
may occur. There will be no occlusal load on these the presence of cavitaion lightly debride the walls of
lesions so plaque will not be forced into the develop­ the enamel cavity with a very small chisel to clean
ing cavitation as happens on the occlusal surface, fragile enamel prisms. The cavity is now reatty for
so progress through tooth structure may be quite restoration and the preferred material is a glass
slow. In the absence of cavitation there is always a ionomer. It can be syringed and tamped into place
chance that the lesion can be healed through and bn the assumption that there are clean wlls
remineralisation so the current recommendation is to around the full circumference of the cavity, these will
keep an early lesion under careful observation be­ be a complete seal and the potential for
fore proceeding to surgical intervention. remineralization of the pulpal wall if required (Fig.
7.24a, b).
Q0 I TEXTBOOK OF PEDODONTICS

Fig, 7.24a Tunnel cavity preparation in upper Fig. 7.24b The cavities were restored with resin
second molar and slot cavity preparation modified glass ionomer
in the first molar

Fig. 7.25a A cavity prepared on second molar

dictated by carious lesion

Fig. 7.25b A short length of mylar strip has Fig. 7.25c Glass ionomer has been syringed
been pre formed to shape and is gently into the conditioned cavity and tamped on to
supported by a wooden wedge the floor and axial wall to ensure good
adaptation
 SECTION 7 : PEDIATRIC RESTORATIVE DENTISTRY | ÎCTÊV

Internal preparation (Partial or blind tunnel) SMART MATERIALS

If the approximal enamel in relation to the lesion is
demineralised but not cavitated, it is not necessary While the quest for the ‘ideal restorative material’
to break through the enamel because it is likely that, goes on a newer generation of materials are being
- With good preventive follow up, it can be released. These materials, though some may not be
remineralised. commercially available, have the potentiai to replace
the currently used ones.
Slot cavity/Minibox restoration
The next alternative could be the preferred design
for the small proximal lesion in all deciduous teeth. It
has been loosely titled slot or box cavity and in­ that support the remaining tooth structure to theex­
volves approaching the lesion through the crest or tent that cavity preparation can be doneinthe most
outer surface of the marginal ridge. Entry should be conservative way. Some of these materials arc
very conservative in the beginning and it should be ‘biomimetic’ in nature, wherein there may beproper-
extended only as dictated by the extent of the lesion. ties that ‘mimic’ natural tooth substance such as
Confine the cavity to the extent of the caries only enamel or dentine better and one step further in die
and retain as much tooth structure as possible. The concept of tissue regeneration, wherein the tissues
restorative material of choice is the glass ionomer. can be regrowri in the oral cavity. Along these lines
BRAX -1 gene has been isolated, which is thought
As there will be a greater exposure to occlusal load
to be responsible for the control on enamel growth.
with this design there will be a greater need to con­
sider the advantages of lamination with composite
Even the current developments in existing materials,
resin (Fig. 7.25a, b, c)
notably composite and GIC, can also be applied to
make the materials ‘smarter’. To overcome some of
Proximal approach their deficiencies by use of CAD/CAM can make
The third potential approach to the proximal lesion designing of cavity preparation much easier and more
becomes possible only if the adjacent tooth is miss­ adaptable to each tooth, rather than a generalized
ing or else has a fairly extensive cavity already pre­ approach
pared in it This will allow a direct access to the le­
sion and can lead to a very conservative cavity with Self-Assessment
no involvement of the marginal ridge at all. Remove
only the completely broken down enamel sufficient 1. Whatisresin modified glass ionomer?
to allow access to the dentin, use a small round bur 2. What is the setting reaction for glass ionomer
to clean the walls but leave the axial walls alone. Use cement?
a radioopaque restorative material because it will need 3. What is ion exchange adhesion?
to be visible to another operator who may other wise 4.
mistake it for a carious lesion. 5. What is the difference between conditioning and
etching?
The advantages of above preparations in comparsion 6. What is meant by a smear layer?
with conventional Class II preparation are: 7. What are the pre requisites for etching?
■ it is conservative, maintains marginal ridge which 8. What is ‘zinc free’ alloy?
contributes to conserve the tooth strength. 9. What is amalgam?
■ Prevent the risk for iatrogenic damage to the ad­ 10. What is the indication of ART?
11. What are the merits and demerits oftunnel cavity
jacent approximal surface is minimised.
preparation? 1|||
■ A normal contact area is maintained
12. What is slot cavity?
 7.5 Semipermanent Restorations

Mount G J, Batra R, Tandon S

The alarming rate of failure for extensive class 2 res­ Polycarbonate crowns are designed to provide vari­
torations in primary molars and class 3 in primary ous advantages:
anterior teeth has compelled the researchers to dis­ ■ they save time
cover the semipermanent restorations The ■ are easy to trim and
polycarbonate crowns and the stainless crowns are ■ can be easily adjusted with pliers
one of these moderately recent advances. The semi­
permanent restorations are recominended to restore Technique for construction (Fig. 7.26a, b.c):
the lost tooth structure and stabilize it with these 1. Crown is selected according to mesiodistal width
prefabricated crowns.. and cervico-mesial length of the tooth while keep­
ing in mind the shade of the tooth.
POLYCARBONATE CROWNS 2. The tooth is reduced by about 0.5 mm to allow
space for the crown form labio-Iingually.
In pedodontic practiceJhe most common lesion in 3. Mesio distally the reduction removes the contacts.
anterior teeth is likely to be the result of nursing 4. 1 -2 mm of incisal reduction is carried out
bottle caries. These lesions will occur beginning on 5. Crown is selectively ground at gingival aspect
t he labial face of all anteriors and they progress rap­ 6. It is then lined with acrylic or composite material
idly as a diffused demineralisation of the entire sur­ 7 The preparation and the surrounding gingiva is
face of all existing teeth. The best that can be offered lubricated with water or saliva and the crown is
at this time is the stabilisation of the lesion without then seated. As the acrylic starts to set the crown
much in the way of a complete rebuild of the coronal is removed from the preparation and reseated a
anatomy. It is suggested that the first step should be number of times. This dissipates the heat during
to develop a clean periphery around the lesion using polymerization and prevents blocking into under­
a smallround bur whilst leaving the central portion cuts.
of the affected dentin intact and undisturbed for fear 8. The margins are trimmed and finished and the
of producing a pulp exposure. Tins will make it pos­ crown is cemented with luting acrylic cement.
sible to develop the ion exchange with glass ionomer Blanching of gingival tissues should be checked
and allow development of an effective seal. to avoid over extension into the sulcus.
Polycarbonate crowns are temporary crowns which
can be given as fixed prosthesis to deciduous STAINLESS STEEL CROWN
anteerior teeth which will get exfoliated in future.
These are contraindicated in: Stainless steel crown is a semi-permanent restora­
• severe bruxism tion used in the primary and young permanent teeth.
■ deep bite It was introduced as chrome-steel crown by
■ excessive abrasion Humphrey in 1950, which proved to be a favour to
 SECTION 7 : PEDIATRIC RESTORATIVE DENTISTRY | 31^

Fig. 7.26a Polycarbonate crown for anterior Fig. 7.27 Crown forms - Aluminium crowns on
teeth (Courtesy: 3M Product) left and 3M stainless steel crowns on right

Fig. 7.26b Cervical crimping of polycarbonate Fig. 7.28a Caries is excavated before the
crown to improve the adaptation placement of stainless steel crown
(Courtesy: 3M Product)

Fig. 7.26c Cementation of polycarbonate crown Fig. 7.28b Stainless steel crown in place
on left central incisor following cementation
 ! TEXTBOOK OF PEDODONTICS

clinical pediatric dental practice. Now it is commonly ■ Pretrimmed crowns (eg.Unitek stainless steel
called stainless steel crown. crowns,3M Co.,st. paul,MN;and Denvo
crowns,Denvo Co. Arcadia,CA).
The requirement of stainless steel crown is more fre­
These crowns have straight, non-contoured sides
quently found in deciduous dentition than in perma­
but are festooned to follow a line parallel to the
nent dentition because of 2 reasons:.
gingival crest. They still require contouring and
* First in a relatively small deciduous teeth ne­
some trimming.
glected caries can destroy the tooth’s integrity
faster than in the larger teeth of the permanent ■ Precontoured crowns (eg.Ni-Chro Ion crowns
dentition. and Unitek stainless steel crowns,3M
■ Second the deciduous teeth pulp is larger than Co.,stpaul,MN).
permanent pulp in relation to it dentin and enamel These crowns are festooned and are also
envelope. Thus it is difficult to make the dentinal precontoured though a minimal amount of
stump for a gold casting or to use a pin system of festooning and trimming may be necessary. (Ta­
retention for more extensive amalgam restoration. ble 7.27)

Thus, stainless steel crown is an efficient and reli­

COMPOSITION
able method of restoration of deciduous dentition. It
is also a most advantageous system of restoration ■ Stainless steel crowns (18-8)Austentic type of
because of its retention and resistance. alloy is used. For example Rocky mountain and
Unitek.
Advantages 17-19% ciiromium
« These crowns are far superior to multisurface 10-13% nickel'
amalgam restorations with respect to both life 67% iron and
span and replacement also and a most advanta­ 4% minor elements. *
geous system of restoration because of its reten­ The austentic types provide the best corrosion
tion and resistance. resistance of all the stainless steel.
$
■ They are acceptable to both the patient and the
■ Nickel-base crowns They are Inconel 600 type
dentist.
of alloy.
« They are also more cost effective because of com­
72% nickel
paratively simple procedures involved in restor­
14% chromium
ing even severely affected primary molars.
6-10% Fe
0.04% carbon
Objectives
0.35% manganese and
Objectives of using stainless steel crown restoration
0.2% silicon.
are:
• to achieve biologically compatible, masticatorily These alloys have good formability and ductility
competent and clinically acceptable restoration. necessary for clinical adaptation of crowns an 1 wear
■ to maintain the form and function and where pos­ resistance to resist opposing occlusal forces. The
sible, the vitality of the tooth should be main­ metallurgical characteristics ofNi-Chrome crown al­
tained. lows these crowns to be fully shaped and strain hard­
ened without a defect during manufacture.
DIFFERENT TYPES OF STAINLESS STEEL CROWNS
INDICATIONS
■ Un trimmed crowns (eg. Rocky mountain) these
crowns are neither trimmed nor contoured, require ■ Extensive decay in primary and young^perma-
lot of adaptation, thus are time consuming. nent teeth (Fig. 7.28a, b)
 SECTION 7 : PEDIATRIC RESTORATIVE DENTISTRY | flQ

Primary teeth with caries on 3 or more surfaces or For instance, developing class 5 lesion is a sign
where caries extends beyond the anatomic line an­ of poor oral hygiene and cariogenic diet When
gles. For example caries on mesial surface ofthe max­ this occurs in the preschool age child who also
illary and mandibular first molar. The proximity ofthe has class 2 lesion in the same tooth, the stainless
pulp on the mesial side make placement of an accept­ steel crown is indicated particularly in the first
able amalgam restoration difficult. primarymolar.

Primary incisors with class 4 lesions occuring me- ■ As an abutment:

sially and distally, along with a class 5 lesion on the For a space maintainer or prosthetic .appliance,
same tooth i.e. the primary anterior teeth that are for example a restoration for a first primaiy molar
extensively decayed from the nursing bottle syn­ when it is tobe the abutment for a distal extension
drome. appliance.
■ For teeth deformed by developmental defects or
anomalies: ■ Temporary restoration of a fractured tooth
Stichas enamel dysplasias or dentinogenesis im­
perfecta. ' ■ In severe cases of bruxism:
s i. The teeth may be soab reded that stainless steel
■ For teeth with hypoplastic defects: r crowns are required to restore the interarch verti­
They may be more susceptible to caries because cal dimension and prevent traumatic pulpal expo­
retention of the plaque occurs in hypoplastic de­ sure.
>
fects. In the placement of stainless steel crowns
on hypoplastic teeth, treatment may involve the In the mixed dentition phase, the stainless steel
crowning of the teeth in all 4 quadrants (often all crown adapted to the primaiy molars will assist in
posterior teeth). Thus there is a danger of alter­ preventingundue wear ofthe first permanentmb-
ing the vertical dimension by impinging on the
freeway space. So the crowns should be fitted
quadrant wise. Only when the previous crown is ■ Single tooth crossbite:
cemented then proceed with preparation of the In case wherFalbwer mandibular incisor lias been
tooth in the next quadrant. previously displaced labially, a reversed stainless
steel crown or a banded metal incline on the
If extensive abrasions have already resulted in a inlocked incisor with a guide plane at a 45 degree
loss of the vertical dimension, then a slight (less angle to the occlusion plane can be used. With
then 2mm) opening of the bite is acceptable. If the use of stainless steel crown correction oc­
the bite is opened more than 2mm,it will result in curs in lto2 weeks.
tenderness of the treated tooth and possibly in
an adverse pulp response. For replacing prematurelylost anterior teeth:
Double stainless steel crowns on abutment teeth
■ Following die pulp therapy
can be used for replacing the lost maxillary ante­
^Tnbbfliffieprimary and permanent teeth as pulp
rior teeth.
therapy leaves the treated tooth more brittle be­
cause of fluid loss, it is likely to fracture.
Factors To Be Considered In Pre-Operative
■ Asa preventive restoration Evaluation
If the patient has a high susceptibility to caries
manifesting it either by numerous gross carious ■ Dental age of the patient
lesions or by rampant caries and in a handicapped This is recorded by the root development of the
child whose lack of oral hygiene may encourage underlying tooth. When a primary tooth can be
further decay. expected to exfoliate within 2 years of restore-
 CTEl I TEXTBOOK OF PEDODONTICS

t io it, amalgam restoration can be done. However, approximates the M-D width of thé crown. The
failure of extensive amalgam restoration in the pri­ smallest crown that completely covers the prepa­
mary teeth can be frustrating. This can be over­ ration should be chosen.
come by an initial placement of stainless steel
crown. To produce steel crown margins of similar shapes,
examine the contours of the buccal and lingual
■ Co-operation of the patient marginal gingivae (Fig. 7.30a,b).
If the patient is uncooperative, whether it is due ■ Buccal and lingual marginal gingivae of the
to age(i.e <3yrs.) or due to negative behavior. If second primaiy molar resembles smiles with
the child is stubborn and does not want to coop­ greatest occlusal-gingival height of the clini­
erate, first a positive behavior has to be instilled. cal tooth crown about midway on the buccal
If child is unable to co-operate because of age(i.e and lingual surfaces.
<3yrs ) then a chair side GA may have to be con­ ■ Buccal marginal gingivae of the most mandibu­
sidered. In this case, since it is difficult to check lar first primary molar and many maxillary first
the correct occlusion so it is always better to keep molars is similar to a stretched out "S’, having
the stainless steel crown at the level or slightly greatest occlusal-gingival height located at the
below the level of the adjacent tooth. So that the mesiobuccal.
child does not have disturbed occlusal due to ■ The contour of the lingual marginal gingivae
premature contact. of all the first primaiy molars resembles smile.
« The occlusal-gingival height is located about
■ Motivation of the parents midway in bucco-lingual direction.
Whether the parents are willing to come for den­
tal visits for the follow-up. ■ Tooth preparation
L. A should be administered.
• Medically compromised/disabled children
For example in children with a heart problem, Isolation
prophylaxis has to be taken as in tooth reduction, Isolation has to be done with ¿otton rolls, which are
-subgingival procedure is done or in poor general held in position by cotton roll retainer. Use of rubber
condition of the child chair side GA has to be dam for isolation is mandatory. When it is not possi­
taken into account. ble to use rubber dam, as in case of terminal teeth in
arch, a gauze oral screen should be used to prevent
CLINICAL PROCEDURE the possible aspiration of a crown form.
■ Evaluate the preoperative occlusion Remove the decay
a. Take the alginate impression of U/L dental arch Decay is removed with a large round bur in a slow
of the patient. speed handpiece or with a spoon excavator.
b. Pour the cast in the dental stone. *
c. Note the dental midline and the cusp fossa
relationship bilaterally.
■ Selection of crown
The correct size crown may be selected prior to
the tooth preparation by the M-D dimensions of
the tooth to be restored, and a Boley gauge can
be used for this purpose
If the crown is not selected before the tooth re­ Fig. 7.30a,b (a) Proxmial marginal gingival
duction, after the tooth reduction it can be tissues of second deciduous molar appears to
selected as a trial and error procedure which frown and (b) Buccal surface appears to smile
 SECTION 7 : PEDIATRIC RESTORATIVE DENTISTRY |

After caries removal and pulp therapy, if necessary, and occlusolingual line angles are rounded by hold­
the previously carious area can be built up with a ing the bur at a 30-45° angle to the occlusal surface
quick setting reinforced ZnOE cement and/or zinc and moving it in a mesio-distal direction.
oxyphosphate cement.
RECOMMENDATIONS FOR PREPARATION
Steps in reduction
The aims of tooth reduction are: « How much occlusal reduction should be done?
a to provide sufficient space for the steel crown. Though various views have been expressed re­
■ to remove the caries. garding the occlusal reduction it is found that
a to leave sufficient tooth for retention of the about 1.5-2mm of reduction have to be done to
crown. obtain occlusal clearance. However as much of
the tooth structure as possible must be left for
Occlusal reduction (Fig. 7.31a) retention.
A 69L OR 169L bur is used to reduce the occlusal
surface by 1.5 to 2.Omm,following the cuspal outline ■ Which su rface should be reduced first, proxi­
and maintaining the original contour of the cusps. mal or occlusal?
Reduction of occlusal surface can be judged by com­ If the proximal reduction is done at the initial step,
parison with the marginal ridges of the adjacent teeth. even with utilization ofwedged rubber dam, some
a mount of gingival bleeding will occur. If blood
Proximal slices (Fig. 7.31b)
gets on the preparation, it will make the diagnosis
Place the wooden wedges in the interproximal em­
ofvery small pulp exposure difficult.
brasures. The wedges separate the adjacent teeth,
thus minimize the risk of damaging the tooth enamel.
Thus the best plan is to reduce the occlusal as
The bur (69L or 169L) is moved B-L across the proxi­
the initial step, removing any caries as part of
mal surface, beginning at the marginal ridges and at
that step. Next perform the necessary pulp therapy
an angle (10 degree) slightly convergent to occlusal
then proceed with proximal surface reduction.
surface. The depth of slice should be sufficient to
break contact with the adjacent tooth and it should
■ Considerations for retention capability of the
develop a finish-line below any existing caries. Prepa­
crown
ration should be taken gingivally far enough to avoid
It is not only mechanical preparation which is re­
the development of the ledge, whi h would make it
quired for the retention but the cementing me­
difficult to seat the crown properly (Fig. 7.31c). Be­
dium also plays an important role for the reten­
cause of cervical constriction of the primary tooth,
tion of stainless steel crown.
adequate depth of the proximal preparation will re-
s|^|ri^^ther edge finish line.
■ Special recommendations for preparation of
tooth
^^®^^Wthe buccal and lingual surface is either One has to concentrate on making the stainless
very minimal. Natural undercuts of steel crown more physiologically acceptable to
dBOOri^ce^'assists the retention of the stainless the gingiva as it is seen in our clinical practice
However; in some cases; as the first and also that cement increases the retentive
piiiif iholar, it is necessary to reduce the large buc­ capacity of all types of preparations. Reducing
calbulge. supragingival bulge with reduction extending
0.5mm below7 the gingival crest helps to obtain an
Round all the line angles acceptable gingival response.
Using a side of the bur or diamond, the occlusobuccal
 I TEXTBOOK OF PEDODONTICS

Fig. 7.31a Preparation of tooth to receive Fig. 7.32 Contouring done at middle 1/3rd of
stainless steel crown - 1.0 to 1.5 mm occlusal crown to produce belling effect
reduction

Fig. 7.31b Mesial and distal contact points Fig. 7.33 Crimping done at cervical 1/3rd of
are cleared crown to aid in tight marginal fit

Fig. 7.31c Cross-section showing crown Fig. 7.34 Stainless steel crown in place.
margin located approximately 1 mm Excess cement is removed using explorer and
subgingivally knotted dental floss
 SECTION 7 : PEDIATRIC RESTORATIVE DENTISTRY |

It is especially significant when the Ion crowns crown and bridge scissors or with a corborundum
are used because of hardness and difficulty of wheel on a slow speed straight handpiece, which
manipulating the nickel steel. When the softer shapes the margins simultaneously.
metal crowns(Rocky-mountain) are used, rnain-
tainingthe cervical bulge may be the preparation ■ For shapingthe ciown margins, mark 3 light points
of choice. on the metal at the mesiobuccal, buccal and
distobuccal and at the mesiolingual, lingual and
EVALUATION CRITERIA FORTOOTH PREPARATION distolingual surfaces at the crest of respective
marginal gingiva without compressing the mar­
■ The occlusal clearance is 1.5 to 2mm. ginal gingiva. These marks on the metal corre­
■ The proximal slices converge toward the occlusal sponds to the greatest diameter of the tooth. Fi­
and lingual, following the normal proximal con­ nal finished margins are placed approximately 1mm
tour. below these marks. The correctly shaped finished
■ An explorer can be passed between the prepared crown margins are parallel to the contours of the
tooth and the proximal tooth at the gingival mar­ marginal gingiva of the tooth, about 1.0mm into
gin of preparation. the gingival crevice.
■ The buccal and lingual surface are reduced at least
0.5mm with the reduction ending in a feather edge, SEATING THE CROWN
0.5 to 1mminto the gingival sulcus.
■ The buccal and lingual surfaces converge slightly Now the crown is tried on the preparation by seating
towards the occlusal. the lingual first and applying pressure in a buccal
■ All the point and line angles in the preparation direction so that the crown slides over the buccal
are rounded and smoothed. surface into the gingival sulcus. Resistance should
■ The occlusal third of buccal and lingual surfaces be felt as the crown slip over the buccal bulge.
are gently rounded.
Each time the crown is placed on the tooth, gingival
INITIAL ADAPTATION OF CROWN tissue should be carefully examined so that the mar­
gins are in the gingival sulcus. They shouldnot com­
Two principles related to stainless steel crown length press and produce blanching of the marginal gingival
and crown margin shapes that are based on an un­ tissue.
derstanding of the tooth morphology and gingival
tissue contours were presented by Spedding(1984). CROWN CONTOURING (Fig. 7.32)

• The crown should be of a correct length and its Initial crown contouring is performed witha 114plier
margins can be adapted closely to the tooth. This (ball and socket pliers)in the middle l/3rd ofthe crown
can be achieved when the finished crown is cor­ to produce a belling effect. This will give the crown a
rectly seated on the prepared tooth vith its oc­ more even curvature. Contouring of proximal metal
clusal surface in the occlusal plane and its mar­ surface is not done with these pliers as they are al­
gins placed just apical to the marginal gingival ready in contact with the adjacent teeth. Though,
crests. occasionally the #112(Abell) pliers are used to con­
tour a proximal surface to establish correct contact.
After the correct size crown is placed on the pre­ Adaptation of the gingival 1/3 rd of the crown is done
pared tooth, the crown height can be reduced by with the 137 Gordan pliers.
removing about 1mm of the crown initially with a
 I TEXTBOOK OF PEDODONTICS

CROWN CRIMPING (Fig. 7.33) polished prior to cementation with a rubber wheel to
remove all scratches.
Any marked gingival crimping of the crown can also
be done with Unitek 800-412 pliers. The tight mar­ Procedure ofpolishing
ginal fit aids in: While polishing the crown, margin should be blunt
■ mechanical retention of the crown. since knife edge finish produces sharp ends which
• protection of the cement from exposure to oral act as areas of plaque retention. A broad stone wheel
fluids. should run slowly, in light brushing strokes, across
» maintenance of gingival health. the margins towards the center of the crown. This
During the trial fitting and cementation, the crown will draw the metal closer to the tooth without reduc­
should be placed from lingual and rolled towards ing the crown height and thus improves the adapta­
buccal surface. In this way, maximum undercut tion of crown.
on the buccal surface is more easily covered.
A wire brush can be used to polish the margins to a
high shine. To give a fine lustre to crown, Rouge,
CHECKING THE FINAL ADAPTATION OF
whiting or a fine polishing material can be used.
THE CROWN
RADIOGRAPHIC CONFIRMATION OF THE
• The crown must snap into place. Should not be
GINGIVAL FIT
able to be removed with finger pressure.
■ The crown should fit so tightly that there is no
Before cementation, a bite wing is taken to verify
rocking on the tooth. Moderate occlusal displace­
proximal marginal integrity. If the crown is too long,
ment forces at the margin do not displace the
there is still an opportunity to reduce the length. If it
crown.
is too shorty then add an orthodontic band or adap­
■ The properly seated crown will correspond to the
tation of another crown is indicated.
marginal ridge height of the adjacent tooth and is
not rotated on the tooth.
CEMENTATION (Fig. 7.34) f
■ Crown is in proper occlusion and should not in­
terfere with the eruption of the teeth. Stainless steel crown should be cemented only on
« There should not be any high points when clean dry tooth. Isolation of teeth with cotton rolls is
checked with an articulating paper. recommended.
• The crown margin extends about 1 mm gingival to ■ Rinse and dry the crown inside and out and pre­
gingival crest. pare to cement it. A ZnPO4,polycarboxylate or
« No opening exists between the crown and the GIC is preferred.
tooth at the cervical margins. Crown margins « If ZnPO4 is used, 2 coats of cavity varnish should
closely adapted to the tooth and should not cause be applied on vital tooth before cementation and
gingival irritation. cement should be of consistency so that it strings
• Restoration enables the patient to maintain oral about 1 1/2 inches from mixing pad with the
hygiene. spatula. Cement is filled in approximately 2/3rd of
crown, with all inner surface covered.
FINISHING AND POLISHING ■ Seat the crown completely on dried tooth surface
preparation. Final placement should follow an
Accumulation of the plaque and inflammation of established path of insertion of the crown. Ce­
gingiva is commonly seen in practice of restorative ment should be expressed around all margins. To
dentistry due to rough and unpolished restoration. ensure complete seating of the crown, handle of
To avoid these complications, the crown should be mirror or band pusher may be used.
 SECTION 7 : PEDIATRIC RESTORATIVE DENTISTRY |

■ Before the cement sets, ask the patient to close ment of the crowns and interproximal approxima­
into centric occlusion by applying pressure tion. (Fig. 7.35a,b)
through a cotton roll and confirm that the occlu­ ■ both crown should be trimmed, contoured and
sion has not been altered. prepared for cementation simultaneously to al­
■ ZnPO4, cement can be easily removed with an low for adjustments in the interproxtmalspaces
explorer or scaler. After the polycarboxylate ce­ and establish proper contact areas.
ment is partially set, it will reach a rubbery con­
sistency. Excess cement should be removed at To get these adjustments, adapt and seat the crown
this stage with a explorer tip. The interproximal on the most distal tooth first and proceed mesially.
areas can be cleaned by passing the dental floss
through these areas. Crowns in areas of space loss (Me Evoy 1977)
■ Rinse the oral cavity and before dismissing the When there is an extensive and long standing caries,
patient reexamine the occlusion and the soft tis­ the primary teeth shift into the interproximal contact
sues. areas. As a result the crown required to fit over the
B-L dimensions will be too wide a M-D to be placed
Among all the cements used for cementation the GICs and the crown selected to fit over the M-D space will
are quite new and very promising. Cementing Stain­ be too small in cirumference.
less steel crown with GIC have some benefits. These ■ Select a larger crown which will fit over the tooth’s
cements have comparable strengths as ZnPO4, re­ greatest convexity
lease fluoride as do the silicophosphates chelate or ■ Reduce the M-D width by grasping die marginal
bond to the tooth structure and compatible to the ridges of the crown with Howe utility pliers and
pulp as do the polycarboxylates. But the response to squeezing the crown.
GIC was characterized by gingival enlargement and « Recontour the proximal,buccal and lingual walls
sulcular bleeding with no tooth sensitivity. The rea­ of the crown with theNo. 137 or No. 114 pliers.
son for this is unknown. It could be due to excess ■ Do the additional reduction of buccal and lingual
material in the gingival sulcus. Hence the most ver­ surface of tooth and select a smaller crown, if this
satile, retentive and least irritating cement available crown is difficult to place.
at present time appears to be polycarboxylate.
Preparing a Stainless steel crown adjacent to a
SPECIAL CONSIDERATIONS FOR STAINLESS class H amalgam (Mc Evoy 1985)
STEEL CROWNS ■ Place the rubber dam.
■ Crown reduction is completed and the crown is
Quadrant dentistry adapted.
When the quadrant dentistry is practiced, stainless ■ Next a matrix band and wedges are placed. Amal­
steel crowns are to be placed on the adjacent teeth. gam is inserted and carved.
Few points which are to be considered here are(Nash ■ With the matrix band in place, the crown is re­
1981): moved safely without fracturing the amalgam.
■ prepare the occlusal reduction of one tooth com­ ■ Then remove the matrix band and the final carv­
pletely before beginning the occlusal reduction ing of amalgam is done, .as there is good visibility
of the other tooth as their is tendency to under­ and access to the proximal box area.
reduce both ,when reduction on both the teeth is ■ Now complete die crown adaptation and cement
done simultaneously. the crown.
• reduce the adjacent proximal surface of the teeth The advantage of this approach is that, because
being restored more than when only one tooth is the crown and clas& II amalgams are prepared and
restored. The greater reduction will ease the place restored concurrently better restorations may
 r TEXTBOOK OF PEDODONTICS

The crown is tried on the tooth and amount of

overlapping necessary is marked on the crown.
The overlapped edges are then spot welded. The
crown js polished with a rubber wheel and fine
abrasives. '

■ The oversized tooth or the undersized c rown

Separate the edges as needed and weld a piece of
Fig. 7.35a Buccal marginal gingival tissues of 0.004 inch orthodontic band material across the
second deciduous molar appears to ‘smile’ cut surface. After contouring, apply the solder to
and first deciduous is 'streched-out S’ fill any microscopic deficiency in seal. Polish the
soldered crown.

■ Deep subgingival caries

One approach is to complete the indicated pulp
treatment and then restore the cavity preparation
with silver amalgam.

Now the silver amalgam is considered substitute

for the tooth structure. The proximal areas are
sliced as in a routine crown preparation. Stain­
less steel crown is adapted with amalgam substi­
tutes for tooth structure at the interproximal fin­
ish line. If the subgingival caries occurs
interproximally, the unfestooned Rocky moun­
Fig. 7.35b Proximal reduction is more when 2 tain crown will be deep enough to coyer the prepa­
adjacent crowns has to be placed than a
ration.
single crown

Another method is to solder an extension on in­

result and it helps to overcome the nuisance of
terproximal areas of the crown.
placing 2 rubber dams.
■ The open contact
STAINLESS STEEL CROWN MODIFICATION
If the closed contact area (except for the primate
space)is not established, it will result in food pack­
In 1971 ,Mink and Hill reported several ways of modi­
ing, increased plaque retention and subsequently
fy! ng the stainless steel crown when the crowns are
gingivitis.
either too large or too short.
This problem can be solved by selection of a larger
■ Undersized tooth or the oversized crown
crown or exaggerated interproximal contour can
This commonly occurs when due to a long stand­
be obtained with a 112 (ball and socket)plier to
ing interproximal caries,space loss has occurred.
establish a close contact. Interproximal contour
To reduce the crown circumference ,a cut is made
can also be build by addition of a solder.
up of the buccal surface to the occlusal surface.
The cut edges are re-approximated to overlap one
■ Open faced stainless steel crowns
another making the crown circumference smaller.
The-stainless steel crown can be modified in
 SECTION 7 : PEDIATRIC RESTORATIVE DENTISTRY |

anterior teeth by a open faced stainless steel Chances of plaque retention and subsequent gin­
crown, which is simply a stainless steel crown givitis increases with marginal discrepancy. The
with the labial surface trimmed away to leave a tolerant potential ofyoung periodontal ligament
crown perimeter which is then restored with a resin tissues is very high to an extreme amount of zinc
veneering. (Croll 1998) „_ phosphate cement pushed into lingual sulcus
This has 2 advantages- during the cementation procedure. The foreign
- esthetic are often improved. body was incorporated without any signs of gin­
- tooth structure is accessible for pulp testing. givitis and discomfort to the patient

Tnhalatjnnorjiigestinn nf cr
COMPLICATIONS
To prevent such mishaps, the rubber dam should
Common complications that can arise with stainless remain in place until cementation. It prevents ac­
steel crown preparation are: cidental swallowing or aspiration of a crown.
Sometimes sudden movement may result in in­
■ Interproximal ledge ____ — halation or ingestion of the crown.
Sledge will be produced instead of a shoulder - If this occurs, attempt can be made to remove
free interproximal slice, if the angulation of the the crown by holding the child upside down
tapered fissure bur is incorrect. Failure to remove as soon as possible.
this ledge will result in difficulty in seating the - If this is unsuccessful, medical referral should
crown. be done for an immediate chest X-ray.
- If the crown is in bronchi or lung, medical con-
When the adjacent tooth is partially erupted and sultation will probably result in an attempt to
the contact area is poorly established, the inter­ remove it by bronchoscopy.
proximal slice is difficult to prepare. To clear the - The presence of cough reflex in the conscious
child wil l reduce the chances of inhalation and
contact area, extensive subgingival tooth reduc­
tion is requi red which may result in formation of a ingestion of the crown is more likely. Inges­
ledge or damaging the erupting tooth. In such a tion is of less consequence as the crown will
case, it may be wise to delay crowning until con­ usually pass uneventfully through the alimen­
tact areas are properly established. tary tract within 5-10 days. But it should be
diagnosed by absence of the crown on a chest
« Crown tilt_ radiograph.
-—Complete lingual or buccal wall may be destructed
Self-Assessment
by caries or improper use of cutting instrument.
This may result in finished crown tilting toward
the deficient side. Placement of restoration prior 1. What is the use of polycarboxylate crowns?
to crowning provides a support to prevent crown 2. What are the indications of stainless steel crowns?
tilt, the alloy acting as a core. The clinical signifi­ 3. What are the different types of stainless steel
cance of crown tilting is minimal unless it occurs crowns?
on young permanent molars where supra-erup- 4. What are the modifications of stainless steel
tion of the opponent tooth may occur. crowns?
5. How much of occlusal reduction should be done?
■ Poor margins, 6. Which surface should be reduced first, occlusal
When the crown is poorly adapted, its marginal or proximal?
integrity is reduced. Recurrent caries may occur 7. What is snap fit’ of a crown?
around open margins.
 | TEXTBOOK OF PEDODONTICS

8. What are the complication's associated with stain­ 12. Greener EH. Amalgam - yesterday, today and to­
less steel crowns? morrow. Operative Dentistry. 4;24-35,1979
13. Hamid A, Hume WR. The effect of dentin thick­
Further Suggested Reading For Section - 7 ness on diffusion of resin monomers in vitro. Jour­
nal of Oral Rehabilitation. 24;20r25,1997
1. Akinmade AO, Nicholson JW. Review - GI^ss 14. Hilton TJ. Cavity sealers, liners and bases; cur­
ionomer cements as adhesives. Part I. Fundamen­ rent philosophies and indications for use. Oper.
tal aspects and their clinical relevance. Journal of Dent. 21:134-146,1996
Material Science in Medicine. 4,95-101,1993 15. Hollist NO. Clamp usage when applying rubber
2. Bonella E, White SM. Fatigue of resin bonded dam.BrDent J,27;184(12):579,1998
amalgam restorations. Oper. Dent., 21,122-126, 16. Hume WR, Gerzina TM. Bioavailability of com­
1996 ponents of resin-based materials which are ap­
3. Bortolozzi CF, Pimenta LAF. Evaluation of the plied to teeth. Critical Reviews of Oral Biology
compressive strength of teeth with Class II con­ and Medicine. 7; 172-179,1996
servative restorations. Ji Dent. Res. (Abstr.97) 17. Hunt PR. Micro conservative restorations for
77;1155,1998 approximal carious lesions. Journal of the Ameri­
4. Browning WD, Denninson JB. A survey of fail­ can Dental Association. 120;37-40, Î990
ure modes in composite resin restorations. Oper. 18. J. American Academy of Pediatric dentistry,Special
Dent. 21;160-166,1996 Issue,Ref.Manual. Vol.2.1,106,1999-00
5. Bryant RW, Hodge K-LV. A clinical evaluation of 19. Marshall K. Rubber dm: Br' Dent J, 184(5);218-9,
posterior composite resin restorations. Austral­ 1998
ian Dental Journal, 39177-81,1994 20. Martin J. Tyas, Kenneth J. A, JoE Frencken,
6. Clemens A,.Full Jerry, D.Walker, Jimmy Graham J. Mount, Minimal intervention dentistry
R.Pinkham,stainless steel crowns for deciduous - a review, Int. Dent. J. 50:1:141,2000
molars, JADA 89:360-364,August 1974. 21. Mc.Evoy Susan A.,A new tech, sequence for
7. Croll T. P, Primary incisor restoration using resin- approximating a stainless steel crowp and a class
veneered stainless steel crowns, ASDC-J-Dent- II amalgam. J.Pedo,9;250-256,1985.
Child;65,89-95,March-April 1998. 22. McLean JW, Nicholson JW, Wilson AD. Proposed
8. Dawson AS, Makinson OF, An alternate philoso­ nomenclature for glass-ionomer dental cements
phy and some new treatment modalities in opera­ and related materials. Guest editorial, Quintes­
tive dentistry, Part II, Australian Dental Journal, sence International, 25:587-589,1994
32;205-10,1992 23. McLean JW. Dentinal bonding agents versus
9. Frenken JE, Makoni F, Sithole WD, Hackenitz. glass-ionomer cements. Quintessence Interna­
Three year survial of one surface ART restora­ tional. 25;659-667,1996
tions and glass ioniser sealants in a school oral 24. McMaster DR. House RC, Anderson MH, Pelleu
health program in Zimbabwe. Caries Res. 32:119- GB. The effect of slot preparation length on the
126,1998 transverse strength of slot retained restorations.
10. Frenken JE, Makoni F, Sithole WD. Atraumatic Journal of Prosthetic Dentistry. 67;472-477,1992
restorative treatment and glass-ionomer sealants 25. Mount GJ, Hume WR. A revised classification of
in a school oral health programme in Zimbabwe: carious lesions by site and size. Quint. Inter.,
Evaluation after 1 year. Caries Res. 30:428-433, 28;301-303,1997
1996 26. Mount GJ, Hume WR. Preservation and restora­
11. Friedman MJ. New light curing options for com­ tion of tooth structure. Mosby International, Lon­
posite resin restorations. Compend. Contin. Educ. don, 1998.
Dent. 20:122-135,1999
 SECTION 7 : PEDIATRIC RESTORATIVE DENTISTRY |

27: Mount GJ, Makinson OF, Peters MCRB. The 36. Protocols for clinical pediatric dentistry, Vol.4;80,
( strength of auto-cured and light cured materials. Annual 1996.
The shear punch test. Aust. Dent. J., 41 ;118-23, 37. Robert H.Speeding, Two principles to produce
1996 well adapted stainless steel crown, DCNA,
28. Mount GJ. Clinical performance of glass- 157,Jan. 1984.
) ionomers. Biomaterials. 19:573-579,1998 38. Savide N.L.Caputo and Luke L.S; The effect of
\ 29. Mount GJ. Clinical placement of modem glass tooth perforation on retention of stainless steel
j ionomer cements. Quintessence International. crowns, J.Dent. Child, 46;25,1979.
| 24; 107-111,1993 39. Simonsen RJ. Cost effectiveness of pit and fis­
\ 30. Mount GJ. The use of amalgam to protect remain- sure sealant at 10 years. Quintessence Interna­
i ing tooth structure. New Zealand Dental Journal, tional, 20;75-84,1989
i 73:15-20,1977
£ * - 40. Strand GV, Nordbo H, Tveit AB, Espilid I,
| 31. Nash,David A.,The nickel-chromium crown for Wikstrand K, Eide GE. A three year clinical study
i restoring post. Primary .teeth, J AD A, Vol. 102:44- of tunnel restorations. Eur. J. Oral Sci. 104;384-89,
| 49,Jan., 1981 1996
| 32. Ngo H, Marino V, Mount GJ. Calcium, Strontium, 41. Strand GV, Tveit AB. Gjeidet NR Marginal ridge
J Aluminium, sodium and fluoride release from four strength of tunnel prepared teeth restored with
i glass-ionomers. J. Dent. Res. 77, Abstr. 75, page various adhesive filling materials. In press.
641,1998. 42. Van Meerbeck B, Peumans M, Verschueren M,
f 33. Ngq H, Mount GJ, Peters MCRB. A study of
Gladys S, Braem M, Lambrechts P, Vanherle G.
glass-ionomer cement and its interface with the Clinical status of ten adhesive systems. Journal
enamel and dentin using a low-temperture, high of Dental Research. 73,1690-1702,1995
resolution scanning electron microscope tech­ 43. Whitehouse RL. Dosages of inter patient cross­
nique. Quint Int 28;63-69,1997 contamination from saliva ejector suck back. J Can
' 34. Olmez A, Oztas N, Basak F, Erdal S. Comparison
Dent Assoc. Jun 62(6):499-500,1996
of the resin-dentin interface in priniaiy and per-
44 Willems G, Lambrechts P, Braem M, Celis JP,
manent teeth. J. Clinical Pediatric Dent. 22:293 -
Vanherle G. A classification of dental composites
298,1998
according to their morphological and mechanical
35. Pashley DH. Clinical correlations of dentine struc­
characteristics. Dental Materials, 8;310-319,1992
ture and function. J. Prosth. Dent 66;777-781,1991
 SECTION - 8

Pedia tric Endodontics

8.1 Objectives and Diagnostic Procedures
Gopinath V R, Tandon S

Introduction Treatment planning should include:

■ Is the child a reasonable patient?
Pediatric endodontics is a relatively new terminol­ Consider the value of the involved tooth in rela­
ogy, which deals with the management of pulpally tion to the child’s overall development and abil­
involved teeth in children. The pulp therapy in chil­ ity to co-operate in the dental chair.
dren is still a subject of controversy due to mainly
the lack of efficacious medicaments and skill, which ■ Is the child medically fit?
requires a lot of patience on the part of the operator Medical histoiy is of great importance as, those
in handling this group of patients. Despite increased children who are more susceptible to infection
awareness regarding the importance of deciduous like children with congenital heart disease or
teeth and emphasis on the prevention of dental car­ immuno-suppressed patients or children with
ies, pre-mature loss of primary and young permanent poor healing potentials (diabetes) wifi always be
teeth continues to be common in dental practice. questionable cases for a successful pulp therapy.
Therefore, this chapter highlights the dynamics of
dental pulp, its pathologies affecting it with clinical ■ Is the tooth restorable?
features and its diagnostic procedures. It also dis­ A tooth with extensive caries leading to gross
cusses in detail about the various treatment modalities, destructi on of the coronal portion or a tooth which
has caries penetrating the floor of the pulp cham­
the primary objective of which is to preserve the tooth.
ber is unrestorable.
Factors Influencing Appropriate Pulp Therapy
■ Is it necessary to keep the tooth?
The amount of root remaining and the extent of
It is desirable to attempt to maintain the vitality of
bone loss that has occurred in the supporting
the pulp of a tooth affected or infected by caries,
structure will have a significant bearing on pre­
traumatic injury or other causes. However, a tooth
serving thé tooth.
can remain functional without a vital pulp. It is pos­
sible to reduce pulp autolysis or eliminate it entirely
■ Are parents co-operative and do they understand
without significantly compromising the function of
the importance of treatment options?
tooth. The successful pulp therapy is predictive upon
Parents’ consent in accepting the treatment and
the acquisition and analysis of appropriate diagnos­
preventive program, including periodic evalua­
tic data. tion should always be given prior consideration.
 SECTION 8 : PEDIATRIC ENDODONTICS |

Goals of Pulp Therapy Histology

The primary objective of pulp treatment is to main­ The pulp is described as having two regions, central
tain the integrity and health of oral tissues. This and peripheral zones.
may be achieved by keeping the following goals in
the mind: ■ Central pulp zone: The main body of the pulp
■ to allow a tooth to remain in the oral cavity in a occupies this area, which contains a core of loose
non-pathological state connective tissue (stroma) bearing large nerves
■ to maintain the arch length and tooth space and blood vessels and branch out to supply to
■ to restore a tooth to its functionally efficient form outer pulp layers. Outlining the central zone is an
■ to present the development of aberrant habits area that is richly populated with undifferentiated
and speech abnormality mesenchymal cells (reserve cells) and fibroblasts,
■ to maintain the child’s esthetics and thereby pre­ and is referred to as the cell rich zone. The princi­
vent any psychological trauma ple extra cellular components are ground sub­
stance and collagen.
Prior To Any Treatment Option A Sound Knowl­
edge About The Dynamics Of Physiology And Pa­ ■ Peripheral zone: Peripheral to the central area is
thology Regarding Pulp Is Mandatory For A Suc­ the sub-dentinoblastic region of the pulp or zone
cessful Clinician of Weil. This appears as a cell free zone which
may diminish in size or temporarily disappear.
Pulp Physiology Plexuses of capillaries and small nerve fibers
Dental pulp may be defined as a special organ with a ramify in this layer deep to the odontoblastic layer.
-unique environment of the unyielding dentin sur­ The nerve fibers do not have their outer wrap­
rounding a resistant, resilient soft tissue of mesen­ ping (myelin sheath) and terminate into naked,
chymal origin reinforced with a ground substance. It free fibers as dendrites (free nerve endings), act­
has a close relationship between its peripheral cells, ing as specific receptors for pain. On account of
the odontoblasts and dentin therapy making it a func­ these free nerve endings, pulp demonstrates pain
tional entity, sometimes referred to as the pulp den­ as the only sensation irrespective of the stimu­
tin complex. lus.

The dental pulp has a high circulatory force because Structural Elements of the pulp are given in Table
of the fluid interchange between capillaries and tis­ 8.1
sue, which maintain a hydrostatic pressure within
Histopathology and Clinical Symptoms
this non-compliant chamber. This pressure is called
as intra pulpal pressure, which is normally 10 mm of ■ Normal:
Hg and varies with each arterial pulse. The pulp does A normal tooth is asymptomatic and exhibits a
not have a consistent effective collateral circulation, mild to moderate transient response to thermal
even though the teeth have accessory canals. Hence, and electric pulpal stimuli, the response subsides
a pulpal injury irrespective of different causes is fre­ almost immediately where such stimuli are re­
quently irreversible and painful. moved. The tooth and its attachment apparatus
do not cause a painful response when percussed
Nerve fibers responsible for transmitting pain are A or palpated. Radiographs usually reveal aclearly
delta (fast pain) and polymodal fibers (slow pain). delineated canal that tapers toward the apex. There
is no evidence of canal calcification and the lamina
dura is intact.
 330 I TEXTBOOK OF PEDODONTICS

Table 8.1 : Structural elements of the pulp

Cellular Components

Cell Location Function

1. Fibroblast Throughout the cell rich zone Produces matrix and collagen

2. Reserve cell Capillaries and cell rich zone Pleuripotent

3. Histiocyte Connective tissue Phagocytosis

4. Odontoblast First cell type as pulp is Glycoprotein synthesis

approached from the dentin (predentin matrix)
Extracellular Components
Components Distribution Function

1. Fibres Throughout Provides support for structural

elements

2. Ground Makes up the bulk of the pulp Gel like medium in which all
substances elements are placed.

3. Nerve fibres Transmit pain impulses only

(A-delta and C) (because of the presence of
free nerve endings only)

4. Arterioles,
venules and
lymphatics

• The diseases of the pulp can be classified as: irritant. The exudative (acute) force is hyperactive
1. Hyperemia and the painful symptoms are indicative of an
- reversible intrapulpal pressure increase that has surpassed the
- irreversible threshold limits of pain fibers.
2. Pulpitis
- Acute pulpitis Reversible pulpitis:
- Chronic ulcerative pulpitis ■ The pulp is inflamed to the extent that thermal
- Chronic hyperplastic pulpitis stimuli cause a quick, sharp, hypersensitive re­
3. Pulp degeneration sponse that subsides as soon as the stimulus is
- Calcific removed; otherwise the tooth is asymptomatic.
- Fibrous Any irritant that can affect the pulp may cause
- Atrophic reversible pulpitis, e.g. caries.
- Internal resorption ■ Reversible pulpitis is not a disease but merely a
4. Necrosis of pulp symptom. If the cause can be removed, the pulp
should revert to an uninflamed state and the symp­
Painful pulpitis tom should subside. A reversible pulpitis can be
Painful pulpitis is a clinically detectable inflamma­ clinically distinguished from a symptomatic irre­
tory response of the pulpal connective tissue to an versible pulpitis by two methods.
 SECTION 8 : PEDIATRIC ENDODONTICS | €EE>

1. Pain in reversible pulpitis subsides almost imme­ large carious exposure or by a previous traumatic
diately after the stimulus is removed while in an injury that resulted in a painless pulp exposure of
irreversible pulpitis there is a sharp painful re­ long duration.
sponse to thermal stimuli and the pain lingers
even after the stimulus is removed. Hyperplastic pulpitis
2. With a reversible pulpitis there is ho spontane­ One form of asymptomatic irreversible pulpitis is a
ous pain as there often is with a symptomatic reddish cauliflower-like overgrowth of pulp tissue
irreversible pulpitis. through and around a carious exposure. This is at­
tributed to a low-grade chronic irritation and to the
Irreversible pulpitis increased vascularity ofthe pulp that is characteris­
Irreversible pulpitis may be acute, subacute or tically found in young people.
chronic; it may be partial or total. The pulp may be
infected or sterile. Clinically, the acutely inflamed pulp Internal resorption
is thought to be symptomatic and the chronically The asymptomatic irreversible pulpitis can also be
inflamed pulp asymptomatic. With pulpal inflamma­ present in the form of internal resorption. This is
tion there is an exudate, if the exudate can be vented characterized by the presence of chronic inflamma­
out to relieve pain that accompanies edema, the tooth tory cells in the granulation tissue. It is diagnosed
may remain quiescent. Conversely, if the exudate that by radiographs.
is being continuously formed remains within the hard
confines of the root canal, pain will probably occur. Necrosis
Necrosis, death of the pulp, may result from untreated
Symptomatic irreversible pulpitis irreversible pulpitis or may occur immediately after a
Characterized by spontaneous intermittent or con­ traumatic injury that disrupts the blood supply to
tinuous paroxysms of pain. “Spontaneous” means the pulp. The necrotic remnants maybe liquefied or
that no stimulus is evident. Sudden temperature coagulated. Regardless of the type of necrosis, the
changes induce prolonged episodes of pain. There endodontic treatment is the same.
may be a prolonged painful response to cold (i.e.
remaining after the stimulus is removed) that can be Diagnostic Procedures
relieved by heat, and painful response to heat which Before initiating treatment, one must first assemble
is relieved by cold. Continuous spontaneous pain all the information regarding signs, symptoms and
may occur merely by a change in posture (eg, when history. That information is then combined with re­
the patient lies down or bends over). Pain from the sults from the clinical examination and test to obtain
symptomatic irreversible pulpitis tends to be moder­ the diagnosis. A diagnostician must have a Working
ate to severe, depending on the severity of inflam­ knowledge of examination procedures - percussion,
mation. It may be sharp or dull, localized or referred palpation, probing and pulp testing; a knowledge of
(eg., referred from the mandibular molar towards the pathosis, itsradiographicandclinicalmanifestation;
ear or up to the temporal area), intermittent or con­ an awareness of the various modalities of treatment;
stant. and above all, a questioning mind. A methodical and
disciplined approach, along with a good measure of
Asymptomatic irreversible pulpitis patience, will help establish an accurate diagnosis.
Asymptomatic irreversible pulpitis may develop on
the conversion of a symptomatic irreversible pulpitis History
into a quiescent state, probably because the inflam­ Recollecting is the first step towards establishing a
matory exudate was quickly vented. This can be due diagnosis. A complete history will net determinetieat-
to any type of injury, but it is usually caused by a ment but may influence modification in endMrt"* irk-
 €33 I TEXTBOOK OF PEDODONTICS

treatment modalities, especially if there have been lesions, discolorations and other obvious abnormali­
any changes in the patient’s health status. ties associated with the teeth should be noted.

Detailed history ofpain Coronal Evaluation

Children are not good historians. Their symptoms Done by using a mouth mirror and explorer and pos­
are often misleading because of their apprehension sibly a fiber optic light source. The dentist carefully
and parent involvement. It is not uncommon to see a and thoroughly examines the suspected tooth or
child with a large carious lesion in the primary tooth teeth for caries, defective restoration, discoloration,
with no complaint and sometimes without any deep enamel loss or defects that allow direct passage of
lesion the child will complain of pain due to fear. stimuli to the pulp. Vertical and horizontal fractures
Therefore, a detailed history of the pain should be are located by transillumination.
evaluated with very simple, subjective questions like:
1. Do you have any discomfort on eating ice cream Pulpal Evaluation
or drinking hot soup? The clinical condition of the pulp can be evaluated
.2. What happens when you eat anything sweet like by thermal stimuli, percussion, palpation and vitality
a candy bar? tests. The various method of pulpal evaluation, pro­
3. Does your tooth bother you at the night when vide information which can be used with the child’s
you go to sleep? history and radiograph to establish diagnosis.
4. How long does the pain last?
5. Does your tooth jump when you hit it with tooth Conventional Pulp Testing Methods are given in
brush or spoon? Table 8.2
6. How often do you get this pain?
Newer methods

The above questions are an attempt to see if the ■ Laser Doppler Flowmetry
tooth is influenced by any thermal, chemical stimuli The laser doppler flowmetei; developed in the
or percussion. Spontaneous pain at night indicates 1970s to measure the velocity of red blood cells
trouble. These questions may give a clue as to in capillaries, is a noninvasive, objective, pain­
whether a tooth is mildly inflammed, chronically less alternative to traditional neural - stimulation
inflammed or necrotic. methods, and therefore a promiring test for young
children. The flowmeter produced regular signal
External Examination fluctuations for vital teeth. Nonvital teeth showed
The child must be examined for localized swelling, no such synchronous signal but produced irregu­
changes in colour or bruises, abrasions, cuts or scars lar fluctuations or veiy steep spike traces that
and similar signs of disease, trauma or previous treat­ were attributed to a movement artifact. This in­
ment. The extraoral examination includes the face, strument has demonstrated its value for ongoing
lips, and neck, which may need to be palpated if the assessment of post - traumatized permanent inci­
patient reports soreness. Enlarged lymph nodes are sors.
of importance in denoting the spread of inflamma­
tion. ■ Pulse oximetry in evaluation of vitality
Since pulp vitality is purely a function of vascu­
Intraoral Examination lar health, a vital pulp with an intact vasculature
Examination of oral vestibules, buccal and lingual may test nonvital if only its neural component is
mucosa, palatal soft tissues for localized swelling injured as in a recently traumatized tooth. For elec­
and sinus tract or color changes is carried out. tric and thermal testing to be effective, the pulp
Finally, as part of the general inspection, carious must have a sufficient number of mature neurons.
 SECTION 8 : PEDIATRIC ENDODONTICS |

Table 8.2: Conventional Pulp Testing

Method Technique/Material Symptom/lnterpretation
1. Thermal ■ Ethyl chloride, ice, air ■ Lingering pain: Irreversible pulpitis
- Cold blast, hot water, heated ■ Hypersensitivity or subsiding pain:
- Heat gutta percha (used for Reversible pulpitis.
location of symtomatic
tooth).
2. Electric ■ Instrument such as « Higher current required (nonvital or
odontometer chronic inhammation)
(Fig. 8.1) ■ Lower current required (acute pulpitis)
Unreliable in:
Children
Recently traumatized teeth
Multirooted teeth
3. Percussion « Vertical ■ Apical periodontitis
(Irreversible pulpitis if due to caries)
■ Lateral ■ Lateral periodontal space inflartimation
4. Radiograph IOPA • Furcation involvement
■ Thickening of the PDI space: Indicates
periapical infection (usually accompained
with irreversible pulpitis)

A direct measurement of pulp circulation is the

only real measure of pulp vitality. Pulp oximetry is
a completely objective test, requiring no subjec­
tive response from the patient, that directly meas-
. ures blood oxygen saturation levels. To deter­
mine oxygen saturation, the pulse oximeter meas­
ures and compares amplitudes of the ratios of
transmitted infra-red with red light This ratio var­
ies with relative fractions of oxygen saturated to
unsaturated hemoglobin and used to calculate
oxygen saturation. These characteristics infer that
die pulse oximeter is also capable of evaluating
Fig. 8.1 Odontometer for pulp testing. the blood vasculature status within a tooth and
therefore pulp vitality.
However, both primary and immature permanent
teeth may not exhibit full alpha myelinated axon The dependence on a pulsatile blood flow ap­
innervation until 4-5 years after eruption. This pears to be a disadvantage of the use of the pulse
reduced number of pain receptors makes them oximeter.
less responsive to stimuli. Considering all these
limitations, present pulp testing with thermal and ■ Dual wavelength spectrometry
electric methods cannot be considered reliable This measures blood oxygenation change within
vitality tests for children.
 | TEXTBOOK OF PEDODONTICS

the capillary bed of dental tissue and thus not 2. What are the important factors to be considered
dependent on a pulsatile blood flow. for planning pulp therapy?
■ Hughes probeye camera: 3. What are the primaiy objectives of pulp therapy?
This is used in detecting temperature change as 4. What is the Zone of Weil?
small as 0. Io C hence been used to measure pulp 5. What are the functions of dental pulp?
vitality7 experimentally. 6. What is meant by the util ity of pulp?
7. How will you differentiate clinically reversible
Self-Assessment pulpitis and symptomatic irreversible pulpitis?
8. Why electrical pulp tester is unreliable in chil­
1. What is dental pulp and what is so special about dren?
it?
 8.2 Treatment Modalities

Tandon S, Gopinath V K

INDIRECT PULP CAPPING THERAPY complete removal of caries would probably cause
a pulp exposure. Careful diagnosis of the pulpal
■ Definition: The procedure involving a tooth with status is completed before the treatment is initi­
a deep carious lesion where carious dentin re­ ated.
moval is left incomplete, and the decay process is
treated with a biocompatible material for some time The tooth is anesthetized and isolated with rub­
in order to avoid pulp tissue exposure is termed ber dam. All the caries except that immediately
indirect pulp capping. overlying the pulp is removed. Care must be taken
to eliminate all the caries at the dentin - enamel
■ A radiopaque base is placed over the remaining junction. If there is a communication of the caries
affected dentin to stimulate healing and repair. with the oral cavity, the carious process will con­
tinue, resulting in failure of treatment.
The tooth then is restored with a material that
seals the involved dentin from the oral environ­
Care must also be taken while removing the car­
ment.
ies to avoid exposure of the pulp. The use of a
large round bur is best to remove the caries. The
Justifications:
utilization of a spoon excavator when approach­
■ Reduction of hyperemia in pulp.
ing the pulp may cause an exposure by removal
■ Remineralization of carious or precarious dentin.
of a large segment of decay and hence should be
■ Reduction of anaerobic bacteria. used cautiously. Not all undermined enamel is
■ Formation of reparative dentin. removed, for it will help to retain the temporary
■ Pulp vitality maintained. restoration.
■ Continued normal root closure in immature per­
manent teeth. After all the caries, except that just overlying the
pulp, has been removed, a sedative filling of ei­
Indication and contraindications and objec­ ther zinc oxide - eugenol (ZOE) or calcium hy­
tives of indirect and direct pulp are given in droxide is placed over the remaining carious den­
table. 8.3 and 8.4 respectively tin and areas of deep excavation. The tooth may
then be restored with ZOE or amalgam (Fig-1). If
Procedure (Fig. 8.2) the remaining tooth structure is insufficientto
retain the temporary filling, a stainless steel band
■ Indirect pulp therapy is utilized when pulpal in­ or temporary crown must be adapted to the tooth
flammation has been judged to be minimal and to maintain the dressing within the tooth.
 I TEXTBOOK OF PEDODONTICS

Table 8.3: Indications and contraindications of pulp capping

INDIRECT PULP CAPPING DIRECT PULP CAPPING

^Indications Indications
» Ideally, used when pulpal inflammation ■ Small mechanical exposures less than
has been judged to be minimal and 1mm which is surrounded by sound
complete removal of caries would cause dentin.
a pulp exposure. ■ Light red bleeding from the exposure
site that can be controlled by cotton
pellet.
■ Traumatic exposures in a dry, clean
field, which report to the dental office
within 24 hours.
Contraindications Contraindications
■ Any signs of pulpal or periapical ■ Pain at night.
pathology. ■ Spontaneous pain
« Soft leathery dentin covering a very large ■ Tooth mobility
area of the cavity, in a non restorable ■ Thickening of Periodontal membrane
tooth. ■ Intraradicular radiolucency
■ Excess bleeding at the exposure site
■ Purulent or serous exudate

Table 8.4: Objectives of indirect and direct pulp capping

INDIRECT PULP CAPPING DIRECT PULP CAPPING

■ The restorative material should seal ■ The vitality of the tooth should be
completely the involved dentin from the maintained.
/ oral environment. ■ No prolonged post - treatment signs or
* The vitality of the tooth should be symptoms of sensitivity, pain, or
preserved. swelling should be evident.
■ No prolonged post-treatment signs or ■ Pulp healing and tertiary dentin
symptoms of sensitivity, pain or formation should result.
swelling should be evident. ■ There should be no pathologic
• The pulp should respond favourably changes.
and tertiary dentin or reparative dentin
should be formed, as evidenced by
radiographic evaluation (1.5 microns/day
after 30 days of pulp capping).
■ There should be no evidence of internal
resorption or other pathologic changes.
 SECTION 8 : PEDIATRIC ENDODONTICS |

Amalgam

Remaining
caries

A - The pulp will be exposed if all the caries is removed.

B - All decay is eliminated except that just overlying the pulp. Calcium hydroxide -
ZOE is placed over the remaining caries.
C - The tooih is sealed with amalgam.

Fig. 8.2 Indirect pulp therapy.

Fig. 8.3 Dentinal barrier formed following indirect pulp capping

on deciduous second molar.
 | TEXTBOOK OF PEDODONTICS

« If this preliminary caries removal is successful, procedure of pulpal protection with adequate base
the inflammation will be resolved and deposition is, of course, mandatory before placement of per­
of reparative dentin beneath the caries will allow manent restorations.
subsequent eradication of the remaining caries
without pulpal exposure. ■ The reentry restorative procedure is still ques­
tionable. Research has shown that carious den­
• The sedative dressing to be used in indirect pulp tinwill remineralize with the initial restoration. If
therapy may be either calcium hydroxide or ZOE. the restoration has a good margin and at the re­
call visit a layer of secondary dentin is evident,
« The treated tooth is reentered in 6 to 8 weeks, and reentry is not necessary (Fig. 8.3).
the remaining caries is excavated. The rate of re­
parative dentin deposition has been shown to Infected Vs Affected Dentin is given in Table 8.5
average 1.4 microns per day following cavity
preparations in the dentin of human teeth. The ■ DIRECT PULP CAPPING
rate of reparative dentinformation decreases mark­ Definition: The procedure in which the small ex­
edly after 48 days. posure of the pulp, encountered
■ During cavity preparation or
• If the initial treatment was successful, when the ■ Followingatraumatic injury or
tooth is reentered the caries will appear to be ar­ ■ due to caries, with a sound surrounding den­
rested. The color will have changed from deep tin, is dressed with an appropriate
red rose to light gray or light brown. The texture biocompatible radiopaque base in contact with
will have changed from spongy and wet to hard, the exposed pulp tissue prior to placing a res­
and the caries will appear dehydrated. Practically toration is termed as a direct pulp capping.
all bacteria are destroyed under ZOE and calcium ■>

hydroxide dressing sealed in deep carious lesions. • Direct pulp capping in Primary teeth
Traditionally, direct pulp capping in the primary
« Following removal of the remaining caries, the teeth has been viewed with skepticism. The rea­
tooth maybe permanently restored. The usual** sons cited were, the abundant blood supply and

Table 8.5: Infected Vs Affected dentin

Infected dentin Affected dentin

■ Highly demineralized ■ Intermediately demineralized

■ Unremineralizable ■ Remineralizable
■ Superficial layer ■ Deeper layer
■ Lacking sensation ■ Sensitive
• Stained by 0.5% fuschin or 1.0% acid ■ Does not stain
red solution in 0.2% propylene glycol
■ Ultrastructure: Intertubular dentin ■ Ultrastructure: Inter-tubular dentin
greatly demineralized, with irregularly partially demineralized, but apatitie
scattered crystals. crystals bound like fringes to the sound
Presence of deteriorated collagen collagen fibers with distinct cross bands
fibers that have only indistinct cross and interbands.
bands and no interbands.
■ Should be excavated. ■ Should be left to remineralize.
 SECTION 8 : PEDIATRIC ENDODONTICS |

a consequent faster inflammatoiy response, and tin chips. In addition, microorganisms may be
poorer localization of infection. forced into the tissue. The resulting inflammatory
reaction can be so severe as to cause a failure.
Limitation in Primary Teeth:
■ Staining carious lesions was proposed many years
Reasons for limitation of direct pulp capping in cari- ago by Fusayama to allow differentiation of
jus exposure is as follows.
remineralizable and non-remineralizable dentin.
■ Internal resorption. These harmless dyes demonstrate non-
■ Calcification. remineralizable dentin. Parts ofthe tooth that stain
i Chronic pulp inflammation. should be removed. Any tooth structure that
i Necrosis. does not stain can remain, since this soft dentin
■ Intraradicular involvement. will remineralize. Examples ofsome brands are Cari-
Recently however, animal studies have suggested D Test (Gresco products Inc), Caries Detector (J
that healing of the pulp may take place even in Morita USA Inc), Caries Finder (Danville Engi­
the presence of inflammation. Several studies neering) and Sable Seek (ultra dent products). This
have found varying success rates (Table 8.6). method will limit the removal of decay to non-
remineralizable dentin during direct and indirect
» Procedure: pulp capping.
When pulp capping is done, care must be exer­
■ Location of the pulp exposure is an important
cised while removing the deep carious dentin over
consideration in the prognosis. If the exposure
the exposure site to keep to a minimum the push­
occurs on the axial wall of the pulp, with pulp
ing of dentin chips into the remaining pulp cham­
tissue coronal to the exposure site, this tissue
ber. Studies have shown decreased success when
may be deprived of its blood supply and undergo
dentin fragments are forced into the underlying
necrosis, causing a failure. Then, a pulpotomy or
pulp tissue. Inflammatory reaction and formation
pulpectomy should be performed rather than a
of dentin matrix are stimulated around these den­
pulp cap.

Table 8.6: Success rate in direct pulp capping using different materials (Primary Teeth)

Year Author Age Filling material Observation period Success%

1963 Sawusch Dycal 10-63 months 80

1970 Weine 8-19 Dycal 18.6 months 90
1971 Jepperson 2-7 Ca(OH)2 paste 1-7 years 78
1977 Schroder et al Ca(OH)2 paste 12 months 83
1984 Garcia Godoy 4-9 ZOE & FC 18 months 96
1984 Jerrel et al 6-10 Dycal 7-63 days 95
1987 Turner 6-10 Life 63 days 22
Dycal 33
Ca(OH)2 85
 «El» I TEXTBOOK OF PEDODONTICS

■ Flush out dentinal debris and control bleeding at Pulp capping agents
the exposure site. No clot should form on the ex­ Many materials and drugs have been employed as
posed site. The pulp-capping agent should come pulp capping agents. Materials, medicaments, anti­
in contact with the vital pulp tissue. Marginal seal septics, anti-inflammatory agents, antibiotics and
over the pulp-capping procedure is of prime im­ enzymes have been utilized as pulp-capping agents;
portance since it presents ingress of bacteria and but calcium hydroxide is generally accepted as the
reinfection. Healing and the formation of sec­ material of choice for pulp capping.
ondary dentin are inherent properties of the pulp.
Factors promoting healing are conditions of the ■ Calcium hydroxide (Table 8.7)
pulp at the time of amputation, removal of irri­ Herma/?[1930] introduced calcium hydroxide for
tants, and proper postoperative care such as pulp capping. In 1938 Teuscher and Zander intro­
proper sealing of the margins. duced calcium hydroxide in the United States.
They histologically confirmed complete dentinal
« After pulpal injury, reparative dentin is formed as bridging with healthy radicular pulp under cal­
part of the repair process. Although formation of cium hydroxide dressings.
a dentin bridge has been used as one of the crite­
ria for judging successful pulp capping, bridge When calcium hydroxide is applied directly to pulp
formation can occur in the teeth with irreversible tissue, there is necrosis of the adjacent pulp tis­
inflammation. Moreover, successful pulp capping sue and an inflammation of the contiguous tis­
has been reported without the presence of a re­ sue. Dentin bridge formation occurs at the junc­
parative dentin bridge over the exposure site. tion of the necrotic tissue and the vital inflamed
tissue. Although calcium hydroxide work effec­
Salierit features ofsuccessful pulp capping: tively, the exact mechanism is not understood.
« Maintenance of pulp vitality. Compounds of similar alkalinity (pH of 11) cause
• Lack of undue sensitivity or pain. liquefaction necrosis when applied to the pulp
• Minimum inflammatory response. tissue. Beneath the region of necrosis, cells of
• Lack of internal resorption and iritraradicular pa- the underlying pulp tissue differentiate into
thosis. odontoblasts and elaborate dentin matrix.

Table 8.7: Calcium hydroxide: advantages and disadvantages

Advantages Disadvantages

• Initially bactericidal then bacteriostatic ■ Does not exclusively stimulate dentinogenesis.

■ Promotes healing and repair ■ Does exclusively stimulate reparative dentin.
• High pH stimulates fibroblasts ■ Associated with primary tooth resorption
■ Neutralizes low pH of acids ■ May dissolve after one year with cavo surface
■ Stops internal resorption dissolution
• Inexpensive and easy to use ■ May degrade during acid etching
■ Parti cl esm ay obturate open tubules ■ Degrades upon tooth flexure
■ Marginal failure with amalgam condensation
■ Does not adhere to the dentin or resin restoration

Cox and Suzuki, 1994

 SECTION 8 : PEDIATRIC ENDODONTICS I

Commercially available compounds ofcalcium hy­ cess rate of 89% when compared to calcium hy­
droxide in a modified form are known to be less droxide which gave a success rate of 68% only.
alkaline and thus less caustic on the pulp. The
reactions to Dycal, Prisma VLC Dycal, Life and ■ Other materials
Nu-cap have been shown to be similar The chemi­ Several other materials used as pulp capping
cally altered tissue created by application of these agents have included antibiotics, corticosteroids,
compounds is resorbed first, then the bridge is polycarboxylate cements, dentin, albumin, acid
formed in contact with the capping material. and alkaline phosphatase, chondroitin sulfate,
chondroitin sulfate and collagen, calcium - eug­
It was postulated that calcium would diffuse from enol cement, calcitonin, barium and strontium hy­
a calcium hydroxide^ressing into the pulp and droxide, native enriched collagen solution and
participate in the formation of a reparative (fentin. hydroxyapatite.
Experiments with radioactive ions, however, have
shown that calcium ions from the calcium hydrox­ PULPOTOMY
ide do not enter into the formation of new dentin.
Radioactive calcium ions injected intravenously Definition: pulpotomy can be defined as the com­
were identified in the dentin bridge. Thus, it was plete removal of the coronal portion of the dental
established that calcium for the dentin bridge pulp, followed by placement of a suitable dressing or
comes from the blood stream. medicament that will promote healing and preserve
vitality of the tooth [Finn, 19950
Isobutyl cyanoacrylate
It has been reported to be an excellent pulp -cap­ PRIMARY TOOTH VITAL PULPOTOMY.
ping agent because of its hemostatic and bacte­
riostatic properties; at the same time it causes Pediatric dentists still consider pulp therapy particu­
less inflammation than calcium hydroxide. How­ larly the vital pulpotomy to be controversial. While
ever, it cannot be regarded as an adequate thera­ pulpotomy therapy evolved slowly over the first 50
peutic alternative to calcium hydroxide since it years, the pace of change since the 1960s has con­
does not produce a continuous barrier of a re­ tinued to accelerate dramatically.
parative dentin following application to the ex­
posed pulp tissue. ■ Pulpotomy therapy can be classified according
to the following treatment objectives as devitali­
Resin bonding agents (Hybridization) zation (mummification, cauterization), preserva­
In the recent years, research has supported the tion (minimal devitalization, noninductiveX or
use of resin bonding agents on potentially heal­ regeneration (inductive, reparative].
able exposed pulps. Supeibond C & B and clearfil
liner bond system have been observed to induce PULPOTOMY
a secondary dentin formation when used as a di­
I. VITAL PULPOTOMY TECHNIQUE
rect pulp capping agent. Studies have supported
using 4-methacryloxyethyl trimellitate anhydride 1. Devitalization
(4 - META) bond (Amalgam bond, Parkell) on ex­ ■ Single sitting 1. Formocresol
2. Electrosurgery
posed pulp.
3. Laser
■ Two stage 1. Gysi Triopaste
Laser 2. Easlick’s
Andreas Moritz (1998) evaluated the effect of CO2 Formaldehyde
laser on direct pulp capping and reported a sue
 €2E) I TEXTBOOK OF PEDODONTICS

3. Paraform devitalising ■ Radiographic interpretation can give some clues

paste
as to the extent of the carious lesion, status of the
2. Preservation
1. Glutaraldehyde lamina dura, presence of abnormal resorptive proc­
2. Ferric sulphate esses or interradicular rarefaction’s, which can
give an indirect clue to the relative presence or
3. Regeneration 1. Bone morphogénetiç absence of inflammation that may exist.
protein.
A. DEVITALIZATION (Single sitting):
II. NON-VITAL PULPOTOMY
(Mortal pulpotomy) 1. Formocresol pulpotomy technique:
1. Beechwood cresol ■ The formocresol pulpotomy technique was
2. Formocresol first advocated by Sweet [1930]. He used a
multiple sitting technique , which has been
Indication and contraindication for subsequently modified to either a single or two
pulpotomy stage technique.
Indication:
■ Formocresol is a solution of 19% formalde­
1. Vital tooth with healthy periodontium.
hyde, 35% cresol in a vehicle of 15% glycerine
2. Pain, if present, is neither spontaneous nor per­
and water. To prepare a 1:5 concentration of
sistent.
this formula, first thoroughly mix 3 parts of glyc­
3. Tooth which is restorable.
erin with 1 part of distilled water, then add 4
4. The tooth that possesses at least 2/3rd of its root
parts of this preparation to 1 part Buckley’s
length.
formocresol, and thoroughly mix again.
5. Hemorrhage from the amputation site is pale red
and easy tojcontrol.
Mechanism of action
6. In mixed dentition stage primary tooth is prefer-.
■ The proposed mechanism of action of formal­
able to a space maintainer.
dehyde is that it prevents tissue autolysis by
Contraindication bonding to protein. In particular, the chemical
1. Evidence of internal resorption. binding is thought to be peptide groups of
2. Presenceof interradicularbone loss.- certain side chain amino acid groups. This is a
3. Existence of abscesses~or fistula in relation to the reversible process and is accomplished with­
teeth. out changing the basic overall structure of the
4. Radiographic signs of calcific globules seen in protein molecules.
the pulp chamber.
5. Caries penetrating the floor of the pulp chamber. Procedure (Fig. 8.4a, b, c)
6. Tooth close to naturafexfoliation.- ■ In the pulpotomy procedure, the tooth should
first be anesthetized and isolated with rubber
Diagnostic consideration: dam. A surgically clean technique should be
■ Examination of the literature shows overwhelm­ used throughout the procedure. All remaining
ing evidence of the importance of performing the dental caries should be removed, and the over­
pulpotomy on teeth in which inflammation has hanging enamel should be planed back to pro­
been confined to the coronal pulp when radicular vide a good access to the coronal pulp.
pulp is free of inflammation. Teeth selected ac­ ■ The entire roof of the pulp chamber should be
cording to these criteria will have a successful removed with a bur. No overhanging dentin
prognosis.
 SECTION 8 : PEDIATRIC ENDODONTICS

A. Cariously involved primary B. Access cavity and removal of

molar coronal pulp tissue

C. Placement of a cotton pellet D. Pulp chamber filled with ZOE and crown is
moistened with formocresol. buildup with glass-ionomer before placement
of stainless steel crown.
Fig. 8.4a Method of performing a Pulpotomÿ.

Fig. 8.4b Pulpotomy on deciduous molar - Fig. 8.4c Pulpotomy on deciduous molar -
pre treatment post treatment
€НЭ I TEXTBOOK OF PEDODONTICS

from the roof of the pulp chamber should ■ The formula of each agent used are as follows:
remain. A sharp discoid spoon excavator may
1. Gysi Triopaste: Tricresol 10ml
be used to amputate the coronal pulp. The pulp
Cresol 20ml
stump should be cleanly excised with no tag Glycerin 4ml
of the tissue extending to the floor of the pulp Paraformaldehyde 20ml
chamber. Zinc Oxide 60gm
2. Easlicks Paraformaldehyde 1gm
■ The pulp chamber should then be irrigated Paraformald- Procaine base 0.03gm
with a light flow of water from the water sy­ ehyde Powdered asbestos
ringe and evacuated. Moist cotton pellets paste: 0.05gm
should be placed in the pulp chamber and al­ Petroleum Jelly 125gm
lowed to remain over the pulp stump until a Carimine to colour
clot forms. 3. Paraform Paraformaldehyde 1gm
Devitalizing Lignocaine O.Oógm
« If the hemorrhage is controlled readily and the Paste: Propylene glycol 0.50ml
pulp stump appears normal, it may be assumed Carbowax 1500 1.30gm
that the pulp tissue in the canals is uninflamed Carmine to Colour
hence it is safe to proceed with the pulpotomy.
The pulp chamber is dried with a sterile cotton Technique
pellet Next, a pellet of cotton moistened with First appointment
1:5 concentration of Buckley’s formocresol and Step I:
blotted on a sterile gauze to remove the ex­ - Preparation of instruments and materials.
cess, is placed in contact with the pulp stump - Isolation of the affected teeth with rubber dam.
and allowed to remain for 5 minutes. The pel­ - Preparation of the cavity.
lets are then removed and the pulp chamber is - Excavation of the deep caries dentin.
dried with new cotton pellets.
Step II:
- When pulp exposure is encountered during
« A thick paste consisting of zinc oxide and excavation of deep caries, ensure that the ex­
eugenol is prepared and placed over the pulp posed site is free of debris. Ideally, enlarge the
stump. A zinc poly carboxy late cement is exposure with a round bur. Prepare a cotton
placed over the paste and the tooth is restored pellet large enough to cover the exposure but
with stainless steel crown. small enough to clear the cavity margin. Incor­
porate the paraformaldehyde paste into the pel­
DEVITALISATION PULPOTOMY let, and place it over the exposure, Seal the
(Two stage): tooth for 1 to 2 weeks. Formaldehyde gas lib­
This is a two stage procedure involving the use erated from the paraformaldehyde permeates
of paraformaldehyde to fix the entire coronal and through the coronal and radicular pulp, fixing
radicular pulp tissue. The medicaments used to the tissues.
devitalize the exposed primaiy pulp are similar, in
that they contain some formalin or paraformal­ Second Appointment:
dehyde. The medicaments used have a devitaliz­ - On the second appointment, pulpotomy is car­
ing, mummifying and bactericidal action. ried out with the help of local anesthesia. The
roof of the pulp chamber is removed and
 SECTION 8 : PEDIATRIC ENDODONTICS

cleaned with saline and dried with a cotton pel­ the treatment or to extract the tooth. If there are no
let. The pulp chamber is filled with antiseptic symptoms the pulp chamber can be filled with a anti
paste and the tooth is restored. Note that on septic paste. While filling the pulp chamber the anti­
the second appointment, after removal of septic paste can be firmly pushed into the root ca­
dressing if the pulp is found to be vital, repeat nals with cotton pellets. The tooth can be restored
the dressing for one more week or do a vital with stainless steel crown.
pulpotomy under local anesthesia.
1. Minute pulpotomy
MORTAL PULPOTOMY (NON-VITAL PULPOTOMY) ■ Garcia Godoy, Novakovic, Carvajal have sug­
gested that a shorter application time (1 minute)
Ideally, a non-vital tooth should be treated by pulpec­ may be adequate and perhaps superior to the
tomy and root canal filling. However, pulpectomy of recommended 5 minutes.
a primary molar may sometime be impracticable due
to non-negotiable root canals and also due to limited Clinical & Radiographic Evaluation:
patient’s cooperation. Hence, a two stage pulpotomy 1. Absence of pain, fistula, abscess & mobility.
technique is advocated. 2. Absence of periradicular or periapical pathol­
ogy-
Selection Criteria: 3. Absence of internal or external resorption.
■ History of spontaneous pain.
■ Swelling, redness or soreness of mucosa. Histologic Evaluation:
■ Tooth mobility. Massler and Mansokhani described the tissue
■ Tenderness to percussion. reaction to formocresol as a progressive fixation
■ Radiographic evidence of pathological root re­ followed by degeneration. Three distinct zones
sorption or periradicularbone destruction. noted between 7 to 14 days are as follows.
■ Pulp at the exposed site does not bleed. 1. Broad acidophilic zone of fixation.
2. Broad pale staining zone of atrophy.
Now-a-days the tooth with the above mentioned se­ 3. Broad zone of inflammatory cell.
lection criteria is considered for pulpectomy rather
than Mortal pulpotomy A progressive apical movement of these zones
was described with only an acidophilic zone left
First Appointment at the end of a year
In the first appointment the necrotic coronal pulp is
removed. The pulp chamber is irrigated with saline Formocresol toxicity:
and dried with cotton pellet, infected radicular pulp The toxic properties of formocresol reported are;
is treated with a strong antiseptic solution such as ■ Permanent tooth hypoplasia
beechwood cresol. Dip the pellet in beechwood ■ Systemic distribution
cresol and remove the excess by damping it on a « Antigenicity
sterile cotton and place it in the pulp chamber over ■ Mutagenicity and carcinogenicity
the radicular pulp. Seal the cavity with a temporary ■ Occurrence of dermatitis and pharyngitis
cement for one or two weeks.
2. Electrosurgical pulpotomy (Mack and Dean,
Second Appointment 1993)
During the second appointment isolate the tooth and It is a non-chemical devitalization, whereas mum­
remove the temporary dressing and the pellet con­ mification eliminates pulp infection and vitality
taining beechwood cresol. Note that if the symp­ with chemical crosslinking and denaturation. Etec-
toms persist or if there is no signs of resolution of trocauteiy carbonizes and heat denatures the pulp
the sinus, a decision must be made either to repeat and bacterial contamination. Electrosurgery does
 Г TEXTBOOK OF PEDODONTICS

little to improve on the formocresol pulpotomy 1. Glutaraldehyde

but does not use any chemicals. Glutaraldehyde introduced by Kopel (1979) has
received attention in the recent years as an alter­
After amputation of the coronal pulp, the pulp native to formocresol for pulpotomy in primary
stumps are cauterized through this method. After teeth in view of its superior fixative properties,
completion, the pulp chamber is filled with zinc self-limiting penetration, low antigenticity, low tox­
oxide and eugenol paste. The tooth is restored icity and elimination of cresol. The histologic pic­
with a stainless steel crown. ture of a glutaraldehyde treated pulp shows ini­
tial zone of fixation that does not migrate apically.
3. Laser Pulpotomy The tissue adjoining the fixed zone has the cellu­
In an effort to find a more biologically acceptable lar details found in normal pulp tissues The clini­
and effective alternative to formocresol, other cal success rate when glutaraldehyde was not
agents and techniques have been examined. Non- overzealously blotted from the pellet before use
pharmacologic hemostatic techniques for the pul­ was high (Table 8.8).
potomy procedure, such as electrosurgeiy and
■ In vitro, antimicrobial and cytotoxic concentra­
laser therapy have been suggested. Jeng-fen Liu
tions of glutaraldehyde and formocresol showed
et al in 1999 studied the effect on Nd: YAG laser
an effective antimicrobial activity at a concentra­
for pulpotomy in primary teeth and noted 100%
tion of 3.125% glutaraldehyde and 0.75%
success with no signs or symptoms, and only
formocresol. Thus gluturaldehyde was seen to
one tooth had internahroot resorption at the six-
exert a less cytotoxic effect on the immediate and
month follow up visit.
surrounding tissues when used as a pulpotomy
agent.
B. PRESERVATION
■ The cytotoxic effect of glutaraldehyde and for­
Included in this category are chemicals which in­ maldehyde was studied, in relation to the time of
duce minimal insult to the tissue. While not capable exposure and concentration. Cytotoxic effects of
of initiating an inductive process, they helped to formaldehyde occurred over a narrow concentra­
conserve vitality of the radicular pulp. Chemicals in­ tion range from non-toxic to maximally toxic, and
cluded under this section are glutaraldehyde and fer­ the range was little affected by the time of expo­
ric sulfate, which have an obvious effect on the su­ sure. In contrast, glutaraldehyde exerted its effect
perficial tissue but differ from formocresol and elec­ over a wider concentration range, and a longer ex­
trosurgery by virtue of their properties, actions and posure time were necessary for maximal toxicity.
rationale for use.

Table 8.8: Clinical studies with Glutaraldehyde

Investigators Clinical success Radiographic Duration (in months)

Guillaría (1989) 96 96 12
Prakash et al (1989) 100 100 6
Fuks et al (1991) 96 82 25
Garcia godoy (1991) 100 98 42
Tsai et al (1993) 98 78.7 36
Alacam (1996) 96 92 12
 SECTION 8 : PEDIATRIC ENDODONTICS | €ZB

■ Gluteraldehyde application in 2 to 5% concentra­ exposed dentin pulp of four adult miniature pigs
tion was advocated safe for clinical success. was seen to cause a substantial amount of hard
tissue formation (osteodentin and tubular den­
2. Ferric sulfate tin) thereby completely bridged the delect. Hence,
This npnaldehyde hemostatic compound was hop-1 is a collagen carrier matrix which appeared
proposed on the theory that it might prevent prob­ to be a suitable bio-active capping agent.
lems encountered with clot formation and thereby
minimize the chances for inflammation and inter­ ■ We will be entering a new era, when commercially
nal resorption. Ferric sulfate forms a metal-pro­ available recombinant human BMPs will be made
tein clot a t the surface of the pulp stump and this available for experimentation and clinical trials. A
acts as a barrier to irritating components of the combination of BMPs may be necessary to en­
sub-base. If true, the ferric sulfate may function sure maximal and predictable reparative dentino­
solely in a passive manner. genesis, but there are details to be determined in
logical steps. If this material is proved to be fruit­
C. REGENERATION ful in human clinical trial this product could be an
ideal material of choice for vital tooth pulpotomy
An ideal pulpotomy treatment should leave the in primary teeth.
radicular pulp vital, healthy and completely enclosed
within an odontoblast lined dentin chamber. In this Pulpotomy with commonly used materials
situation, the tissue would be isolated from noxious is given in Table 8.9
restorative materials in the chamber, thereby dimin­
ishing the chance of internal resorption. Addition­ PULPECTOMY IN PRIMARY TEETH
ally, the odontoclasts of the uninflamed pulp could (Fig. 8.5a, b, c,d,e)
enter into the exfoliative process at the appropriate
time. Implied in this scenario is the induction of re­
^Pulpectomy involves removal of the roof and con­
parative dentin formation by the pulpotomy agent. tents of the pulp chamber in order to gain access to
■ Unlike the other two categories for pulp treat­ the root canals which are debrided, enlarged and dis­
ment, the rationale for developing this field of infected. The canals are filled with resorbable mate­
regeneration is actually based on sound biologic rial. Indications and contraindictions of pulpectomy
principles. in primary teeth are given in table 8.10.

« This exciting new era was founded when Urist Objectives:

(1965) concluded that the bone matrix contains a ■ Following the treatment, the infectious process
factor capable of autoinduction and named this should resolve.
factor bone morphogenetic protein (BMP). Only ■ There should be radiographic evidence of a st-
recently, with the techniques of molecular biol­ cessfiil filling without gross over-extension or
ogy we now know that there is a family of pro­ underfilling.
teins that has bone inductive properties and BMP ■ The treatment should permit resorption of the
is a generic term for this family. primary root structures and filling materials at the
appropriate time to permit normal eruption of suc-
« The effect of recombinant human BMP-2 and cedaneous tooth.
BMP-4 when capped with inactivated (fentin ma­ ■ There should be no radiographic evidence of fur­
trix on an amputated canine pulp have been seen ther breakdown of the supporting tissues
to imply that recombinant human BMP2 and BMP ■ Treatment should alleviate and prevent further
4 induce differentiation of adult pulp cell into sensitivity, pain or swelling.
odontoblast. The recombinant human osteogenic ■ There should be no internal or external root re­
protein 1 (hop-1) when placed on artificially sorption or other pathology.
€E0 I TEXTBOOK OF PEDODONTICS

Table 8.9: Pulpotomy with commonly used materials

Formocresol Calcium Hydroxide Glutaraldehyde

■ Tissue fixation is evident ■ Calcium bridge formation • Better and non reversible
■ Potent germicides— ■ Germicidal activity fixation of the tissues.
■ Vital tissue remains at the ■ Vital pulp remains. ■ Excellent antimicrobial ----- -
apex. ■ Reported clinical success « Pulp tissue remains vital1___
■ Reported clinical success to be 65% ■ Reported clinical success
about 95% after 2 years. ■ Histological success 35% 98-100%
■ Histological success .70% ■ Associated with internal « Comparitively less
after 2 years. resorption in deciduous .dystrophic calcification^
« Reported toxicity and teeth. ■ Less pulpal necrosis
periapical leakage due to « Bridging may make further
the smaller molecule size. endodontic treatment
complicated.

1
Table 8.10: Deciduous tooth pulpectomv

Indications Contraindications

^«.Strategically important tooth, (e. a: ■ Systemic conditions

in case of the deciduous second ■ Lack of patient cooperation
molar where the permanent first ■ Excessive mobility
molar has not erupted) ■ Non-restorable
. . . tooth
.... ■ Irreversible pulpitis
■ Minimal periapical changes with
. sufficient bone support
■ At least 2/3 rd of the root length
available
■ Internal resorption withoutany
obvious perforation
.......... —\----- I *
 SECTION 8 : PEDIATRIC ENDODONTICS | €EE>

Fig. 8.5a Pulpectomy in deciduous Fig. 8.5b Pulpectomy in deciduous

anterior tooth - pretreatment anterior tooth - post-treatment
following obturation

Fig. 8.5c Pulpectomy in deciduous

molar tooth - Pretreatment

Fig. 8.5d Check X-ray Fig. 8.5e Pulpectomy in deciduous ‘

molar tooth - Post obturation
 €E0 r TEXTBOOK OF PEDODONTICS

TECHNIQUE (Fig. 8.6A-F) ■ Primary Molars

The primary molars normally have the same
Access opening for pulpectomy in number of roots and positions of the roots as the
primary teeth corresponding permanent molars. The maxillary
molars have three roots, two facial and one pala­
Primary Root Canal Anatomy ? tal; the mandibular have two roots, mesial and
To complete endodontic treatment on primary teeth distal. The roots of the primary molars are long
successfully, the clinician must have a thorough slender compared with the crown length and
knowledge of tile anatomy of the primary root canal width, and they diverge to allow fona permanent
systems and the variations that normally exist. tooth bud formation.

■ Primary anteriors ■ Maxillaryfirst primary molars

The form and shape of the root canals of the pri­ The maxillary7 first primary molars have from two
mary anterior teeth resemble the form and shape to four canals that roughly correspond to the ex­
of the exteriors of tjie teeth. terior root form with much variation. The palatal
root is often round; it is often longer than the two
« Maxillary incisors facial roots. Bifurcation of the mesial-facial root
The root canals of the primary maxillary central into two canals occurs in approximately 75% of
and lateral incisors are almost round but some the maxillary7 first primary7 molar.
what compressed. Normally, these teeth have one
canal without a bifurcation. Apical ramifications ■ Maxillary second primary molars:
or accessory7 canals and lateral canals are rare The maxillary7 primary molar has two to five ca­
but do occur. nals, roughly corresponding to the exterior root
shape. The mesial-facial root usually bifurcates
« Mandibular incisors or contains two distinct canals. This occurs in
The root canals of the primary7 mandibular central approximately 85% to 95% of the maxillary sec­
and lateral incisors are flattened on the mesial ond primary molars.
and distal surfaces and sometimes grooved,
pointing to an eventual division into two canals. ■ Mandibularfirst primary molars:
The presence of two canals is seen less than 10% The mandibular first primary molar usually has
of the time. Occasionally, lateral or accessory ca­ three canals, roughly corresponding to the exter­
nals are observed. nal root anatomy but may have two to four ca­
nals. It is reported that approximately 75% of the
■ Maxillary and Mandibular Canines mesial roots contain two canals, whereas only
The root canals of the maxillary and mandibular 25% of the distal roots contain more than one
canines correspond to the exterior root shape, a canal.
rounded triangular shape with the base toward
the facial surface. Sometimes, the lumen of the ■ Mandibular secondprimary molars
root canals is compressed in the mesial-distal di­ The mandibular second primary molar may have
rection. Bifurcation of the canal does not nor­ two to five canals but usually has three. The me­
mally occur. Lateral canals and accessory canals sial root has two canals approximately 85% of the
are rare. time, whereas the distal root contains more than
one canal only in 25% of the times.
 SECTION 8 : PEDIATRIC ENDODONTICS |

B. Use an endodontic file to remove

A. Access opening
the infected pulp

C. Dry the canals with cotton pellets D. Obturate the canals with ZOE
and paper points mixture

E. Apply constant pressure to the F. An alternative method using a

ZOE mixture moist cotton pellet to condense the
mixture
Fig. 8.6 Pulpectomy on primary teeth
 && I TEXTBOOK OF PEDODONTICS

Access opening for primary anterior teeth: Canal Cleaning And Shaping:
Access opening for endodontic treatment on primary
or permanent anterior teeth have traditionally been Isolation (Fig. 8.7)
through the lingual surface. This continues to be the ■’ Use of the rubber dam is essential in any endo­
surface of choice except for the maxillary primary in­ dontic procedure as it is the best method of iso­
cisors. Because of the problems associated with the lating the tooth from the oral cavity. First intro­
discoloration of endodontically treated primary inci­ duced by Barnum (1864), it is useful in providing
sors, it has been recommended to use a facial ap­ a clean, dry and sterilizable field. (Refer isolation)
proach followed by an acid etch composite restora­
tion to improve aesthetics.

The anatomy of maxillary primary incisors is such

that access may successfully be made from the facial
surface. The only variation to the opening is more
extension to the incisal edge than with the normal
lingual access in order to give as straight an approach
as possible into the root canal.

Access openingfor primary posterior teeth:

Access opening into the posterior primary root ca-
nalsare essentially the same as those for the perma­
nent teeth. Fig. 8.7 Isolated primary maxillary first molar
during pulpectomy
Important differences between the primary and per­
manent teeth are the: Debridement \
• Length and the bulbous shape of the crowns
■ Canal cleaning and shaping is one of the most
■ A very thin dentinal wall at the pulpal floor and
important phases of primary endoddntic therapy.
the root.
The main objective of the chemica l - mechanical
« The depth necessary7 to penetrate into the pulp
preparation of the primary tooth is debridement
chamber is quite less than that in the permanent
of the canals. Although an apical taper to the
teeth.
canals is desirable, it is not necessary to have an
■ Likewise, the distance from the occlusal surface
exact shape to the canals. The biomechanical
to the pulp floor of the pulp chamber is much less
preparation in the primary7 teeth can be said to be
than in permanent teeth. In the primary molars,
different enough to warrant the following con­
care must be taken not to grind on the pulpal
siderations:
floor since perforation is likely.
1. Relative pulpectomy'. Due to the tortuous
When the root of the pulp chamber is perforated and course of the canal coupled with the numer­
the pulp chamber is identified, the entire roof should ous accessory canals, the complete removal
be removed with a bur. Since the crown of the pri­ of pulp in the primary teeth may often be diffi­
mary teeth are more bulbous, less extension towards cult , if not impossible. Thus, all such proce­
the exterior of the tooth is necessary to uncover the dures can be regarded as partial pulpectomy
openings of the root canals than in the permanent procedures.
teeth.
 SECTION 8 : PEDIATRIC ENDODONTICS |

2. Selective filling'. Resorption in the primary the pulp chamber with temporary cement. At a
teeth may have started at thetime of treatment. subsequent appointment the canal is reentered.
Also, the slender roots, with thin apical ends As long as the patient is free of all sighs and
may predispose the tooth to a root fracture in symptoms of inflammation, the canals are again
cases of excessive preparation. Thus the pro­ irrigated w ith sodium hypochlorite and dried pre­
cedure of selective filing of the canals should paratory to filling.
be followed.
FILLING OFTHE PRIMARY ROOT CANALS
It is important to establish the working length to
ROOT FILLING MATERIALS
prevent over extension through the apical
foramen. It is suggested that the working length Developmental, anatomic and physiologic differ­
be shortened, 2 or 3mm short of the radiographic ences between the primary and permanent teeth calls
root length, especially in the teeth showing signs for differences in the criteria for root canal filling ma­
of apical root resorption. terials. The ideal requirements of a root-filling materi­
als for the primary teeth are as follows.
Instruments should be gently curved to help
negotiate canals. This helps in maintaining the Ideal requirements:
original shape of the canal and thus lessens the ■ Resorb a t a similar rate as the primary root.
risk of perforation. Shaping of the canals proceeds ■ Should beTSrmiess to the periapical tissues and
in much the same manner as is done to receive a to the permanent tooth germ; resorb readily if
gutta-percha filling. The canals are enlarged sev­ pressed beyond the apex.
eral file sizes past the first file that fit snugly into ■ It should have a stable disinfecting power.
the canal, with a minimum size of 30 to 35. ■ It should be inserted easily into the root canal
and be removed easily if necessary)
Since many of the pulpal ramification cannot be ■ Should adhere to the walls of the canal and should
reached mechanically, copious irrigation during not shrink.
cleaning and shaping must be maintained. Debri­ ■ It should not be soluble in water.
dement of the primary root canal is more often ■ Be radiopaque and not discolour the tooth.
accomplished by chemical means than mechani­ No material currently available meets all these cri­
cal means. The use of sodium hypochlorite to teria. The filling material most commonly used for
digest organic debris and RC-prep to produce primary pulp canals are_Zinc_feide^=^g@ad^
effervescence must play an important part in re­ paste, iodoform paste and calcium hydroxide.
moval of the tissue from the inaccessible area of
the root canal system. ZINC OXIDE - EUGENOL PASTE

If the inflammation is beyond the coronal pulp Zinc oxide - eugenol paste (ZOE) is probably the
with only inter radicular but no periapical radiolu- most commonly used filling material for primaiy teeth.
cency, a single visit pulpectomy is preferred. On Camp in 1984 introduced the endodontic pressure
the cither hand, if the pulp is necrotic with peri­ syringe to overcome the problem of underfilling, a
apical involvement, filling procedure is delayed relatively common finding when thick mixes ofZOE
until a later time. After canal debridement, the ca­ are employed. Under-filling, however, is frequently
nals are again copiously flushed with sodium hy­ clinically acceptable. Overfilling, on the other hand,
pochlorite and are then dried with sterile paper may cause a mild foreign body reaction. Another
points; a pellet of cotton is barely moistened with disadvantage of ZOE paste is the difference between
camphorated parachlorophenol and sealed into its rate of resorption and that of the tooth root.
 €E2) I TEXTBOOK OF PEDODONTICS

IODOFORM PASTE radioopaque. For these reasons, the calcium hy­

droxide - iodoform mixture can be considered to
Several authors have reported the use of KRI paste, be a nearly ideal primary tooth filling material.
It resorbs rapidly and has no undesirable effects on Other preparation with a similar composition is
succedaneous teeth when used as a pulp canal medi­ available mthe United States with the trade name
cament in abscessed primary teeth. FurtheyKRIpaste ofEndoflas (Sanlon Laboratories, A. A 7523 Cali,
that extrudes into the periapical tissue is rapidly re­ Colombia S. A).
placed with anormal tissue. It is also found to have a
long lasting bactericidal potential. Since iodoform « Chawla et al (1998) carried out apilot study in the
paste does not set into a hard mass, it can be re­ mandibular primary molars using calcium hydrox­
moved if retreatment is required. KRI was found to ide paste as a root canal filling material and found
have a success rate of 84% as compared to ZOE, it to be a success.
which showed a success rate of only 65%.
■ We have also observed almost a 100% clinical
* A paste developed by Maisto has been used success in 10 endodontically treated primary
clinically for many years, and good results have molars which were filled with vitapex (calcium
been reported with its use. This paste has the hydroxidised idoform).
same composition as the KRI paste with addi­
tions. GUTTA PERCHA
Since gutta percha is not a resorbable material its
Composition of commonly used root canal mate­ use is contraindicated in the primary teeth.
rials are given in Table 8.11 for primary teeth
Comparison of materials used for pulpectomy
in primary teeth is given inTable 8.12
CALCIUM HYDROXIDE
Obturation techniques
» This material is generally not used in pulp therapy ■ Several techniques have been used fpr the filling
for primary teeth. However, several clinical and of materials into the deciduous teeth canals.
histopathologic investigations of calcium hydrox­ 1. The primary teeth with their larger canals can
ideand iodoform mixture (Vitapex, Neo Dental be filled with the thin mix coating the walls of
Chemical Products Co. Tokyo) have been pub­ tire canal with the help of a reamer in a anti­
lished by Fuchino and Nishino (1980). This mate­ clock wise direction while taking it out slowly
rial was found to be easy to apply and resorbs at followed by the placement of the thicker mix
a ¿lightly faster rate than that of the root. It has which is then pushed manually.
t W-
no Toxic effects on permanent successor and is
* i’

le 8.11: Composition of commonly used root canal materials for primary teeth

Walkhoff paste KRI paste Maisto paste Vitapex (Fig. 8.8)

■ Parachlorophenol ■ Iodoform 80.8% ■ Zinc Oxide 14 gms « Calcium hydroxide

■ Camphor ■ Camphor 4.86% ■ Iodoform 42 gm ■ Iodoform
■ Menthol ■ Parachlorophenol ■ Thymol 2 gm ■ Oily
2.025% ■ Chlorophenol additives
Camphor 3cc
■ Menthol 1.215% ■ Lanolin 0.50 gms
 SECTION 8 : PEDIATRIC ENDODONTICS |

Fig. 8.8 Vitapex material for obturating root Fig. 8.9 Lentulo spiral used to obturate
canals in primary teeth root canals

Fig. 8.10 Endodontic instrument holder Fig. 8.11 Over obturation seen following ZOE
obturation of mandibular second
molar (Distal Root)
 J TEXTBOOK OF PEDODONTICS

Table 8.12: Comparison of materials used for'pulpectomy in primary teeth

Properties ZOE Ca[OH]2with KRI
Iodoform paste
[VITAPEX]
*

1. Resorbs at the same rate as the tooth.

2. Harmless Y Y Y
3. Overfill resorbs Y Y
4. Antiseptic Y Y Y
5. Easily applied Y
6. Adheres to the wall Y Y Y
7. Easily removed Y Y
8. Radiopaque Y Y Y
9. No discolouration Y Y Y

Y-Yes *Vitapex - Neo Dental Chemical Products Co. Ltd., Tokyo, Japan (2000)

2. Pastes can also beifilled by means of a Lentulo chamber to seal over the ZOE canal filling. The
spiral mounted on the micromotor hand piece. primary tooth is restored with a stainless steel
The direction of rotation needs to be checked crown.
for the material to properly flow into the canal.
FOLLOW-UP AFTER PRIMARY PULPECTOMY
(Figs. 8.9, 8.10). I

■ The rate of success following^rimary pulpectomy

3. The endodontic pressure syringe is also effec­ is high. However, these teeth should pe periodi­
tive for placing the ZOE into the canals. The cally checked for success of the treaXipent and to
Vitapex system also uses a syringe with the intercept any problem associated with failure.
material in it. The syringe is introduced upto While resorbing normally without interference
1/5 the distance from the apex of the canal and with eruption of the permanent tooth, the primary
the material is slowly injected as the syringe is tooth should remain asymptomatic, firm in the al­
withdrawn from the canal. veolus, and free from pathosis. If evidence of
pathosis is detected, extraction and conventional
« Regardless of the method adopted to fill the ca­ space maintenance are recommended.
nals, care should be used to prevent extrusion of
the materials into the periapical tissues. The ad­ « It has been pointed out that pulpally treated pri­
equacy of the obturation is checked by radio­ mary teeth may occasionally present a problem
graphs. In the event a small amount of the ZOE is of overretention. After normal physiologic resorp­
inadvertently forced through the apical foramen, tion of the root reaches the pulp chamber, the
it is left alone since the material is resorbable (Fig. large amount of ZOE present may impair the re­
8.11). sorption and lead to prolonged retention of the
■ When the canals are satisfactorily obturated, a crown. Treatment usually consist of simple re­
fast - set temporary cement is placed in the pulp moval of the crown and allowing the permanent
tooth to erupt
 SECTION 8 : PEDIATRIC ENDODONTICS |

YOUNG PERMANENT TOOTH barrier at the apex of the tooth, against which a
GP root filling can be condensed without the pos­
APEXIFICATION AND APEXOGENISIS (Table 8.13) sibility of sealant or GP going through the apex
into the periapical tissues.
Endodontic management of infected or non vital of
young permanent tooth with a wide-open blunder­ APEXIFICATION
buss apex has long presented a challenge. An imma­
ture permanent tooth is defined as one where the Indications
apex can be considered to be open. This procedure is indicated for nonvital permanent
teeth with incompletely formed roots.
Problem oftreating immature incisor with a necrotic
pulp Objectives
This procedure should induce root end closure at
The anatomy of the non-vital immature incisor the apices of immature roots, as evidenced by peri­
presents several problems. odic radiographic evaluation. Post treatment, adverse
1. There is an open apex hence no hard tissue stop clinical signs or symptoms such as a prolonged sen­
against which gutta percha can be packed. sitivity, pain, or swelling should not be evident There
2. The open apex of the root canal tends to be should be no evidence of abnormal canal calcifica­
shaped like a blunderbuss making it difficult to tion or internal or external root resorption, lateral root
obturate the apex with root filling material. pathosis, or breakdown of periradicular supporting
3. Apicectomy is not advisable because the walls tissues during or following treatment.
of the immature roots are likely to fracture when
sealing the root apex. Adaterials
A number of materials and procedures have been rec­
■ Root canal treatment of these teeth requires a root ommended for apexification procedure: antisepticand
end closure technique to form a complete calcific antibiotic paste (as reported by Frank), Zinc oxide

Table 8.13: Apexogenesis and Apexification

APEXOGENESIS ^APEXIFICATION (Fig. 8.12a, b. C, d)

■ It is the physiologic process • It is the method of inducing

of root development in vital the development of root apex
infected tooth. in an immature pulpless tooth
« Normal or pulp tissue with by formation of osteocementum
minimal inflammation is or other bone like tissue.
present: ■ Indicated in cases where there
1. Completely (direct pulp is no normal pulp tissue i.e.,
capping) where the pulp has undergone
2. In the radicular portion irreversible pulpal necrosis.
(pulpotomy) ■ Normal root development takes
■ Normal root end development place rarely. More commonly,
takes place. calcific barrier is formed clinically,
on a radiograph or both.
 <cFF> I TEXTBOOK OF PEDODONTICS

f r*

Fig. 8.12a Apexification pretreatment Fig. 8.12b Calcium hydroxide placed

showing open apex in the pulp chamber following
removal of pulp

Fig. 8.12c Check X-ray - Apical Fig. 8.12d Post-treatment obturated

constriction formed by 12-13 months with gutta percha
 SECTION 8 : PEDIATRIC ENDODONTICS 1 359J

A. Immature tooth with periradicular B. Working length measured

disease

Ç. The canal is filled with calcium hydroxide

Fig. 8.13 Apexification

 I TEXTBOOK OF PEDODONTICS

and metacresylacetate-camphorated para-chloroph- 8. On a 6 month recall, you should see radiographic

qnol, tricalcium phosphate, collagen-calcium phos­ evidence of an apical closure. Weine, 1976 noted
phate gel, resorbable tricalcium phosphate, ceramic, five alternatives evident at this time.
calcium hydroxide, empty canals and even no treat­ ■ No apparent apical closure, but a resistance
ment at all. - point when a file is inserted.
■ Radiographic evidence of a calcified bridge at
• Calcium hydrô^3^ ^:
the apex.
This is available in many forms and is the most
■ Apical closure without canal space changes.
widely used and tested material. Dry powder can
■ Normal continuance of apical closure.
be packed into the canal; powder can be mixed
■ Increased radiographic evidence of resolution
with water; or powder can be mixed with intracanal
of apical pathology.
medicaments or with methyl cellulose. Recently,
9. When you have accomplished apical closure, the
calcium hydroxide points (58% calcium hydrox­
root canal filling is completed.
ide, 42% guttapercha and colouring agent) have
10. If apexification has not been completed, repeat
also been used. There seems little justification,
the cleaning and insertion of a calcium hydroxide
however, for mixing the powder with an intracanal
and CMCP paste.
medicament. Most medications are clearly cyto­
toxic. The antibacterial effect is provided by cal­
Treatment Evaluations:
cium hydroxide.
« The first evaluation of the apexification proce­
Procedure dure may be done after 3 months. Radiographs
’Frank in 1966 was one of the first to describe the may show hard tissue deposition, but such evi­
clinical methods using calcium hydroxide paste and dence is not considered reliable. It is necessary
camphorated monochorophenol (CMCP), to stimu­ to test the quality of the apical barrier with a size
late root closure. 35 file. If the file easily penetrates, so too will the
obturation material It will therefore be necessary7
The procedure for apexfication is as follows (Fig 8.13):
to continue the apexfication by reapplying cal­
1. The tooth is isolated with rubber dam, and ac­
cium hydroxide.
cess is gained into the pulp chamber.
2. Using large reamers and files, remove the debris
■ If the 3 months radiograph shows little or no api­
from the coronal half of the pulp and establish
cal changes, reschedule the patient for another 3
the file length radiographically.
months recall. There is no need to change the
3. Clean the canal, irrigate it and then dry it with a
calcium hydroxide if it appears to occupy the root
paper point. Repeated gentle use of sodium hy­
canal space adequately, and if the coronal tempo-
pochlorite assists debris removal.
raiy seal appears satisfactoiy. Any question about
4 Seal a pellet of CMCP in the pulp chamber with a
either condition requires replacement of both the
provisional restorative material.
calcium hydroxide and the coronal seal. Shalini
5. On recall, in 1 to 3 weeks, remove the restoration
Gupta et al in 1999 reported a continuing root
and clean the canal.
formation in a carious non-vital and immature
6. Take care to avoid any instrumentation of the walls
mandibular second premolar after a single visit
of the dentin near the apex.
calcium hydroxide apexification treatment. An
7. Mix a paste of calcium hydroxide and CMCP on a
apical hard tissue barrier was formed, accompa­
glass slab. Cany the paste to the canal and force
nied by a separate, mesioapically growing root,
it into the apex with a large plugger or cone-
in 7 months post treatment. Treatment was con­
shaped instrument. The objective is to fill the ca­
cluded with gutta percha root canal restoration.
nal completely. Obtain a radiograph to check the
The success of this single visit apexification treat
accuracy of the root canal filling.
 SECTION 8 : PEDIATRIC ENDODONTICS |

ment supports the contention thatfrequent chang­

ing of the calcium hydroxide dressing is not al­
ways required to induce an apical closure.

■ The follow-up evaluation is repeated even 3

months until successful apical bridging has oc­
curred .This may take as little as 3 months or as
long as ayear or more, depending on the degree
of apical destruction and the ability of the apical
tissue tb repair.

Obturation of the root canal

Because the root canal wall does not change during
Fig. 8.14a Root canal treatment in permanent
apexification, the shape of the canal will remain the
first molar - pre treatment
same after the apical barrier has formed, namely a
reverse taper. These canals are probably best suited
for obturation by a thermoplasticized technique. (Fig
8.14a, b, c).

Recall andfollow-up
A routine recall evaluation should be performed to
determine the outcome of the root canal procedure.
Teeth treated in this manner are more likely to de­
velop root fractures due to the thin root canal avails.
Therefore, the more developed the teeth before
apexification, the better their prognosis.

Alternative to conventional apexification

■ A primary objective in endodontic therapy is the
complete obturation of the root canal space. A
good apical stop is an essential factor in achiev­
ing this goal. It effectively confines the filling
material to the canal space and allows the appli­
cation of adequate condensation forces to yield
ait acceptably dense filling. Immature pulpless
teeth present special problems in adherence to
this objectives. These teeth have parallel or di­
vergent walls in the apical third which make a
normal development of an apical stop impossi­
ble. This leads to an inability to confine the filling
material to the canal space.

■ Mineral trioxide aggregate or MTA, is a new ma­

terial developed for endodontics that appears to Fig. 8,14c Post-obturation
be a significant improvement over other materials
 I TEXTBOOK OF PEDODONTICS

for procedures in bone. It is the first restorative Further Suggested Reading For Section - 8
material that consistently allows for the
overgrowth of cementum, and it may facilitate the 1. Berger IE. Pulp tissue reaction to formocresol
regeneration of the periodontal ligament. and zinc oxide-eugenol. J.Dentchild: 13; 32,1965
2. Cappuccino C.C & Sheehan R.F. The biology of
m Schwartz et al [1999] reported the lise of MTA the dental pulp. In text book of oral biology. Edi­
as: tion by J.H. Shaw, E.A Sweeney, C.C Cappuccino
1. First appointment - Calcium hydroxide was and S.M. Meller. Philadelphia, WB. Saunder &
used and the tooth was temporized Co., 1978.
3. Chawla H.S. etal. Calcium hydroxide as a root ca­
2. Second appointment! 3 weeks later] - The tooth
nal filling material in primaiy teeth- A pilot study.
still had a sinus tract
J. Indian Soc Pedo PrevDent: 16(3); 90-91,1998
3. Third appointment - The sinus was healed. A 4. Curt Goho. Pulse oximetry evaluation of vitality
thick mix of MTA and saline was introduced in primaiy and immature permanent teeth. Pediatr
into the canal, and left to set overnight. The Dent-: 21 (2); 125-127,1999
next day the tooth was obturated with gutta 5. Ehrenreich D.W A comparison of the effect of
percha. The tooth was found to be asympto­ Zinc oxide and eugenol and calcium hydroxide
matic with normal periapical structure at 9 and on carious dentin in human primar/ molar. J. Dent
20 months recall . Child: 35; 451,1968
6. Eliyahu Mass. Endodontic treatment of infected
Self-Assessment primaiy teeth using Maisto’s paste. J. Dent Child:
56:117,1989
1 What role do the radiographs play in the man­ 7. Fei A,Udin R.D Johnson R. A clinical study of
agement of deep caries? ferric sulfate as a pulpotomy agent in primary
Z Give the objectives, indications, contra indica­ teeth. Pediatr Dent: 13; 327-332,1991
tions of indirect pulp capping? 8. Garcia-godoy et al, Pulpal response to different
3. Describe the treatment procedure for pulpotomy application time of formocresol. J.Pedod: 6; 170-
and pulpectomy? 193,1982
4. What is the difference between the infected and 9. Gideon Holán & Anna B Fuks. Comparison of
affected dentin? pulpectomies using ZOE and KRI paste in pri­
5. What are the materials used for indirect pulp cap­ mary molar. Pediatr Dent: 15(6); 403,1993
ping, direct pulp capping, pulpotomy and pulpec­ 10. Glass R.L & Zander H. A. Pulp healing. J. Dent
tomy? Res: 28; 97,1949
6. What are the reasons for the relative low success 11. Sun HW et al. Cytotoxicity of glutaraldehyde and
rate of direct pulp capping in primary teeth? formadehyde in relation to time of exposed and
7. What are the differences between formocresol and concentration. Pediatr Dent: 12; 3^)3-307,1990
glutaraldehyde pulpotomy? 12. Jeng-Fen Liu, Liang-Ru-Chen, Shou-Yee Chao.
8. What is mortal pulpotomy? Laser pulpotomy of primary teeth. Pediatr Dent:
9. What are the materials used for obturation of pri­ 21(2); 128-129,1999
mary teeth? 13. Kopel H.M¡. etaíl The effects of glutaraldehyde
10. What is the difference between apexogenesis and on primary pulp tissue following coronal ampu­
apexification? tation, an m vivo histologic study. J.Dent.Child:
47; 425-430,1980
 SECTION 8 : PEDIATRIC ENDODONTICS |

14. Machido Y. Root canal therapy in deciduous teeth. 23. Roberts S.G & Brilliant J.D. Tricalcium phosphate
Jap Dent Assoc J: 36; 796-802,1983 as an adjunct to apical closure in pulpless penna-
15. Mack R.B, Dean J. A. Electrosurgical pulpotomy: nent teeth. JOE: 1;263,1975
a retrospective human study. J.Dent.Child: 60; 107- 24. S.D Hill etal. Comparison of antimicrobial and
114,1993 cytotoxic effects of gluteraldehyde and
16. Mack R.B, Halterman C.W. Labial pulpectomy formocresol. Oral Surg Oral Med Oral Pathol: 71;
access followed by esthetic composite resin res­ 89-95,1991
toration for non-vital maxillary deciduous inci­
25. Stewart D. J and Kramer IRH. Effects of calcium
sors. J. Am Dent Assoc: 100; 374,1980
hydroxide on the unexposed pulp. J. Dent Res:
17. Mount G. J. Some physical and biological proper­
37; 758,1958
ties of glass ionomer cement. Int. Dent. J. 45;135-
26. Tomeck C.D, Smith J, Grindall P. Biologic effects
140,1995
18. Mesic N - Par etal. Clinical and histological exami­ of endodontic procedures on developing incisor
nation of young permanent teeth after vital am­ teeth. Effect of pulp injury and oral contamina­
putation of the pulp. Acta Stomatologica tion. Oral Surg: 35; 378,1973
Croatica: 24; 253-262,1990 27. Tsai TP, Su H.L, Tseng L.H. Glutaraldehyde prepa­
19. Nakashima .M. Induction of dentin formation on rations and pulpotomy in primaty molar. Oral Surg
canine amputated pulp by recombinant human Oral Med Oral Pathol: 76; 346-350,1993
bone morphogenetic proteins (BMP)2 & 4. J. Dent. 28. Wilkerson M, Hill S, Arcoria C. Effect of the or­
Res: 73(9); 1515-1522,1994 gan laser on primaiy tooth pulpotomies in swine.
20. Nevins A etal. Induction of hard issue into J. Clin Las Med & Suf: 14; 37-42,1996
pulpless open apex teeth using collagen calcium 29. Suneda YT et al. A histopathological study of di­
phosphate gel.. JOE: 4; 76,1978 rect pulp capping with adhesive resins. Oper Dent:
21. Nishino M etal. Clinico-roentgenographical study
20; 223-229,1995
of iodoform-calcium hydroxide root canal filling
30. Zander H. A. Reaction of the pulp to calcium hy­
aterial Vitapex in deciduous teeth. Jap. J.
droxide. J. Dent Res: 18; 373,1939
Pedodont: 18; 20-24,1980
22. Olgart L, Gazelius B, Lindh- Stromberg. U. Laser
Doppler flowmetry in assessing, vitality in luxated
permanent teeth. IntEndod J: 21; 300-306,1988
 SECTION - 9

Developing Malocclusion
and its Management
9.1 Incipient Malocclusion
Tandon S

Introduction Incipient malocclusion

The responsibility of early detection and manage­ A incipient malocclusion may be defined as a con­
ment of developing malocclusion rests with the dition which shows atendency ip develop into a
pedodontists, because they see the patient at a very deviation from the normal dentofacial or occlusal
young age and at various intervals like preschool relationship. }
age, school age and the teenage period. Many ir­
regularities or deviations from the normal may be Types of incipient malocclusion (Table 9.1)
observed while they just begin to exist and they are
diagnosed early. This chapter is aimed to discuss The early recognition of such problems requires the
principles of diagnosis of incipient malocclusion knowledge of what is normal and also classifying
which is sometimes present as early as in predentate both normal and abnormal for a successful plan­
ning of preventive or interceptive treatmerft. There­
period, deciduous dentition or mixed dentition. The
fore, a cursory examination is required at the first
diagnosis of these deviations is of prime importance
visit to collect information, classify occlusion, or­
for a dental practitioner to prevent before they start
ganize the facts gathered and reach a tentative di­
to come into existence or to refer such problems to
agnosis. This provides a basis for a more definitive
the concerned specialist for the timely intervention
treatment plan, and a line of action to prevent ini­
to minimize the corrective treatment
tial occlusal problems to develop into malocclusion.

definitions Concept of diagnosing incipient malocclusion

Incipient: Beginning to exist or coming to exist­ Diagnosis is the study and interpretation of data
ence. concerning a clinical problem in order to determine
the presence or absence of an abnormality.
Malocclusion: Such malposition and contact of The traditional approach in diagnosing a normal
maxillaiy and mandibular teeth as to interfere with occlusion was to view the normal occlusion as fa­
the highest efficiency during excursive movements vourable, functional and acceptable esthetically, but
ofjaws which are essential for mastication and nor­ the modem concept is entirely changed. It is now
mal functions. mainly stressing on prevention oriented early de­
tection of problems.
 SECTION 9 : DEVELOPING MALOCCLUSION AND ITS MANAGEMENT |

Table 9.1: Types of incipient maloclusion

Dental Skeletal Dento-skeletal

Involving tooth or a group of teeth When mandible or maxilla Combination of both

Example: are in abnormal réíatign to Example:
i) Crowding in deciduous dentition 4 each other or to the anterior i) Deficient mandibular
ii) Rotation of teeth interfering with cranial base. growth with lower
mastication Example: anterior crowding.
iii) Dental caries causing mesio- 1 ncipien£problemjuxuxs
distal spacelogs during growth of the individual
iv) Space loss with a premature loss i) Developing mandibular
of deciduous teeth . growth in class III relation
v) Anterior and posterior cross bite. ii) Maxilla developingjn...
class ÍI relation

Recently Graber (1994) expressed his view regard­ ESSENTIALS OF DIAGNOSIS

ing the diagnosis ' the goal of the diagnostic proc­
ess is to produce a list of all the patient’s problems I. GENERAL EVALUATION
and to state them clearly and concisely” which seem
to be a very simple way of detecting deviation espe­ Initial patient contact:
cia lly related to the incipient one. Data collection starts with the first encounter with
the patient and/or parent. First contact may be via
Incipient malocclusion is the result of a develop­ die telephone - one gets to know the patient’s age,
mental process, not pathologic, and the objective source of referral, parents awareness, etc. It can
signs typically measured by the dentist are morpho­ also reveal whether the parents’ orientation is pri­
logic characteristics rather than the physiologic marily cosmetic or whether their greatest concern
measurements of function used by the physician to is with function and oral health, in the first inter­
treat an illness. Therefore, a clinician must keep in view when one questions “What problem concerns
mind that orthodontic diagnosis is based on the you the most”?
symptoms of impaired functions and/or psychologi­
Chief complaint:
cal acceptance that has let the patient to seek treat­
There are two logical reasons for concern about the
ment, not the morphological signs per se.
alignment and occlusion of teeth, impaired
dentofacial esthetics that can lead to psychological
The growth of the child is not static in nature and is
problems, and impaired function. It is important to
constantly under dynamic changes from birth until
establish their relative importance to the patient.
the early stage of teenage. It is thus, essential to
The dentist may or may not agree with the patient’s
obtain a good rapport between the dentist, the child
assessment - that judgement'comes later. At this
and parent and it should be made clear that a nor­
stage, the objective is to find out what is important
mal occlusion may not develop always. The parent
to the patient.
should be made to understand how things can go
wrong, and how much easier it is to prevent and
Medical history:
intercept the incipient problems rather than correct
Orthodontic problems are almost always the culmi­
them at a later date.
nation of a developmental process, not the resum e#
 ÆSŒI I TEXTBOOK OF PEDODONTICS

a pathologic process. A careful medical history is Age:

needed to provide a proper background for under­ Chronological age recorded, certain treatment
standing the patient’s overall situation and to evalu­ changes occur at certain ages that are normal for
ate specific orthodontically related concerns. that age, thus knowing the age helps identify and
anticipate this condition. Growth modification pro­
Dental history cedures using functional and orthopedic appliances
Can evaluate any problems plus the patients atti­ are carried out during the growth period. Surgical
tude towards dental treatment. procedures are carried out after growth cessation.
Can also question the parents, whether they have
had any orthodontic treatment before. This will shed Sex:
some light on the possible hereditary component of Growth spurts are different in males and females.
the child’s problem and it provides an insight into Females usually precede males in the onset of growth
how much, the parents already know about his type spurts at puberty and termination of growth.
of treatment.
Prenatal history:
Genetic history Information on condition of the mother during preg­
A genetic history can begin with an inquiry as to nancy (drugs like thalidomide and German mea­
whether any siblings have required orthodontic sles can result in congenital deformities of the child).
treatment and a discussion about the nature of their Information on the type of delivery (forceps deliv­
problems. Inquiries should also be made into ery predispose to TMJ injuries which can manifest
whether the parents/close relatives have had ortho­ as marked mandibular growth retardation).
dontic treatment, which may indicate the child’s pre­
Family history:
disposition towards malocclusion.
Skeletal class II/III malocclusions are inherited.
When examining, be alert to facial characteristics
II. STRUCTURAL ASSESSMENT
that might be associated with a craniofacial syn­ £
drome. Extra oral examination:

Social-behavioural history A. General health, body type, and posture

This information may be difficult to obtain, as par­ 1. Physical growth status:
ents are often reluctant to speak about a child’s emo­ It is important to judge the general physical
tional problems. Questions on progress in school development in relation to the amount of
should be made. If the child is slow or has a learn­ growth that has occurred and the potential of
ing disability it may be better to, whenever possi­ future growth that remains. This is achieved
ble, to reduce the patient’s responsibility in carty- by recording height and weight of the child.
ing out treatment, e.g. a fixed rather than a remov­ 2. Body type
able appliance is preferable. Ectomorphic, mesomorphic and endomorphic
have certain implications regarding somatic
Attempt to elicit the patient’s feelings of self worth. growth and development.
If facial protrusion is the problem, how does it af­
fect the child’s self evaluation? Do the children in B. Facial features:
school call the child by funny names that relate to 1. Facial type (mesofacial, brachyfacial and
the appearance? Does the family focus, inadvert­ dolicofacial).
ently, on one or more of the child’s facial features?
 SECTION 9 : DEVELOPING MALOCCLUSION AND ITS MANAGEMENT |

. Shape of the head (dolicocephalic, mesocephalic - Position of the upper and lower lips with re­
and brachycephalic) (Fig. 9.1) spect to maxillary and mandibular incisors
Profile analysis (anteroposterior and vertical re­ during mastication, deglutition, respiration
lationship) (Fig. 9.2) and speech.
a) protruded/retruded mandible - Tongue position and pressures exerted dur­
b) prbtfudedfretruded maxilla ing functional movements.
c) relationship of maxilla and mandible to cra­
nial structures. III. FUNCTIONAL ASSESSMENT
Lip posture at rest (colour size, mentolabial sul­
cus) (Fig. 9.3) Respiration
. Relative symmetry of facial structures Mouth breathing or interference with nasal respi­
(Fig. 9.4a, b, c) ration have important effects on craniofacial growth.
a) size and shape of nose
b) chin button size and contour Methods of examination

ntra Oral Examination: 1. Study the patient’s breathing unobserved. Nasal

- breathers usually show the lips touching lightly
) Jaw relationship
during relaxed breathing, whereas mouth breath-
- Ant-post relationship (overjet) (Fig. 9.5)
ers keep the lips apart.
- Vertical relationship (ovefbite) (Fig. 9.6)
- Lateral relationship (crossbite) 2. Ask the patient to close the lips and take a deep
breath through the nose:
) Open mouth examination of the teeth
Nasal breathers normally demonstrate a good re­
- Number of teeth present and absent
flex control of alar muscles and control the size
- Identification of teeth present
and shape of the external nares, they dilate the
- Record any abnormality of size, shape/posi-
externalnares on inspiration. MoutfibreaffiSST'
tion
even though they are capable of breathing
- Restorative status
through the nose, A) not change the size and
- Tooth to bone ratio
shape of the external nares and occasionally even
- Oral hygiene
contract the nasal orifices during inspiration.
- Centric occlusion, molar and canine relation­
ship 3. Mirror test: A double sided mirror is held be-
- Overjet and over bite _ - tween the nose and the mouth. Fogging on the
- Midline nasal side of the mirror indicates nasal breath­
ing while fogging towards the oral side indicates
) Soft tissue appraisal
mouth breathing.
- Gingiva (color, texture, hypertrophy)
- Labial frenum, upper and lower Cotton test: (Butterfly test): A butterfly shaped
- Tongue size, shape, posture piece of cotton is placed over the upper lip be­
- Palate, tonsils, adenoids low the nostrils. If the cotton flutters down it
- Vestibular mucosa indicates nasal breathing. This test can be u^ed
-• Lip morphology, color, texture, and charac­ to detect an unilateral nasal blocking.
ter of tissue, hypotonic, flaccid, hypertonic,
.J. Water test: The patient is asked to fill his mouth
functionless, redundant, short, long etc).
with water and retain it for a period of time.
- Clicking, crepitus or popping of TMJ
While nasal breathers accomplish this with ease,
- Excessive mobility of individual teeth
mouth breathers find the task difficult
 TEXTBOOK OF PEDODONTICS

A. Mesocephalic B. Brachycephalic C. Dolicocephalic

Fig. 9.1 Shape of Head.

A convex profile indicates A Straight A concave profile indicates

cl. II malocclusion usually profile (Normal cl. Ill malocclusion which may
from a mandible that is placed profile) be due to the maxilla too far
too far posteriorly. back or the mandible too
forward.

Fig. 9.2 Facial profiles

 SECTION 9 : DEVELOPING MALOCCLUSION AND ITS MANAGEMENT |

Competent lips
Incompetent lips

Assessment of mentolabial sulcus Assessment of nasolabial angle

Normal - No contraction of muscle Normal angle - 110°
Hyperactive - Puckering of chin Prognathic maxilla - < 110°
Retrognathic maxilla - > 110°

Fig. 9.3

A. Symmetric face B. Asymmetric face

Fig. 9.4a Symmetry of face

J
{SO) | TEXTBOOK OF PEDODONTICS

Natural head position while facing- Thirds of the face are roughly
the examiner equal in vertical dimension

Intercanthal distance is about Mouth is as wide as the distance

equal to alar nasal base width from right to left medial limbus

Fig. 9.4b Normal facial proportions.

A. Upper apical zone

B. Upper coronal zone
C. Lower apical zone
D. Lower coronal zone

Fig. 9.4c Relationship of facial zones.

 SECTION 9 : DEVELOPING MALOCCLUSION AND ITS MANAGEMENT

Fig. 9.5 Assessment of anterior posterior jaw relationship with ‘A’ and ‘B’ points
Normal - The hand is at an even level
Prognathism - The middle finger is ahead of index finger, hand points downward
Retrognathism - Index finger is ahead with hand pointing upward

Fig. 9.6 Assessment of the vertical facial height with the angle formed between
lower border of mandible and the Frankfort horizontal plane
 I TEXTBOOK OF PEDODONTICS

Differential Diagnosis Differential diagnosis of swallowing types are

1. Nasal breathers: lips touch lightly at rest, nares illustrated in Table 9.3
dilate on command inspiration.
2. Mouth breathers: Lips are parted at rest, nares Occlusal interference.
maintain size/contact on command inspiration In various positions (centric or eccentric), there may "
with the lips held together. be occlusal interferences, leading to a deviated path
of closure and consequently forcing an imbalance
Speech difficulties indicating dental problems of musculature. This may in turn have a potential
(Bell 1980) are given in Table 9.2 . for affecting future growth and imbalance in cranio-

Table 9.2: Speech difficulties indicating dental problems

Speech Sound Type Dental problems

Zs/ZzZ Sibilant Lisp related to large gap between

incisors or missing incisors, openbite.
ZtZ ZdZ Lir jo Difference in production related to alveolar
stop irregular incisors (especially lingual
• position of max incisors or supernumerary
teeth; tongue tie).
ZfZ ZvZ Linguodental Distortion related to excessive protrusion of
mandible fricative.
ZthZ ZchZ ZshZ Linguodental Distortion related to severe openbite, missing
voiced or fricative incisors.
voiceless
ZIZ Linguo Distortion related to tongue tie.
alveolar
continuant £

Table 9.3: Differential diagnosis of swallowing types

Swallowing Tongue thrusting
Retained
Signs and symptoms infantile Mature Simple Complex infantile
swallowing
Tongue between teeth Yes No Yes Yes Yes
Endogenous Yes No No No Yes
Mandibular stabilization
by facial contractions Yes No No Yes Yes
Teeth-together swallow No Yes Yes No No
Lip and mentalis
contractions Yes Ño Yes Yes Yes
Enlarged tonsils and No No No No Yes
adenoids or history of
low gag reflex threshold
 SECTION 9 : DEVELOPING MALOCCLUSION AND ITS MANAGEMENT I G&

facial skeleton as well as distorting the form of al­ b) Preterm birth (Gestational age under 37
veolar arches. For example, pseudo class III due to weeks):
functional disturbance in occlusion, bilateral cross Prematurely bom infants are subjected to a vari­
bite appearing as unilateral cross bite due to func­ ety of metabolic stresses and exhibit a higher
tional adaptation. These problems may also have an prevalence of oral dental disturbances than nor­
impact on TMJ growth and normal function. mal full term infants. These developing prob­
lems can be prevented if timely care is provided
Recent methods of orthodontic evaluation: to the infant
Following may be considered as an index to de­
1) RMO’S Jiffy orthodontic evaluation veloping probable malocclusion problems.
2) PorDios (purpose on request digitizer Input-Out­
put system) is an IBM compatible system. Palatal grooves and cleft formation:
3) Dentofacial planner ■ A prolonged orotracheal intubation of infants
4) Quick ceph image is seen to be associated with airway damage,
5) Digigraph (synthesis of wider imaging, comp palatal groove formation, defective primary
tech, and 3 D sonic digitizing). incisors and an acquired cleft palate.

POTENTIAL PROBLEMS OF INCIPIENT Primary incisor defects

MALOCCLUSION ■ Intubated infants exhibit a fourfold increase
In the present era, dentistry is prevention oriented in primary incisor defects, which occur in ap­
and the child in the first year of life is a most desir­ proximately 85% cases. Nearly 2/3Td of tire
able patient to recognize the potential problems of maxillary incisors affected are located to the
incipient malocclusion. Following details may be left of the midline, corresponding to the
able to elicit some of the anticipated incipient greater prevalence of right handed intubation
malocclusions. technique.

I. Predentate period:
Alveolar ridge groove formation
a) Types of delivery: It is observed that the method
Greenberg and Nowak (1984) reported 47.6%
of delivery at the time of birth is of serious con­
incidence of palatal/alveolar ridge groove for­
cern for a dentist.
mation with orotracheal intubation in preterm
■ A high incidence of crossbite is seen in a
infants for a period of 1 to 62 days. Incidence of
group of children who were bom with for­
palatal groove formation increased to 87.5% in
ceps delivery.
infants who were intubated 15 days or more. This
■ An increased asymmetric molar occlusion was
observed with traumatic breach delivery. palatal grooving can be prevented with the use
■ A tendency for abnormal dental arch dimen­ of an intraoral derice that prevents tire endo tra­
sion, larger height of the maxilla and greater cheal tube from directly pressing on the palate.
length of the mandibular arch was observed Delayed eruption of primary teeth:
to occur as a result of forceps delivery. Fadavi (1992) noticed delayed eruption in pre­ y
■ Fewer bilaterally stable occlusions, corre­ mature infants.
sponding more asymmetric molar and canine
occlusions and a tendency for the asymmet­ Viscardi (1994) found that first primary teeth
ric occlusion were found in the difficult
erupts at the usual chronologic age in healthy
forceps deli ven’ group. The children also had
premature infants, but eruption may be delayed
a tendency for a narrower shape of arch, sug­
in premature infants who require a prolonged f
gesting early constructive forces. ' -'S'-
 tfcYZI | TEXTBOOK OF PEDODONTICS

mechanical ventilation for neonatal illness/or lature. One thrusts the tongue strongly between
who experience inadequate nutrition. the teeth in front and on both sides, particularly
noticeable are the contractions of the buccinator
c) Neonatal jaw relationship muscle. Such patients may have the following in­
Although upper and lower gum pads touch dications to developing incipient mal-occlusion.
throughout much of tire arch circumference, in ■ Inexpressive faces, since the 7th cranial nerve
no way is a precise bite or jaw relationship yet muscles are not being used for the delicate
seen. Generally, the forward relationship of the purpose of facial expression but rather for the
maxillary gumpad seen at birth gets corrected ma ssive effort of stabilizing the mandible dur­
itself with the growth of mandible. But, an an­ ing the swallow7.
terior open bite associated with it may not be a ■ Serious difficulties in mastication, for ordi­
transient relationship. It is seen that 2% of all narily they occlude only on one molar in each
neonates have an anterior openbite relationship. quadrant.
The oral habit also has a definite influence on ■ Their gag threshold is typically low.
the infant’s gumpads, resulting in a significant ■ These children may restrict to themselves to
increase in the incidence of anterior openbite re­ a soft diet and frankly stating they do not en­
lationship by the age of 4 months. Sometimes, it joy eating.
may remain with the tongue thrust habit at a ■ Mastication often occurs between the tongue
later stage also. tip and palate because of the inadequacy of
occlusal contact.
d) Infantile swallowing
During the normal infantile swallow the tongue f) Inadequate breast feeding
lies between the gumpads and the mandible is It is observed that in children whose mothers
stabilized by an obvious contraction of the fa­ have introduced an early weaning and w7ho had
cial muscles. The buccinator muscles is particu­ vety short breast feeding, a low impact muscu­
larly strong in infantile swallow as it is during lar activity interfered with the normal develop­
nursing. The normal infantile swallow is seen ment of alveolar ridges, hard palate and hence
in the neonate and gradually disappears with the lead to posterior cross bite in primaiy dentition.
eruption of the incisors in the primary dentition. Karjalainen (1999) has also suggested that early
It, therefore, is less often seen in the dental ex­ introduction of bottle feeding is an indication of
amination of children. The cessation of the in­ low muscular activity which may result into de­
fantile swallowing and the appearance of the ma­ veloping malocclusion problems.
ture swallowing pattern is not a simple on and
off phenomenon. Sometimes, they are an inter­ Therefore, early diagnosis of such potential prob­
mix of primary dentition and mixed dentition lems may be of great help to the dental practi­
swallowing pattern is as transitional swallow tioner to guide the child and intervene to break
causing an open bite. Therefore, this transition the habit. Sometimes, a prognosis for condition­
of swallowing should be observed carefully. ing of such a primitive reflex is very poor. It may
be associated with skeletal craniofacial develop­
e) Retained infantile swallowing mental syndromes and/or neural deficits for
This is seen due to persistent presence of this w hich dentist may be the first to recognize the
swallowing reflex even after the arrival of per­ problem to refer the case timely.
manent teeth. There is a demonstration of very
strong contraction of the lips and facial muscu­
 SECTION 9 : DEVELOPING MALOCCLUSION AND ITS MANAGEMENT |

II. Deciduous dentition Crowding or overlapped teeth in the primary denti­

tion may occur, although it is rare. True crowding
The main value of observing children during the in the primary dentition almost always guarantees
deciduous dentition is to prevent and intercept a crowded permanent dentition.
malocclusion.
Spacing in Chances of crowding
Serial examinations, cephalograms, lateral jaw and deciduous dentition in permanent dentition
intra oral radiographs and casts must be taken in
order to record dentofacial maturation progress. Crowding 10 in 10
No spaces 7 In 10
Diagnostic records should be obtained at the fol­ Below 3 mm total
lowing intervals: spacing 5 in 10
1. Before the permanent mandibular incisors be­ 3-6 mm 2 in 10
gin to erupt (age 5). Over 6 mm None
2. After the permanent maxillary incisors begin to (Leighton 1971)
erupt (age 6.5).
3. After the permanent maxillary lateral incisors Crowding of isolated teeth, however, is sometimes
begin to erupt (age 7.5 to 8). indicative of a sucking habit. Lower anterior teeth
can be tipped lingually into a crowded position as a
Dental arches result of constant pressure from a finger.

A child’s primary dentition without spacing results Transverse relationship

in crowding of the permanent dentition in almost
40% cases. Therefore, spacing is desirable in the One should look out for any midline discrepancies
primary dentition (Fig. 9.7). and posterior plane. A large midline discrepancy is
unusual in the early primary dentition, and one
should be suspicious of a mandibular shift, which is
often indicative of a posterior crossbite.

It is important to check that the mandible is in

centric relationship because a bilateral cr ite
will appear to be unilateral, if the mandible drifts
laterally into maximum intercuspation. Thechild
shifts the jaw because the teeth do not fit well
together and the bite is uncomfortable.

« A true unilateral crossbite that is due to unilat­

eral maxillary constriction in the primary denti­
Fig. 9.7 Mild crowding in the lower anteriors tion is rare but can occur.

Although the presence of primate and developmen­ ■ Maxillary constriction in primary dentition may
tal spacing does not ensure that the permanent den­ be due to an active thumb sucking habit, although
tition will erupt without crowding, these spaces usu­ there are many cases in which the origin of the
ally alleviate some crowding. crossbite is undetermined. In a small number of
cases, the mandibular shift is due to an interfer-
 GEt I TEXTBOOK OF PEDODONTICS

ence caused by the primary canines (selective ■ If the patient’s eruption pattern deviates from
removal of enamel in both arches eliminates the the normal sequence and there are differences
interference and the lateral shift into crossbite). between the contralateral sides of the mouth, fur­
ther investigation is warranted to determine
« Anterior crossbite may occur due to over retained whether the teeth are missing or are impeded
primaiy teeth. from erupting.

u A crossbite in the primary dentition usually will ■ If a tooth is missing (often maxillaiy lateral in­
be present in the perma nent dentition, and if cor­ cisors) or prevented from erupting, it could be
rected in primaiy dentition it may not reappear an indication of the development of an incipient
in the permanent dentition. Untreated functional malocclusion.
posterior crossbite gradually brings about a com­
pensatory structural change of the mandible and ■ A missing primary molar could lead to discrep­
sometimes of the condyle. ancies in arch length at a later date (i.e, during
eruption of the permanent 1st molar). Similarly
Vertical dimension with an impacted primary tooth.

Overbite: is approximately 2 mm in the primaiy Habits:

dentition. Anterior openbite is usually indicative of Thumb and finger sucking, pacifier habits, lip hab­
a sucking habit in this age group. its, tongue thrust, mouthbreathing, nail biting, brux-
ism and self-mutilation are some habits that can be
If the patient and the parent deny the existence of a seen during the primaiy dentition period.
sucking habit, further investigation into the cause
of the open bite is needed. Skeletal malocclusion Thumb sucking (4 to 6 hrs/day) pan cause
condylar fracture, and degenerative diseases such • anterior openbite
as juvenile rheumatoid arthritis may account for the ■ facial movement of the upper incisor and lin­
openbite and should be investigated. gual movement of the lower incisors.
■ maxillary constriction.
Overjet: Excessive overjet in the primary dentition
is usually due to a non-nutritive sucking habit or to Changes that occur during the primaiy dentition
a skeletal mismatch between upper and lower jaws. are okay so long as the habit extinguishes itself prior
to eruption of the permanent teeth.
Delay of eruption
Primary dentition terminus
■ Children with delayed dental eruption may ei­ By 3 years of age the occlusion of the 20 primary
ther have a veiy slow but normal sequence of teeth is usually established and the relationship of
eruption or some isolated eruption problem. the distal terminal planes of the second primaiy mo­
lar teeth is represented by one of the three planes,
« To distinguish the eruption sequence of the child, straight flush terminal plane, mesial and distal step.
it is compared with the normal sequence of erup­
tion and the eruption pattern on the right side is These primary molar relationships again can give
compared with that on the left. us an insight into the future permanent molar rela­
tionships and whether any malocclusion will de­
« If the sequence seems appropriate, dental devel­ velop or not.
opment is slow (probably).
 SECTION 9 : DEVELOPING MALOCCLUSION AND ITS MANAGEMENT |

Table 9.4: Second primary molars relationship indicative of

developing occlusion

Primary terminal plane Initial permanent Final occlusion

1st molar occlusion
49% mesial step 1% class III 3% class III
27% class I
37% flush terminal 49% end on 59% class I
14% distal step 23% class II 39% class II

Second primary molars relationship indicative of mild mesial step terminus exists during the pri­
developing occlusion (Table 9.4) mary dentition stage.
• Chances are very good but less predictable that
Second molar relationship in non spaced decidu­
a class I will develop from a flush terminal plane.
ous dentition
■ The opportunity for a class I developing from a
Mesial step: When the distal surface of the man­ distal step terminus is virtually non existent
dibular second molar is mesial to that of the maxil­
lary second molar it may develop to class III molar Impacted primary teeth
relationship in permanent dentition which depends Prolonged impaction of primary incisors is unusual.
on: Magnitude of Leeway space In history of trauma they may be present but usu­
Magnitude of Mesial step ally reerupt again and do not remain impacted.
Differential growth of jaw-s These impacted teeth can cause a delay in the erup­
tion of the permanent tooth.
Distal step: When the distal surface of mandibular
second molar is distal to that of maxillary second Congenital absence of primary teeth:
molar, a class II molar relationship is attained by Hypodontia of primary teeth (incisors), is usually
the permanent molars. This relationship will not associated with agenesis of the corresponding per­
be able to get changed even with the utilization of manent incisor in children w'hen early extraction
Leeway space or differential growth of mandible. or tooth avulsion takes place.
Molar relationship in non-spaced mandibular and
The likely rationale fortheir observation is that the
spaced maxillary deciduous arch
successional tooth buds of permanent incisors de-
■ A poor combination which is accompanied by a
velop just lingual to the buds of their primaiy pred­
distal step in primary1 dentition leading to disto-
ecessor and therefore it is very likely to be impaired
occlusion immediately after the eruption of per­
by an abortive development of the primary incisor
manent first molar.
tooth bud.
■ If the flush terminal plane exists, but maxillary
first permanent molar erupts prior to the first Infected Primarv teeth:
permanent mandibular molar, it w ill close the The close association of an infected apex to an
spaces in maxillary arch and develop into disto- unerupted tooth may cause the unerupted perma­
occlusion. nent tooth to become ankylosed. The process fol­
lows the irritation of the follicular/periodontal tis­
Changes of developing malocclusion
sue resulting from chronic infection. In the
« The likelihood of developing a class I perma­
unerupted tooth, enamel is protected by enamel epi-
nent dentition relationship is greatest when a
 €H3 I TEXTBOOK OF PEDODONTICS

thelium. The enamel epithelium may disintegrate incisors cause permanent lateral incisors to erupt
as a result of infection (or trauma), the enamel may in crossbite. At the time of eruption of permanent
subsequently be resorbed, and bone or coronal cc- incisors, if the primary teeth show no sign of exfo­
mentum may be deposited in its place. The result is liation (check on a xray) and then extract to pre­
a solid fixation of the tooth in its uncrupted posi­ vent development of a malocclusion. u ..
tion. Malocclusion can be initiated by the child w hen
he favours one side of his jaw to avoid chewing on Maxillary primaiy canine can cause labial/lingual
carious teeth. eruption or impaction of permanent canine.

Retained primary teeth: (Fig. 9.8a, b) Ankylosis of primary teeth

■ Primaiy teeth, particularly molars, may become
Retained mandibular incisors cause permanent lat­ ankylosed (fused) to the alveolar process and
eral incisors to erupt lingually. Retained maxillary their eruption is prevented. Primary teeth are
more likely to get ankylosed in the lower arch
twice as often as the upper one.
• Ankylosis can lead to malocclusion because
when it occurs late in the resorption of the pri­
mary roots, even then it can interfere with the
eruption of the underlying permanent tooth.
■ Henderson (1979) pointed out that ankylosis
should be considered as an interruption in the
rhythm of eruption.
■ Nagan (1990) suggested that ankylosed tooth that
has failed to erupt or is submerged well below
the occlusal plane of the adjacent tooth should
be extracted and be replaced with a suitable space
Fig. 9.8a Lingually erupting mandibular central maintainer as it may cause supra eruption of the
incisors due to retained primary teeth. opposing tooth and space loss by tipping of the
adjacent teeth.

Loss of primary tooth

If the primary tooth is lost and the crown of its suc­
cessor tooth is completed (Nolla’s stage 6) and root
formation has begun, then the permanent succes­
sors will be accelerated in its eruption. On the other
hand if the crown of a successor tooth is not com­
pleted at the time of loss of the primary tooth, the
eruption of the permanent tooth will be delayed be­
yond its normal eruption time. Therefore, antici­
pated problem and their management should be as­
sessed accordingly.
1 Fig. 9.8b Properly aligned permanent cenuat
incisor after primary teeth extraction and Premature loss of primary teeth
proximal stripping. Primary teeth act as space maintainers for the per­
manent teeth. Proper timing of the exchange of
 SECTION 9 : DEVELOPING MALOCCLUSION AND ITS MANAGEMENT |

primary with permanent teeth is an important fac­ Important considerations

tor in tire proper disposition of the permanent teeth Therefore, the extraction of a primary tooth can have
in the dental arch. The effects of an early loss of a profound effects on the developing permanent den­
primary:^qqth-may be as follows: tition. A tooth should never be extracted before first
- “ Shorteningof arch length. assessing its likely effects and then plan treatment
- Tipping of the adjacent permanent teeth to prevent or eliminate those effects.
- Supraeruption of the opposite tooth
Since an important factor that determines drifting
Factors influencing mesial/distal drift: of teeth is the degree of crowding in the arch, it is
essential to assess this before appropriate treatment
Degree of crowding can be planned.
- It is directly related to the rate and extent of drift.
- In an uncrowded arch there may be little or no Gingival conditions
movement of teeth but in a crowded arch adja­ The gingival conditions should also be considered
cent teeth quickly move into the spaces provided from the point of view of a developing malocclusion.
by the extraction of teeth. ■ Generalized prepubertal periodontitis: In the pri­
mary teeth prepubertal gingivitis may show root
Tooth extracted resorption with clefting and inflammation ofthe
■ Loss of 2nd primary7 molar allows mesial drift gingiva, rapid destruction of the alveolar bone
of the 1st permanent molars, especially if it is and a premature loss of the primary teeth that
unerupted; however a center line shift occurs may affect the eruption and drifting of perma­
only in very7 crowded arches. nent teeth and lead to a malocclusion.
■ In contrast, extraction of a primary7 canine, al­ ■ Children with hypophosphatasia may show pre­
lows permanent incisors to drift distally, but me­ mature exfoliation of their primary teeth (due to
sial drift of teeth is minimal. failure of anchorage of periodontal fibers) which
■ Extraction of a primary 1st molar allows some may affect alignment of the permanent teeth
mesial and distal drift to occur. which are known to be normal on eruption,
■ Relative amount of mesial and distal drift of teeth ■ Loss of attachment with breakdown of alveolar
is expected following extraction of a primary tooth. bone, exposure of root, tooth mobility and pre­
mature tooth loss may occur in dentin dyspla­
Primary tooth sia, juvenile periodontitis, papillon leferve syn­
extracted drome, leukemia, neutropenia, scurvy, diabetes,
2nd molar hypophosphatasia, mercury toxicity and radia­
1st molar tion.
Canine
Supernumerary teeth
Age of patient Counting of teeth will reveal the presence of super­
The earlier a primary tooth is extracted, the greater numerary teeth. Approximately, 0.3% of children
the opportunity7 for drifting of teeth, but overeruption have extra teeth in the primary dentition.
of opposing teeth may limit movement.
Functional relationships and TMJ
If a primary molar is extracted before eruption of There is a possible or potential functional element
the permanent 1st molar, mesial drift of the latter is in every7 malocclusion. The patients usual occhisal
inevitable, even in arches that are not crowded. position may be due to occlusal interferences in the
 Î TEXTBOOK OF PEDODONTICS

««deviated path of closure. Any interference may wherein the deciduous second molar roots are
prompt a reflex shifting of mandible during closure resorbed. The other region where this may be ob­
to an occlusal position dictated by cusps and forc­ served is the mandibular anterior teeth.
ing an imbalance of musculature. Such
malocclusions may be termed as functional Self-Assessment
malocclusions. 1. What does the word incipient indicate?
2. What is the rationale of incipient malocclusion?
They arc important because of their potential for 3. Name some of the incipient malocclusion con­
affecting future growth and imbalance in craniofa­ ditions?
cial skeleton as well as distorting the form of the 4. What is ectopic eruption and how does it lead to
alveolar arches. the malocclusion problem?
5. What are the important steps in early diagnosis
Ectopic eruption: of incipient malocclusion problems?
The situation where the erupting permanent tooth 6. What is retained infantile swallow and what will
causes resorption of primary tooth due to improper happen if it is not checked on time?
direction of eruption can be termed as ectopic erup­ 7. What arc the different facial forms?
tion. This condition is more commonly seen during 8. List out the various anomalies in predentate, pri­
the eruption of the upper first permanent molar mary dentition and mixed dentition?
 9.2 Orthodontie Prevention

Shetty N., Tandon S

Introduction ■ We prefer to define preventive orthodontics as a

comprehensive monitoring of the developing
In the quest for providing optimal dental care, the dentition in a child and applying suitable meas­
age-old maxim of ‘prevention is better than cure’ ures to guide it to normal occlusion.
holds true. In this endeavor the Pedodontist is most
evenly poised to carry the mantle of providing the B. Interceptive orthodontics
required services.
■ The American Association of Orthodontists
For the preventive approach to be truly effective it (1969) defined interceptive orthodontics as that
needs to apply at its earliest i.e. at the primary pre­ phase of science and art of orthodontics employed
vention level. However this may not always be pos­ to recognize and eliminate the potential irregu­
sible and the treatment provided early in the progress larities and malpositions in the developing
of the problem may also limit the damage caused or dentofacial complex.
sometimes even revert ft back to normal.
■ Profitt and Ackerman [1980] have defined it as
Thus the key difference between ‘Prevention’ and the elimination of existing interferences with the
Interception’ lies primarily in the matter of tim­ key factors involved in development of denti­
ing. This chapter presents a brief preview as to the tion.
modalities of treatment for the clinician, which can
go a long way in preventing the development of ■ Our clinical experience defines Interceptive or­
malocclusions or at least minimizing them. thodontics as an early intervention in the devel­
oping dentition to minimize the developing
Definitions malocclusion or eliminate the potential factors
interfering with normal occlusion.
A, Preventive orthodontics
"'Importance of deciduous dentition
■ Graber [ 1966] has defined preventive orthodon­ No other factor plays a more significant role in
tics as the action taken to p? ¿serve theintegrity7 preventive and interceptive orthodontics than the
of what appears to be normal occlusion at a spe- preservation of the deciduous dentition till its
• cifictime’?) normal time of exfoliation. The deciduous teeth
provide a ‘mold’ for the proper growth of jaws,
■ Profitt and Ackerman [1980] have defined it as so that the permanent teeth may have an adequate
prevention of potential interference with occlu­ space for aligning themselves.
sal development.
 l-TEXTBOOK OF PEDODONTICS

Premature loss of a deciduous tooth or a group Preventive measures to be considered

of teeth may lead to the following wide range of (Role of Pedodontist)
implications .
A pedodontist is often the first person to encounter
• Space loss: The premature loss of the deciduous the above mentioned effects of premature loss of
tooth will lead to the imbalance of forces main­ deciduous teeth. Thus it is essential on the part of
taining the tooth in the mouth, leading to an un­ the pedodontist to take early measures in prevent­
controlled force causing space loss. Also, the ing the profound effects on future developing den­
guidance of the first permanent molar is a prime tition, psychology and personality of the child. The
consideration, for the deciduous dentition. following tiniety measures should be instituted.

A. Parent education:
• Speech: Specially, primary7 anterior teeth have
~"Pedodontists are largely responsible for the pre­
a role to play in the development of speech ar­
vention in orthodontics. They first see the child
ticulation in children. Premature loss may lead
patient. This provides the best opportunity to
to abnormal tongue position as well.
educate the parents to the realization that de­
ciduous teeth are fully as important as the per­
• Esthetics: A child may feel ashamed to smile manent ones, arid insomeTSpect^^xiT rriore
or laugh with his peers because of embarrass­ so. An investment in their early care will be of
ment. immediate benefit to the child as well as be of
priceless value later.
« Psychological effect: The child may sometimes
have a more withdrawn attitude due to the In this age where the opportunity exists to start
anaesthetic appearance. care for the child even before birth, the role of
antenatal diagnosis and education cannot be de­
» -Mastication: It may lead to loss of masticatory nied.
efficiency and hence improper assimilation of £

food. Thus general health gets affected. Genetic counselling involves the determination
of the risk of an individual acquiring a particu­
_Growth stimulation: for the development of lar disease existing in the family tree and advis­
dentofacial structures will be absent. ing the parents as the potential problems that
may arise. For example, the growth of the jaws,
Rao (1998) has stated premature tooth loss may lead the mandible in particular, has been seen to fol­
to certain specific effects such as: - low a genetic trend.
Changes in dental arch length and occlusion
B. Caries control:
, ■ Misarticulation of consonants in speech
Dental caries of the deciduous teeth, when ne­
Development of oral habits
glected or when not given proper dental care is'
■ Psychological trauma.
the principal cause of malocclusion of the per­
manent dentition. Thus, all measures that play
A Pedodontist frequently comes across such cases,
a role in cariesprevention and treatment play a
assesses its effect and thus has a profound effect on
major, albeit indirect, role in preventive ortho­
the future dental and may be psychological status
dontics.
of an individual.
 SECTION 9 : DEVELOPING MALOCCLUSION AND ITS MANAGEMENT |

L^Tri this context Nutritional_jand_ Diet Nature and prevalence ofspace loss
Counselling, Fluoride applications and water While recording the prevalence of space loss or clo­
fluoridation, pit and fissure sealants play an sure the following observations are recorded by most
important role. Tertiary preventive measures of the clinicians.
such as the pulpectomy procedures also in their ■ Incidence of premature loss of deciduous
own way manage to maintain the tooth in the molars
arch for the required time and prevent space ■ Rate of space closure
loss. ■ Time of space closure
■ Amount of space closure
C. Maintenance oftootitshedding time table ■ Direction of space closure.
A difference of more than 3 months in shedding
and eruption in one quadrant, compared to oth­ A. Premature loss of deciduous molars
ers, should be viewed with suspicion and inves­ Majority of reports indicate that frequently the
tigated thoroughly. premature extraction of the deciduous molars
will cause crowding of teeth due to space loss
D. Maintenance of dental arch integrity associated with either rotation, tipping or bod­
Preventive orthodontics to a large extent is re­ ily movement. We have also observed that by
sponsible for the maintenance of arch integrity, the age of 7-8 years, almost 50-60 % children
most commonly following the premature loss of start showing mutilated occlusion due to the early
a deciduous tooth. loss of primary teeth. The maximum number of
cases were due to caries of deciduous molars. (Ta­
E. Other measures ble 9.4a, b).
Many other factors like care of the deciduous
teeth, maintenance of occlusal equilibration if B. Rate and Time of space closure
there is any functional reason, extraction of su­ ■ Unger (1938) proposed that the earlier a tooth
pernumerary tooth, ankylosed tooth, monitoring is lost the greater the initia l rate of space loss.
of incipient malocclusion are important part of ■ Seward (1965) found that a continual rate of
preventive orthodontics in Pediatric dental prac­ closure 13 mm. per year in the maxilla ex­
tice apart from space management. isted and all individuals demonstrated space
loss. In the mandible, the mean rate of clo­
SPACE LOSS sure was 1.0 mm per year, with individuals
varying widely in the timing of closure.
In the arch, every tooth is like a unit, which is main­ « Northway (1984) has stated that more space
tained in place by a host of factors and also it, in was lost in the first year following an extrac­
turn, maintains the arch integrity. Should there be tion than in successive years. The rate of space
any imbalance of the forces acting on the tooth, the loss in maxilla is age related. Thus at the age
opposing unrestricted force causes a movement of of 6 years: total space loss is 4.1mm, 7 years:
tooth/teeth. 2.1mm and at an older age, <L5mm. In the
E.g.: a) In cases where proximal contact is lost due mandible, there was no relation between age
to caries or even loss of a tooth as a whole, the me­ and the amount of space loss. Average loss
sial component of force (generally) is unbalanced was from 2.6 to 3.2 mm in 4 years (Table 9.4c)
and may cause mesial drifting, more so during the
eruption of the first permanent molar.
I TEXTBOOK OF PEDODONTICS

NATURE AND PREVALENCE OF SPACE LOSS

Table 4a: The percentage of malocclusions due to the premature

extraction of deciduous molars

1 Lyons 1924 65%

2 Brandhorst 1932 20%
3 Willets 1933 28%
4 Tandon 1985 50%

Table 4b: Prevalence of premature loss of deciduous molars

0/
Authors Age /0 Year

1 Brandhorst N.A 37% 1932

2 Pringle 6 yrs 70% 1937
3 Charbeneau 7-8 yrs 35% 1950
4 Foster 4 yrs 11% 1958
5 Simons N.A 15% 1972
6 Pedersen 8 yrs 50% 1978
7. Tandon et al 7-8 yrs 48% 1987
Northway (1984)

Table 4c: Unilateral space loss due to premature extraction

MAXILLA MANDIBLE
D E D+E D E D+E
Liu (1949) 2.3 2.5 2.3 1.4 1.4 1.3
Jarvis (1952)- - M 0.1 4.2 • 1.9 2.7 -
- F - 2.1 - - 2.9 -
“Breakspeary (1961) 0.8 2.2 2.0 0.7 1.7 1.3
Ronnerman and 0.5 - 3.7 - 1.7 6.8- -
Thilander (1977) 1.4 4.5 3.1 2.1
Rao and Sarkar (1999] 1.11 2.05 2.58 0.40 1.23 1.38.
 SECTION 9 : DEVELOPING MALOCCLUSION AND ITS MANAGEMENT I

C Amount of space closure Sequelae

Several studies have found that the maximum ■ The primary canine shows a distal shift in
space loss occurred in the maxillary region due the 1st year (if at all)
tu the premature loss of the second deciduous ■ The deciduous second and the permanent first
molars. molars shift mesially depending on age and
■ Contrary to the other reports space loss in our duration of absence
patients was found to be maximum in the man­ ■ The first premolar is mesially directed along
dible with the total space loss being more than the mesial surface of the second molar
2.5 mm. ■ The permanent canine has no place and is
blocked out of the arch.
D. Direction of space closure
There has been a generalization of the direction B. Maxillary second primary molar loss:
of space closure. Sequelae
« Earlier studies have reported that maxillary7 « The molar shifts mesially. It was observed that
extraction sites close primarily by mesial if the extractions were performed prior to the
movement of posterior teeth, and mandibular emergence of the first molars, it resulted in a
extraction sites by distal migration of ante­ permanent space loss, more in the upper.than
rior teeth. lower.
■ The second most deleterious period has been
■ Based on Kronfeld’s theory7 that neutral areas found to be after emergence of the second
are located between the bicuspids in maxilla molar but before the emergence of the first
and just mesial to the first molar in mandi­ bicuspid.
ble, the teeth anterior to the neutral area «re ■ The period of emergence of the second molar
expected to erupt to the distal, while the distal is thought to be crucial, as distal to the first
teeth migrate forward. molar a growth centre exists.
■ The cuspid and the first deciduous molar shift
■ North way et al (1984) stated that for both distally.
arches, the greatest space loss occurred as a « The first bicuspid generally erupts first and
result of the molar movement forward towards erupts into this space distally, sometimes even
mesial. causing impaction of the second bicuspid.

E. Effect of caries C. Maxillary first and second molars loss:

It has been reported that in both the arches, se­ Under these circumstances, a host of factors ex­
vere caries resuhs in a space loss of about 1- ist and the outcome depends on the interaction
mm. In our patients, the Ioss~3ue to caries, was” between them.
observed to be from 1.5 to 2.5mm
D. Mandibular tooth loss
INDIVIDUAL TOOTH LOSS The effect of mandibular extractions tends to be
similar for all the 3 situations i.e - D loss, E loss
A. Maxillary first primary molar loss: and D + E loss
Though measurements of D+E show not much ■ The permanent molar tips forward. If D is
arch length loss after premature loss of D /D, in lost, the E may tip as well.
these cases the incidence of canine (permanent)
being blocked out from the normal alignment is
high.
 Îtfcfcl J TEXTBOOK OF PEDODONTICS

■ The developmental orientation of bicuspid ■ Mandibular - In case where mandibular cus­

tooth buds is an important variable and so is pid is extracted, an abnormally strong men-
the sequence of eruption. talis musculature may cause distal drifting of
■ In severe cases again, the second bicuspid has the lateral incisor, shift of midline and a deep­
got a maximum chance of being impacted due ening of the bite.
to lack of space.
2. Timelapsedsinceext faction
E. Anterior region The time elapsed since extraction must be con­
■ Most studies agree that the loss of the ante­ sidered, as a maximum space lossLwill occur in
rior teeth are rarely associated with any space the first six months. Thus when a choice exists,
loss, especially so when the primary canines appliances must be placed immediately follow­
have already erupted. ing extraction.

■ The premature loss of canine on one side of 3. Dental age, Eruption pattern & Bony covering
the arch, in the mandibular region, is associ­ Decisions are to be based upon the normsüssô-
ated with the shift of the midline in the same ciated with dental age rather than chronological
direction. age.
■ Eruption patterns may also vary and thus may
« There is a linguo - distal inclination of the impede the placement of the appliance as
teeth, causing a collapse of the anteriors lin­ such. Also, ectopic eruption and root resorp­
gually, apart from closure of the space and tion (atypical) may also delay or hasten exfo­
shift of midline, [Barber, 1987]. liation time.
■ Eruption of the first molar causes a bodily
VARIABLES INFLUENCING SPACE CONTROL space loss in maxillary and tipping in man­
PROGRAMS ——- — dibular arch. It is observed that space in man­
dibular arch is difficult to regain.
• Most growth studies are in general agreement ■ In cases where a tooth has been lost due to
that once the primary dentition has been estab­ infection the overlying bone may not be a good
lished, the arch length i.e. the measurement from guideline to follow. In such situations, the
the distal surface of the second primary molar amount of root formation should also be con­
around the arch to a similar position on the op­ sidered (3/4 of root development).
posing side is constant until the permanent den­
tition is established. The preservation of the 4. Available space .
same in the primary and mixed dentition is of Though space loss may occur after the tooth has
utmost importance, for it allows the dental units exfoliated prematurely, it might sometimes be
to 'fit’ into their relative positions. Wright and present before due to interproximal caries. Thus,
Kennedy (1978) have discussed the following key the amount of space available and required
variables and their importance. should be measured and thus space maintenance
/regaining should be instituted.
J^-Oral musculaturejind habits (Fig. 9.9)
■ "Maxillary arch - Anterior teeth may be 5. Interdigitation
proclined and thus arch length or perimeter Increased cuspal height along with proper in­
is increased. Thus clinician should check and terdigitation will help to stabilize the occlusion.
evaluate where the teeth should be as well as Thus, it has been postulated that these factors may
where they are at the initial examination. help prevent the space loss.
 SECTION 9 : DEVELOPING MALOCCLUSION AND ITS MANAGEMENT |

2
Lip
force force

6.6 g/cm2
10.0 g/cm2 buccinator
(Large variability) 11.6 g/cm2

Fig. 9.9 Balance of forces

6. Anomalies^ 1. Intra-oral examination to:

These may hamper the eruption of the teeth such a. Assess the overall oral health status
as the supernumerary tooth and thus it is essen­ b. Determine the status of patient’s occlusion
tial that a complete radiographic survey be done 2. Facial analysis
before the selection of the appliance. a. Determine the asymmetric growth patterns
and or lateral deviations of the mandible
7. Sequence of eruption b. Determine dental, skeletal growth
A situationmayansewhere the second decidu­ c. Dental and skeletal (occlusal) abnormalities.
ous molar is lost prematurely and the eruption 3. Functional assessment
of the second molar is taking place. Though a. Functional factors
other factors may not warrant space mainte­ b. Habits
nance, it may be required for this purpose. c. Detect TMJ dysfunction

CLINICAL ASSESSMENT FOR SPACE Apart from above guidelines, the following factors
MANAGEMENT should also be considered before deciding the treat­
ment plan such as:
Clinical assessment can be carried out following the
■ Position of incisors. This gives an indication as
guidelines laid down recently by the American
to the amount of space actually present.
Academy of Pediatric Dentistry.
 | TEXTBOOK OF PEDODONTICS

■ Crowding: This would indicate 1 mm minimum ■ The equation used is:

requirement
« Depth of curve of Spee: The correction of 1- Erupted tooth size in the mouth Unerupted
mm depth on either side of the arch yields a 1 x tooth size
mm linear space per side. Erupted tooth size in X-ray - in X-ray
■ Midlines: Shift of the midline may require ad­
ditional space. - Correct tooth size
■ Leeway space: Whether it is maintained I re­
gained depends on the arch - length analysis C. Hixon and Oldfather have suggested a method,
done. which has been stated to be the most accurate. It
involves the following measurements.
Space discrepancy analysis Sum of the maximum mesio - distal diameter of
Any space management measures should be carried one permanent central incisor and one lateral
out only after a space discrepancy analysis is done incisor, with the diameter of the unerupted first
for which the two factors to be considered are: and second bicuspids measured on the radio­
1. Space required < graph taken by the paralleling technique (using
2. Space available a 16-inch cone). The following prediction chart
can be used:
It can either be done by a radiographic method or
on study model or combination of both. Though sev­ Measured value Estimated tooth size
eral authors have recommended different analysis,
23mm 18.4mm
we suggest that at least two of the following be per­ 24 19.0
formed rather than rely on a single analysis. 25 19.7
26 i 20.3
A. Arch perimeter or Moyer’s analysis 27 *21.0 ,
The perimeter of the arch is measured from the 28 21.6
mesial surface of one permanent molar around 29 22.3 *
to the mesial surface of the opposite molar. The 30 22.9
arch can be measured in 4 - 6 segments.
« ,Size of unerupted teeth: A special case in- D. Tanaka and Johnson used the following meas­
*volves computation of the size of unerupted urement:
teeth, either from radiographs or by ratios ■ Half the Mesio-distal width of 4 lower inci­
based upon correlations between the sizes of sors +10.5 « Mandibular 3+4+5 in one quad­
permanent teeth. The Moyers analysis is the rant.
most commonly used mixed dentition analy­ ■ Half the Mesio-distal width of 4 lower inci­
sis. sors + 11.0 = Maxillary 3+4+5 in one quad­
rant
B. Radiographic method:
It requires clear x-ray films of the unerupted teeth SPACE MAINTENANCE AND MANAGEMENT
and of the overlying primary æeth. The enlarge­
ment ratio for each unerupted permanent tooth By tradition and repetition, preventive orthodon­
is computed by measuring the nearest erupted tics is to many people limited to the procedurei
tooth first in the mouth and then in the radio­ implied by the term space maintenance. Thus it if
important to place in proper perspective tin
graph.
terms space maintenance and management.
 SECTION 9 : DEVELOPING MALOCCLUSION AND ITS MANAGEMENT |

■ Space maintenance can be defined as the pro- « Modifiability: Anticipation of future modifica­
visïôïïofaïïappliance (active or passive) which tions is essential.
is concerned only with the control of space loss « Limitations: Loss of the 1st primary molar be­
without taking into consideration, measures to fore eruption of the second premolar while us­
supervise the development of dentition. ing the band and loop.
■ Cost: Directly bonded are the best as time is
■ Space management (control) includes measures saved.. As laboratory time increases, labour
that diagnose and prevent/intercept situations, charges increases.
so as to guide the development of dentition and
occlusion. CLASSIFICATION OF SPACE MAINTAINERS

SPACE MAINTAINERS > REMOVABLE

■ Space maintainers can be defined as appliances
used to maintain space or regain minor amounts
of space lost, so as to guide the unerupted tooth Cast partial Wrought partial
into a proper position in the arch.

Ideal requirements: Passive Active

The space maintainers used should meet the fol­
lowing conditions.
■ Maintain the desired mesiodistal dimension of Functional Non-functional
the space (intra-arch space maintenance)
. ■ Should not interfere with the vertical eruption ------------------- ► FIXEl)
of the adjacent teeth I inter arch space mainte- / ;
nance]
■ Should not interfere with the eruption of the per­ Banded Bonded
manent teeth ; ■
._■« Provide mesiodistal space opening when it is re­
quired. Passive Active
■ Maintain individual functional movement of 1
teeth.
Functional Non-functional
Factors governing the selection of appliance:
■ Patientcooperation: With removable appliances,
greater cooperation is required as compared to
the fixed appliances. Band and loop
■ Appliance integrity: In general all types of ap­ Lingual arch
pliances suffer breakage. But as per Wright and Distal shoe space maintainer
Kennedy [1968] the mandibular removable ap­ Nance palatal arch
pliance is the most susceptible to breakage and Transpalatal arch
that the integrity of fixed appliances is better. Prefabricated space
■ Maintenance: The length of time and the pro­ maintainer (3D)
jected maintenance should be considered. Bonded space maintained
 ^ETt> I TEXTBOOK OF PEDODONTICS

FIXED SPACE MAINTAINER ■ Should not extend subgingivally any more than
necessaiy
Construction of space maintainer ■ Band material should resist deformation under
The fixed space maintainer generally are constituted stresses in the mouth.
of the following components: ■ Resist tarnish
a. Band ■ Inherent springiness
b. Loqp/archwire ■ Cause no occlusal interference
c. Solder joint _
d. Auxiliaries Steps in band formation
A. Separation
Band: The band forms an important part of the con­ B. Band fitting [band pinching]
struction of the various fixed appliances. Several C. Welding
bands are employed such as: D. Soldering
1. Loop bands
a. Precious metal (first introduced by Johnson) A. Separation: Adequate separation of the teeth is
b. Chrome alloy bands. an essential prerequisite for any banding tech­
nique.
2. Tailored bands
a. Precious metal Methods
b. Chrome alloy. ■ Brass wire - 0.015 inch - 0.020-inch soft brass
wire. It works well in young patients with
3. Preformed seamless bands thick periodontal membrane, but can be quite
a. Chrome alloy/precious metal which are painful.
adopted, festooned and stretched to fit. ■ Elastic threads - These prqyide a gentle force
over a prolonged period and are painless at
« A range of preformed bands from 1-32 depend­ the time of insertion.
£
ing on the mesiodistal width of the tooth for the
maxillary and mandibular arch are available B. Band formation: Various techniques of band for­
commercially. mation are known. These can be:
a. Direct formation
Band material: Depending on the tooth to be b. Preformed bands
banded, they can be classified as: c. Indirect band technique
■ Anterior teeth 0.003 by 0.125 by 2 inches
• Bicuspids 0.004 by 0.150 by 2 inches Direct formation of the band in the mouth in­
■ Molar region 0.005 by 0.180 by 2 inches volves:
(deciduous) i) Band pinching
• Molar region 0.006 by 0.180 by 2 inches ■ The band strips are first contoured in an
(permanent) inciso - gingival or occluso - gingival
direction using the Johnson’s contouring
Technique for band construction pliers. The ends of the strip of the band
Every band should possess a few ideal criteria such material are welded and then a loop is
that - made for the reception of Howlett band
■ It should fit the contours of the tooth as closely forming pliers. This contoured strip is
as possible, thereby enhancing the placement of located on the tooth in the desired posi­
the attachment in relationship to the tooth. tion (Fig. 9.12, 13, 14)
 SECTION 9 : DEVELOPING MALOCCLUSION AND ITS MANAGEMENT |

Fig. 9.10 Pliers for band pinching and crown adaptation

 I TEXTBOOK OF PEDODONTICS

iii) Trimming
This involves reducing on the buccal and lin­
gual side if required. This primarily adjusts
the occluso-cervical length of the band.

iv) Folded flap method

■ After the formation of the seam, the
excess is cut off, leaving a small remnant
The band is then returned to the toothand
the small remnant is folded neatly against
the lingual surface of die tooth.
■ This should be done directly on the tooth;
Fig. 9.11 Band forming pliers - anterior band otherwise the band will be made smaller
forming plier on the left side and posterior during the process of folding over the tag.
band forming plier on tie right The folded over remnant is then spot
welded. The band may sometimes require
■ The bands should be pinched on the cuspal crimping to produce a rolled retentive edge
area and not on the groove areas. This is to the band.
because, it is difficult to adapt a double ■ The occlusal margins of a completely
thickness of the band in the groove areas. seated band should be slightly below the
■ The upper molar band is usually pulled proximal ridges (1-mm).
from the palatal side, whereas the lower ■ Gingival margins should extend 0.5 to
molar band is pulled from buccal side. 1.0 mm into the gingival sulcus (Owen et
■ The seam of the upper band will be kept al 1984). A better criterion is to check
at the mesioloingual line angle whereas clinically for the blanching and relieve the
for the lower, at the mesiobuccal line angle. areas where it is seen.
■ The two edges of the seam should be ■ Buccally it should be just below the level
parallel to each other so that the band rests where the opposing cusps touch the
uniformly on the tooth surface. grooves.
■ In cases where a sufficient clinical crown ■ Lingually, it should be placed just below
is available, the peak band - forming the deepest portion of the lingual devel­
pliers may be employed on the teeth. opmental groove.
These are available as right and left.
A partially indirect technique involves the con­
ii) Festooning struction of the bands and then taking impres­
■ This constitutes the countouring of the sions to form the appliance on the cast. Atotally
band in order to follow the gingival indirect technique is where the bands are also
margin proximally. The level of the band constructed on the cast. This is useful as it pro­
at the marginal ridge is also adjusted in vides a more efficient and faster method.
the process.
« The distal side may require more trimming C. Welding: Welding is the process during which a
because of the lower position of the portion of the metal being joined is melted and
marginal ridge as well as due to the raised flowed together. Bands are generally joined by
position of the gingiva (especially during welding. Electric spot welding is carried out with
eruption of the distal tooth) (Fig. 9.15) electric current being forced to flow through a
 SECTION 9 : DEVELOPING MALOCCLUSION AND ITS MANAGEMENT |

Fig. 9.12 Welded band material with eyelet Fig. 9.13 Howlett band forming plier engaging
fie welded band material

Fig. 9.14 Contoured strip placed on tooth Fig. 9.15 Band showing the festooning
 icEEl I TEXTBOOK OF PEDODONTICS

limited area on the materials to be welded. The - Where loop is welded to the crown
resistance of the materials to electric current gen­ - Where the band is adapted over the crown and
erates an intense localized heat and brings about the loop is soldered to it.
fusion of the two surfaces.
4. Reverse i.e. Banding the first primary molar for
D. Soldering: It is the process by which the two
guidance. This appliance has been used in cases
metals are joined together by an intermediary
where the second molar is lost before the erup­
metal of a lower fusion temperature. The most
tion of the first permanent molar(Gellin 1990)
common solder used is the silver solder contain­
ing silver, zinc, copper and tin.
5. A cast crown with a tube on the canine and a
Flux is used to increase the flow and prevent cast crown with a bar and post can be cemented
oxidation. The solder is applied to the joint after on the molar, such that the post fits the tube.
which finishing is done with a green stone, while
polishing with a rouge. 6. Techniques for constructing a functional vari­
ant of space maintainer, either by direct or indi­
I. BAND AND LOOP (Fixed, non functional, pas­ rect technique have also been described.
sive space maintainer)
II. LINGUAL ARCH SPACE MAINTAINER (Fixed,
Construction nonfunctional,passive mandibular arch appli­
The larger tooth, the second deciduous molar, is used ance)
for anchorage of the appliance. A loop (0.030 inch
to 0.035 inch) is soldered to the band and spans the ■ They belong to those group of space control ap­
edentulous space to contact the abutment tooth be­ pliances which not only contiol anteroposterior
low the contact point. The loop is contoured to rest movements but also are capable of controlling
on the tissue on both sides of the ridge, with an and preventing an arch perimeter distortion, by
opening in the loop sufficient to permit the erup­ controlling the lingual collapse of single tooth
tion of the cusps of the underlying permanent tooth. or segments of the arch. *
The loop should contact the mesial abutment at the
contact point (Barbar, 1982). If it is constructed ■ The lingual arch in essence consists of a round
below it, the chances of it slipping gingivally are stainless steel or precious alloy wire, 0.32 to 0.40
high. (Fig. 9.16). inches in diameter closely adapted to the lin­
gual surfaces of the teeth and anchored to bands
Modifications on the first permanent molars. Rarely, second
1. The loop can be made only on one side, but it is deciduous molars may also be used. The means
less stable (Meyers). used to anchor the archwire to the bands will
define whether the lingual arch is of a remov­
2. Sometimes an occlusal rest is given on the tooth. able or fixed type (Fig. 9.17a, b, c, d).
This modification is to overcome the disadvan­
tage of the appliance slipping gingivally. But this Removable lingual arch
may hamper the proper eruption of the tooth to ■ It has precision made vertical posts soldered at
its occlusal plane (Wright and Kennedy, 1978). right angles to distal extensions, which fit pre­
cision - made tubes on the lingual surfaces of
3 Crown - loop: Where abutment requires a crown the molar bands and are held together by means
this appliance may be used. Two techniques can of lock wire.
be used -
 SECTION 9 : DEVELOPING MALOCCLUSION AND ITS MANAGEMENT

Fig. 9.16 Space maintained for missing Fig. 9.17a Pre-formed lingual arches
primary first molars using the crown and loop
on left side, band and loop on the right

Fig. 9.17b Fixed lingual arch space maintainer

with banded first first permanent molars

Fig. 9.17c Lingual arch with ‘U’-loop Fig. 9.17d Modified lingual arch
 I TEXTBOOK OF PEDODONTICS

■ More used for active movement when tipping of ■ The wire should maintain a 3 - 4 mm contact
the molar is less than 5 degrees as it allows for with the lingual surface of the band to provide
an easy removal and adjustment. for a long solder joint
« Lingual tubes are placed in the center of the lin­ ■ Konstantinos et al (1998) have suggested that
gual surfecepftjbiehand anterio-posteriorly and in the canine region 2 omega bends need to be
aligned with the lingual groove, such that they given. This is to prevent interference between
are parallel to the long axis of the tooth and at the arch wire and the cuspids, which migrate
right angles to the occlusal margin. distally into the primate spaces.
■ In the original design by Hotz, 2-inch adjust­
Modifications of removable lingual arch ment loops are given so as to allow for some
a) Auxiliary springs can be incorporated to bring adjustment ofthe length. They may also be used
about minor individual tooth movements. for regaining space.
t>) Loop lingual archwire: used as 2 loops or 1 loop
mesial to the first permanent molar. It is used Passivation
for limited tooth movements i.e. either The lingual archwire should be completely passive.
posteriorly or even buccal movement of the tooth. This is done by heating the wire to a dull brownish
c) Lingual Horizontal tube: This is used, as the ver­ appearance, while keeping the wire gently in place
tical tube on the unaffected side will provide a on the cingula with an old instrument.
greater resistance to its movement than on the
affected side. III. DISTAL SHOE SPACE MAINTAINER
d) Ellis loop lingual archwires: These are preformed (Intra-alveolar, Eruption guidance appliance)
arch wires. Along with this, Ellis Vertical lin­
gual tubes are used. It has the advantage that it « The fixed distal shoe space maintainer, was first
is time saving. Since it is preformed, possible reported by Willets (1932). The appliance is con­
fracture points are reduced to a minimum. structed when there is a premature loss of the
I- second primary molar, prior to the eruption of
fixed lingual arch the first permanent molar. This wai a cast gold
This is soldered or welded to the band. It is used appliance and soon fell into disfavour due to the
mostly where an active tooth movement is not increased cost.
planned. The addition of canine ‘spurs’ distal to
the deciduous cuspids, is a simple modification that ■ The commonly used one is that described by
helps to maintain a anterio-posterior length at both Roche [1942], a crown or band and bar appli­
ends of the arch. ance. The major difference between the two ap­
pliances in the gingival extension. The Roche
Idngual arch construction variety had a ‘V’ shaped gingival extension while
■ The wire should be made to contact the cingula the Willets one had a bar type (Fig. 9.18a,b,c,d)
of the mandibular incisors slightly above the
gingival papillae. The wire should also lie in Classification
the gingival third of the primary molar, while
extending posteriorly to rest passively on and 1. Fixed
parallel to the middle third of the molar i) Functional
bands[Kapala, 1985] Advantage - durable, maintains occlusion, can
• In case of edentulous ridge, the wire is curved be used after removal of extension.
down to the lingual approximately 1 mm away Disadvantage - costly, time consuming, diffi­
from the soft tissue. cult construction and adjustment.
 SECTION 9 : DEVELOPING MALOCCLUSION AND ITS MANAGEMENT |

Fig. 9.18b Modified distal shoe

Fig. 9.18c Distal shoe placed intraorally Fig. 9.18d Radiographic view of distal shoe

Fig. 9.19 Nance space holding applicance to Fig. 9.20 Trans palatal arch - upper fixed
maintain space for maxillary pre-molars bilateral space maintainer
 I TEXTBOOK OF PEDODONTICS

ii) Non-functional the 1st molar, this may not be possible. Thus a
Advantage - easy fabrication, low cost and groove placed in the mesiofacial surface with a
single abutment. 691 bur will aid in developing retention.
Disadvantage - more breakage chance, less b) For non-functional as it is not able to establish
retentive and new appliance required after the occlusion, the first molarmay tip over the
eruption of tooth. plane, at the time of eruption.

2. Removable IV. NANCE ARCH or NANCE SPACE HOLDING

APPLIANCE (Fixed, nonfunctional, passive,
Criteria for appliance fabrication
maxillary arch appliance)
A. In the lower arch, the contact area of the distal
extension should have a slight lingual position ■ Discussing the limitations of the orthodontic
over the crest of the alveolar ridge. By contrast, treatment, Nance (1947) described the ‘preven­
the area of distal extension of the maxillary ap­ tive lingual wire’. It consists of bands on the
pliance should be slightly facial. This is impor­ upper molars, with the arch wire extending for­
tant to prevent rotation of tooth and appliance. ward into the vault.
Construction (Fig. 9.19)
B. Width
■ The acrylic button is present on the slope of the
If no adequate width is provided, the tooth may
palate and provides an excellent resistance
slip. It should be approximately the width of
against forward movement (U loop). The wire
the contact area.
should extend from the lingual of bands to the
C. Length of the distal extension: deepest and most anterior point in the middle of
■ Ideally, measure the second molar before ex­ hard palate.
traction and remove the same from model. ■ ‘U’ bend is given in the wiw for the retention of
« If the second molar is already missing, a rec­ the acrylic 1 -2 mm away from the soft tissue.
ommended practice is to measure on a radio­
graph, the distance between distal surface of V. TRANSPALATAL ARCH (TPA)
first primary molar to the first permanent (Fixed, non-functional, passive appliance)
molar. This carries the disadvantage of the
It is used in the maxillary arch. The arch is sol­
appliance being over extended, especially in
dered to both sides, straight, without a button and
the maxillary arch as the molar erupts from a
without touching the palate. (Fig. 9.20)
more distal direction to swing mesially.
■ The basis of the appliance is that the migration
• Thus the best way is to measure M- D width
and rotation is caused by rotation around the lin­
of the second primary molar on opposite side.
gual root By preventing this, space loss is pre­
D. Depth ofgingival extension vented by the appliance. Also, it is thought that
The gingival extension of the appliance should one molar will provide some stability to it’s an­
be constructed to extend 1 mm below the mar­ timere. However, cross arch anchorage can be
ginal ridge so as to just ‘capture’ the mesial used if onty one of the primary molars is lost
marginal ridge of the tooth and both the permanent molars are erupted.

Special considerations: BONDED SPACE MAINTAINERS

a) For the functional type if cast gold appliance is
1) These were suggested by Palmer (1979) as they
used, better to use 2 abutments, as it is func­
would be helpful in reducing the time for appli­
tional. But with space between the canine and
ance construction.
 SECTION 9 : DEVELOPING MALOCCLUSION AND ITS MANAGEMENT | icSEl

■ A triangular mesh pad is adapted to the me­ - upper right + lower left and
sial surface of distal abu tment and to the distal - upper left + lower right
surface of anterior abutment. For additional
retention, the mesh can be contoured to ex­ ■ The .030" truchrome construction is said to
tend onto a small area of the lingual and buc­ resist distortion. The 3Dpost - tube provides
cal aspects. a secure fit. It also allows to be tightened with
■ The space maintainer tube is welded on the a slight adjustment. The bar position is ad­
post mesh, while the wire with the correct justed to the first bicuspid just below the con­
length is welded anteriorly. tact point Features include an instant plug in
■ A vacuum molded template is then formed and removal, secure lock in, resist deforma­
over the space maintainer. After removal of tion, removable for hygiene, can be used for
the template, the appliance is cleaned and space regaining, time and cost - saving and
bonded. can also be converted to a functional space
maintainer.
2) A variation was suggested by Artum and
Marstander (1983). They found a round, 5) Modified bonded space maintainer
multistrand orthodontic wire 0.032 inch diam­ ■ Coican (1992) has presented a case report
eter to be more satisfactory4*7 than an ordinary where the conventional band and loop was
round wire. They also used an autopolymerizing contraindicated because the first molar was
composite resin. partially erupted. A removable appliance was
rejected due to lack of retention, short clini­
3) A new universal space maintainer has been sug­ cal crowns and the patient’s age. A second
gested by Athanasios (1984). molar bracket was bonded to the buccal sur­
It consists of a solid steel foil pad bases and 2 face of the erupting first molar. A full size
sections rectangular wire segment is used to span the
a) Round retainer wire edentulous space and provide light contact
b) Stainless steel tubing. against the deciduous first molar.
■ Liegeois et al [1999] have also described a
Only 2 variations - left and right - are sufficient. modified bonded space maintainer. Slots and
The pads can be used for direct bonding after occlusal shores are prepared on the primary
the wire length is marked and the excess is cut. teeth and a sanitary pontic is placed in the
edentulous area to make it functional. The
Advantages stated are: alloy used is chrome cobalt.
1. Easy, fast and economical to produce
2. No bands or impressions are necessary DISADVANTAGES OF THE FIXED SPACE
3. It can be completed in one appointment MAINTAINERS
4. Can be used for posterior spaces of any length
■ Maximum failures are encountered with the
5 Possibilities of decalcification and periodon­
placement of lingual arches.
tal damage is decreased.
■ Cement loss and solder failure are found to be
6 Can be used on partially erupted teeth and is
high in all appliances.
esthetic.
■ Tissue lesions are high with the band and loop.
■ Another important disadvantage is the eruption
4) A 3D instant space maintainer which is patented
interference caused by lingual arch in a few cases.
by Rocky Mountain has been described by
Wilson and Wilson[1984]. It is pre-fabricated
Management by fixed space maintainers illus­
and available in 2 forms.
trated in Table 9.5
 Table 9.5: Management by fixed space maintainers
Appliance Indications Contraindications Limitations/Disadvantages
■f
1. Band 1. Premature loss of any Extreme crowding or 1. Seldom used for space
and primary first molar. space loss loss of more than one tooth.
loop 2- Where the unerupted High caries activity 2. Nonfunctional
premolar is more than 3. Migration of the loop
' \ -*L~ >' 2 years from clinical gingivaily (semi fixed)
eruption and root 4. Loss of E before eruption
. length is less than 1/2 of 4
2. Lingual T. Bilateral loss of posterior 1 .Before the eruption of 1. Loss of cementatibn and
arch teeth (rarely used in the mandibular incisors solder are most commonly
wires . primary dentition) (can be modified) associated with this
V'" 2. Minor movement of the appliance.
anterior teeth. 2. May cause untoward
3. Maintenance of leeway movement
space.
4. Space regaining
3. Distal Early loss or removal of the 1. Inadequate abutments 1. Over extension causes
shoe second primary molar prior due to multiple loss injury to the permanent
space to the eruption of the first 2. Poor patient/parent tooth bud i.e., second
mainta­ permanent_molar is the cooperation premolar.
iner prime indication. 3. Congenitally 2. If under extended, it
In the maxillary arch with missing first molar may allow the molar to
bilateral space loss, 2 4. Medical conditions such tip into the space or over
appliances may be used. as blood dyscrasias, the band.
CHD, Rh: fever, 3. Prevents complete epithe-
di^b^tes or generalized lialization of the extraction
debilitation socket. ?
4. Ronnermann and Thiiander
(1979) have discussed the
path of eruption and stated
that the drifting takes palce
only after eruption through
the bony covering. The
lower first molar normally
erupts occlusalward to
contact first the distal crown
surface and uses that butt­
ress for uprighting. Isolated
cases should be considered
ectopic eruption.
4. Nance 1. Bilateral loss of the 1. Palatal lesions 1. May cause tissue hyper­
palatal deciduous molars. 2. If either of the molars plasia and infection due to
arch 2. Combined with a habit has not erupted poor oral hygiene.
breaking appliance
-,
(on the acrylic button)
5. Trans­ 1. Best in cases where 1. Bilateral loss 1. May cause both the molars
palatal unilateral loss of space to tip together.
arch is seen.
 SECTION 9 : DEVELOPING MALOCCLUSION AND ITS MANAGEMENT I

REMOVABLE SPACE MAINTAINERS

Indications:
1) When premature loss of primary molars takes
place and space maintenance with restoration of
masticatory fonction is impdæhf.
2) In cas® Where supra-eruption has already taken
place, a non-fonctional one may be used.
3) In the anterior region, premature loss may have
deleterious effects on speech and esthetics. For
this purpose, replacement of the anterior teeth
may be done by R.P.D.
4) When a multipletpoth loss is seen, where fixed Fig. 9.21a Functional removable space
appliances may not serve the purpose. maintainer - upper arch
5) When permanent molars have not erupted,are-
movable guiding plane may also be used.
6) In high-risk caries child, maintenance is poor
. j and fixed appliances are contraindicated. The
key disadvantage of all removable appliances lies
in the heavy dependence on patient compliance.

■ In a majority of clinical conditions, a removable,

partial denture, with an acrylic denture base,
wrought wire clasp and artificial teeth will serve
the purpose. Rarely, in cases of prolonged use,
a cast, chrome - cobalt alloy framework may be
considered. (Fig. 9.21a, b)
Fig. 9.21b Functional removable space
Classification: maintainer lower arch

A simple classification that includes the various 4. It may irritate the underlying soft tissues.
clinical situations in which removable appliances 5. It may not maintain space during the eruption
may be given in the primary/mixed dentition are: of the tooth.
I - Unilateral Maxillary posterior Self Assessment
II - Unilateral Mandibular posterior
III - Bilateral Maxillary posterior 1. Define preventive orthodontics
IV - Bilateral mandibular posterior 2. What are the common procedures done in pre­
V - Bilateral maxillary anterior and. Posterior ventive orthodontics?
VI - Bilateral mandibular anterior posterior 3. Define space maintainer, space maintenance and
VII - Primary/permanent anterior r space management
VIII - Complete primary teeth loss. 4. Classify space maintainers and give the indica­
tions, advantages and disadvantages of the same
Demerits: 5. What factors are considered before instituting a
1. It depends entirely on patient co-operation and space maintainer program?
compliance. 6. Write short notes on
2. It may be lost or can be broken by the patient. a. Willet’s appliance
3. The lateral jaw growth may be restricted, if clasps b. Band and loop space maintainer
are incorporated. c. Proximal stripping
 9.3 Early Orthodontic Interventions
J

Mehta S, Vanka A, Tandon S

Introduction relations. Thus, use of devices such as utility arch

wire , can reduce the complexity of the treat­
Early orthodontic intervention by the pediatric den­ ment at a later date. It can be considered a su­
tist is a highly controversial issue generated by a pervised neglect on the part of specialists if in­
section of specialists. Though comprehensive treat­ cipient malocclusions are not resolved as soon
ment may be required at a later date, the need for as they are seen in the developing dentition
early intervention cannot be denied. The problem (Carpezza ,1997)
can be prevented from occurring in the first place ■ The early occlusal guidance trains the tongue to
or it's complexity can be reduced to an extent that act like a functional appliance and produces
the further procedures are simplified. Clinical ex­ unique arch development.
periences of various Pedodontists show that empha­ « Majority of the class II problems which are of­
sis should be placed on guidance of growth, early ten 3.5 mm or less in molar relation if treated
interception of developing malocclusion and elimi­ early can be corrected within-^ 6-8 months.’
nation of the first symptom. « Clinical studies have shown the ‘Andrews six
keys to normal occlusion" can be more consist­
Reasons for earlv interventions ently attained with early intervention than late
treatment.
Several reasons that favour early intervention are: « Extraction of permanent teeth can be reduced
■ It does not impede normal growth of the denti­ with early intervention and hence more
tion rather it helps in facilitating the guidance esthetically accepted profile is achieved.
of developing occlusion. ■ Non compliance of adolescent years can be
■ Crowding progressively gets worse if not inter­ avoided with early treatment.
vened, early, with the secondary effects being ■ Children and patient’s support is overwhelming
more complicated than primary problem. as functionally and esthetically accepted occlu­
■ Premature loss of primary teeth if not prevented, sion can be achieved before the traditional start­
can cause asymmetry of the arch form, with com­ ing time for late orthodontic treatment.
plex mechanics required to treat this problem
Benefits of early diagnosis and treatment:
later. (Fig. 9.22a, b)
• Rotated teeth if not corrected early and left for a) The possibility' of achieving better results?
long duration may also affect stability of correc­ b) Some forms of treatment can only be done at an
tion later. (Fig. 9.23a, b, c) early age.
• Early intervention also allows for more favour­ c) Early treatment of serious deleterious habits is
able condylar position and growth by unloading easier than treatment after years of habit rein­
the mandible in cases of developing class III forcements.

~ 4*
 SECTION 9 : DEVELOPING MALOCCLUSION AND ITS MANAGEMENT |

Fig. 9.22a Radiograph showing unilateral Fig. 9.22b Radiograph showing bilateral
space loss space loss

Fig. 9.23a Derotation of maxillary left central

incisor by semi fixed appliance, a) Banded
central incisor

Fig. 9.23b Derotation of maxillary left central Fig. 9.23c Derptated central incisor
incisor by semifixed appliance, b) Use of
elastics for derotation
 Cßö I TEXTBOOK OF PEDODONTICS

d) Psychologic advantage to early treatment in some efficient orthodontic treatment. Following condi­
children. tions may need a thorough evaluation with an early
intervention.
Difficulties in early treatment: a) Loss of primary teeth endangering available
Before starting treatment, however, one must evalu­ space in the arch,
ate the drawbacks such as: b) Closure of space due to premature loss of de­
1. Misperceptions exist about the goals of early ciduous teeth. The lost space in the arch must
treatment be regained
2. Improper early treatment can be harmful c) Malpositions of teeth that interfere with normal
3. Diphasic treatment may lengthen the chronologi­ development of occlusal function, faulty pattern
cal treatment time. of eruption, mandibular closure or endanger the
4. Early diagnosis and treatment planning are more health of teeth.
tentative during active growth and tricky to pre­ d) Supernumerary teeth that may cause
dict whereas when growth diminishes the fac­ malocclusions (Fig. 24a, b).
tors of malocclusion are clearly seen.

Conditions that need early intervention:

In Primary dentition:
a) Anterior and posterior crossbite
b) Cases in which teeth have been lost due to car­
ies and loss of space may result.
c) Unduly r^^ned primary incisors which inter­
fere withformal eruption of permanent incisors.
d) Malpositioned teeth which interfere with nor­
mal occlusal function or induce faulty pattern of
mandible closure.
e) All habits or malfunctions which may distort Fig. 9.24a Mesiodens resulting in midline
growth. diastema

Contra-indications to early intervention:

a) There is no assurance that treatment results will

be sustained.
b) A better result can be achieved with less effort
at another time.
c) Social immaturity of the child makes treatment
impracticable.
d) Patient unwilling to co-operate for treatment.

In Mixed dentition period:

The mixed dentition period is the time of the great­
est opportunity for occlusal guidance and intercep­ Fig. 9.24b Diastema resolving following
tion of malocclusion. At this time, the dentist has extraction of mesiodens
the greatest challenges and finest opportunities for
 SECTION 9 : DEVELOPING MALOCCLUSION AND ITS MANAGEMENT |

e) Crossbites of permanent teeth. to the development of occlusal disharmonies. How­

f) Malocclusions resulting from deleterious hab­ ever, when the space is progressively lost, as we
its. have discussed in space closures following early loss
g) Oligodontia - if closure of space is preferable to ofjprnnary teeth, the therapy should be considered
prosthesis. to regain it so that additional disharmonies do not
h) Localized spacing between the maxillary cen­ develop. Then the regained space is maintained.
tral incisors for which orthodontic treatment is
indicated. Diagnosis
i) Neutro occlusion with extreme labio version of For regaining space or any movement of teeth, the
maxillary teeth. most important procedure is diagnosis. Attention,
j) Class II (disto occlusion) cases of functional type limited to the segment id which the tooth is miss­
k) Class II (disto occlusion) of dental type ing, is a frequent cause of the failure in attempting
l) Class II (disto occlusion) cases of skeletal cases to regain space. Considérations for treatment should
m) Space supervision problems. include;
n) All malocclusions accompanied by extremely ■ The alignment and space needs ofthe other teeth
large teeth. If serial extraction is to be under­ in the arch,
taken, treatment must be instituted in mixedden- ■ The relationships of teeth to the denture base,
tition. ■ The transverse and sagittal denial relationships,
o) Gross inadequacies of disharmonies of apical ■ The vertical relationships, aid
bases. ■ The profile of the soft tissue
The various diagnostic aids necessary are study
These problems can be either completely eliminated models, radiographs of all the periapical struc­
by the preventive measures or can be corrected in turés, clinical assessment of facial symmetry and
their inception before they cause irreparable dam­ proportions, and possibly cephalometric analy­
age. sis.

INTERCEPTIVE ORTHODONTICS Dental and skeletal relation

Hie concept of interceptive orthodontics revolves Clinically we have to make quick assessments
around the minor problems present during devel­ to determine unfavourable skeletal patterns or
opment Of dentition, which if left untreated mayin­ dental malocclusions. Thus, clinical assessment
creasein terms of complexity and be, consequently should rule out the presence of a dental or skel-
difficult to treat at a later date. Thus (he procedures etal class II, class III, openbite or dosed bite re­
are instituted once the problem is detected? albeit at lationship.
an early stage. It may thus be considered at the Certain variations in class I malocclusion may
secondary level of prevention. also exist in which simple measures at refin­
ing space should not be the only consideration.
The common problems, which can be intercepted, Dentil alignment considerations that affect thé
would be space regaining, crowding, crossbites, regaining of фасе include estimation of rota­
midline diastemas, and orthopedic guidance tion, slipped contacts, and fecial-lingual dis­
placement of teeth frorii arch circumference.
REGAINING THE SPACE ------ Assessment of the soft tissue profile will help to
identify cases in which a relative protruriotipr
Space maintenance is necessary in early loss of pos­ retorsion of the central alveolar structures’dééis
terior primary teeth because early loss contributes complicate evaluation of available space,
 | TEXTBOOK OF PEDODONTICS

Radiographs and study models Construction: A molar band is fitted to the first
Radiographs and study models will aid significantly permanent molar. Molar tubes are soldered or spot
in assessing space needs and consideration of tooth welded in a horizontal position both buccally and
alignment. It is important to recognize whether lingually to the band. Impressions will be taken
teeth have moved bodily into the space or have with alginate.
tipped axially, because forces applied to tip teeth
back into a proper alignment are easier to manage A stainless steel wire which is slightly smaller than
than forces required to move the teeth bodily. the tube size is selected and bent into a ‘U’ shape.
The base of the ‘U’ should contain a reverse bend
Visualizing the proximity of adjacent erupting teeth to contact the distal surface of the first premolar.
(especially second molars) and estimating their po­ As the wire comes out of the tube it should aim
tential impact on the teeth that have crowded the toward the first premolar at a point just below the
space should also be done. Radiographs of the peri­ greatest distal convexity of the first premolar. A
apical structures are necessary. stop should be placed on both arms where the
straight part meets the bend of the wire. A spaced
Mixed dentition analysis coil spring is selected which will slide on the wire
Moyer’s mixed dentition analysis will give an esti­ and is cut about 2 to 3 mm. longer than the distance
mate of the amount of the space to be regained. It is from the anterior stop to the molar tube. The band
however safer to do at least another analysis [Tanaka is cemented with the coil springs compressed.
and Johnson] to confirm the exact amount of space
loss that has taken place. Sometimes even if there Gerber space maintainer (Fig. 9.25)
is a loss bf space, one may need only to maintain This type of appliance may be fabricated directly in
the space if it is sufficient for the permanent succes­ the mouth during one relatively short appointment
sors to erupt into good alignment. and requires no lab work. A assembly, which
may be welded of soldered in place with silver sol­
Ànchorage considerations der and fluoride flux is fitted in the tribe, the appli­
When appliances are used to reposition the first per­ ance placed and wire section extended to contact
manent molars, there will be reciprocal force ex­ the tooth mesial to the edentulous area.
erted to thé teeth and the supporting tissues ante­
rior to the space, and the result may be an undesir­
able flaring of the anterior teeth. Thus if favourable
conditions exists, an attempt to regain space is cer­
tainly indicated. Several fixed and removable ap­
pliances for space regaining procedures have
evolved for thé tipping of the first molars. How-
ever, the distal movement other than minimal tip­
ping can most satisfactorily be achieved by head
gearappliance.

FIXED SPACE REGAINERS

Open coil space regainer

Fig. 9.25 Space regainer to regain space due to
A reciprocal active fixed regainer can be used to
early loss of 74, 75 teeth
good advantage in the mandibular arch when the
first premolar has erupted into the oral cavity.
 SECTION 9 : DEVELOPING MALOCCLUSION AND ITS MANAGEMENT | CEd

The length of the push coil springs is established maintainer, since it facilitates frequent removal
by placing the band-tube-wire assembly in the of the arch for the purpose of activation.
mouth, extending the wire to the desired length, in
contact with the mesial tooth and measuring the Sectional arch technique
distance bet^en the tube stops on the wire and the K sectional arch technique can also be used to re­
end of the "LT tube. To this distance, add the'amount gain the lost arch length. Upto 4 millimeters of space
of space needed in the regainer, plus 1 to 2 mm, to can be regained In an effective and efficient man-
ensure spring activation and cut springs to this ncr by the method described. It can be used in the
length. The springs are compressed enough to al­ cases where the second molar is erupted.
low the assembly to fit the edentulous area.
Lip bumper/plumper (Fig. 9.27a, b)
Hotzlingual arch (Fig. 9.26) The appliance is most easily used for the space re­
Another method for moving the molar distally uti­ gaining procedures in which bilateral movement is
lizes the looped Hotz lingual arch. This is appro­ desired. It consists of a heavy labial arch wire over
priate in a situation where the lower first perma­
nent molar has drifted mesially, but the premolar or
.cuspid has not drifted distally But there must be x-
ray evidence that there is sufficient space between
the first molar and the developing second molar.

Fig. 9.27a Lip bumper to distalize molars and to

align lower incisor, by relieving lip pressure and
allowing guidance under tongue pressure, a) Pre­
treatment witt) appliance in place

Fig. 9.26 Lingual arch space maintainer with

U-loop to regain space loss in the 74 .region

■ Anchorage for the movement is achieved as the

arch contacts all the teeth. Besides, spurs across
the canines can also be used to the same effect.
■ After adjustment, the posts in the passive posi­
tion should be approximately 1 mm distal to their
passive positions over the lumen of their tubes.
The arch is then forced forward and the posts
slipped down into place.
■ As mentioned earlier, it is advantageous to use
Fig. 9.27b Post treatment
the removable type of lingual arch space
 CHi) I TEXTBOOK OF PEDODONTICS

which an acrylic flange is prepared in the anterior appliance, since the distalizing force is produced
region such that it does not contact the lower by the elastic stretched on the middle of the lingual
anteriors. Instead, it is used to relieve the lip pres­ surface of the molar to be moved. The other is ar­
sure. This pressure can be used to distalize the mo­ ranged in the same position on the buccal surface
lars by: of the molar. The elastic caiibechanged once each
1. Incorporating loops in the arch wire just before day.
it enters the buccal tube.
2. Utilizing a coil spring. Jack screw
It can also be used unilaterally. It is another type of removable appliance used for
space regaining which will incorporate an expan­
Anterior space regainer sion screw in the edentulous space. Space is opened
A technique described is the use of an anterior space by expanding the plates anteroposteriorly.
regainer utilizing direct bonding. To the lateral in­
cisors was attached labial tubes. A 0.014” round wire CROWDING
was then inserted in an open coil spring and
activated. [Bayardo (1986)] Crowding is a common problem encountered at vari­
ous stages of development and in varying degrees
REMOVABLE SPACE REGAINERS of severity. Crowding in the mandibular region may
Several designs of space maintainers have been de­ be seen in the early mixed dentition and is a find­
scribed. The correct selection of the appliance de­ ing of importance for the Pedodontist.
pends on the case, particularly the compliance of
the patient. In the pre-eruption stage of the incisors, crowding
is seen to be present There exists a situation called
Free end loop space regainer ‘incisor liability’ where the permanent incisors be­
It utilizes a labial archwire for stability and reten­ ing larger than their deciduous counterparts, may
tion, with a back-action loop spring constructed of have an impact on the crowding.
No. 0.025 wire. The base of the appliance is made a) In the maxillary arch, the laterals ate more pala-
of acrylic resin. Movement of the permanent molar tally placed.
is achieved by activating the free end of the wire b) In the mandibular arch, the teeth may be lin­
loop at specific intervals of time. gually placed accompanied by some amount of
rotation.
Split saddle/split block space regainer
It is also called split saddle space regainer. It dif­ Will crowding resolve on its own?
fers from the free end spring type in that the fiinc-
tional part of the appliance consists of an acrylic This is dependent on several factors such as -
block that is split buccolingually and joined by 1. Interdental spacing - the eruption of the per- ’
No.0.025 wire in the form of a buccal and a lingual manent incisors brings about the lateral shift of
loop. The appliance is activated by periodic spread­ the deciduous canines so as to align themselves.
ing of the loops. The activator block is split with a Should interdental spacing be absent, this shift
disk after the appliance has been processed. is not possible and may decrease the chances of
a better alignment. Thus, Leighton’s prediction
Sling shot space regainer of permanent teeth crowding based on presence
This consists of a wire elastic holder with hooks or absence of interdental spacing can be a good
instead of a wire spring that transmits a force against predictor.
the molar tor be distalized. This is called sling shot
 SECTION 9 : DEVELOPING MALOCCLUSION AND ITS MANAGEMENT |

2. Intercanine arch width - the intercanine arch disking the mesial surfaces of the canines will
width increase can also help in resolving the help to align the incisors.
incisal crowding. The intercanine width in­
creases to about 6mm in maxilla and about 4mm
in mandible from 2 years of age to maturity.
Hagberg (1994) has used this measurement and
predicted that an intercanine distance of 28 mm
or more shows little risk of crowding, while that
less than 26 mm may be associated with some
crowding upto 10 years of age at least.
3. Inclinations of the permanent incisors - the
more forward inclination of the permanent inci­
sors may help increase the arch circumference.
4. Ratio of the size between the permanent and pri­
mary teeth will give an indication as to whether
adequate space will be available or not. Fig. 9.28 Proximal stripper can be used for
better control over proximal stripping
Considering the above factors and keeping in mind
goals of interceptive orthodontics being to make Disking may either becarried put either by means
adequate space available at tine right time, observa­ of a169L bur or a disking stri|’ In cases where
tion or intervention may be required. minimal disking is required, the strip may be
preferred for better control The disked surfaces
Options in the management of crowding need to be protected with a fluoride application.

The various options that exist in the management Once space is made available, the teeth may
of crowding are: spontaneously correct themselves by tongue pres­
1) Observe sure. Should the laterals be locked behind the
2) Disk primary teeth centrals, however, modification of the lingual
3) Extraction of teeth arch (withauxiliaiy springs) may be used to align
4) Referral the incisors. Should an adequate space not be
provided by disking the canines, the primary mo­
1. Observation lars may be disked later.
In cases where spacing exists in the primary den­
tition with the incisor position having an addi­ 3. Extraction of teeth
tional space creating effect, crowding (less than The extraction of teeth in order to create space
2 mm) will in most cases correct themselves with is a well established procedure. The most rec-
normal dentition and occlusion establishment
(apart from late incisor crowding). Concomi­ yiiVi ’s ex­
traction, timely extraction and Wilkinson
tantly, if a space analysis, coupled with the meas­ traction.
urement of intercanine width shows a favour­
able situation, the patient should be kept under Serial extraction
observation. Though the concept was initiated way back by
Bunon (1743) the catchy term serial extraction
2. Disking ofprimary teeth'. (Fig. 9.28) was coined by Kjellgren (1929) and was popu­
The primary teeth may sometimes prevent the larised by Nance (1940), who has been called
incisors from aligning themselves. If the space the 'father of serial extraction’ philosophy in the
required is not more than 3-4 mm, the grinding/ US. The extraction of teeth is often carried but
 СЮ I TEXTBOOK OF PEDODONTICS

without proper diagnostic aids or further com­ Assessment - It includes

prehensive orthodontic correction is not taken ■ Clinical examination
into consideration. Thus the term/Guidance of ■ Occlusion study (models)
eruption ‘[11012,1970 ] would sound more ap­ « X-rays - ЮРА, OPG, cephalograms with cepha­
propriate. lometric tracings
■ Mixed dentition analysis
Definition ■ Facial photographs
Serial extraction can be defined asjthe correctly
timed, planned removal of certain deciduous and Rules to be followed:
permanent teethm mixed dentition cases with dento 1) There must be class I molar relationship bilater­
alveolar disproportion i.e., teeth to supporting bone ally
imbalance in order to: 2) The facial-skeletal relation must be balanced
a) Alleviate crowding of the incisor teeth for ex­
anterior-posteriorly, vertically and mesio distally.
ample to provide space for spontaneous align­
3) Discrepancy should be at least 5 mm in all quad­
ment of incisors, when the lateral incisors are
rants
erupted at 7-8 years, deciduous canines may be
4) Dental midline should coincide
extracted
5) There must be neither openbite nor deepbite
b) Allow unerupted teeth to guide themselves into
improved positions. For example, deciduous first
Procedure and rationale
molar is extracted to speed eruption of first
premolar, when root development of the first
premolar is halfway. Several sequences of treatment have been advocated
c) Lessen the period of active appliance therapy or with the most common ones being those of Dewel
eliminate it. and Tweed.

Indicationsfor serial extraction ■ Dewel [ 1978 ]: The sequence proposed by

1) Class I with anterior crowding (space discrep­ Dewel is the extraction of CD4
ancy 10mm or more)
2) Lingual eruption of the lateral incisors A. Extraction of deciduous canines - the decidu­
3) Midline shift potential due to unilateral canine ous canine space is utilized for aligning the
loss crowded incisors. The resorption of the canine
4) Crowded arches accompanied with extreme by a lateral incisor can provide an indication to
proclination the same (Age 8.5 years).
5) Abnormal primaiy canine root resorption
4) Lack of developmental spacing B. Extraction of the first deciduous molars - At
7) ¿ Anomalies such as ankylosis, ectopic eruption the age of 8.5 years, the unerupted permanent
premolar will not have reached 1/2 root length.
Contraindications Once this happens (at about 9 1/2 yearsV Же
1) Mild to moderate crowding (about 8 mm or less) deciduous first molar may be extracted to pro­
2) Congenital absence of teeth providing space mote the eruption of the first premolar. At this
3) Where extensive caries of permanent first mo­ stage, it would 3d well to note that the incisor
lars requires their removal.
crowding may have got resolved. Should the
4) Accompanying deep or openbites without cor­
eruption sequence be unfavourable, with the ca­
rection
nine erupting before the premolar, enucleation
5) Severe class IL III of dental/skeletal origin
can be carried out. The extraction of the second
4) Cleft lip and palate cases
 SECTION 9 : DEVELOPING MALOCCLUSION AND ITS MANAGEMENT |

deciduous molar with the placement of a lingual Thus mechanotherapy and retention may be
arch is another alternative, wherein the first unavoidable.
premolar is encouraged to shift distally. At a later 2) It may be used only selectively in class II
date, once the canines erupt the first premolars malocclusions.
are removed. 3) Psychological trauma and lack of the patient co­
operation may affect the future dental treatment.
It is important that before extracting the first 4) Caries may affect the second premolars, neces­
premolars, a reassessment of the existing prob­ sitating their removal.
lem is made. 5) Impacted canines-even after removal of premo­
lar, the canine may remain impacted.
■ Tweed (1966) proposed the extraction sequence
as DC4: Timely extraction: (Fig. 9.29a, b)
This is similar to serial extractions wherein se­
a) At 8 year of age, all the deciduous first molars quential removal of deciduous teeth is carried
are extracted. The deciduous canines are main­ out, but differs in that no permanent teeth are
tained to hamper the eruption of permanentjca- removed. The term Timely extraction has been
nines. recommended by Stemm [1973].

*b) After the premolars (crowns) are through the al­

veolar bone, the premolars along with the de­
ciduous canines are extracted.

■ Dale (1985) has proposed the same technique in

cases of alveolodental protrusion. Here after ex­
traction of the premolar and canine, no effort is
made to prevent the lingual movement of teeth.

Advantages of serial extraction procedure

The key advantage in serial extraction lies in the

fact that by timely extraction of the teeth, further Fig. 9.29a Timely extraction a} Pre-treatment
appliance therapy is minimized or eliminated. It will
also reduce the complexity of treatment need.

Disadvantages of serial extraction procedure

1) Unfortunately, quite too often the serial extrac­

tion procedure will have to be followed by fixed
appliance therapy. This is particularly so in cases
of Class I with crowding, where the procedure
is accompanied by
a) Relatively deep oveibite
b) Distoaxial inclination of the canines and
mesioaxial inclination of the second
Fig. 9.29b Post-treatment
premolars. This has been termed as ditching.
 I TEXTBOOK OF PEDODONTICS

Timed extractions have been advocated in cases should be evaluated, as it may incline further
where: distally & get impacted below the second molar.
a) There is a gingival recession due to labial posi­
tioning of the lower incisors, coupled with an CROSS BITE
inadequacy of dental arch length.
b) There is ectopic eruption of the lateral incisors ■ An anterior crossbite is an abnormal labiolingual
or the first permanent molars. Apart from the relationship between one or more maxillary and
locking of the tooth below the deciduous coun­ mandibular anterior teeth while a posterior
terpart (especially in maxillary molar), space loss crossbite is an abnormal buccolingual relation­
may also be present. ship of a tooth or teeth in the maxilla or mandi­
ble, or both, when the two dental arches are
Hie plain removal of the canines will cause lateral brought into a centric occlusion
and lingual shift ofthe mandibular incisors. Though
this will help in repositioning, it may create arch Classification
length deficiency where none existed before and thus
should be accompanied by space maintenance to Cross bite
preserve the alignment. The best indication to use
J
the so called timed extractions of primary teeth
would be when the crowding is 4-9 mm. This is Anterior Posterior
because the alignment of the incisors after the per­
manent canines have erupted is a difficult task. I I
Unilateral Bilateral
• Incisor extraction
Occasionally, extraction of an incisor tooth may I I
give a good result. This can be done in cases True Functional
where the jaws are narrow and the teeth are fanned
out laterally. Any pathology of the lateral inci­ Combination of above
sors, where it cannot be saved or if it is excluded
from the arch, may favour its extraction. Anterior Vs Posterior cross bite is depicted in Ta­
ble 9.6
• Wilkinson’s extractions
While serial extractions are primarily indicated The modalities of treatment for anterior cross bite
in cases where the crowding exists in the ante­
rior region for relief of crowding in the posterior A differential diagnosis must be made to determine
teeth segments, the first molar extractions can whether the problem is of skeletal or dental origin.
be carried out The prognosis is much better if a plain dental prob­
lem exists.
The criteria to be evaluated would thus be quite
similar to serial extractions. The dental age of Other factors that need to be evaluated are:
an individual needs to be assessed. For the sec­ ■ Axial inclinations of the upper and lower inci­
ond molar to assume a normal relationship, the sors
first molar should be extracted preferably before ■ The absolute size of the mandible and maxilla
eruption of the second molar (especially in the and their relationship to each other and to cra­
mandibular arch). Before extracting the first mo­ nial base.
lars, the inclination of the second premolar ■ Profile of the patient'
 SECTION 9 : DEVELOPING MALOCCLUSION AND ITS MANAGEMENT | CIO

Table 9.6: Anterior Vs Posterior cross bite

Anterior cross bite Posterior cross bite

Etiology: 1. Traumatic injuries to the primary 1. Ectopic eruption of the permanent

It can be dental, dentition that cause a lingual dis­ first molar. *
skeletal or a placement of the permanent tooth 2. Prolonged thumb or finger sucking.
combination bud. 3. Prolonged retention of primary
of the two. 2. Supernumerary tooth. teeth.
3. An inadequacy of arch length 4. Occlusal interferences.
causing the lingual deflection of the 5. Skeletal: They may be caused due to:
permanent tooth during eruption. a) Deficient lateral growth of the
4. AJiabit of biting the upper lip. maxilla as seen in deft palate
5. A repaired cleft lip. repair.
6. A functional cross bite caused due b) Increased growth of mandible or
to premature tooth contact during c) Combination of both.
centric closure.
7. Skeletal: An anterior cross bite of
skeletal origin generally results from
an excessive abnormal mandibular
growth that produces a true class
III malocclusion. It has got a genetic
background.

■ The molar and cuspid occlusion c) Lower inclined plane: This was introduced by
■ The extent of root formation (if root formation Catalan. Treatment of dental anterior crossbite
is not complete lighter forces to be applied) involving one or two teeth may be accomplished
■ Adequate mesiodistal space should be available by using a cemented lower acrylic inclined plane.
Sufficient overbite for retention purpose The inclined plane should be contoured and pol­
ished at a 45-degree angle to the long axis ofthe
Corrective measures and appliances lower incisor teeth prior to cementation. The
steeper the angle, greater the force applied (Fig.
a) Occlusal equilibration: Correction of a pseudo 9.31a, b, c).
class III anterior crossbite may require only the It lias the disadvantage that:
removal of premature tooth contacts by incisal ■ the possibility of opening the bite by wearing
grinding of the maxillary and mandibular incisors. it longer than two or three weeks.
■ exact amount of labial movement is unpre­
b) Tongue blade therapy: It is ideally suited for dictable and uncontrollable. \
cases where a simple one tooth anterior dental
crossbite exists, with the teeth in the early stages d) Stainless steel crown: A reverse stainless steel
of eruption. Using the lower incisor as the ful­ crown is best suited for single tooth crossbites
crum, the locked tooth can be pushed out by plac­ in which the lower mandibular incisor has been
ing the tongue blade 45 degrees behind the tooth. previously displaced labially.
It should be used 1-2 hours daily for 10-14 days
• (Fig. 9.30d).
 Ci£> | TEXTBOOK OF PEDODONTICS

Fig. 9.30a Left central incisor in cross-bite - Fig. 9.30b Post-treatment

Pre-treatment

Fig. 9.30c 2’ - spring for correcting anterior Fig. 9.30d Tongue blade therapy for correcting
cross bite *
developing anterior cross
bite
 SECTION 9 : DEVELOPING MALOCCLUSION AND ITS MANAGEMENT |

Fig. 9.31a Lower inclined plane to correct Fig. 9.32a Correction of anterior segmental
anterior cross bite with 21, 22. cross bite. Pre-treatment
teeth in cross bite

Fig. 9.31b Lower inclined plane in place i Fig. 9.32b Appliance placed to open the
/ bite in order to correct the cross bite

Fig. 9.31c Corrected bite Fig. 9.32c Post-treatment

 Cí£> i TEXTBOOK OF PEDODONTICS

e) Composite inclines: Another simple technique ■ The midline should be checked to determine if
is to build up a composite incline on the lower unilateral mandibular shift is present.
teeth directly in the patient’s mouth. Croll [ 1999] ■ A facebow transfer may sometimes confirm the
has suggested the use of a bonded compomer functional shift, however, by observing the pa­
dope based on the assumption that a compomer tient closing from rest into centric occlusion, a
having lessstrengththan a composite can be eas­ lateral deviation can be frequently observed.
ily removedwhen desired.
Corrective measures and appliances
f) Removable Hawley appliance: A maxillary
Hawley appliance with Z springs incorporated a) Occlusal equilibration: A dental bilateral lin­
into the acrylic resin is usefid in the correction gual crossbite in the primary or mixed dentition
of a dental anterior crossbite involving'single or may be simply corrected by removing occlusal
more than one tooth. Retention can be obtained interferences, usually in the cuspid areas. How­
by the use ofball clasps, Adams or C type clasps. ever, this may sometimes need to be accompa­
Movement of the inlocked incisors is accom­ nied by some appliance.
plished by activating the springs 1.5 mm to 2
mm every one or two weeks. Patients are in­ b) Removable W-arch appliance: This appliance
structed to wear the appliance 24 hours a day. If should be limited to only bilateral dental crossbite
the bite is deeper than normal, or if correction is conditions because of the reciprocal action. Cau­
taking longer than expected, then a slight open­ tion should be exercised since a precise control
ing of the bite may be desirable by means of a of the force being applied to the teeth is difficult.
bite plane (Fig. 9.30a, b, c and 9.32a, b, c).
c) Cross elastic appliance: Cross elastic therapy is
g) fixed appliances: Lingual arch may sometimes useful in correction of dental unilateral crossbite
be indicated in case of space control programs. involving one or two teeth. Bands are adapted
Auxiliary springs can be used along with the lin­ and cemented to the teeth involved. A hook or
gual or palatal arches for the purpose of correct­ button spot is welded to the bands. The two teeth
ing the crossbites. are engaged by means of an elastic. Reciprocal
movement of both the upper and lower teeth oc­
Modalities for the Correction of Posterior curs. The disadvantages are patient cooperation
crossbite and increased armamentarium (Fig. 9.33a, b, c).

The important consideration is to determine whether d) Removable Hawley appliance: A removable

the crossbite is unilateral or bilateral, and which maxillary Hawley appliance with an offset
has got a functional component to it. Following jackscrew embedded in the acrylic resin, may be
points can be considered in differential diagnosis: useful in the correction of two teeth unilateral
• Study models using a wax bite can be an asset to dental crossbite. The appliance offers good con­
diagnosis. It also helps in detecting abnormal trol of the amount and direction of force being
inclination of teeth, symmetry of the dental applied to the teeth. The activation of the screw
arches to certain extent the growth pattern. is done at 1/4 turn every week (Fig. 9.34a, b, c).
« Cephalometric analysis will show gross skeletal
abnormalities. When the crossbite is corrected, the appliance
• An occlusal radiograph can also be taken pre- should be worn in passive retention for an addi­
operatively to compare with the post-operative tional three to six months as a retentive appli-
x-ray. anee.
 SECTION 9 : DEVELOPING MALOCCLUSION AND ITS MANAGEMENT |

Fig. 9.33a Maxillary molar in lingual Fig. 9.34a Complete posterior and left central
cross bite incisor in cross bite

Fig. 9.33b Correction utilizing interarch Fig. 9.34b Correction with appliance incorpo­
elastics rating screw and Z-spring

Fig. 9.33c Post-treatment Fig. 9.34c Post-treatment

 Table 9.7: Midline Diastema
Etiology Treatment plan
1. Normal developing dentition ■ Resolves by itself with the eruption of the
[Ugly Duckling Stage] permanent canines.
* ■ Spontaneous closure seems to occur with
less frequency in ,
a) Generalized spacing
b) Initial diaste&atf&more than 3 mm.
2. Familial incidence ■ Appliance therapy
3. Parafunctional habits i) Correction of the habits has been known to
• Flaccid lips and a poor muscle tone spontaneously correct the diastema
• Tongue thrust (simple) may Cause within limits.
anterior open bite and diastema ii) In cases of excessive diastema, correction
• Thumb/digit sucking over a prolonged of the diastema can be simultaneously
period carried out with the habit breaking appliance.
4. Tooth size discrepancies ■ First intrusion of the maxillary incisors,
a) Excessive anterior vertical overlap followed by retraction of the incisors
b) Excessive vertical maxillary alveolar to close the diastema.
growth. Retrognathic mandible or a ■ If however cephalogram indicates an
prognathic mandible. excessively long lower face or a Class III
growth trend, functional therapy may be
the treatment of choice.
5. Frenum attachments ■ Generally advocated that the diastema
should be closed as far as possible before
going in for frenectomy. The reason cited
is that should the surgery be performed
before, the surgical scar tissue maintains
the diastema. %
(xMesio-distal angulation of teeth ■ The correction of the crown angulation
(tipping) will close the diastema. *
7. Tooth anomalies (supernumerary tooth, ■ Supemumerary:Removal of the super­
peg shaped laterals, absence of laterals). numerary followed by a closure of the
diastema is done.
■ Peg shaped laterals: The diastema can be
corrected orthodontically followed by esthetic
restoration of the peg shaped laterals.
■ Absence of laterals:
i) The space for the missing laterals, if
detected early, may initially be maintained
and at later date replaced with fixed
prosthesis.
ii) Another option is to orthodontically move the
canines into the space of the missing
laterals, followed by a careful recontouring
of the cuspid and the first bicuspid (if
required) to simulate the lateral and
cuspid respectively.
8. Pathological (Juvenile periodontitis) ■ Systemic phase [if required ] followed by
appliance therapy
 SECTION 9 : DEVELOPING MALOCCLUSION AND ITS MANAGEMENT |

Skeletal correction: It may be carried out in two

forms:
a) Slow palatal expansion
b) Rapid palatal expansion

The various appliances used are:

- Minnesota expander
- Hyrax jackscrew
- Fixed split palate acrylic appliance

MAXILLARY MIDLINE DIASTEMAS

Maxillary midline diastemas are one of the com­ Fig. 9.35a Diastema correction of lower
mon complaints encountered. It has been defined incisors using elastics
as a space greater than 0.5 mm between the proxi­
mal surfaces of adjacent teeth. The incidence of di­
astema varies both culturally, racially and with age.

Midline diastema, etiology and treatment plan

are illustrated in Table 9.7

Appliance therapy for the correction of diastema

The correction of diastema can be carried out by
various fixed or removable appliances. The princi-
pie applied here is of reciprocal anchorage (in fixed).
The types of movement are either bodily or more
commonly by tipping. (Fig. 9.35a, b, c, d).

Removable appliances Fig. 9.35b Post-treatment

a) An active plate can be utilized for this purpose.
The plate incorporates palatal finger springs Inherent in the use of removable appliances is
passing between the central and lateral, such that the drawback that only tipping movements can
the loop is opposite to the direction of move­ be achieved. For optimum angulation of the teeth,
ment. A modified cantilever spring may be used a further correction is required.
to the >ame effect.
Fixed appliances
b) A split labial bow is a modification which can a) A stainless steel band with a bracket or more
be utilized to close the diastema. It may be ac­ commonly a bracket may be banded to the tooth
companied by the disadvantage that space may and elastics utilized to bring.the centrals towards
be created between the laterals. each other. Tubes may be welded and an archwire
used, so that the teeth may slide. In this case
c) In cases where there is an increased overjet ac­ more control can be achieved over movement
companying the diastema, a Hawleys plate with b) For a more esthetic treatment, a lingual button
an active labial low can be used to retract the may be bonded and an elastic applied. Even these
incisors and thus close the space.
CSS I TEXTBOOK OF PEDODONTICS

Fig. 9.35c Diastema correction of upper Fig. 9.35d Post-treatment

incisors using arch wire

Fig. 9.36a Myofunctional appliance and Fig. 9.36b Appliance showing orthodontic
their modifications prevention and interception
 SECTION 9 : DEVELOPING MALOCCLUSION AND ITS MANAGEMENT |

may bring about only a tipping movement, and has been termed hybrid appliance. The three basic
not true bodily movement. components included are:
c) For the purpose of bodily movement of the teeth,
it is suggested that an Edgewise bracket with a b Eruption - biteplanes. These may be anterior,
simple looped partial arclwiiemade from a rec­ flat, or inclined and constructed out of either
tangular wire be tied under ffie^ehsion into both acrylic or wire. They act by encouraging a dif­
brackets. ferential eruption of teeth and by removing
intercuspal interferences.
Retention
In order to prevent a relapse, a long term retention • Linguo-facial muscle balance - shields or
is required in these cases. A small multistranded screens. The equilibrium theory of tooth posi­
wire may be used lingually and held in place by tion states that over time tooth movement oc-
means of composite. curs in response to any alterationhuthe
homeostatic relationship existing betweenthe
FUNCTIONAL JAW ORTHOPAEDICS forces from the tongue on one side and the lips
and cheeks on the other. The vestibular shields
In achieving dentofacial effects, fixed orthodontic and lip pads of the functional regulator hold the
appliances generate mechanical forces that are trans­ lips and cheeks away from the teeth, thereby dis­
mitted to teeth. In functional orthodontic appli­ rupting the equilibrium and permitting an un­
ances, the neuromuscular activity is tapped to alter opposed buccal movement of the teeth.
stresses on teeth and jaw bones.
■ Mandibular repositioning - construction or
Definitions working bite. All functional appliances are con­
■ Frankel (1974) A functional appliance can be structed to a ‘construction’ or ‘working’ bite.
defined as a removable or fixed appliance which Such registrations are based on theassumption
favourably changes the soft tissue environment. that, by displacing the mandible from its rest
position and stretching the muscles attachedto
b Mills (1991 j: A functional appliance can be de­ it, reflex activity will restore the mandible to a
fined as a removable or fixed appliance which posture determined by the unstretched muscles.
changes the position of the mandible so as to
transmit forces generated by the stretching of Indications
the muscles, fascia and/or periosteum, through
the acrylic and wirework to the dentition and Use bf functional appliances alone
the underlying skeletal structures. Some patients can be treated by use of functional
appliances only, so that an acceptable occlusion can
Classification: be established. These cases generally have a mild
Functional appliances can be removable or fixed and skeletal discrepancy, proclined upper incisors and
can also be classified as: (Fig. 9.36a) no dental crowding.
- tooth borne passive - eg. bionator
- tooth borne active - eg. Clark twin block Use of functional appliances in combination with
- tissue borne, eg. Frankel functional regulator fixed appliance
This is used most commonly to improve the
The appliances have also been classified, depend­ anteroposterior relationship before starting the fixed
ing upon the components used. Such an appliance appliance treatment. In particular, they are extremely
 | TEXTBOOK OF PEDODONTICS

useful in Class II cases and go a long way in reduc­ Effects on soft tissues
ing the amount of a comprehensive fixed therapy
required. It may also reduce the need for These include:
orthognathic surgery7 at later date. ■ removal of the lip trap and improved lip compe­
tence
Interccptive treatment ■ removal of adaptive tongue activity
Early intervention with functional appliances may ■ lowering of the rest positidí üfTlie mandible;
be indicated when one wishes to utilize their growth­ and
enhancing effect. In addition, (hey are extremely ■ removal of soft-t issue pressures from the cheeks
effective at reducing the relative prominence of the and lips.
proclined upper incisors, which are particularly sus­
ceptible to dentoalveolar trauma. COMMON APPLIANCES IN USE

Rationale for use Activators (Fig. 9.37a, b, c, d)

The theoretical basis behind the functional appli­ The "monobloc", designed by Robin (1902), was
ance therapy is that a new pattern of function within the first reported functional appliance. This was
the orofacial system (i.e., in the tongue, lips or modified by Andresen in 1936 and later termed ac­
muscles of mastication), directed by the appliance, tivator in 1957.
leads to the development of a new' morphologic pat­
tern (i.e, an altered dental or skeletal relationship). Indications
Evidence for these theories come from both animal Partial or total correction of Class II div I, Class II
experimentation and human cephalometric studies. div II, Class III, open bites in a mixed and early
permanent dentition. A typical indication would be
Effects on the dento-skeletal complex Class II div I with deep bite.
The skeletal, dentoalveolar and soft-tissue effects '4

of these appliances have been reviewed by Dare and Contraindication

Nixon (1999). It is not advisable to use the appliance in cases of
crowding or where individual tooth movements are
Skeletal effects required.
Il has been reported that growth takes place at the
condyles during the growth of the mandible by Bite registration
means of a functional therapy. Some amount of Based on the amount of horizontal and vertical open­
growth restriction of the maxilla has also been re­ ing
ported recently. a) Schwarz (1956) suggests the optimal is a half of
the individuals maximum range.
Dentoalveolar effects b) Woodside (1977) states that mandible registered
The dentoalveolar effects of functional appliances in a position protruded 3.0mm distal to the most
include: protrusive position that the patient can achieve.
• inhibition of the downward and forward erup­
tion of the maxillary teeth; As a general rule the horizontal advancement is kept
■ retrod i nation of the upper incisors edge to edge or 2 mm less than the maximum pro­
■ proclination of the lower incisors trusion. Vertical opening is kept 5 mm posteriorly.
■ lower labial segment intrusion; and It is also advocated that in cases where the overjet
■ leveling of the curve of Spee and tipping of the is more than 10 mm, a stage-wise advancement is
occlusal plane. to be carried out.
 SECTION 9: DEVELOPING MALOCCLUSION AND ITS MANAGEMENT |

Fig. 9.37a Class H div. 1 malocclusion Fig. 9.37b Correction with activator therapy
with a retruded mandible

Fig. 9.37c Post-treatment photograph showing Fig. 9.37d Post-treatment photograph

molars in Class I relationship showing change in profile
 I TEXTBOOK OF PEDODONTICS

Duration of use Frankel functional regulator

In general, an overjet of 8mm may require 10-12 The functional regulator is the only true tissue-bome
months of wear. Though originally designed as a appliance; however, wirework does extend onto the
night wear appliance only, the time taken for cor­ occlusal surfaces of the maxillary canines and the
rection may be reduced if the patient compliance is first permanent molars. Much of the appliance is
good and the patient can wear for more than 14 located in the vestibule and the appliance is said to
hours a day. work by altering both mandibular posture and the
contour with the dentition. This appliance can be
Several modifications have been suggested for the used to enhance dental eruption as well as correct
activator, which can be used for a variety of situa­ anteroposterior and lateral arch discrepancies.
tions. Frankel advocates advancing the mandible 2 to 3
mm every 4 to 5 months, and notching the maxil­
Bionator lary teeth to aid retention.
Originally designed by Balters in 1964, these have
been termed ‘open activators’ in view of their re­ Horse shoe appliance
duced bulk. Three basic types of bionators have been The horse shoe appliance is used for the correction
used as per their indications. They are of class III molar relationship. Originally developed
• The standard appliance is used in cases of a de­ by Schwarz (1997), the appliance has the advan­
ficient mandible and is made up of an acrylic tages that it is easy to construct, and it does not
flange extending posteriorly. The palatal bar with allow for the eruption of teeth due to the presence
a loop [ to control tongue position] and the modi­ of acrylic resin over the upper and lower teeth.
fied labial bow[ with buccal extensions, that re­
duce the muscle forces] are used. With selective Head gear
trimming, desired eruption of the teeth can be In cases where a skeletal overgrowth is present in
achieved. the maxillary arch, extra-oral foVce may be required
■ The open bite appliance, which is used to in­ to restrict the growth of the maxilla. The most
hibit any abnormal posture or function of the commonly used appliance for this purpose is the
tongue. head gear appliance.
■ The reversed/class III appliance, which is used
to stimulate the growth of the under developed A significant factor for the success of the head gear
maxilla. The loop of the palatal bar is in the appliance is the determination of whether it is the
opposite direction and the trimming differs in maxillary overgrowth that is the problem [and if it
that some acrylic is left between the teeth. The is, how much] or if the mandible is lacking in growth
maximum benefit is obtained when the appli­ (and if it will catch up).
ance is worn day and night
The forces applied are through the teeth. These
Clark twin block forces have a horizontal and vertical component.
This type of appliance was introduced by Clark in Should these forces be improperly applied, as in
1988, and consists of upper and lower removable where there is an excess of the vertical component,
plates with acrylic hooks trimmed at an angle of 70 it may lead to molar extrusion. This may not only
degrees with a midline expansion screw in the up­ harm the molar but has the undesirable effect of
per plate to allow a simultaneous expansion. They impeding mandibular growth as well.
were originally designed for high angle cases and
are often constructed with an attachment inserted Anchorage for the appliance is derived from vari
into the upper block for high-pull headgear. ous regions [cervical, occipital, parietal regions].
 SECTION 9 : DEVELOPING MALOCCLUSION AND ITS MANAGEMENT |

As with all the removable appliances, the patient s

cooperation is of paramount importance.

Specifications for use

K duration of 12-16 hours a day is the minimum
requirement for an effect to occshb^Qisnerally a force
of 400 gms on either side is applied.

Pendulum Appliance
This appliance has also been termed as non-com­
pliance therapy for molar distalization. The pendu­
lum applicance is a hybrid that uses a larger Nance
acrylic button in the palate for anchorage along with
0.032 TMA springs that deliver a light continuous Fig. 9.38a Skeletal Class III malocclusion
force to upper first molar. This appliance produces intercepted using a chin cap
a broad swinging arc or pendulum of force from
midline of palate to the upper molars.

This is mostly used in the patient with Class 1 skel­

etal relationship and Class II dental malocclusion.

Chin cap (Fig. 9.38a, b, c)

It is used in cases of excessive grow th of the mandi­
ble. The use and efficacy of the chin cap is not ac­
cepted by all the clinicians, but can be considered a
valuable aid.

Two philosophies exist to its use. They are concerned

with the direction of force applied.
1. They are used such that the force is applied Fig. 9.38b Chin cap in frontal view
through the condyle. Though animal experi­
ments may have substantiated this, clinical find­
ings are disappointing. This could, in part, be
attributed to the basic difference in the mecha­
nism of growth of the maxilla and the mandi­
ble.
2. They are used with the forces directed below’ the
condyle. The effect is that the chin is rotated
downward and backward which is caused by the
rotation of the mandible. This type of an appli­
ance is ideal in cases with short vertical height.

The pre-orthodontic trainer

The starting (blue) trainer imparts only a light force
on the teeth, then after 6-8 months the firmer (pink) Fig. 9.38c Chin can in lateral view
 I TEXTBOOK OF PEDODONTICS

trainer, which imparts a much higher force on the upper arch and lower arch, and has the advan­
malaligned anterior teeth, is implemented. This is tages of easy construction, and prevents extru­
the principle behind the straight wire technique, sion and individual movements ofteeth as it cov­
starting with a light wire then progressing to a firmer ers the whole of upper and lower dentition.
wire as the teeth come into a better alignment.
Limitations and complications offunctional
When to treat? appliances
Several factors should be taken into consideration
They can be listed out as:
before deciding to go ahead with the appliance
therapy. ■ Discomfort, as both the upper and lower teeth
are joined together.
■ The best time to start the functional therapy is
in the late mixed dentition. Thus several func­ ■ It mainly depends on the patient’s compliance.
tional appliances- for example, the medium ■ It can be used only if a favourable horizontal
opening activator for an early reduction of a deep growth pattern is present in cases of Class II cor­
rection.
overbite as well as for sagittal correction can be
■ It has to be removed during mastication, par­
used in this period. Rather than a generaliza­
ticularly when strongest forces are applied.
tion, girls and boys, along with early maturers
■ It may interfere with speech
should be assessed individually.
■ Treatment is often increased - the two-stage treat­
• Advantage can be taken of the pubertal growth
ment may prolong treatment by upto 18 months.
spurt so that this active growth phase can be
■ Laboratory and technical resources are required
harnessed to optimize the amount of growth re­
for construction and adjustment
straining effect or growth enhancing effect.
■ High cost
■ In the maxilla, generally the growth needs to be
retarded and thus if the growth spurt is not over
Self-Assessment
even after appliance therapy, some amount of
growth may lead to a recurrence of the problem. 1. Define interceptivo orthodontics
In the mandible on the other hand the growth 2. What are the common procedures done in inter­
needs to be enhanced by taking the help of the ceptivo orthodontics?
growth spurt. However, as the growth spurt 3. What is serial extraction? Discuss in detail the
measured by a longitudinal monitoring of stat­ methods, indications, advantages and disadvan­
ure, cannot be predicted with any great clinical tages of serial extraction
accuracy, some authors have questioned the use 4. Write short notes on:
of this appliance. a. space regainer
b. management of developing cross bite
• Yang [1997] has suggested the use of a Horse­ c. Rationale for interceptivo orthodontics
shoe appliance for the treatment of Class III d. Mixed dentition analysis
malocclusion., originally suggested by Schwarz 5. What is non-compliance therapy for distalization
[1966]. It consists of 2 separate plates for the of molars?
 9.4 Commonly Occuring Oral Habits
in Children and their Management
I
Tandon S, Sajida B, Bhat M,

Oral habits maybe a part of normal development; a Buttersworth (1961): defined a habit as a frequent
symptom with a deep rooted psychological basis or or constant practice or acquired tendency, which has
may be the result of abnormal facial growth. A wide been fixed by frequent repetition.
array of oral habits has been a subject under discus­
sion for many years. Digit sucking, lip and nail bit­ Mathewson (1982): Oral habits are learned pat­
ing, bruxism, mouth breathing, tongue thrusting etc. terns of muscular contractions.
may be considered as some of the common habits
seen in children. These habits bring about harmful With our clinical experience we have defined a habit
unbalanced pressures to bear upon the immature, as a settled tendency in response to a specific cause
highly malleable alveolar ridges, the potential resulting from repeated learning.
changes in position of teeth, and occlusions, which
may become decidedly abnormal if these habits are Classification
continued for a long time. The data on the etiology, We have attempted to classify the commonly ob­
age of onset, self-correction and treatment served oral habits in our practice based on their
modalities for the various habits differ greatly. Hence causative factors (Refer flow chart 9.1).
for a successful management of the habit, an un­
derstanding of the dental implications and mani­ Development of habit
festations of the habit should be pursued. One of The newborn develops some instincts, which are
the most valuable sendees that can be rendered as composed of elementary reflexes. An instinct is one
part of the interceptive orthodontic procedures is where the pattern and order are inherited, while in
elimination of the abnormal habits before they can a habit the pattern and order are acquired if con­
cause any damage to the developing dentition. Since stantly repeated during the lifetime of an individual.
the pedodontist is at an advantage in that he can At the beginning the infant makes an effort by fre­
see the child during the period that the habit is de­ quent learning and practice, later on the muscles
veloping, he gets the opportunity to examine the start responding more readily. At the outset it takes
child before the detrimental effect of the habit mani­ a long time for the impulses to pass along the affer­
fests itself as derangement in occlusion and unfa­ ent nerves to the brain and back along the efferent
vourable esthetics. nerves to the muscles involved. It has been stated
that unconscious mental pattern of childhood
Definitions develops from five sources namely instinct, insuffi­
cient or in correct outlet to energy, pain or
Dorland (1957): habit can be defined as a fixed or discomfort, abnormal physical size of parts, imitation
constant practice established by frequent repetition. of or imposition of others.
 СЕЭ I TEXTBOOK OF PEDODONTICS

Flow chart 9.1 Oral habits can be classified as:

Obsessive Non-obsessive
(deep rooted) (easily learned and dropped)

;
Intentional Masochistic Unintentional Functional Habits
or or or e.g. Mouth breathing,
Meaningful, Self-inflicting Empty, e.g. Tongue thrusting,
e.g. Nail biting, injurious habit Abnormal pillowing, Bruxism
Digit sucking, e.g. Gingival Chin propping
Lip biting. stripping

Author James (1923) Kingsley (1958) Morris and Klein (1971) Finn (1987)
Bohanna
(1969)

Classifi­ a. Useful habits a. Functional oral a. Pressure a. Empty habits I. a. Compulsive

cation b. Harmful habits. habits non­ b. Meaningful habits
habits b. Muscular habits pressure habits b. Non-compu-
c. Combined ones habits Isive habits
b. Biting JI.a. Primary
habits habits
b. Secondary
' habits

THUMB SUCKING _ Classification

Based on our clinical observation, thumb sucking
Thumb sucking is a habit of concern to specialists can be classified:
in various fields, such-as psychiatrists, psycholo­
gists, pediatricians, pediatric dentists, orthodontists, 1. Normal Thumb Sucking
speech therapists and plastic surgeons. Despite ex­ The thumb sucking habit is considered normal
tensive research considerable controversy still ex­ during the first and second year of life. Such a
ists regarding sucking habits. habit is usually seen to disappear as the child
matures. The habit at this age does not generate
Thumb sucking and finger sucking can more gen­ any malocclusion.
erally be termed as digit sucking. A broader cat­
egory of sucking habits includes any form of 2. Abnormal Thumb Sucking
nonnutritive sucking that involves pacifiers, hair, etc. When thumb-sucking habit persists beyond the
preschool period then it could be considered as
Definition an abnormal habit. If the habit is not controlled
Thumb sucking can be defined as placement of the . or treated during this stage, it may cause delete­
thumb into various depths into the mouth (Fig. rious effects to the dentofacial structures.
9.39a, b)
 SECTION 9 : DEVELOPING MALOCCLUSION AND ITS MANAGEMENT | Cffi)

Fig. 9.39a Finger sucking Fig. 9.39b Thumb sucking

This can again be divided into: Type B: This type is seen in almost 13-24% of the
a. Psychological children wherein the thumb is placed into the oral
The habit may have a deep-rooted emotional cavity7 without touching the vault of the palate, while
factor involved and may be associated with at the same time maxillary and mandibular anteriors
insecurities, neglect or loneliness experienced contact is maintained.
by the child.
Type C: This type is seen in almost 18% of the chil­
b. Habitual dren where in the thumb is placed into the mouth
The habit does not have a psychological bear­ just beyond the first joint and contacts the hard pal­
ing, however the child performs the act out of ate and only the maxillary incisors, but there is no
habit. The habit is a cause for concern due to contact with the mandibular incisors.
its potential to cause malocclusion.
Type D: This type is seen in almost 6% of the chil­
Sucking habits can also be classified as: dren wherein very little portion of the thumb is
a. Nutritive sucking habits placed into the mouth.
eg. Breast feeding, bottle feeding
b. Non-nutritive sucking habits (NNS habits) Johnson (1993): Classified NNS habits based on
eg. Thumb or fmger sucking, pacifier sucking factors that influence the severity of the habit (Ta­
[O’ Brien, 1996] ble 9.8).

Subtelny (1973) : has graded thumb sucking into 4

The Sucking Reflex
types:
The process of sucking is a reflex occurring in the
Type A: This type is seen in almost 50% of the chil­ oral stage of development and is seen even at 29
dren, where in whole digit is placed inside the mouth weeks of i.u., and may disappear during normal
with the pad of the thumb pressing over the palate, growth between the ages of 1 and 3 1/2 years. It is
while at the same time maxillary and mandibular the first co-ordinated muscular activity of ^■ in­
anteriors contact is present. fant. It is important for meeting both psyc cal
 CEß) I TEXTBOOK OF PEDODONTICS

Table 9.8: Classification of NNS habits.

Level Description

Level 1 (+/-) Boys or Girls of any chronological age with a habit that occurs during sleep.

Level ll(+/-) Boys below age 8 with a habit that occurs at one setting during waking hours.

Level lll(+/-) Boys under age 8 years with a habit that occurs at multiple settings during
waking hours.
Level IV(+/-) Girls below age 8 or a boy over 8 years with a habit that occurs at one setting
during waking hours.

Level V (+/-) Girls under age 8 years or a boy over age 8 years with a habit that occurs
across multiple settings during waking hours.

Level VI (+/-) Girls over age 8 years with a habit during waking hours.

(+/-) designates willingness of the parents to participate in treatment.

and nutritive needs during feeding and apart from pleasurable erotic stimulation of the lips and
seeking nutritional satisfaction they also experience mouth. One of the concepts of thumb sucking
pleasurable stimuli from lips, tongue and oral mu­ brought about by this theory is that humans pos­
cosa and learn to associate these with enjoyable sen­ ses a biologic sucking drive. An infant associ­
sations such as fondling, closeness of a parent. Ba­ ates sucking with pleasurable feelings such as
bies who are restricted from sucking due to a dis­ hunger, satiety and being held. These events will
ease or other factors become restless and irritable. be replaced in later life by transferring the suck­
This deprivation may motivate the infant to suck ing action to the most suitable object available,
the thumb or finger for additional gratification. namely the thumb or fingers. *

Finger and tongue thrusting habits are normal for ■ The learning theory: Davidson (1967)
the first year and half of life and will disappear spon­ This theory advocates that non-nutritive suck­
taneously by the second year with proper attention ing stems from an adaptive response. The infant
to nursing. If it continues beyond 3 years, associates sucking with such pleasurable feel­
malocclusion will result. ings as hunger. These events are recalled by suck­
ing the suitable objects available mainly thumb
Influence of different variables on incidence and or finger.
prevalence of thumb sucking habit is given in
Table 9,9 ■ Oral drive theory: Sears and Wise (1982)
They suggested that the strength of the oral drive
Theories
is in part a function of how long a child contin­
Various theories have been proposed by psycholo­
ues to feed by sucking. Thus, thumb sucking is
gists to explain noil-nutritive digital sucking
the result of prolongation of nursing;' and not
■ Classical Freudian theory (1905) the frustration of weaning. This theory agrees
The psychoanalytical theory holds that this origi­ with Freud’s theory that sucking increases the
nal response arises from an inherent psycho- erotogenesis of the mouth.
sexual drive suggesting that digit sucking is a
 SECTION 9 : DEVELOPING MALOCCLUSION AND ITS MANAGEMENT I ¿jklB

Table 9.9: Influence of different variables on incidence and prevalence of thumb sucking habit

Variables Relationsh ips Study

Age No evidence of thumb sucking in neonates. Levin and Kaye 1964

2- 5 years - 17.3%
upto 7 years - 45% Singhal and Bhatia 1988
Garathini et al 1990

Relatively low incidence in preschool children. Traisman and Traisman,

Robert, Brazelton
1956-1958

Even distribution in school going children except in Backlund 1963

six years or older children who were engaged in
slight sucking habit.

Gender No correlation in gender in neonates. Levin and Kaye 1964

In infants and children no significant difference Traisman and Traisman

between boys and girls. 1958

Even distribution among boys and girls in school Backlund 1963

going children

Race Significantly low incidence found in Negroid races. Brenchley 1992

Pacifier Related to low incidence of thumb sucking at 5 years Ravn 1976

Feeding Increase incidence in a low duration breast feeding Levy 1928

methods Longer feeding leads to habit
Significant relationship between duration and Robert 1944
intensity of thumb sucking and amount of time Yarrow 1954
spent in feeding sessions

Siblings No correlation between level of the habit and number Larsson et al. 1971
of siblings with the habit.

Parental High incidence among children of professionals Popovich and Thompson 1973
status

No incidence of thumb sucking Dahlborg, Qwen and

Moghall 1969.
 CE9 I TEXTBOOK OF PEDÔDONTICS

Non-nutritive

Frustration

Fig. 9.40 Etiology of different sucking habits

■ Johnson and Larson (1993) nomic status are blessed with ample sources of
They believed that it is a combination of psy­ nourishment. The mother is in a better position
choanalytic and learning theories which explains to feed the baby and within a short time the ba­
that all children posses an inherent biologic drive by's hunger is satisfied. Mothers belonging to
for sucking. The rooting and placing reflexes are the low socio-economic group is unable to pro­
merely a means of expression of this drive. En­ vide the infant with sufficient breast milk. Hence,
vironmental factors also may contribute to this in the process the infant suckles intensively for
sucking drive to nonnutritive sources such as a long time to get the required nourishment,
thumb or fingers. (Fig. 9.40) thereby also exhausting the sucking urge. The
development of a sucking habit is said to be as a
Maintenance of the habit way of rechanneling the surplus sucking urge.
Most children would cease digit sucking early in This theory explains the increase in incidence
their developmental process by the age of three to of thumb sucking in industrialised areas when
four years. But an acute increase in the child's level compared to rural areas. The African children
of stress or anxiety due to some underlying needed to suck intensively for a long time to get
psychologic or emotional disturbances can account sufficient nourishment. Thus they exhausted the
for continuation of a digit sucking habit, with con­ whole of their sucking urge.
version of ah empty habit into a meaningful stress
■ Working mother
réduction response. Therefore, direct therapy has
The sucking habit is commonly observed to be
been linked to unfavourable results, such as symp­
present in children with working parents. Such
tom substitution. This makes it very clear that be­
children brought up in the hands of a caretaker
fore initiating treatment try to grasp the possible
may have feelings of insecurity. Therefore, they
psychologic disturbances, whereas with a learned
use their thumb to obtain a secure feeling.
habit it follows that direct and aggressive treatment
of the habit would not place the patient at risk for ■ Number of siblings
symptom substitution. The development of the habit can be indirectly
related to the number of siblings. As the number
Causative factors increases the attention meted out by the parents
to the child gets divided. A child neglected by
« Parent’s occupation
the parents may attempt to compensate his feel-
This can be related to the socioeconomic status
ings of insecurity by means of this
of the family. Families living in high socioeco­
habit.
 SECTION 9 : DEVELOPING MALOCCLUSION AND ITS MANAGEMENT I

Order of birth of the child difficult to break it until the child is 4-5 years.
It has been noticed that the later the sibling rank Thus it was suggested that the habit should be
of a child, the greater the chance of having an viewed by the clinician as a behavioural pattern
oral habit. It has been speculated that to some of multivariate nature. Thumb sucking may be­
extent siblings imitate one another in sucking gin for one reason and be sustained by other fac­
tors at different ages.
Social adjustment and stress
Digit sucking has also been proposed as an Diagnosis of digital habits
emotion based behaviour related to difficulty with
social adjustment or with stress. Although suck­ ■ History
ing for psychological satisfaction as well as for Determine the psychological component in­
food is considered normal in infancy, digit suck­ volved
ing in older children has been told to be associ­ Question regarding the frequency, intensity
ated with abnormal psychological development. and duration of the habit
The psychological effects may be compounded Enquire the feeding patterns, parental care of
by the emotional impact of peer pressure and the child.
punitive and scolding parents. The presence of other habits should be evalu­
ated.
Feeding practices The diagnosis of a digit habit can also be obvi­
Various controversies exist in this regard as to ous when the child is actively performing the
the influence of feeding modes to the develop­ habit. However, during a dental appointment a
ment of the habit. Thumb sucking is seen to be child may seldom indulge in his habit.
more frequent among breast-fed children. Yet
abrupt wdaning from the bottle or breast has also ■ Extraoral examination
been hypothesized to contribute to acquiring an Various key areas to be noted include the fol­
oral habit A negative relation is also seen be­ lowing:
tween breast-feeding and the development of
dummy or finger sucking. The digits (Fig. 9.41)
Digits that are involved in the habit will ap­
Age °f child pear reddened, exceptionally clean, chapped
The time of appearance of digit sucking habit has
significance.
In the neonate’. Insecurities are related to
primitive demands as hunger.
During the firstfew weeks of life’. Related to
feeding problems.
During the eruption of the primary molar. It
may be used as a teething device.
Still later. Children use the habit for the re­
leases of emotional tensions with which they
are unable to cope, taking refuge in regress­
ing to an infantile behaviour pattern.
In spite of contrasting views regarding the
etiology there is some agreement that if the habit Fig. 9.41 Callus formation on the thumb as a
result of thumb sucking
continues beyond the age of 6-7 months it is
 | TEXTBOOK OF PEDODONTICS

and with a short fingernail i.e. a clean dishpan ■ Intra oral examination
thumb. Fibrous roughened callus may be Tongue
present on the superior aspect of the finger Examine the oral cavity for correct size and
The habit is also known to cause deformation position of the tongue at rest, tongue action
of the finger. duringswallowing.

Dento alveolar structures

Lips
Individuals with severe finger or thumb suck­
Upper lip may be short and hypotonic. Note
ing habits, where the digit applied an ante­
the position of lips at rest whether they are
rior superior vector to the upper dentition and
held together or apart. The position of the lips
palate, will have flared and proclined maxil­
during swallowing should also be observed.
lary anteriors with diastemas and retroclined
Chronic thumb suckers are frequently char­
mandibular anteriors (Fig. 9.42).
acterized by a short, hypotonic upper lip. Rela­
tive tensions of the upper and lower lips also
plays a role during swallowing. Upper lip
passive or incompetent during swallowing.
Lower lip is hyperactive and this leads to a
further increase in the proclination of upper
anteriors due to its thrust on these teeth.

Facial form analysis

Check for mandibular retrusion, maxillary
protrusion, high mandibular plane angle, and
profile.

When swallowing, the patient is observed for

presence of a facial grimace or an excessive
Fig. 9.42 Forces acting on teeth while thumb
mentalis muscle contraction, a normal place­ sucking
ment of the tongue against the teeth and pal­
ate and whether the pa ttern of speech of the Other intraoral symptoms will include a high
child is essentially normal. Facial profile is probability of buccal crossbite, particularly in
either straight or convex. those children who suck their digits with a
pronounced constriction of their buccal mus­
Other features culature and a tendency to narrow palates.
Features caused due to the presence of other
Observe the symmetry of incisal position of
habits along with thumb sucking. Associated
upper central and lateral incisors. Asymmetry
symptoms that should be watched for during
indicates that the child sucks the right or left
the initial examination are habitual mouth
thumb or finger by preference. Measure di­
breathing and tongue thrust swallow, particu­
mensions of over-jet and open bite if present.
larly in children with anterior openbite. Ac­
tive thumb suckers also have a higher inci­ Gingiva
dence of middle ear infections and frequently Look for evidence of mouth breathing;
have enlarged tonsils accompanied by mouth gumline etching, decayed or excessive stain­
breathing. Features of secondaiy habits have ing on the labial surface of the upper central
to be noted. and lateral incisors.
 SECTION 9 : DEVELOPING MALOCCLUSION AND ITS MANAGEMENT I <№>

Clinical Findings ■ Constriction ofmaxillary arch

A digit sucking habit can present without ill effects. This may be because of the failure of the maxil­
However various malocclusions can occur in the pri­ lary arch to develop in width due to an altera­
mary and permanent dentitions. tion in the balance between cheek and tongue
pressures. If the thumb is placed between the
The type of malocclusion produced by digit suck­ teeth, the tongue must be lowered, which de­
ing is dependent on a number of variables (Nanda creases pressure by the tongue against the lin­
1989) gual surfaces of the upper posterior teeth. At the
1. Position of the digit same time, cheek pressure against the teeth is
2. Associated orofacial muscle contractions increased as the buccinator muscle contracts dur­
3. Mandibular position during sucking ing sucking. Cheek pressures are greatest at the
4. Facial skeletal pattern corners of the mouth and this probably explains
5. Intensity, frequency and duration of force ap­ why the maxillary arch tends to become 4V’ -
plied. shaped with more constriction across the canines
than the molars.
Commonly observed clinical problems
■ Posterior cross bite
■ Maxillary anterior proclination and mandibu­ This occurs as a consequence of constriction of
lar retroclination the maxillary arch. The unbalanced muscle
When a child places a thumb or finger between forces on the maxilla exerted by the cheek mus­
the teeth, it is usually placed at an angle so that cles are unmet by the pressure from the lingual
it presses lingually against the lower incisors and musculature which are normally present. While
labially against the upper incisors. This direct this results in a maxillary constriction, there is
pressure is responsible for the displacement of no restriction to the mandibular growth eventu­
the incisors. There can be variation depending ally leading to a cross bite.
on which teeth are affected, how much, which
teeth are contacted, and the number of hours per Dentofacial changes associated with prolonged
day of sucking and the magnitude of pressure. nutritive sucking habits are given in Table 9.10
Intermittent vigorous sucking does not cause as
much malocclusion as that seen in a habit of 6 Prevention
hours or more, especially as seen in children who
sleep with the thumb or finger between the teeth ■ Motive based Approach
all night long. The etiology of thumb sucking focusses on a pre­
dominant psychological background. It’s preven­
■ The anterior open bite tion should be directed towards the motive be­
This type of malocclusion arises due to a combi­ hind the habit Histoiy serves as an important
nation of factors tool for diagnosing the etiology, whether the
1. Interference with normal eruption of incisors habit is meaningful or empty
due to an interposed thumb.
2. Excessive eruption of posterior teeth due to ■ Child’s engagement invarious activities * |
separation of the jaws, which alters the verti­ Parents when questioned may reveal that the
cal equilibrium on the posterior teeth, 1mm child practices the habit when bored and left to
of elongation posteriorly opens the bite by himself or it could be just before he goes to ^fjp<
about 2mm anteriorly In such cases, the parents can be c<
keeping the child engaged in various :,'S
■ '■ S-
СЕЭ I TEXTBOOK OF PEDODONTICS

Table 9.10: Dentofacial changes associated with prolonged nutritive sucking habits
Effects on the maxilla Increased proclination of the maxillary incisors
Increased maxillary arch length
Increased anterior placement of apical base of the maxilla
Increased SNA
Increased clinical crown length of the maxillary incisors
Increased counterclockwise rotation of the occlusal plane
Decreased SN to ANS-PNS angle
Decreased palatal arch width
Increased atypical root resorption in primary central incisors
Increased trauma to maxillary central incisors
Effects on the mandible Increased proclination of mandibular incisors
increased mandibular intermolar distance
Increased distal position of B point.
Effects on the interarch Decreased maxillary and mandibular Incisal angle
relationship Increased overjet
Decreased overbite
Increased posterior cross-bite
Increased unilateral and bilateral Class II occlusion
Effects on lip placement Increased lip incompetence
and function Increased lower-lip function under the maxillary incisors
Effects on tongue Increased tongue thrust
placements and function Increased lip to tongue resting position
Increased lower tongue position
Other effects Risk to psychologic health K
Increased risk of poisoning
Increased deformation of digits
Increased risk of speech defects, especially lisping *
(Johnson and Larson 1993)

This gives little chance for the child to practice

the habit. The child can be encouraged to follow ■ Duration of breast feeding
his hobbies of interest such as painting or en­ Care should be taken w7hen feeding infants in
gaging in outdoor activities with his fellow that the duration of feeding should be adequate
mates. These measures can be followed when the so as to enable the child to exhaust his sucking
parents are working. urge and feel completelly satisfied.

Parent’s involvement in prevention « Mothers presence and attention during bottle

When the parents are at home they should be feeding
advised to spend ample time with the child so as Bottle-fed babies should be held by the mother
to put away his feeling of insecurity. At night and enough attention should be given in the proc­
this can again be reinforced by playing soothing ess. This will promote a close emotional union
music or by telling good bedtime stories till the between the mother and the baby similar to that
child falls asleep. seen in breast-feeding.
 SECTION 9: DEVELOPING MALOCCLUSION AND ITS MANAGEMENT J

■ Use of a Physiological nipple digit sucking continues after 6 years or into

A physiological nipple should be used for bot­ mixed dentition, the malocclusion will not self-
tle-feeding and the size and number of the hole correct.
should be standardized to regulate a slow and
steady flow of the milk. ■ Motivation of the child to stop the habit
It is also important to assess the maturity of the
■ Use of a dummy or pacifier child in response to new situations and to ob­
Acquiring a digit sucking habit can be prevented serve the child’s reactions to any suggestion. The
by encouraging the baby to suck a dummy in­ treatment approach for the digit sucking habit
stead. If the child has already found his thumb should deal directly with the child. The first
or fingers, it will not be easy to introduce the ingredient needed to stop the habit is the child’s
dummy. Because not all babies start to suck their desire to stop.
thumbs, it is only necessaiy to offer a dummy to
a child whose behaviour indicates an urgent de­ ■ Parental concern regarding the habit
sire to suck a digit or dummy. Dummies are easier If the parent is unable to cope with the situation
to dispense with at an earlier age than is digit positively then both the parent and the child
sucking. should be dealt with during treatment. The par­
ents should become silent partners. It is impor­
Treatment considerations tant that the child should not be embarrassed or
criticized, rather help should be offered to deal
■ Psychological status of the child with this difficult liabit. Negative reinforcements
Diagnosis and management of any psychologi­ in the form of threats, nagging and ridicule
cal problem should be planned before treatment would only entrench the habit.
of any potential or present dental problem. The
frequency, duration and intensity of the oral liabit ■ Otherfactors
are important in evaluating the psychological Self-correction again depends on the severity of
status of the child. The events that precede the the malocclusion, anatomic variation in the
habit such as the use of a security blanket, the perioral soft tissue, and the presence of other oral
dependency on a favourite toy; problems with habits, such as tongue thrusting, mouth breath­
sleep, nightmares, nervousness and anxiousness ing and lip biting habits.
will yield information concerning the possible
psychological stimuli of the habit. If the oral Treatment
habit was associated with an emotional problem The treatment plan can be broadly divided into the
this would suggest the need for psychological following:
consultation.
1. Psychological therapy
» Age factor « Screen the patient for the underlying psycho­
If the child desists with the finger sucking habit logical disturbances that sustain a thumb suck­
within the first three years of life, the damage ing habit Once psychological dependence is
incurred such as open bite, is temporary provided suspected, the child is referred to profession­
the child’s occlusion is normal. No treatment is als for counselling.
provided in this age group. If a malocclusion is ■ Thumb sucking children between the ages of
caused by digit sucking and the habit is discon­ 4 and 8 years of age need only reassurance,
tinued between the age of 4 and 5 years, self­ positive reinforcement and friendly remind­
correction of the habit can be expected. When ers.
 I TEXTBOOK OF PEDODONTICS

« Awareness of the habit can be accomplished

by emphasizing the positive aspects of habit
cessation. Various aids are employed to bring
the habit under the notice of the child such as
study models, mirrors, etc.
« Children and parents are informed about ex­
isting dentofacial deformities and the long­
term risks of a sustained habit. Patients should
be presented with positive mental and visual
images of the dentofacial ideals expected from
habit cessation and subsequent orthodontic
treatment.
■ During the treatment adequate emotional sup­
port and concern should be provided to the
child by the parents.
Fig. 9.43a Thumb sucking habit
■ Destructive approaches in the form of nag­
ging, shamming and belittling ought to be
strictly avoided.
• Constant reassurance and encouragement
should be provided to the patient to gain his
confidence.
• The use of positive behaviour modification
techniques and even hypnosis has been effec­
tive in digit habit therapy. When the habit is
discontinued, the child can be rewarded with
a favourite new toy or special outing.
■ Dunlop’s beta hypothesis: He believed that if
a subject can be forced to concentrate on the
performa nce of the act at the time he practises Fig. 9.43b Thumb sucking habit corrected with
it, he can learn to stop performing the act. thumb cap
Forced purposeful repetition of a habit
eventually associates it with unpleasant reac­ Thermoplastic thumb post was devised by
tions and the habit is abandoned. The child Allen in 1991 where a thermoplastic mate­
should be asked to sit in front of a mirror and rial was placed on the offending digit. A total
asked to suck his thumb, observing himself of 6 weeks of treatment time was required for
as he indulges in the habit. elimination of habit.

2. Reminder therapy ■ Intraoral appproaches

This can be divided into the following: Various orthodontic appliances are employed
• Extra oral approaches (Fig. 9.43a, b) to attenuate and eventually break the habit.
It employs hot tasting, bitter flavoured prepa­ Removable appliances used may be palatal
rations or distastefill agents that are applied crib, rakes, palatal arch, lingual spurs.
to finger or thumbs. For example, Cayenne Hawley’s retainer with and without spurs.
pepper, quinine, asafoetida. This is effective Fixed appliances such as upper lingual tongue
only when the habit is not firmly entrenched. screens appear to be more effective in break-
 SECTION 9 : DEVELOPING MALOCCLUSION AND ITS MANAGEMENT | gRIjl

ing these habits. If the child has made appre-. The lower jaw of the infant is usually behind the
ciable changes in his habit by 3 months, the upper jaw. Vertically a space is present between the
appliances can be safely removed for a test­ gum pads. During the infantile swallow the tongue
ing period. If gross signs of anxiety are is between the gumpads in close apposition with
aroused e.g. bed wetting, bad dreams, etc, the lips and its contraction plus those of the facial mus­
appliance should be removed. cles help to stabilize the mandible. The mandibular
elevators show a minimal activity.
3. Mechanotherapy
Fixed intra-oral anti thumb sucking appliance During the latter half of the first year of life, sev­
Most effective mechanical deterrent to thumb eral maturational events occur that alter the func­
sucking is an intraoral appliance attached to the tioning of the orofacial musculature. With the ar­
upper teeth by means of bands fitted to the pri­ rival of incisors the tongue assumes a refracted pos­
mary second molars or the first permanent mo­ ture and initiates the learning of mastication. As
lar. A lingual arch forms the base of the appli­ soon as bilateral posterior occlusion is established,
ance to which are added interlacing wires in the true chewing motions are seen to start and the learn­
anterior portion in the area of the anterior part ing of the mature swallow begins. Gradually the fifth
of the hard palate. It works by preventing the cranial muscles assume the role of mandibular
patient from putting the palmer surface of the stabilization during the swallow. The muscles of fa­
thumb in contact with the palatal gingiva, cia t expression begin to learn the delicate and
thereby robbing the pleasure of sucking. .complicated functions of speech and facial
expression.If the transition of infantile to mature
Blue grass appliance swallow does nottake place with the eruption ofteeth,
Haskell (1991) introduced this appliance, for then it leads to what is known as the tongue thrust
children with a continued thumb sucking habit, swallow.
which is affecting the mixed or permanent den­
tition. It consists of a modified six sided roller Definitions
machined from Teflon to permit purchase of the
■ Brauer - 1965 A tongue thrust was said to be
tongue. This is slipped over a 0.045 stainless
present if the tongue was observed thrusting be­
steel wire soldered to molar orthodontic bands.
tween, and the teeth did not close in centric oc­
This appliance is placed for 3-6 months. Instruc­
clusion during deglutition.
tions are given to turn the roller instead of suck­
ing the digit. Digit sucking is often seen to stop
■ Tulley 1969 - States tongue thrust as the for­
immediately.
ward movement of the tongue tip between the
teeth to meet the tower lip during deglutition
Quad helix
and in sounds of speech, so that the tongue be­
This appliance prevents the thumb from being
comes interdental
inserted and also corrects the malocclusion by
expanding the arch. Barber 1975 - Tongue thrust is an oral habit .S
pattern related to the persistence of an infantile |
TONGUE THRUSTING swallow pattern daring childhood and adoles- |
cence and thereby produces an open bite and pro- |
In embryonic life, the developing tongue is consid­ trusion of the anterior tooth segments. |
ered disproportionately large in comparison to the
developing mandible and it fills the embryonic na­ Schneider 1982 - Tongue thrust;
sal cavity. placement of the tongue between
 I TEXTBOOK OF PEDODONTICS

teeth and against the lower lip during swallow-- Functional adaptability to transient change in
¿ng. anatomy j
The tongue can protrude when the incisors are j
Classification missing. Following the loss of deciduous teeth j
and prior to full eruption of the permanent inci- J
1. Physiologic
sors, there exists a natural opening for the |
This comprises of the normal tongue thrust swal­
tongue. The tip of the tongue may protrude into I
low of infancy.
the open area during swallowing. It has been |
2. Habitual
observed that this protrusive activity will change |
The tongue thrust swallow is present as a habit
with the full eruption of the permanent incisors. |
even after the correction of the malocclusion.
3. Functional
Feeding practices and tongue th rusting j
When the tongue thrust mechanism is an adap­
The development of improper swallowing hab­
tive behaviour developed to achieve an oral seal,
its has been attributed to bottle-feeding. How- J
it can be grouped as functional.
ever there is a controversy as to whether bottle- J
4. Anatomic
feeding is more contributory than breast-feed- i
Persons having enlarged tongue can have an an­
ing to tongue thrust development. The consist­
terior tongue posture.
ency of the infant’s diet may also be a factor in
the development of an adult swallow pattern.
Etiology
i
The cause of tongue thrust remains controversial. Induced due to other oral habits !
Several theories have been proposed based on clini­ During these stages of development, thumb and
cal observation and existing research result. finger sucking habits may still be prevalent in
many children. When this habit has created a
■ Retained infantile swallow malocclusion such as an anterior open bite, the '
There is a considerableamountof evidence which tongue is seen to protrude between the anterior
suggests that tongue thrust is merely a retention teeth during swallowing. With correction of the
of the infantile suckling mechanism. With the habit and with normalisation in occlusion, a
eruption of the incisors at six months of age, the change in the protrusive tongue activity can take
tongue does not drop back as it should and place.
continues to thrust forward. Tongue posture dur­
ing rest is also forward. Hereditary
The type of maxillary structure that favours the
« Upper respiratory tract infections
development of tongue thrust may be heredita ry
Upper respiratory tract infections such as mouth
For example, inherited hyperactivity of orbicu­
breathing, chronic tonsillitis, allergies, etc. pro­
laris oris with specific anatomic configuration
mote a more forward tongue posture due to pain
and neuromuscular activity.
and decrease in the amount of space which brings
about a tongue thrust swallow. It may also be
Tongue size
present due to the physiological need to main­
Tongue size as well as tongue function is an im­
tain an adequate airway.
portant consideration. Conditions such as con­
■ Neurological disturbances genital aglossia and macroglossia can have an
Hyposensitive palate, moderate motor disability, effect on the dentition.
disruption of sensory control and coordination
of swallowing can lead to tongue thrust.
 SECTION 9 : DEVELOPING MALOCCLUSION AND ITS MANAGEMENT | CEÔ

Clinical Manifestations rior open bite present and also because of the
longer period of time required for the tongue tip
Clinical manifestations noted in patients with tongue to move from rest to second stage of swallowing
thrust swallow will depend on variables such as the in the tongue group.
intensity, duration, frequency and type of tongue
thrust. ■ Malocclusion
Various malocclusions have been reported to be
Extra caused due to tongue thrust. These can further
be subdivided as
« Lip posture a. Features pertaining to the maxilla
Tlpsepâratïoh was greater in the tongue thrust rod ¿nation of maxillary anteriors result-
group and this was a consistent finding both at s ing in an increase in over-jet.
rest and in fonction. This observation may sug­ - Generalised spacing between the teeth.
gest some lack of compensatory lip activity dur­ Maxillary constrictiQn.— ^
ing swallowing in these subjects. b. Features pertaining to the mandible
- Retroclination or procl ¿nation of mandibu­
■ Mandibular nwyenients
lar teeth depending on the type of tongue
The mandibular movements during swallowing
thrust present.
in the tongue thrust group were more erratic,
c. Intermaxillary relationships
and no correlations could be found between the
- Anterior or posterior open bite based on
movements of the tongue tip arS of the mandi­
x^Tlie posture of the tongue.
ble itselfrin the tongue thrust group, the aver­
- - Posterior teeth crossbite.
age path of mandibular movement was upward
and backward with the tongue moving forward.
DIAGNOSIS
^Speech
Tongue thrust children are more likely to have ■ History
various speech disorders, such as sibilant distor­ History should include questions pertaining to
tions, lisping, problems in articulation of /s/, /n/, the relevant details.
/t/, Zd/, /1/, /th/, /z/, Zv/ sounds. - Determine the swallow pattern of siblings and
parents to check for hereditary etiologic fac­
■ Facialform tor.
Increase in anterior face height - Determine whether or not remedial speech
was ever provided
Intra oralfindings - Information regarding upper respiratory in­
fections, sucking habits and neuromuscular
■ Tongue mpvemerits
problems.
The swallowing sequences are seen to be jerky
- Finally past and present information regard­
and inconsistent in the tongue thrust group. The
ing the overall abilities, interests, and moti­
movements are also irregular from one swallow
vation of the patient should be noted.
to another within the individuals. The chin point
was found to be posterior in the tongue thrust
■ Examination
group as compared to the normal position.
The perverted swallowing habit should be de­
■ Tongue posture tected and corrected early to facilitate normal
The tongue tip at rest was lower in the tongue development of the palate and dentitions.
thrust group. This could be because of the ante­
CE0 I TEXTBOOK OF PEDODONTICS

- Study the posture of tile tongue while the man­ Complex tongue thrust: generalised open bite
dible is in postural position. This can be done with the absence of contraction of lip and mus­
if lips rest apart. Tongue posture can also be cle and teeth contact in occlusion
noted in the lateral cephalogram of the man­
dibular posture. Lateral tongue thrust: posterior open bite with -
tongue thrusting laterally s >
Observe the tongue during various swallowing
- Observe the role of the tongue during masti­
procedures, the unconscious swallow, the com­
cation and speech.
mand swallow of saliva, and the command swal­
- Intrinsic and extrinsic muscle action of the
low of water, unconscious swallow during chew­
tongue is to be checked.
ing. The complexity of the tongue thrust has to
- Presence of grimace during swallowing is as­
be observed carefully whether it is a simple
certained.
tongue thrust, lateral tongue thrust or a complex
- Function of the posterior pharyngeal wall, soft
tongue thrust. The following clinical features
palate is noted.
should be checked during swallowing: (Fig. 9.44)
Simple tongue thrust: Treatment considerations
normal tooth contact in posterior region
anterior open bite ■ Agf
contraction of the lips, mentalis muscle and Tongue thrust often self-corrects by 8 or 9 years
mandibular elevators of age by the time the permanent anterior teeth
completely erupt The self-correction occurs be­
cause of an improved muscular balance during
swallowing as the mature swallow is adopted.
However it is seen that orthodontic correction is
usually more successful if initiated during the
early mixed dentition stage of dental develop­
ment or between ages 9-11 years.

■ Presence/absence of associated manifestations

Treatmëhns^genëfâiry not recommended when
tongue thrust is present without malocclusion
Simple tongue thrusting or a speech problem.
■ Malocclusion
if the tongue thrust is present wit h malocclusipn
but no speech problem, orthodontic corrections
of the malocclusion will usually eliminate the
tongue thrust.
■ Speech defects
For tongue thrust and speech problem, speech
therapy during Jhe elementaiy school years is
indicated. Normal mandibular growth and a si­
multaneous diminishing in the size of the pha­
ryngeal lymphoid masses results in improved
speech because of less anterior displacement and
Complex tongue thrusting more space to accommodate the tongue during
Fig. 9.44 Trngue thrusting habit articulation.
 SECTION 9 : DEVELOPING MALOCCLUSION AND ITS MANAGEMENT | CJQ

If tongue thrust is present along with b. Using appliances as a guide in the correct
malocclusion and a speech problem, speech positioning of tongue
therapy and orthodontic treatment are needed. The correct method of swallowing should be
practised once or twice a day. Once the pa­
■ Associated with other habits tient is familiar with the new tongue position
Ifthe patient has both thumb sucking and tongue an appliance is given for training the correct
thrusting, the thumb sucking should be treated positioning of the tongue.
first.
Pre orthodontic trainerfor myofunctional
Treatment training (Fig. 9.45)
The treatment of tongue thrust can be divided into This appliance aids in the correct positioning of the
various steps: tongue with the help of tongue tags. The tongue
■ Training ofcorrect swallow and posture of the guards prevent longue thrusting when in place.
tongue
a. Myofunctional exercises
The patient can be guided regarding the cor­
rect posture of the tongue during swallowing
by various exercises:
1. The child is asked to place the tip of the
tongue in the rugae area for 5 minutes and
is asked to swallow.
2. Orthodontic elastic and sugarless fruit drop
exercise. These can be held by the tongue
tip against the palate on the rugae area dur­
ing practice.
3. 4S exercises. This includes identifying the Fig. 9.45 Pre orthodontie Vainer for
spot, salivating, squeezing the spot and myofunctional training
swallowing.
Nance palatal arch appliance
Use the pressure point oii the papilla to
In this the acrylic button can be used as a guide to
show where the spot is. The tip is against
place the tongue in the correct position.
this spot at rest position. The child then
■ Speech therapy
learns the 2S exercise; spot and squeeze.
The first step towards speech therapy should be
Spot should be the rest position for the tip
to train the correct positioning of the tongue. This
ofthetongue. ‘Squeeze’ is done by squeez­
tongue posture is more conducive to the articu­
ing the tongue vigorously against the spot
lation of speech and to the normal alignment of
with the teeth closed, followed by relaxing.
the teeth. However such therapy is not indicated
When the child has done the 2S exercise,
before the age of 8 years. The child is asked to
have him do the 4S exercise.
repeat simple multiplication tables of sixes and
Place the tongue on the spot, salivate,
to pronounce words beginning with ‘s’ sounds.
squeeze against the spot and swallow, ■ Mechano therapy
4. Other exercises. The child is asked to per Bothfixed and removable appliances can be fab­
form a series of exercises such as whistling, ricated to restrain anterior tongue movement dur­
reciting the count from sixty to sixty nine, ing swallowing with the objective of restraining
gargling, yawning, etc, to tone the respec­ the tongue to a more posterior superior position
tive muscles. in the oral cavity.
 444 | TEXTBOOK OF PEDODONTICS

Purpose of the tongue thrust appliance

The tongue thrust appliance tends to force the tongue
downward and backward during swallowing. The
spurs which are placed palatally are bent down so
that they form a sort of picket fence behind the lower
incisors during full occlusal contact of the posterior
teeth, a more effective barrier to tongue thrust is
attained.

The appliance also re-educates tongue position so

that the dorsum of the tongue approximates the pala­
tal vault and the tip of the tongue contacts the pala­
tal rugae during deglutition. As the tongue is forced
back within the confines of the dentition, it spreads Fig. 9.46a Tongue thrusting habit - Pre treatment
laterally, with the peripheral portion overlying the
occlusal surfaces of the posterior teeth. Interocclusal
clearance is maintained and in this manner,
overeruption and narrowing of the maxillary buccal
segments is prevented. The mature swallowing act is
stimulated by this type of appliance, as the tongue
adapts to the new position and function.

Removable appliance therapy

A variety of modifications of Hawley’s appliance can
be used to treat tongue thrust.

The advantages of this appliance system are

1. The anchorage value gained from the acrylic cov­
ering the entire palate and contacting the entire Fig. 9.46b Habit breaking appliance with
maxillary dentition at its lingual surface. tongue cribs
2. The capability of using the Hawley to close the
anterior openbite through the use of the labial
bow.
3. The crib can serve as a reminder.

The acrylic should be removed from the gingival

marginal area of the lingual surfaces of the maxillary
anteriors to allow the incisors to be moved lingually
when the labial wire is activated. The loops of the
tongue crib are removed one by one as the patient is
weaned from the habit appliance over a 6 month
period.

Fixed Habit breaking appliance (Fig. 9.46a, b, c)

Crowns and bands are given on the first permanent Fig. 9.46c Habit corrected - Post treatment
molar and a 0.040 inch stainless steel ‘U’ - shaped
 SECTION 9 : DEVELOPING MALOCCLUSION AND ITS MANAGEMENT I

lingual bar is adapted by starting on one side ex­ For the complex tongue thrust, swallow active
tending to the canine anteriorly at the level of the orthodontic treatment is recommended followed
gingival margin. The base wire is then adapted to by myofunctional therapy during the retention
follow the contour of the palate and carried phase.
posteriorly to contact the metal crown on the first
permanent molar. After the base baFis fabricated ■ Surgical treatment
the crib can be formed. Three or four 'V’ shaped The treatment of the retained infantile swallow
projections extending downward to a point just be­ behaviour is difficult and often consists of
hind the cingulum of the mandibular incisors are orthognathic surgical procedures to correct the
made with the arms of the crib soldered to the base. skeletal malformation as well as myofunctional
Depending on the severity of the open bite, 4-9 therapy. The prognosis is guarded and the re­
months may be required for the autonomous cor­ lapse may occur if the tongue does not adapt to
rection of the malocclusion. When a posterior open the new skeletal environment.
bite is present due to lateral tongue thrust, a modi­
fied habit crib to eliminate lateral tongue thrust, and In cases involving excessive increase in lym­
to allow tire normal eruption of the posterior teeth phoid tissue with resulting abnormality of tongue
is advocated. position, reduction of that lymphoid tissue is fol­
lowed by a spontaneous improvement in tongue
Oral screen position.
Another effective means of controlling abnormal
muscle habits like tongue thrusting and at the same MOUTH BREATHING
time utilizing the musculature to effect a correction
of the developing malocclusion, is the vestibular or For normal dentofacial growth to occur, there should
oral screen or a combination. be normal breathing. Increased resistance to the flow
of air through the nasal passages may be consid­
Tire oral screen is a modified acrylic plate. Either ered to be the primary cause of mouth breathing.
an acrylic or wire loop barrier may be constructed The habit may interfere with the development of
to prevent tongue thrusting. The combined oral and the chest, since niouth breathing is not as deep as
vestibular screen is fabricated to control muscle nasal breathing. This may inturn lead to postural
forces both inside and outside the dental arches. If defects when the muscles of the chest, the back and
constructed in the proper manner, the abnormal the neck do not function properly. This could alter
muscle forces can be intercepted and channeled into the equilibrium of pressures on the jaws and teeth
beneficial activity, reducing the development of and affect both jaw growth andtoothjposition. In
malocclusion. The vestibular and oral screen may order to breathe through the mouth, it is necessary
also be used along with fixed appliances. to lower the mandible and the tongue and extend
the head. If these postural changes are maintained,
■ Correction of malocclusion facial height would increase and posterior teeth
If the anterior tongue placement is tire result of would supraerupt, unless there was unusual verti­
adaptation to the previously existing anterior cal growth of the ramus, the mandible would rotate
open bite, the solution is a correction of the down and back, opening the bite anteriorly and in­
malocclusion. Upon resolution of the creasing the overjet. Increased pressure from the
malocclusion the tongue usually changes its stretched cheeks might cause a narrower maxillary
swallow pattern and adapts to the new tooth po­ dental arch.
sition.
 dS | TEXTBOOK OF PEDODONTICS

Definition 5. Abnormally short upper lip preventing proper

lip seal. j
Sassouni (1971): Defined mouth breathing as ha- 6. Obstruction in the bronchial tree or larynx.
bitual respiration through the mouth instead of the 7. Obstructive sleep apnoea syndrome.
nose. "7~8. Genetically predisposed individuals.
Ectomorphic children having a genetic type of *
Merle (1980) suggested the term oro-nasal breath­ tapering face and nasopharynx are prone for na- i
ing instead of mouth breathing. sal obstruction.
9. Thumb sucking or similar oral habits can be the
Classification instigating agent.

Finn (1987) has classified mouth breathing into: Clinical features

■ General effects
A. Anatomic
- Purification of the inspired air : The nasal air­
The anatomic mouth breather is the one whose
way filters heat and humidifies the air in prepa­
shortupper lip does^pot permit complete clo-
ration for entry into the bronchi and lungs.
sure without undue effort.
, _ . __ ---x . T ■- FL -----

EL Obstructive^ - Pulmonary development: The functional air­

Children who have an increased resistance to, way also creates a proper amount of nasal re­
or a complete obstruction of the normal flow of sistance so that the diaphragm and intercos­
air through the nasal passages. The child is tal muscles must perform work to create the
forced by sheer necessity to breathe through the negative pressure to promote airflow into the
mouth. lungs. With oral respiration the resistance is
lacking and poor pulmondiy compliance is
C. Habitual
seen. This gives the appearance of a pigeon
Habitual mouth breather in a child who continu­
chest. .
ally breathes through his mouth by force of habit,
although the abnormal obstruction has been re­
- Lubrication of the esophagus: Since the
moved.
esophagus contains no mucous glands, the
mucous from the nose and pharynx serves to
Etiology
lubricate the esophagus. In mouth breathers
the oral pharynx is dry and the mucous col­
Most of the children suffer from some degree of na­
lects often to be expectorated. This denies the
sal insufficiency.
esophagus essential lubrication and can pro­
duce a low grade esophagitis.
Allergies, physical obstructions and chronic infec­
tions cause many children to breathe through the
- Blood gas constituents: Blood gas studies re­
mouth.
veal that mouth breathers have 20 percent
*

more carbondioxide, and 20 percent less oxy­

This airway obstruction may be due to
gen in the blood.
1. Enlarged turbinates
2. Deviated septum and other naso-phaiyngeal de­ ■ Effects on dentó facial structures
formities. - Facial form: Patients who mouth breath due
3. Allergic rhinitis, nasal polyps to hypertrophied lymphoid tissue display a
4. Enlarged adenoids or tonsils.
 SECTION 9 : DEVELOPING MALOCCLUSION AND ITS MANAGEMENT | CS®

tendency towards a more vertical growthjpat- drome. On smiling, many of these patients re­
tern. Cephalometric analysis of such patients veal large amounts of gingiva producing the
reveal; ‘gummy smile’. Children who mouth breath
A largefaceheight, have a short thick incompetent upper lip and
-- - Increased mandibular_plane angle, a voluminous curled over hwer lip.
Retrognathic mandible and maxilla.
Allergic children tend to have an increased - External nares: Long standing nasal airway
anterior face height obstruction can lead to a disuse atrophy of the
lateral cartilage. The result is a slit like ex­
- Adenoid facies is a particular type of facial ternal nares with a narrow nose. Sometimes,
configuratiorT frequently associated with after the airway obstruction is removed and a
mouth breathing characterized byalong, nar- patent airway is established, the nose may
row face with an accompanying narrow nose collapse on inspiration, making reconstructive
and nasal passages, flaccid lips with the up­ surgery necessary. Nasal mucosa becomes at­
per lip being shortand-dolico facial skeletal rophied due to a disturbed ciliary action
patterns. Often the nose is tipped superiorly
in front so as an observer can look directly Gingiva : Mouth breathers frequently present
into the nares. The long face is often expres­ with problems like an inflamed and irritated
sion less. The buccal segments of the maxilla gingival tissue in the anterior maxillary arch.
are collapsed, leading to the‘ V’ - shaped and The gingiva is hyper plastic due to continu­
iughpalatalyauLt. ous exposure of the tissues to airdrying.
Chronic gingival condition is due to a de­
- Dental effects: The upper and lower incisors creased salivary flow to remove the debris and
are also retroclined, posterior cross bites^n'e bacterial over growth. The drying effect of
present andthere is a tendency towards an moving air can also lead to heavy deposits of
openbite. Narrow palatal and cranial widths the plaque. Gingiva exhibits a classic rolled
are also associated. This is due to the low set
position of the tongue in order to allow an These occur together with a periodontal dis­
adequate inflow of air through the mouth. ease, where there may be an interproximal
Thus an imbalance of forces exerted by the bone loss with the presence of deep pockets.
tongue and facial musculature on the maxilla
leads to a constricted maxillary arch. There - Other effects: Mouth breathing may lead to
may also be flaring of incisors and a decrease ^tidsGnalia 'Tlle activity of muscles differed
in the vertical overlap of the anterior teeth. in the nose breathers and mouth breathers.
Hie palatoglossus muscle is active in the case
- Speech defects: Abnormalities of the oral and of nose breathers, whereas the levator palatini
nasal structures can seriously compromise activity is lower when nose breathing was
speech performances. Nasal tone in voice is compared with mouth breathing. There is also
seen. a dull sense of smell and loss of taste.

- Lip: These patients frequently have a lip apart Diagnosis

posture, although the lip apart posture should
not be regarded as pathognomonic for nasal ■ History
obstruction. Excessive appearance of the max­ The parents can be questioned whether the child
illary anteriors is a sign of long face syn- adopts frequent lip apart postal.
 CEE) I TEXTBOOK OF PEDODONTICS

occurrence of tonsillitis and allergic rhinitis, oti­

tis media should also be queried.

« Examination
Study the patient’s breathing unobserved. Nasal
breathers usually have their lips touching lightly
during relaxed breathing whereas mouth breath­
ers must keep their lips apart. Ask the patient to
take a deep breath. Most respond by inspiring
through the mouth, although occasionally a na­
sal breather will inspire through the nose with
the lips tightly closed. A mouth breather when
asked to close his lips and take a forced deep
breath will not appreciably change the size and
shape of the external nares and occasionally con­
tracts the nasal orifices while inspiring. A nor­
mal nose breather will usually dilate the nostrils
Fig. 9.47 Clinical test for mouth breathing -
when breathing deeply. This is because nasal
water holding test
breathers normally demonstrate good reflex con­
trol of the alar muscles which control the size
and shape of the external nares. Even nasal It is important to distinguish under which category
breathers with a temporary nasal congestion will does the child with the habit belongs to; whether
demonstrate the reflex alar contraction and di­ habitual, obstructive or anatomic. It is again impor­
lation of the nares during voluntary inspiration. tant to distinguish a habitual mouth breather from
a child who breathes through his nose yet, because
« Clinical tests of a short upper lip, keeps his lips apart.
1. Mirror test &
2. Butterfly test
Treatment considerations
3. Water Holding test (Fig. 9.47)
■ Age of the child
(refer incipient malocclusion for description)
4. Inductive plethysmography As with any other habit, correction of mouth
(Rhinomanometry) breathing could be expected as the child matures.
The only reliable way to quantify the extent This can be attributed to the increase in nasal
of mouth breathing is to establish how much passages as the child grows, thereby relieving
of the total airflow goes through the nose and the obstruction caused due to the enlarged ad­
how much through the mouth using induc­ enoids. Mouth breathing is in many instances
tive plethysmography. This allows the per­ self-correcting after puberty.
centage of nasal or oral respiration to be cal­ ■ E.N. T examination
culated. A minority of the long face children An otorhinolaryngologist examination may be
had less than 40% nasal breathing. advised to determine whether conditions requir­
5. Cephalometries ing treatment are present in the tonsils, adenoids
To establish the amount of nasopharyngeal or nasal septum. In some children mouth breath­
space, size of adenoids and to know the skel­ ing may continue even after the correction of
etal patterns of the patient by taking various the pathologic conditions, in which case it may
cephalometric angles. be habitual.
 SECTION 9 : DEVELOPING MALOCCLUSION AND ITS MANAGEMENT I ¿'EUl

Correction should first aim at removing any inhalation through the nose with arms raised
anatomic or functional causes. To institute a treatment sideways. After a short period, the arms are
of the actual cause, it is important to determine the dropped to the sides and the air is exhaled
type and degree of mouth breathing, whether it is through the mouth.
habitual or obstructive, and whether total mouth
breathing is present or whether it is partial. « Lip exercises
Hypotonicity and flaccidity of the upper lip
Correction of mouth breathing are the most obvious characteristics. The child
Mouth breathing should be treated during the mixed is instructed to extend the upper lip as far as
dentition period to prevent or correct its ill effects possible to cover the vermilion border under
on occlusion. and behind the maxillary incisors. This
exercise should be done 15-30 minutes a day.
Symptomatic treatment for a period of 4-5 months when the child has
The gingiva of the mouth breathers should be re­ a short upper lip. If the maxillary incisors are
stored to normal health by coating the gingiva with protruded, the lower lip can be used to aug­
petroleum jelly, by applying preventive dentistry ment the upper lip exercise. The upper lip is
methods and by clinically correcting periodontal first extended into the previously described
defects that have occurred due to the habit. position. The vermilion border of the lower
lip is then placed against the outside of the
The treatment should be aimed at extended upper lip and pressed as hard as
possible against the upper lip. This type of
1. Elimination of the cause exercise exerts a strong retraction influence
If nasal or pharyngeal obstruction has been di­ on the maxillary incisors, which increases the
agnosed as the cause of mouth breathing, attempts tonicity of both the upper and lower lips.
should be made at treating the etiological factor
Playing a wind instrument actually may be
first Removal of nasal or pharyngeal obstruc­
an interceptive orthodontic procedure.
tion by surgery or local medication should be
sought. If a respiratory allergy is present this A celluloid strip or metal disk held between
should be brought under control. the lips not only necessitate them being closed,
A marked reduction in nasal airway resistance but also makes the child conscious of their
after a rapid maxillary expansion has been re­ opening if the object drops
ported to be achieved.
■ Maxillothorax myotherapy
2. Interception of the habit This was advocated by Macaray 1960. These
If the habit continues even after the removal of expanding exercises are used in conjunction
the obstruction then it should be corrected. with the Macaray activator. Macaray con­
Correction can be done by means of the follow­ structed an activator out of aluminum with
ing: which development of the dental arches and
Exercises dental base relationship could be corrected at
If there is no physiologic cause tire patient the same time as encouraging mouth breath­
should be instructed in breathing and lip ing.
exercises.
■ Physical exercises This stable aluminum activator is incorpo­
This is done in the morning and the night. rated at the angle of the mouth, with hori­
Deep breathing exercises are done with deep zontal hooks to which expanding rubber bands
CTfil | TEXTBOOK OF PEDODONTICS

are attached. The mouth breather holds the Construction of cast

activator in the mouth, and at the same time The cast is covered with a thin even layer of wax
with the left and right arms alternately car­ (24 gauge) to which a large sprue is attached, a
ries out 10 exercises 3 times a day. layer of plaster is then boxed and then poured
on the wax to form a mold. The wax is elimi­
He stands with his back against the wall, rises nated with boiling water. To cast, a level is
and lowers on his toes in time with the ex­ poured full of pure latex and is permitted to stand
pander exercises holding the lips tight together for 12 hours. Another two direct methods
and carries out a lightly forced breathing tech­ 1. Warming Plexiglas to molding stage and
nique in front of an open window. The adapting to the cast.
myotherapeutic exercise are indicated for 2. Painting pure latex over the cast surface
mouth breathers. They also help prevent a The latex is applied to an even thickness of 1/
relapse. The additional myotherapeutic ex­ 8 inch and cured for 10-20 minutes at 130-
pander exercises during bimaxillary treatment 140 F, and due to a shrinkage of a half of its
help to establish physiological nasal breath­ bulk a second coat is applied and cured giv­
ing, as well as correcting maldevelopment of ing a finished overall thickness of l/8inch.
the thorax.
3. Correction of malocclusion
■ Oral Screen Mechanical appliances
The most effective way to reestablish nasal 1. Children with class I skeletal and dental oc­
breathing is to prevent air from entering the clusion and anterior spacing- Oral shield ap­
oral cavity. To do this either the lips or the pliance.
oral cavity must be closed. For this purpose 2. Class II division I dentition without crowd­
an oral screen can be used. Oral screen should ing, age 5-9 years, Monobjoc activator to aid
be constructed with a material compatible with both in the correction of malocclusion and de­
the oral tissues. Reduction in the anterior open terrence of the habit. This appliance when
bite is obtained after treatment for 3-6 months. worn will not allow the air to be breathed
through the mouth.
An effective device during sleeping hours, is 3. Class III malocclusion interceptive methods
a thin rubber membrane either cut or cast to are recommended as a chin cap. The child
fit over the labial and buccal surfaces of the should be evaluated for a sufficient airway be­
teeth and gums included in the vestibule of fore treatment.
the mouth. During the initial phase, windows
are placed on the oral screen so as not to com­ BRUXISM
pletely block the airway passsage.
Definition
Construction of the membrane
1. Impression of the vestibule is taken with the Ramfjord 1966‘. Bruxism is the habitual grinding
teeth in occlusion. This should extend to the of teeth when the individual is not chewing or swal­
posterior limits and above and below the lowing.
mucobuccal-fold.
2. Adapt a 22-gauge rubber sheet over the plas­ Rubina 1986: Bruxism is the term used to indicate
ter cast, remove and trim it to size. nonfunctional contact of teeth which may include
clenching, gnashing, grinding and tapping of teeth.
 SECTION 9 : DEVELOPING MALOCCLUSION AND ITS MANAGEMENT | CSB

Vanderas 1995: Nonfunctional movement of the enon was found in children with cerebral palsy
mandible with or without an audible sound occur­ and mental retardation.
ring during the day or night.
2. Psychological Factors
Types A tendency to gnash and grind the teeth has been
seen to be associated with the feelings of anger
1. Day time bruxism/diurnal bruxism and aggression. Teeth grinding could be a mani­
Diurnal bruxism is the conscious or subconscious festation of the inability to express emotions such
grinding of teeth usually during the day. It can as anxiety, rage, hate, aggression, etc.
occur along with parafunctional habits such as
chewing pencils, nails, cheeks and lips. This type Olkinuora 1972 divided bruxers into 2 catego­
of bruxism is usually silent except in patients ries.
with an organic brain disease. 1. Those whose bruxism was associated with
stressful events
2. Night time bruxism/nocturnal bruxism 2. No such association.
Nocturnal bruxism is the subconscious grinding
of teeth characterized by rhythmic patterns of The non-stress related group had more of he­
masseter EMG activity. reditary influence

Occurrence 3. Occlusal discrepancies

Improper interdigitation of teeth may lead to
* Bruxism may commence in infancy with the bruxism Various occlusal abnormalities that pre­
eruption of the first primary tooth. Infants with vent a stable occlusion of the mandible may be
no teeth to oppose the newly erupted teeth have the cause. This was attributed to the alteration
been seen to lacerate the opposing gum pad. of definite afferent impulses, originating in the
Bruxism may occur throughout life; however, it 'periodontium. A correlation between a deep bite
is seen to increase through the mixed dentition and frontal dental wear has also been reported.
period and then decrease later with age.
4. Genetics
■ One common occurrence is during sleep. Brux- hr
ism can occur at any stage of sleep. However, it tant role in the etiology of bruxism The habit
has been seen to occur during the transition from was reported to be a manifestation of genetically
a deeper stage to a lighter stage of sleep. Brux­ determined behaviour related to the sharpening
ism is also reported to occur during the rapid of teeth for defense. Children of bruxing par­
eye movement stage. Bruxism occurring in this ents had an increased incidence of bruxism.
stage is reported to be the most damaging.
5. Systemic Factors
f The reported incidence of bruxism in children Mg+4- deficiency had been reported as an
varies widely from 7% to 88%. etiological cause for bruxism and had treated sev­
eral cases with therapeutic doses. G.L distur­
Etiology bances from food allergies, enzymatic imbal­
ances in digestion leading to chronic abdominal
1. CNS distress could also be a cause.
The etiology of bruxomania could be from cer­
tain definite cortical lesions. This CNS phenom-
 CE3 I TEXTBOOK OF PEDODONTICS

Various systematic factors, such as intestinal 2. Tooth structure

parasites subclinical nutritional deficiencies al­ Nonfunctional patterns of occlusal wear can be
lergies and endocrinal disorders have also been observed as signs of bruxism. Bruxism can lead
attributed. to an increased tooth sensitivity from an exces­
sive abrasion of the enamel. The enamel prisms
6. Allergies are fractured from high muscle forces generated
Allergies have also been related to nocturnal during sleep and later ground down by the jaw
bruxism. movements. The children who were teeth grind­
ers have atypical wear facets. These may appear
7. Occupational factors as shiny uneven occlusal wear with sharp edges.
Pulpal sensitivity to cold can also be observed.
An over enthusiastic student or compulsive
Sometimes, the pulp may be exposed to attrition
overachievers may also develop the habit. Com­
leading to a dental abscess. Fractures of the tooth
petition sports lead to clenching, and may be sig­
crown, restorations can also result in bruxism.
nificant.
3. Muscular tenderness
Manifestation 1. Tenderness of the jaw muscles, especially to
palpation. Tenderness of lateral pteiygoid a nd
The signs and symptoms of bruxism depend on masseter muscle was seen to be common.
1. Frequency of bruxing 2. Muscular fatigue on waking also seen. <
2. Intensity with which the patient is bruxing. 3. Hypertrophy of the masseter muscle unilater-
3. The age of the patient which may be associated ally/bilaterally.
with the duration of the habit.
4. TM.J. disorders \
The forces of bruxism are transmitted to the struc­ T.M.J. disturbances and pain are in many cases
tures of the masticatoiy apparatus, and depending the result of bruxism. Pain present in the joints
on the resistance of the individual structures, cer­ is usually dull and unilateral. Crepitation and
tain amount of the forces are absorbed and the rest clicking within the joint, restriction of mandibu­
are passed to other structures. lar movements and jaw deviations can be ob­
served. Deviation of the chin during mandibu­
The symptoms and clinical signs ofbruxism in chil­ lar movements occurred more frequently to the
dren are the same as those seen in adults. However, left. These may be in relation to the physiologi­
most of the subjective symptoms are occasional and cal functional asymmetry, eg. right handedness.
mild. The following clinical features may be seen
in children with bruxism. 5. Headache
A common occurrence for chronic headaches
have been reported. The headaches are often of
1. Occlusal Trauma
muscular contraction type, which suggests pain
Bruxism can result in tooth mobility, which may
in the muscle as the underlying cause.
be more in the mornings due to the bruxing ac­
tivities during the sleep period. Bruxism might
6. Other signs and symptoms
be an essential factor for the spread of gingivitis
Sounds-grinding and tapping sounds
into deeper periodontal structures and alveolar
Soft tissue trauma
bone loss. Small ulcerations or ridging on the buccal mu­
cosa opposite the molar teeth.
 SECTION 9 .DEVELOPING MALOCCLUSION AND ITS MANAGEMENT |

Treatment Behavioural modality is initiated by the dentist

through explanation and arousal ofthe patient’s
L Occlusal adjustments awareness of the habit.
This would result in immediate disappearance
of habitual grinding of teeth. Any prematurities 5. Relaxation training
or occlusal interferences in restorations should In this technique, the patient is instructed to tense
be corrected. In case of a patient with CNS dis­ the muscle group in consideration and relax
order, the restoration should be able to withstand thereby training the patient to relax the muscle
the forces ofbruxism. Coronoplasty plays an im­ group voluntarily. Hypnosis, conditioning, etc,
portant role in occlusal treatment However, ex­ are also indicated for subjects in whom bruxism
tensive occlusal adjustments are contraindicated. is due to a central cause.
Before any occlusal adjustments are done the
muscles should be brought back to a relaxed po­ 6. Physical therapy
sition to allow the jaw to resume its normal If musculoskeletal pain and stiffness are associ­
physiologic movements. ated witfi bruxism, a brief course of physical
therapy is appropriate
2. Occlusal splints
Vulcanite splints have been recommended to 7. Drugs
cover the occlusal surfaces ofall the teeth as treat­ Vapocoolants such as ethyl chloride for pain
ment for bruxism. A reduction in the increased within the TMJ area, local anesthetic injections
muscle tone is observed with its use. In the case directly into the TMJ or into the muscles,
of children the use of a soft splint is advisable. tranquilizers and sedatives and muscle relaxants
The splint is made on the mandibular models are used. Placebos maybe used to rule out psy­
using Scher Dental Bioplast material. Little ad­ chological etiology. Medications may be pre­
justment is required in children where scribed for a few days to alter the sleep arousal
intercalation is less. and anxiety level, eg. diazepam. Low doses of
tricyclic antidepressants inay be used to inhibit
The TMJ appliance
the amount of REM sleep.
It is a prefabricated intra oral appliance designed
mainly for the treatment of TMJ disorders. Hab­
8. Bio feedback
its such as bruxism are prevented by the pat­
Ibis is a technique that utilizes positive feed­
ented aerofoil shaped base and a double mouth
back to enable the patient to learn tension re­
guard design.
duction. It is accomplished by allowing the pa­
Restorative treatment tient to view an EMG monitor while the man­
K If the abrasion is so severe that penetration into dible is postured with a minimum of activity.
chamber is imminent, pulpal therapy
coverage stainless steel crowns is indi- 9. Electrical method
Electrogalvanic stimulation for muscle relaxa­
tion is currently being utilized for treatment of
^.Psycdiotherapy bruxism.
Counselling the patient can lead to a decrease in
tension and also create a habit awareness. This 10. Acupuncture techniques for muscle relaxation
may result in an increase in voluntaiy control are also under evaluation.
that can lead to reduced tooth parafunctions.
 I TEXTBOOK OF PEDODONTICS

11. Orthodontic correction habit develops when the child wants to produce
Malocclusions such as Class II and Class III oc­ a normal lip seal during swallowing by placing
clusions frontal open bite and crossbites when the lower lip posterior to the maxillary incisors.
associated with functional malocclusion may cre­
ate a predisposition to bruxism. 2. Habits »
The habit can occur in conjunction with other
LIP HABIT habits such as thumb or digit habit. The digit
habit may result in a large overbite and overjet
Normal lip anatomy and function are important for situation and again the child will attempt to cre­
speaking, eating and maintaining a balanced oc­ ate an oral seal by placing the mandibular lip
clusion. A lip sucking habit is a compensatory ac­ directly behind the maxillary incisors.
tivity that results from an excessive overjet and the
relative difficulty of closing the lips properly dur­ 3. Emotional stress
ing deglutition. This may increase the intensity and duration of
lip sucking. Children in stressful situations have
The lip habit may involve either of the lips, with a an increased salivary output, thus increasing the
higher predominance towards the lower lip. number of swallows and lip seals required. Oc­
casionally, the lip sucking habit becomes a com­
Definition pulsive and gratificational activity during sleep­
ing hours.
Habits that involve manipulation of the lips and
perioral structures are termed as lip habits. Manifestation

Classification ■ Protrusion of maxillary incisors and retrusion

of mandibular incisors (Fig. 9.48)
1. Wetting the lips with the tongue With either of these habits the action is to wedge
2. Pulling the lips into the mouth between the teeth. the lip between the upper and loWer incisors.
(Schneider1982)
An important variant of the lip sucking habit is
the mentalis habit The difference in lip sucking
and mentalis habit is that in lip sucking the en-
’ tire lip, including the vermilion, is pulled into
the mouth whereas in the mentalis habit the ver­
milion border, of the lower lip is often everted
with its lingual aspect elevated into the mouth.
Along with this lower lip eversion, a sublingual
contracture line develops between the lip and the
chin).

Etiology
Fig. 9.48 Up-biting habit
1. Malocclusion
A lip habit may occur in a Class II division 1, Thus, a muscular imbalance is created and if
deep bite malocclusion. In Angle’s Class II di­ practised with a sufficient intensity and frequency
vision 1 with a large overbite and over jet, this will cause the maxillary incisors to move
 SECTION 9 : DEVELOPING MALOCCLUSION AND ITS MANAGEMENT I

labially and upward with interdental spacing and

lower incisors to collapse lingually with crowd-

■
Lip sucking can be recognized by reddened irri­
tated and chapped area below the vermilion bor­
der. The vermilion border may be relocated far­
ther outside the mouth due to constant wetting
of the lips. This is most commonly seen, associ­
ated with the lower lip. The vermilion border
becomes redundant and hypertrophic at rest. In
some cases, a chronic herpes infection with ar­
eas of irritation and cracking of the lip appears.

■ The mentolabial sulcus becomes accentuated,

■ Malocclusion Fig. 9.49a Lip biting with proclination of

Lip sucking and lip biting can maintain an ex­ the upper anterior teeth
isting malocclusion.

Treatment

The lip habit is not self-correcting and may become

more deleterious with age, because of muscular
forces interacting with the child’s growth. Treatment
of a lip sucking habit should be directed initially to­
wards the etiology of the habit (Fig. 9.49a, b).

1. Correction of malocclusion
If there is a Class II division I malocclusion or
an excessive overjet problem, the abnormal lip
Fig. 9.49b Treatment with a oral screen
activity may be adaptive to the dento alveolar
I

morphology. In such cases, it is deemed wise to i

correct the malocclusion before going on to break 2. Treating theprimary habit

die habit The lip habit along with digit sucking can be
* Class I Malocclusion with increased overjet, corrected by aligning the dental arch using
fixed or removable appliance to tip the teeth Hawley retai ner with a labial bow, which can be
back used to retract the maxillary incisors and an
* Class II Growth modification procedures to acrylic plate can be used as a habit reminder.
treat the malocclusion. If the child has an
uncrowded early mixed dentition, an activa­ 3. Appliance therapy
tor may be placed in an attempt to reposition Oral shield is also a useful appliance in Class I
the maxilla to the mandible in a favourable malocclusion. It helps to stop the habit and also
position and allow the child to effect a more in incisal alignment The addition of a small loop
normal lip seal. to the labial oral shield improves the lip tonus
 | TEXTBOOK OF PEDODONTICS

by helping in lip exercises. Performed for 10 min­ NAIL BITING

utes -3 times a day.
Nail biting is one of the most common habits in
Lip bumper
children and adults. It is a sign of internal tension.
A lip bumper may be used as an adjunctive therapy
in both comprehensive and interceptive treatment
Age of occurrence
regimens. The lip bumper is positioncd in the ves­
Nail biting is absent before 3 years of age. The inci­
tibule of the mandibular arch and serves to prohibit
dence rises sharply from 4-6 years and remains at a
the lip from exerting excessive force on the man­
fairly constant level between 7 and 10 year and rises
dibular incisors and to reposition the lip away from
again to a peak during adolescence.
the lingual aspect of the maxillary incisors. This
enables the distal repositioning of the maxillary in­
Etiology
cisors resulting in a decreased over-jet and overbite.

Persistent nail biting may be indicative of an emo­

The lip bumper can be a combined, fixed and re­
tional problem.
movable appliance. Either the second deciduous
molars or the first permanent molars are banded
After the age of 15 the nail biting habit is replaced
and the buccal tubes are soldered to them. The la­
by pencil biting, hair twirling or gum chewing.
bial screen assembly may either be soldered to the
band or crowns or slipped into the buccal tubes. The
Effects
labial shield keeps the wire away from the lower
incisors, preventing it from cushioning to the lin­
■ Dental effects
gual of the maxillary incisors during posture and
The common effects of nailbiting on the teeth
function. With no labial restraining lip habit, the
are crowding, rotation and ^attrition of incisal
tongue will then stimulate the lower incisors to move
edges of the incisors (mandibular).
labially, which increases the arch length, reduces
■ Effects on the nails
crowding and excessive overjet.
Inflammation of the nail beds & also^of the nails.

CHEEK BITING
Management
This is an abnormal habit of keeping or biting the
cheek muscles in between the upper and lower pos­ ■ Mild cases no treatment is indicated.
terior teeth. It may injure the soft tissues and may ■ Avoid punitive methods, such as scolding, nag­
cause an openbite or an individual tooth malposi­ ging and threats
tion in the buccal segment where a persistent cheek ■ Treat the basic emotional factors causing the act.
biting habit exists. ■ Encourage outdoor activities which may help
in easing tension
Clinical features ■ Application of nail polish, light cotton mittens
as a reminder.
1. ulcer at the level of occlusion
2. open bite
SELF INJURIOUS HABITS (masochistic hab­
3. tooth, malposition in the buccal segment.
its, sadomasochistic habits, self-mutilating hab­
its)
Treatment (Fig. 9.50a, b, c, d)
A removable crib may be constructed to break the Self-injurious habits are those in which the patient
habit. A vestibular screen may also be used. enjoys inflicting damage to himself. It is rare in
 SECTION 9 : DEVELOPING MALOCCLUSION AND ITS MANAGEMENT |

Fig. 9.50a Cheek biting habit Fig. 9.50b Trauma to cheek as a result of
the habit

Fig. 9.50d Healing of the traumatized mucosa

foliowing treatment
 tEE) I TEXTBOOK OF PEDODONTICS

normal children but is mostly seen in mentally re­ Frenum thrusting

tarded children (10-20%), children with This habit which is rarely seen is also a form of self
psychological abnormalities. injurious habit. If the maxillary incisors are slightly
spaced apart, the child may lock his labial frenum
Definition between these teeth and permit it to remain in this
position for several hours. On constant repetition
Repetitive acts that result in physical damage to the this may turn into a habit which may displace the
individual. These habits show an increased inci­ tooth.
dence in the mentally retarded population.
Treatment
Etiology
■ Treatment should first be initiated towards psy­
The etiology may either be chotherapy.
a. Organic'. Syndromes and syndrome like mala­ Some children experience a feeling of neglect,
dies such as Lesch-Nyhan disease and De abandonment and loneliness and through the use
Lange’s syndrome in which symptoms such as of self-injurious behaviour attempt to solicit at­
repetitive lip, finger, tongue, knee and shoulder tention and love. Treatment of self-injurious be­
biting are common. haviour generally requires a multidisciplinary
approach. Care should be taken in dealing with
b. Functional: This can further be divided into this form of behaviour because of the underly­
■ Type A ing emotional component. Continued concern for
These are injuries superimposed on a preex­ the habit may support or reinforce the habit
isting lesion. For example, a child with a fin­
ger nail biting habit is under treatment for a ■ Palliative treatment
skin lesion. The lesion shows no evidence of Adjunctive therapy in the form of bandages for
healing as it is perpetuated by this injurious any oral ulcerations will help in healing of the
habit which occurs mainly at the night. wounds as well as serve as a habit reminder.
£

■ Type B « Mechano therapy

They include injuries secondary to another es­ An oral shield will also deter the child from the
tablished habit. The self-injurious habit may unconscious continuation of the habit. Treatment
exacerbate the features existing due to a pri­ for self-mutilation may also include use of re­
mary habit. For example, rotation of the straints and protective padding.
thumb while thumb sucking can harm the soft *
tissues. Bobby pin opening
Usually seen in teen age girls wherein opening bobby
■ Type C pin with anterior incisors is done. Clinically we see
They may be injuries of the unknown or com­ notched incisors and partially denuded labial
plex etiology. This type of behaviour has a enameLAt this age, calling attention to the harm­
greater psychogenic component. There may fill habit is generally all that is necessary to stop the
be a multiplicity of symptoms of greater in­ habit.
tensity. The child may resort to various self-
injurious habits as a form of stress release.
 SECTION 9 : DEVELOPING MALOCCLUSION AND ITS MANAGEMENT |

Self-Assessment 13. Hixon E H, Oldfather, R E; Estimation of the

sizes of unerupted cuspid and bicuspid teeth.
1. Define a habit. Angle Orthod. 28:236-240,1958
2. What are the theories of etiology of thumb suck­ 14. Hotz R P Guidance of eruption Vs serial extrac­
ing? tion . Am J Orthod .58,1-20, 1970
3. What are the types of tongue thrusting? 15. Jackson, JM: Mourino AP: Pacifier use and oti­
4. What are the various clinical tests for the mouth tis media in infants twelve months of age or
breathing habit ? younger. Pediatric dentistry. Vol 21:4: 255-260,
5. List out the various self-injurious habits ? 1999
6. What is a 4 S Exercise ? 16. Jacob S, Shetty S; A Comparison of skeletal and
dental changes concurrent to cervical pull head­
Further Suggested Reading For Section - 9 gear and pendulum appliance for molar
distalization - A Cephalometric study. J Ind.
1. Ahmed R. Bruxism in children. J of Pedodontics. Orhtod. Soc. 33:3-10,2000
10: 105-126, 1986 17. Johnson ED, Larson BE: Thumb sucking: Clas­
2. Athanascion A; Farsaris M; New Universal space sification and treatment. Journal of Dentistry for
maintainer. J. Clin. Orthod: 18(8):870-71,1984 Children (ASDC). Vol 60; No.6: 392-398: No­
3. Barber T.K.; Luke S.L.. Pediatric Dentistry: Post­ vember - December 1993.
graduate Dental Handbook Series, Vol. 17. John 18. Johnson, ED, Larson, BE: Thumb sucking: Lit­
Wright PSG Inc. 1982 erature review Journal of Dentistry for Children
4. Becker. A : The median diastema. Dental clin­ (ASDC) . Vol 60: No.6: 385-391: November -
ics of North America.22(4), 685-710,1978 December 1993.
5. Brauer J, Holt T. Tongue thrust classification. 19. Khinda V, Grewal N. Relationship of tongue
Angle Orthodontics. 35 (2): 106-112,1965 thrust swallowing and anterior open bite with
6. Cash, RG: Bruxism in children: Review of the articulation disorders: a clinical study. J.Indian
literature. The Journal of Pedodontics. Vol 12: Soc Pedo Prev Dent. June 33-39, 1999
107-127, 1988.
20. Klein. Pressure habits, etiological factors in
7. Coican M S: A bonded space maintainer. J. Clin.
malocclusion. Am. J. of Orth. 38(8): 569-587,
Orthod. 26(5):276,1992.
1952
8. Ferdianaku K; Laskon M; Spyrou L: Lingual
21. Larsson E, Dahlin K. The prevalence and
arch appliance fabrication in dental office. J Clin.
etiology of the initial dummy and finger suck­
Pediatr. Dent 22(4):277-80;1998
ing habit. Am. J. of Orth. 87(5): 432-435,1985
9. Foley T F Wright G Z ; Weinberger S J : Man­
22. Levin RS. Briefingpaper: Oral aspects of dummy
agement of lower incisor crowding in early
and digit sucking. British Dental Journal.
mixed dentition . J Dent Child 169-174,1996.
186:108, 1999
10. Gawlik J, N.Ott, G. Mathieu. Modification of
the palatal crib habit breaker appliance to pre­ 23. MartineZ N P: Functional maintenance of arch
vent palatal soft tissue embedment. J. of Dent, length. J. Dent. Child. 190-93,1984
for Children. Nov-Dec 409-411, 1995 24. Mills J R E: The effects of functional appliances
11. Graber T M; Orthodontics Principles and on the skeletal pattern. Br J Orthod.. 18,267-275,
Practice.3 & edition W B Saunders Company, 1991
1998. 25. Moore MB: Digits dummies and malocclusions
12. Haskell, BS: Mink JR: An aid to stop thumb dental update: 415-422. December 1996.
sucking: The "Bluegrass7' appliance. Pediatric 26. Moyer R E: Handbook of orthodontics, Chicago.
dentistry. Vol 13: No. 2: 83-85. March/April Yearbook medical publishers Inc. 1988.
1991.
 ¿13® I TEXTBOOK OF PEDODONTfCS

27. Northway W M; Wainwright- R W: D E space - 32. Simon F J : Regaining space in mixed dentition.
a realistic measure of changes in arch morphol­ Dental Clinics of North America.22(4) 669-683
ogy: space loss due to unattended caries. J. Dent. 1978
Rest. 59(10), 1577-80,1980 33. Vanderas. Relationship between malocclusion
28. O Brien, H.T. et al: Nutritive and Non-nutritive and bruxism in children and adolescents: a re-
sucking habits: A review. Journal of dentistry -Pediatric dentistiy. 17(1): 7-12. 1995
for children (ASDC). Vol: 63. No. 5: 321-327. 34. Vig PS : Vig K W : Hybrid appliances: A com­
September-October 1996 ponent approach to dentofacial orthopaedics. Am
29. Osamu Fukuta et al: Damage to the primary den­ J Orthod Dentofac Orthop. 90;273-285, 1990.
tition resulting from thumb and finger (digit 35. Wasson JL. Correction of tongue thrust swallow­
sucking) Journal of dentistiy for children. Vol ing Habits. J Clin Ortho. 13(1) 27-29, 1989
63. No.6:403-4-7. November - December 1996. 36. Weiss C.E., Van Houten J.T. A remedial pro­
30. Rasmas R, Jacobs R. Mouth breathing and gramme for tongue thrust. Am. J. of Orth 62(5)-
malocclusion: quantitative technique for meas­ 499-506. 1972
urement of oral and nasal air-flow velocities. 37. Wilson W L : Wilson R C : 3 D instant space
Angle Orthodontics. 39 (4): 296-300, 1969 maintainer. J. Clin. Orthod 18(12): 892-93 1984
31. Rubin R. The effects of nasal airway obstruc­ 38. Wright G Z:; Kennedy D B : space control in
the primary and mixed dentitions. DCNA 22(4)
tion. J of Pedodontics. 8:3-26, 1983
579-602. 1978
 SECTION - 10J

Pediatric Considerations
for Oral Surgery
10.1 Local Anaesthesia
Tandoii S

In recent times, there has been a larger degree of endings or an inhibition of the conduction process
acceptance of dental treatment. To a great extent in peripheral nerves.
tliis can be attributed to the relief of pain by the use
of local anesthesia. Various dental procedures re­ Thus the major differentiating feature from general
quire the use of local anesthesia. Adequate local anesthesia being, it produces a loss of sensation with­
anesthesia goes a long way in avoiding discomfort out loss of consciousness.
both to the dentist and the patient and can be one of
the key factors in building a good rapport with the Classification of Local Anesthetics
patient.
The clinically useful local anesthetic agents have
Thus, two facts of significance that can be stated been classified into:
are: I. Esters: They possess an ester linkage between
a) In the absence of adequate pain control, it is dif­ the benzene ring and the intermediate chain.
ficult or even impossible to complete the planned The ester group is the mostly used and is com­
treatment. posed of the following:
a) Matsuura [1989] states that various medical 1. An aromatic, lipophilic group
emergencies may occur during dental treatment. 2. An intermediate chain containing an ester
67% of these occur during extraction or pulp linkage
extirpation. Significantly, these are the two pro­ 3. A hydrophilic secondary or tertiary amine
cedures where obtaining profound local group, which forms water soluble salts when
anesthesia is sometimes difficult. compared with acids.
a) Esters of Benzoic acid: (Ester group)
rhe most widely used method in dentistiy for con- These include, Butacaine, Cocaine, Ethyl
rolling pain is blocking the pathway of painful aminobenzoate, (benzocaine), Hexylcaine,
mpulses. This principle is made use of, in local Piperocaine, Tetracaine.
mesthesia. b) Esters of para-aminobenzoic acid:
Chloroprocaine, Procaine, Propoxycaine.
Definition
II. Amide: They possess an amide link between the
vlalamed (1980) defines local anesthesia as a loss benzene ring and intermediate chain. The amide
>f sensation in a circumscribed area of the body group, which is the newest and the most popu­
:aused by a depression of excitation in nen e lar is composed of the following.
 CS® I TEXTBOOK OF PEDODONTICS

1. An aromatic lipophilic group 1. By constricting blood vessels, vasoconstrictors

2. An intermediate chain containing an amide decrease blood flow to the site of injection.
linkage 2. Absorption of the local anesthetic into the
3. A hydrophylic secondary or tertiary7 amino cardiovascular system is slowed resulting in
group, which forms water soluble salts when lower anesthetic blood levels.
combined with acids. 3. Lower local anesthetic blood levels decrease
Various amides available are Articaine, the risk of local anesthetic toxicity.
Bupivacaine, Dibucaine, Etidocaine, Lidocaine, 4. Higher volumes of local anesthetic agent re­
Mepivacaine, Prilocaine. main in and around the nerve for longer peri­
ods, thereby increasing the duration of action
III. Quinolone of most local anesthetics.
■ Centbucridine 5. Vasoconstrictors decrease bleeding at the site
of their administration and are useful when
Constituents of Local Anesthesia increased bleeding is anticipated.

1. Local anesthetic agents ■ The vasoconstrictors most used in dental lo­

The commonly used local anesthetics in dentistry cal anesthetic solutions can be divided into
and their properties along with the the following three groups:
vasoconstrictors used are given in Table 10.1. a) Pyrocatechin derivatives- epinephrine and
norepinephrine.
2. Vasoconstrictors b) Benzol derivative- levonordefrine
Local anesthetics, except for cocaine have a c) Phenol derivative- phenylephrine
vasodilating effect. To counter this effect, ■ The most commonly used one is Phenyle­
vasoconstrictors are added to the solution. The phrine. It is used in the concentration of
purposes served by vasoconstrictors are: 1:2500 and should be limited to 4 mg at a

Table 10.1: Local anesthetics and their properties

Agents Onset Duration PKa

[minutes] [Hours]

Lidocaine 2% 2-4 1-2 ——

Lidocaine with 1:100,00 epinephrine 2-4 3-4 8.2

Lidocaine with 1:150,00 epinephrine 2-4 3-4 8.2
Mepivacaine 3% 2-4 2-3 7.9
Mepivacaine 2% with 1:20,000 ievonordefrin 2-4 3-4 7.9
Prilocaine 4% 2-4 1.5-2 8.0
Prilocaine 4% with1:200,00 epinephrine 2-4 2-4 7.9
Etidocaine1.5% with1:200,00 epinephrine 2-4 4-9 8.1
Bupivacaine 4% with1:200,00 epinephrine 5-8 4-9 8.2

Higgins (1999)
 SECTION 10 : PEDIATRIC CONSIDERATIONS FOR ORAL SURGERY |

time. In cases suffering from cardiac prob­ b) Calcium displacement theory: Goldman [1966]
lems, one-fourth dose should be kept as the maintained that LA block was due to displace­
limit ment of calcium ions from some membrane site
« These vasoconstrictors are contraindicated in that controlled the permeability to sodium. How­
patients suffering from thyrotoxicosis. ever varying die concentration of the calcium
ion at the site of administration did not alter the
3. Reducing agents LA potency. Thus, this theoiy has also been dis­
Vasoconstrictors are unstable in solution and may carded.
oxidize, especially on a prolonged exposure to
sunlight In an attempt to overcome the problem c) Wei [1969] has proposed the surface repulsion
a small quantity of sodium metabisulphite, which theory. According to him the LA agent acts by
competes for the available oxygen, is included binding to the nerve membrane and changing
in the solution. Since this substance is more read­ the electrical potential at the membrane surface.
ily oxidized than adrenaline or noradrenaline, it But since the resting potential of the cell mem­
protects their stability. brane remains unaltered, this theoiy may not
hold much credibility.
4. Preservatives
The stability of modem local anesthetic solutions d) Lee [1976]: According to him the LA agent acts
is maintained by the inclusion of a small amount by membrane expansion. The agent diffuses to
of a preservative such as caprylhydrocup- hydrophobic regions of the cell, alter bulk mem­
rienotoxin, which is included in Xylotox. Some brane structure and prevents the increased
preservatives, such as methylparaben, have been permeability to sodium that occurs. This mode
shown to produce allergic reactions in sensitized of action is suggested for benzocaine.
subjects.
e) Probably the most accepted theoiy in recent times
5. Fungicide has been the Specific receptor theoiy proposed
A small quantity of thymol is added to serve as a by Strichartz[1987]. According to this theoiy,
fungicide. the LA agent acts by binding to specific receptors
that are present on the sodium channel. The ac­
6. Vehicle tion of the drug has been stated to be direct and
The anesthetic agent and the additives referred involves the binding of the agent to the specific
to above are dissolved in a modified Ringer’s receptor and prevents the entiy of sodium into
solution. This isotonic vehicle minimizes dis­ the cell.
comfort during injection.
Biotransformation
Mechanism of action
Biotransformation essentially means the alteration
Various theories of action have been proposed. of a drug within a living organism.
a) Dett barn [1967] has proposed the acetylcho­ ■ Ester local anesthetics are hydrolyzed in the
line theory where it was stated that acetylcho­ plasma by the enzyme pseudocholinesterase. The
line is involved in neural conduction. This theory rate of hydrolysis has an impact on the potential
has been discarded since there is no evidence toxicity of the local anesthetic. The local
that it plays a role in the conduction of impulse anesthetic that is rapidly hydrolyzed is the least
across the body of the neuron. toxic. Allergic reactions that occur in
 I TEXTBOOK OF PEDODONTICS

response to ester drugs are usually not related to istered above the apex of the tooth to be treated are
the parent compound but rather to para ami­ properly termed field blocks.
nobenzoic acid, which is the major metabolic
product of ester local anesthetics. Nerve block
The term nerve block applie^tethat method of se­
■ The metabolism of amide local anesthetics is curing regional analgesia by depositing a suitable
more complex than that of the esters. The pri­ local anesthetic solution within close proximity to
mary site of biotransformation of amide drugs is a main nerve trunk, thus preventing afferent im­
the liver. Liver function and hepatic perfusion pulses from travelling centrally beyond that point.
therefore significantly influence the rate of Needle used: 1 5/8-inch, 25 gauge needle
biotransformtion of an amide local anesthetic. Solution used Generally 1.8 - 2.0 ml administered.
The rates of biotransformation of lidocaine,
mepivacaine, articaine, etidocaine, and Intraligamentary
bupivacaine are quite similar. Prilocaine under­ Most commonly used for a single tooth. The LA
goes more rapid biotransformation than the other needs to be given under a high pressure. In bleed­
amides. ing disorders or in young handicapped patients
where lip biting may be a problem, 30-45 minutes
Techniques of Local Anesthesia of anesthesia even of the pulp, may be achieved with
this technique.
Local Infiltration ■ The injection technique is as follows: with the
In local infiltration small terminal nerve endings Peri-Press of Ligamaject syringe, the 30-gauge
in the area of the surgeiy are flooded with local needle recommended by the manufacturers is
anesthetic solution, rendering them insensitive to inserted into the gingival siilcus on the mesial
pain or preventing them from beconiing stimulated side. The needle is advanced for local anesthesia
and creating an impulse. In this method, the inci­ into the sulcus as assessed by dentist until re­
sion is made through the same area in which the sistance is met. *
solution has been deposited. ■ The trigger is slowly pulled, depositing approxi­
Needle used: 1-inch, 25 gauge needle mately 0.2 ml of the anesthetic solution.
Amount of solution 0. 6 - 1.0 ml solution buccally,
Intraseptal
just sufficient to cause blanching palatally.
The intraseptal injection may be used to reinforce
the analgesia produced by infiltration, and is pri­
Infiltration anesthesia is usually successful for treat­
marily used for the mandibular primary molars,
ment of the mandibular deciduous canines and in­
when it is wished to avoid giving an inferior dental
cisors and often produces satisfactory anesthesia for
nerve block.
deciduous molars, as the cortical plate is less dense
1. Give a submucosal injection buccally.
in children than in adults.
2. After about 2 minutes, when analgesia of the soft
tissues is effective, inject through the interden­
Field block
tal papilla into the interdental bone mesially and
The field block method of securing regional
distally to the tooth to be treated; about 0.1ml of
anesthesia consists of depositing a suitable local
the solution suffices.
anesthetic solution in proximity to the large termi­
nal nerve branches so that the area to be anesthetized Intrapapillary
is circumscribed to prevent the central passage of The intrapapillary injection may be given to pro­
afferent impulses. Thus maxillary injections admin­ duce analgesia of palatal or lingual tissues, to
 SECTION 10 : PEDIATRIC CONSIDERATIONS FOR ORAL SURGERY |

avoid the need for more painful injections directly Supra periosteal Injection
into palatal or lingual tissues. However only those The suprapenosteal injection is the most frequently
methods or substances that cause a transient and used local anesthetic technique for obtaining pul­
completely reversible state of anesthesia are used in pal anesthesia in maxillary teeth.
clinical practice.
Mandibular injection technique
* Intrapulpal
The intrapulpal technique can be utilized in cases a, Inferior alveolar technique (Fig. 10.2e)
of pulp therapy where the other techniques have
failed. The needle needs to be bent for the purpose
of proper positioning . Also a sufficient amount of
the pulp tissue needs to be engaged for the solution
to be injected into it.
Maxillary Injection Techniques
A number of injection techniques are currently in
use that aid in providing a clinically adequate
anesthesia of the teeth by, soft and hard tissues in
the maxilla. Hie available techniques are as follows:
1. Supraperiosteal(infiltration), recommended for
limited treatment protocols
2. Periodontal ligament injection, recommended as
an adjunct to other techniques or for limited
treatment protocols
3. Intraseptal injection, recommended primarilyfor
periodontal surgical techniques
4. Intra osseous injection, recommended for a sin­
gle tooth when other techniques have failed
5. Posterior superior alveolar nerve block, recom­
mended for management of several molar tooth
in one quadrant (Fig. 10.2a)
6. Middle superior alveolar nerve block, recom­ 6 years at occlusal plane
mended for management of premolars in one
quadrant
7. Anterior superior alveolar nerve block, recom­
mended for management of anterior teeth in one
quadrant
8. Maxillary nerve block, recommended for exten­
sive buccal, palatal, and pulpal management in
one quadrant
9. Greater palatine nerve block, recommended for
palatal and soft osseous tissue treatment distal
to the canine in one quadrant (Fig. 10.2b)
12 years above occlusal plane
10. Nasopalatine nerve block, recommended for
palatal soft and osseous tissue management from Fig. 10.1 Location of the neede for an inferior
canine to canine bilaterally (Fig. 10.2c) alveolar nerve block
 CEO I TEXTBOOK OF PEDODONTICS

Fig. 10.2a Needle advanced upwards, inwards Fig. 10.2d Infra orbital nerve block through
and backwards between the tip of the finger bicuspid approach
and distal surface of the zygomatic process
for the posterior superior alveolar nerve block

Fig. 10.2b The greater palatine nerve block is Fig. 10.2e Needle directed from the opposite
used to obtain palatal anesthesia from side of the arch for anesthetising inferior
the tuberosity to the canine region alveolar nerve

Fig. 10.2c Anesthesia of the palatal region Fig. 10.2f Long buccal nerve block is given
of six anterior teeth is obtained with naso distal and buccal to the last tooth in the
palatine nerve block mandible
 SECTION 10 : PEDIATRIC CONSIDERATIONS FOR ORAL SURGERY (

A syringe with a 1 5/8 inch, 25 gauge needle is Intra Gt al Lignocaine Patch

inserted parallel to the occlusal plane of the man­ Hersh et al [1996] studied the analgesic efficacy and
dibular teeth from the opposite side of the mouth, safety of an intraoral lignocaine patch. Before plac­
at a level bisecting the thumbnail and penetrating ing the patch, the mucosal site was dried with a
the tissues into the pterygomandibular depression. sterile gauze pad. The patch that contained 10% or
The needle is penetrated until gently contacting die 20% lidocaine was placed for 15 minutes on the
bone on the internal surface of the ramus of the buccal mucosa of the maxillary or mandibular
mandible. The needle is then withdrawn about 1mm, premolar region, 2mm apical to the mucogingival
and 1 to 1.8 ml of solution is deposited slowly. junction.
■ In children below five years of age, the man­
dibular foramen lies about 0.5cm below the oc­
Jet Injection
clusal plane, due to the underdeveloped ramus
This is a technique in which a small amount of lo­
of the mandible.
cal anesthetic solution is propelled as a jet into the
® I n chi Idren of about the age group of 6 years the
submucosa wit hout the use of a hypodermic needle.
foramen is at the level of the occlusal plane.
Most of the instruments used for this purpose de­
« In children of more than 6 years the needle
should be placed above the occlusal plane as pend upon the discharge of a small quantity of local
foramen is above the level of occlusion. anesthetic solution from a reservoir. This takes place
when a knob is pressed to release air pressure which
ADVANCES IN THE DRUG DELIVERY SYSTEMS produces a fine jet of solution, which penetrates the
mucosa through a small puncture wound to produce
Iontophoresis (Fig. 10.3)
surface anesthesia. This technique is particularly
Tharian and Tandon [1993] found iontophoresis a
effective prior to palatal injections.
suitable alternative for the application of the drug
for achieving surface anesthesia. Further research
Computer-controlled injection system (Fig. 10,4)
in our department with the use of enhancers has
found the penetration to be improved and the pa-
The Wand Local AnesthesiaSystem is a computer
i nt response to the technique quite encouraging.
controlled injection device, the size of a paperback
It presents a painless modality of administering
anesthesia and further research is warranted. book. It accommodates a conventional local
anesthetic cartridge that is linked by microtubing
to a disposable, lightweight, pen like handle with a
Luer lock needle attached. The computer-control­
led system is activated by a foot control that auto­
mates the delivery of local anesthetic at a precise
pressure and volume ratios, resulting in an effec­
tive and comfortable injection. Patients who haw
experienced an injection with this system report a
virtually imperceptible needle penetration followed
by a sensation of mild pressure. The manufacturer
suggests that needle penetration and advancement
be done very7 .slowly to allow for anesthetic to pro­
ceed the path of the needle.
Fig. 10.3 Iontophoresis - A novel technique of
inducing local anaesthesia
 CE3 I TEXTBOOK OF PEDODONTICS

ingredient is 10% lignocaine hydrochloride in

a water miscible base, which is expelled in small
quantities from an aerosol container. The inclu­
sion of various fruit flavors is intended to make
such preparations more acceptable to children.
It is preferable, after drying the area concerned,
to spray an appropriate quantity of solution on
to a small cotton wool roll which is placed in
the injection site in the sulcus and left in situ for
about a minute prior to insertion bf the needle.
The onset time of anesthesia is approximately
one minute and the duration about 10 minutes.

■ Ointments and Jelly

Ointments containing 5% lignocaine hydrochlo­
ride can be used for a similar purpose, but it takes
3-4 minutes to produce surface anesthesia. Emul­
Fig. 10.4 Wand controlled computerized LA.
sions containing 2% lignocaine hydrochloride
delivery system
are also available.
Electronic dental anesthesia
This method of achieving local anesthesia involves Ethyl chloride when sprayed on to either the skin
the use of the principle of Transcutaneous Electri­ or mucosa volatilizes so rapidly that it quickly
cal Nerve Stimulation [TENS] which has been used produces anesthesia by refrigeration. This phe­
for the relief of pain. It can be used as a supplement nomenon is of clinical value oiily when the spray
to conventional local anesthesia and has been found is directed at a limited area until snow appears.
to be well accepted by the parents. Some limitations This technique is of limited value, but is occa­
would be increased saliva flow, metal instruments sionally used to produce surface anesthesia prior
cannot be used freely, and its use would be contrain­ to the incision of fluctuant abscesses.
dicated in several conditions including heart dis­
ease, seizures, neurological disorders, brain tumours The local anesthetic benzocaine has been widely
and with pacemakers or cochlear implants used as a topical anesthetic since 1903. It is the
[Croll,1994]. ethyl ester of para amino benzoic acid and is an
odourless white crystalline powder soluble in al­
Topical anesthesia cohol, fatty oils and dilute acids. It is one of the
Anesthesia can be obtained by the application of a safest topical anesthetics available. Because of
suitable agent to an area of either the skin or mu­ its low aqueous solubility it is absorbed very
cous membrane which it penetrates to anesthetize slowly from oral tissues and wounds.
superficial nerve endings. It is the most commonly
used to obtain anesthesia of the mucosa prior to in­ ■ EMLA (eutectic mixture of local anesthetics)
jection. Clark et al. in 1986 suggested the use of EMLA
■ Sprays (eutectic mixture of local anesthetics) cream for
Sprays containing an appropriate local anesthetic numbing the skin before inserting the needle as
agent are particularly suitable for this purpose this has reduced the incidence of injection pain.
because of their rapidity of action. The active The EMLA cream is especially designed to
 SECTION 10 : PEDIATRIC CONSIDERATIONS FOR ORAL SURGERY |

go through intact skin. It achieves this because 1. Vasovagal syncope: Though a complication
it contains a mixture of lignocaine and prilocaine present in adults, children rarely suffer from this,
bases, which form the oil phase in the cream. probably due to the constant movement of ex­
tremities coupled with crying out loud which in
COMPLICATIONS effect prevents the pooling of blood in the ex­
tremities.
Problems encountered in children 2. Broken needles: This may be sometimes arise
due to the sudden movement during administra­
A. The numb feeling produced following the tion of anesthesia.
anesthetic procedure can cause a number of post 3. Failure to achieve anesthesia.: Apart from
operative problems. It is a sound practice to ex­ improper technique, normal anatomic variations
plain ahead of time the numb feeling. Failure to may also play a role in the same.
inform the child of this out of the ordinary feel­ 4. Facial paralysis. It may be caused specially in
ing invites the possibility of an unnecessary and the inferior alveolar nerve block due to the in­
unwanted emotional upset on the part of the jection of the solution into the parotid gland ,
child. temporarily paralyzing the facial nerve. The ef­
fect wears off over a period of time during which
B. Lip Biting:
the unaffected eye needs to be protected.
The warning against lip biting should be given
5. Trismus: May be due to the penetration of the
immediately following injecting procedure and
muscle during the administration of anesthesia.
should be repeated again before the young child
leaves the dental chair while in the presence of
Drug dosage dependent reactions
the parent. The parent must know what the child
is told.
A. Local Anesthetics
C) Pulling and rubbing: Local anesthetic solutions can affect the cardiovas­
Another precaution is to be observant and dis­ cular system directly by acting on the cardiac tissue
courage the child from pulling or rubbing the and the peripheral vasculature or indirectly via in­
anesthetized areas. The child may strongly pull hibition of the autonomic nerve fibers which regu­
on the anesthetized area of the lips traumatizing late cardiac and peripheral vascular function. Most
and bruising the tissues. Or the child may rub local anesthetic agents have a depressant.
the anesthetized tissues vigorously with the palm
of his hand, producing uncomfortable inflammed Action on the heart At low concentrations, disin-
tissues. hibition of sympathetic activity will increase heart
rate and cardiac output, at higher (toxic) levels car-?
The anesthetic solutions and their components may
diac output may be reduced, leading to a circula­
cause complications either due
tory collapse. Important factors in preventing the
■ to the method of deposition of the drug [local]
occurrence of these complications is the use of as­
■ to the dosage of the drug or accompanying com­
piration and keeping the amount of agent adminis­
ponents
tered within the toxic limits. The main toxic effect
• hypersensitivity reactions
caused by prilocaine is cyanosis due to methaemo-
Solution deposition: globinaemia. Methaemoglobinaemia has also been
The various problems associated with the deposi­ produced by other local anesthetic agents, for ex­
tion of the anesthetic solution with the injection tech­ ample benzocaine and its derivatives. Toxic reac­
nique include: tions to local anesthetics resulting from an
 I TEXTBOOK OF PEDODONTICS

increased blood level of the drug have four possible Plasma cone. Signs and Symptoms
causes: (mcg/ml) of toxicity
1. An excessive dose of the local anesthetic.
2. Inadvertent intravascular injection. 24 r Cardiovascular
/ Depression
3. Slow detoxification or biotransformation.
20 / Coma
4. Slow elimination or redistribution.
1 16 '
Management of the complications i / Convulsions
I i
I 12 / Unconsciousness
J / Muscular Twitching
The majority of the toxic reactions to local / /

anesthetics require no treatment and are mild, im­ 8

/ Visual and Auditory disturbance
mediate and transient. Toxic reaction can be avoided
4 / Light headedness, numbness of
by close monitoring during the injection, injecting tongue
slowly, and withdrawing the needle at the first signs 0
of an adverse response. The management is quite
similar to that of adults which can be referred from
B. Vasoconstrictors
the respective text books.
The action of vasoconstrictors is to cause local
Table 10.2: Maximum drug dosage for local ischemia and thus retard their own absorption. The
anesthesia side effects of vasoconstrictors are much greater if
injected intravascularly, more so in patients with
Agent Maximum ischemic heart disease and hypertension.
dosage
Hypersensitivity
Lidocaine 2% 4 mg/kg body With the amount of usage of the'drug, tire reported
1: 100,00 epinephrine weight cases of allergy appear to be quite few. Yet should
the patient have urticaria, facial edema or breath­
Lidocaine 2% 4mg/kg lessness, one should suspect the same. The allergy
has also been attributed to Methyl paraben (protein
I Mepivacaine 2% in nature) and due to which it has been replaced in
| 1:20,000 neobynephrine 4 mg/kg the recent time.
I r 1 ■1 ■ ■ 1 f
Self Assessment
Mepivacaine 3% 4-8 mg/kg
1. What different classes of local anesthetic agents
Prilocaine [Citanest] 4% do you know7?
1;200,00 6 mg/kg 2. What are the constituents and their concentra­
tions in a local anesthetic solution?
Prilocaine 4% 6 mg/kg 3. What is the role of vasoconstrictor when given
with a local anesthetic agent?
Etidocaine [ Duranest] 1.5% 4. What are the considerations for an inferior al­
1:200,00 epinephrine 5 mg/kg veolar nerve block in a child?
5. What is the bevel gauge and length of the nee­
I
dle used while administering block and infiltra­
I Bupivacaine [Marcaine] 0.5%
tion in a child patient?
I 1:200,00 epinephrine 1.2mg/kg
1 6. List out the newer techniques in delivering lo­
VIRTS (1999) cal anesthesia.
 10.2 Extraction

Tandon S

introduction
5. When radiograph shows the evidence of peri­
An ideal extraction is the painless removal of the apical pathosis with very poor prognosis.
whole tooth or root or the remaining portion of the 6. When the root is fractured as a result of trauma,
tooth with minimal trauma to the investing tissues, with subsequent development of infection.
so that the wound heals uneventfully and no future 7. When rudimentary supernumerary teeth or
problems are created. For the young child who re­ mesiodens are found in radiograph preventing
quires the removal of a primary tooth, the dentist the eruption of permanent teeth or causing any
should recognize the proper sequence of all the pro­ malalignment.
cedures. The dentist prepares the child by using a
sensitive approach through his selection of words that Contraindications
indicate to the child the nature of the procedure.
1. Local
Indications
1. Acute infections like stomatitis, Vincents in­
1. Teeth that are hopelessly carious and not fection and herpetic stomatitis should be
restorable. eliminated before an extraction is done be­
2. When there is extensive decay, which lias re­ cause if virulence or the number of the or­
sulted in death of dental pulp, and decay reaches ganisms is high, it could result in bacteremia
down into the bifurcation. in the host.
3. When the primary teeth interfere with the nor­ ■ Exception to this condition is acute
mal eruption and alignment of their permanent dentoalveolar abscess with cellulitis,
successors. which requires immediate extraction.
■ Improper resorption of root causing deflec­ Dentoalveolar abscess should be treated
tion of erupting tooth found mainly in lower with pre-operative and post-operative
anteriors. antibiotic medication.
■ Irregular resorption of the roots of molars, one
root being resorbed more slowly than the oth­ 2. Malignancy contra-indicates extraction as
ers. trauma enhances the speed of growth and
■ Retained primary teeth when a permanent spread of tumours. Whereas, extractions are
tooth is present and in normal position to strongly indicated if jaw or surrounding tis­
erupt. sues are to receive radiation therapy.
4. When there is a sinus opening through the mu-
coperiosteal membrane overlying the root.
 I TEXTBOOK OF PEDODONTICS

II. Systemic ■ The parent may be concerned about excessive

1. Acute systemic infections of childhood con­ post-operative bleeding or pain. Reassure the
tra-indicate extractions for a child because of parent that post-operative pain usually does not
lowered resistance. occur when a primary tooth is removed.
■ As blood dyscrasias render the patient « Instruct the parent not to discuss with the child
susceptible to post-operative infection and what the dentist will do, rather let the dentist do
hemorrhage, the extractions should be it. The parent choice of words can be poor and
performed after adequate consultation with they can unintentionally make the child fearful.
a hematologist.
2. Acute or chronic rheumatic heart disease, con­ Preparing the child
genital heart disease and kidney disease re­ ■ The 8 to 10 years old who needs teeth removed
quire a proper antibiotic coverage and con­ should have a working through period. This age
sultation with physician. group adjusts better to the removal of teeth when
3. Diabetes mellitus is another contraindication. they are told four to seven days in advance of
Diabetic child should retain his diet in the the procedure. However, the younger children
same qualitative and quantitative composition should be told on the day of the appointment
after an extraction. The physician should be about the procedure.(Baldwin 1966)
consulted before starting the procedure. ■ Tray containing the armamentarium for the re­
■ Many of these contra-indications are rela­ moval of teeth should be kept behind the chair.
tive and can be overcome with special ■ Never hold the needle in front of the child. It
precautions and premedication should always be hidden with a finger.
■ There are two absolute contra-indications ■ Before giving the L. A, explain to the child that
of extractions sensation of pinching or an ant biting may be
■ Haemangioma felt. x
■ Arterio-venuos fistula ■ It is extremely important that lhe child realizes
the difference between pressure and pain. Den­
In these cases rubber band extractions can be done. tist can push on the child’s shoulder^to explain
A rubber band is tied around the tooth and the tooth the sensation of pressure he will feel.
slowly extrudes out of the socket. ■ Explain the sensation of numbness so that the
child is prepared for it.
P re-Operative Preparation of the Parent and the ■ When checking for anesthesia by placing the
Child elevator into the gingival crevices, note the eye
reaction of the child a s the response of the child
The extraction of a tooth can be emotionally upset­ may not be reliable.
ting to the child and the parents, needing some
preparation. Technique for the removal of Primary Teeth

Preparing the parent: Position of operator: With the introduction of four-

« The dentist must have parental consent before handed dentistry, the operator should try to do the
the procedure is performed on a minor. extraction in sitting position, after taking the ap­
« When there is a doubt whether a carious pri­ propriate position depending on which quadrant he
mary tooth can be restored, the possibility of its is n orking on.
being removed should be discussed with the par­
ents before treatment begins.
 SECTION 10 : PEDIATRIC CONSIDERATIONS FOR ORAL SURGERY |

Fig. 10.5 Armamentarium for extraction

La

Posterior tooth Anterior tooth

Posterior tooth Anterior tooth

Fig. 10.6 Tooth movements during extraction. A. Maxillary arch B. Mandibular arch.
F - Facial, P - Palatal, La - Labial, L - Lingual
 CEE) I TEXTBOOK OF PEDODONTICS

Maxillary right and left -quadrant, mandibular left rotary motion is contraindicated. The initial force
quadrant: operator is positioned in front and to the is slightly to the lingual, then a single sustained
side of the patient. force to the buccal until it is loosened. After it is
loosened, a counterclock wise rotation delivers the
Mandibular right quadrant: operator is positioned tooth from the socket.
in back and to the side of the patient.
Trauma to the Permanent Teeth or Partially
Basic forces exerted in die extraction of pri­ Erupted Permanent Teeth
mary teeth (Fig. 10.6):
■ While extracting the primary teeth, care must
Maxillary and mandibular six anteriors: labial be taken not to place the beaks of the forceps
pressure with mesial rotation and out to the labial. high up on the roots of primary maxillary or
mandibular teeth, as there is a great possibility
Maxillary and mandibular molars: lingual, then of removing the partially formed permanent tooth
buccal pressure with a greater pressure towards the with the primary tooth. If this inadvertently
buccal and out towards the buccal. happens, the partially formed tooth and any sur­
rounding bone should be carefully freed in one
Maxillary anterior teeth: Cross-section of the roots piece from the primary7 roots and replaced in the
of these teeth is round. The initial force is apical alveolus. The soft tissues are then sutured over
then slightly to the lingual. This slight lingual force the alveolus to hold the bone and tooth in
expands the lingual gingival bone. The next force position.
is counterclock wise motion that loosens the tooth
in an unscrewing motion. Then, in a single sus­ « Curettes should not be used to remove periapi­
tained labial force, the tooth, is delivered from its cal granulomas following primary tooth extrac­
socket. tion because of danger df injury to the perma­
nent tooth bud. Instead, post operative radio­
Mandibular anterior teeth: the cross-section of the graph is made six to eight months later to deter­
roots is oval. Therefore, after an initial apical force, mine whether tire granuloma has been replaced
direction of force is to the labial in a single sus­ by bone or cyst. However, the cyst formation is
tained action. After the tooth is loosened, a not a frequent occurrence.
counterclock wise motion delivers the tooth from
its socket. Control Of Hemorrhage in Children

Maxillary primary molars: since the palatal root is ■ Keep the gauze sponge held firmly between the
curved, it dictates the direction of the removal and jaws and over the operative site for a full half-
the initial direction of force is slightly to the lin­ hour after the extraction. Do not use a mouth­
gual. A slight force is applied in order not to frac­ wash for 6 hours after the extraction. Vigorous
ture the curved palatal root. Then, in a single sus­ use of a mouthwash may stimulate bleeding if
tained force to the buccal, the tooth is loosened and used before the blood clots are formed.
counterclock wise motion delivers the tooth out of
socket. ■ If mild bleeding occurs hold hot salt water in
the mouth until it cools to body temperature.
Mandibular primary molars: cross-section of roots Then fill the mouth again with hot salt water
is flat mesio-distally and elliptical. Therefore, any and repeal the procedure. Do this until 1 pint of
hot salt water has been used.
 SECTIO/M 10 : PEDIATRIC CONSIDERATIONS FOR ORAL SURGERY |

■ On the other hand, if bleeding is more and can For the parent:
not be controlled by pressure, bleeding from the ■ Instructions for the parent reinforce what has
alveolar vessels is suspected. The socket should already been told to the child, regarding the home
be packed with hemostatic agents such as: care.
- Adrenaline on a gauzes ■ A light meal with no hard food should be rec­
- Thrombin on a gauze. ommended for that day.
- Gel foam dipped in thrombin; the advantage ■ Analgesicis prescribed ifthe extraction was trau­
being it does not require removal and also matic and antibiotic coverage is done if the area
prevents secondary hemorrhage.. was infected.
■ Blood can appear on the pillow the next day or
Post operative instructions for the Child and so. This represents a slight oozing ofblood from
the Parent the healing socket that gets mixed with saliva,
giving the appearance of a large quantity of
For the child: blood.
■ The child should not be dismissed until a blood ■ ‘Call office if undue symptoms develop.
clot has formed.
■ When changing the blood soaked gauze, the Self-Assessment
gauze is removed from the mouth and immedi­
ately disposed out of sight of the child. 1. What are the pediatric considerations in oral sur­
■ Once the blood has clotted, the child is instructed gery?
to hold a small cotton roll between his teeth for 2. What are the principles of extractions ?
half an hour. 3. What are the indications and contraindication
■ Child is instructed not to bite his.lip. of extraction in children?
■ Do not disturb the area where tooth was removed. 4. What are the complications of extraction of a
■ Do not rinse mouth for 24 hours after the ex­ tooth in children?
traction. 5. What post extraction instructions are given to a
■ Do not take the juices with a straw for that day. child patient?
 10.3 Minor Oral Surgical Procedures
.... < -- r.-'.

Tandon S, Lalani Zahid

The basic procedures involved in carrying out mi­ When the swelling “points”, i.e. it localizes into a
nor oral surgical procedures are the placement of soft fluctuant, palpable mass, it should be incised
incision, and suturing. and drained. Incision and drainage will dramatically
reduce the swelling and pain. The area is anesthetized
Incision and flap with conduction anesthesia (mandibular or inferior
alveolar block) or with peripheral infiltration around,
Most commonly, on the buccal side, flaps raised are not in the swollen tissues, prior to incising. Spray
of the envelope type. The features of this flap are: the topical anesthetic, such as ethyl chloride solution
« A crevicular incision around the neck of the over the swollen area immediately preceding the
teeth, incising the interdental papillae. In an incision. This will prevent the pain from a quick
edentulous area, the incision is continued on the sharp thrust of the scalpel through the center of the
ridge. soft fluctuant mass down to the solid cortical plate.
« The base ofthe flap should be broader, to main­ If the swelling remains hard or indurated, then bathe
tain a good blood supply. This is achieved by the swollen tissue in saline rinses for 5min. every
placing 2 incisions on either end of the flap at hour until it becomes soft and fluctuant and is ready
an obtuse angle (about 100 degrees). No releas­ for incision.
ing incisions are generally placed in the palate.
■ These releasing incisions are placed such that a Incisional Biopsy
complete interdental papilla is included in the
flap. This facilitates proper interdental suturing. Incisional biopsies are performed to confirm a di­
« All incision lines should be, at the end of proce­ agnosis by removing a part of the lesion. It is pref­
dure, backed by bone. erable that the surgeon who is going to treat the le­
• Flaps raised are generally muco-periosteal in sion performs the incisional biopsy and therefore
nature. this procedure is best performed by an oral surgeon
- patients requiring such a treatment should be re­
Incision and drainage ferred.

When the exudate(pus) collection is confined to the Excisional Biopsy of Non-attached Areas of the
hard tissues, a dull, boring, excruciating pressure Mouth
pain develops. However, a swelling occurs and the
pain diminishes as the exudate penetrates the corti­ Small lesions of the oral mucosa are removed by
cal plate. excisional biopsy which involves the removal of an
ellipse of tissue, including the lesion. The long axis
 SECTION 10 : PEDIATRIC CONSIDERATIONS FOR ORAL SURGERY |

of the ellipse is made parallel to the direction of the (not in water) for transport to the laboratory. In a
muscle pull and it is best to hold the specimen with similar fashion, as described above, lesions that are
a suture to avoid crushing, which could render the obviously benign and do not interfere with function
specimen useless for a histological examination All or cause emotional distress can be left in the young
the tissue surgically removed should be sent for his­ child and removed, if desired, at a later date.
tological examination as occasionally the lesion is
not what was suspected clinically. The specimen SUTURE MATERIALS USED IN CHILDREN
should be placed in a solution of 10% formal saline (Refer Table 10.3)

Table 10.3: Suture materials used in children

Suture Indications Size Needle Absorption

Surgical « General closure of most 3/0, Cutting ■ Is completely degraded

silk oral soft tissues.. 4/0 by two years.
■ Where non-resorbable, suture ■ Is a braided material and
is not required and strength is not as dean as new
required. material
Surgical gut « Extraction, suture 3/0 Cutting • Completely absorbed
within 70 days.
■ Effective strength for 2 to
3 days in the oral cavity.
■ Excellent for oral mucosa
when longer life is needed.
Chromic ■ General closure 4/0 Taper • Completely absorbed in
catgut two days.
■ Provides excellent strength
1 for up to 5 days.
Monofilam­ « Large flaps 3/0 Cutting • Non-resorbable.with 15 to
ent nylon '• For extra strength like a 4/0 20% degradation
palate closure « Excellent tissue
■ Skin closure 6/0 compatibility.
■ Very dean
Polyglycolic ■ Alveolar mucosa 4/0 Taper ■ Completely absorbed
acid ■ Attached gingiva. 3/0 Cutting in 90 days.
4/0 ■ Provides exceSent strength
to the oral mucosa for
two weeks.
a Has a tendency to
accumulate plaque
because of its braided
nature.
 CH3 I TEXTBOOK OF PEDODONTICS

Minor surgical procedures in pediatric growth. The ranulas are usually located in the
dentistry sublingual space between the mylohyoid muscle
and lingual mucosa. However, sometimes the
Soft tissue abnormalities swelling extends into the submentalorsub-
mandibular space by perforating through the
L Mucocele (Fig' 10.7 a, b, c, d, e) mylohyoid muscle, a plunging ranula. The over-
The mucocele is an extravasation type of cyst lying tissues achieve a paper thinness and the
(or can also be a retention cyst). The cause com­ lesion becomes blue as it expands.
monly attributed is the trauma to minor salivary
glands with the mucous/fluid spreading into ad­ Treatment: The size of the ranula is difficult to
jacent tissue. This gets covered by a fibrous lin­ assess clinically, as well as radiologically. The
ing. Credence is given to this theory by the fact extent of a ranula can be estimated by injecting
that they most frequently occur on the lower lip a contrast medium into the cyst. The true lateral
area. and postero-anterior view of mandible radio­
graphs should be taken to assess the depth in
Plain puncturing of the lesion is associated with the neck as well as the width of the lesion. Simple
a recurrence and thus enucleation of the lesion incision and drainage ofthe ranula always results
along with removal of the adjacent minor sali­ in its recurrence. Enucleation of a ranula with­
vary glands is the treatment of choice. out rupturing the thin cystic wall is practically
impossible and results in complications. Once the
Excision: Two approaches have been suggested. cyst ruptures, it is difficult to pick up the conti­
a) The incision is elliptical, around the lesion. nuity of lining. The best surgical procedure for
Then the lesion is excised. ranula is marsupilization.
b) The incision, a superficial one, is placed over
the lesion involving the upper layers only. The III. Eruption cyst:
tissue is then separated on either side and the It is seen associated with natal teeth in the new
lesion excised. bom infant, and also occurs in association with
In both cases, the minor salivary glands around the eruption of the deciduous and permanent
the lesion are also excised to prevent recurrence. teeth. Most of the time, natal and neonatal teeth
If the lesion is deep, the tissues are sutured back are normal primary central incisors. These teeth
in layers, to eliminate dead space. should be observed and are to be extracted if they
are extremely mobile. They appear as clear or
II. Ranula: blood tinged, fluid filled masses on the crest of
Another common retention cyst seen in children the alveolar ridge. They interfere with child feed­
is ranula. Ranulas are cavities of cyst like na­ ing or bleed intermittently when traumatized but
ture located in the floor of the mouth. They are otherwise are symptomless. They usually disap­
formed by the retention of fluid in the sublin­ pear when the underlying tooth erupts. It should
gual or submaxillary gland or their ducts. In in­ be unroofed and drained if the lesion becomes
fants and toddlers, ranulas appearing in the floor painful or infected or if the lesion bleeds and the
of the mouth are congenital and those appear­ natal teeth are removed.
ing in the older children and teenagers are usu­
ally post-traumatic. IV. Odontogenic cysts (Fig. 10.8a, b, c, d)
Odontogenic cysts in children are mostly those
It begins its formation on one side of the jaw associated with impacted teeth, such as denti­
and fills the floor of the mouth by slow expansile gerous cyst. However, the canines are more
 SECTION 10 : PEDIATRIC CONSIDERATIONS FOR ORAL SURGERY |

Fig. 10.7a Mucocele on lower lip Fig. 10.7b Incision placed

Fig. 10.7c Specimen

Fig. 10.7e Post treatment

<EFF> I TEXTBOOK OF PEDODONTICS

Fig- 10.8a Occlusal radiograph showing Fig. 10.8b Flap raised

radicular cyst with relation to maxillary left
central incisor

Fig. 10.8c Specimen Fig. 10.8d Sutures placed

 SECTION 10: PEDIATRIC CONSIDERATIONS FOR ORAL SURGERY |

frequently involved in children than the third mo­ ■ Bi-angled spoon excavators are used to sepa-
lars. In the late mixed and early permanent den­ rate the lining from the bone.
tition dentigerous cyst is associated with impacted The adherence of the cyst to a neurovascular
premolars and 12-year molars. In teenagers den­ bundle (which can be separated easily) or to
tigerous cyst mostly involves the impacted wis­ rem teeth should be checked. Thevi-
the adjacent
domteeth. Lateral periodontal and residue Qrsts tality of the adjacent teeth once checked, the
are rare in childhood. need for apicoedomy and root canal treatment

Odontogenic cysts are usually discovered when

■ The keratocysts, with a reported high rate of
a permanent tooth has not erupted on time. In
occurrence, should be treated with care, more
the radiograph the cyst appears as a radiolucent
as the lining is quito thin and friable sb that
areaoutlined by a thin radio-opaque line. To
lovai may be incomplete.
Lslllt
•aO® »Essing a cyst with a deeply impacted
tooth, a panoramic X-ray is most useful.
Treatment of a dentigerous cyst is the enuclea-
■ Two procedures can be carried out in the treat­ $ ' * \ . * 4

ment of cysts.
gilí?«
Marsupialization - The procedure basically in­ without post-operative morbidity should be enu­
volves removal of a part of the lining, to estab­ cleated. However, large dentigerous cysts should
lish drainage, then the lesion re-epitheliazes af­
ter formation of the granulation tissue and might result in the destruction of the nerve and
shrinks in size. The cyst is then enucleated. blood supply to the adjacent teeth or involve ad­
jacent anatomic structures. If the cyst involves
It is indicated in cases where the cyst is very
tire crowns which can serve a useful purpose, it
large and its removal may cause pathologic frac­
should be marsupialized and the teeth should be
ture or devitalizes the adjacent teeth (including
moved into the dental arch with orthodontic aid.
developing teeth displacement), the exposed lin­
ing is sutured to the edge of the mucosa. Arib-
V. Non-odontogenic cysts
The most common non-pdontogenic cyst in
requiredon part of die patient to keep the cavity
childhood is the traumatic bone cyst or also called
extravasation bone cyst or progressive
igyst enucleation - The lesion is removed com- hemorrhage bone cavity.

Etiology'. Trauma

Features: This cyst doos not contain any epithe-

sed. Reflection is done lial lining and is lined by connective tissue.

bone would be perforated by the ex- ity. Simultaneously, there is liquefaction of

trabeculae in the medullaxy bone. Expansion of
the cyst occurs by a progressive infiltrating
O possible, the cyst should be removed edema of the bone marrow that causes further
tttofo^Biunepiece). The cyst lining is sepa- trabecular resorption.
^^db&p^^me and excess bone (if required)
to facilitate its removal.
 CE9 I TEXTBOOK OF PEDODONTICS

Fig. 10.9a Surgical Enucleation of Fig. 10.9b Post-treatment sutures placed

traumatic fibroma. Swelling on the lower left following its surgical removal
gum for past one month associated with
pain and inability to eat

Hg, 10.10a Lingual frenectomy - pre-treatment Fig. 10.10b Post-treatment with sutures
showing tongue tie placed

Fig. 10.11a Frenectomy - Pre- Fig. 10.11b Incision Fig. 10.11c Sutures are placed
operative photograph showing a
wide low attached frenum
resulting in midline diastema
 SECTION 10 : PEDIATRIC CONSIDERATIONS FOR ORAL SURGERY |

Treatment: Surgical exploration followed by cu­ potential of the tooth may be lost and thus the
rettage to establish fresh bleeding. Before pri­ tooth may have to be orthodontically brought
mary closure, gelfoam or bone graft should be into place.
packed into the cavity.

VLFrenectomy (Fig. 10.10a, b) mon area for the impaction of the supernu­
Maxillary labial frenum - a band of fibroelas- merary tooth. (Fig. 10.12a, b, c,
B tic tissue that is present in the midline is the
< maxillary labial frenum. Its high attachment may Removal
®^§tjDEietimes cause persistence of diastema. A ■ Before raising the flap, the bucco-lingual po­
gg^en^ton^ is advocated in these cases. (Fig. sition of the impacted tooth should be as­
|fgl0.11a, b, c) sessed. The parallex technique or the so called
‘SLOB’ rule can be used. When an IOPA is
Indications for frenectomy
■ Gingival recession
■ Diastema formation
■ Accumulation of debris by reflection and
opening of the sulcus

Technique
■ Simple incision of the band is associated with
a high rate of recurrence and should be
avoided. Complete excision is the ideal treat­
ment
■ An incision is made perpendicular to the fre­ « In palatal flaps, it may be sometimes neces-
num, in the muccobuccal fold. Ibis is then saryto divide the nasopalatine nerves orves-
extended around the frenum inbothdirections sels. However; this should again depend on
such that a 'bell shaped defect’ is elaborated. the amount of access present
The incision should be carried to the bone. ■ The supemumerary tooth mayjust have a soft
■ The tissue thus delineated is excised tissue covering it, in which case, raising of
■ In certain cases, where the vestibule is not the flap facilitates its removal. On the other
deep enough, this may need to be accompa­ hand, a bone covering it may have to be re­
nied by a vestibule deepening procedure. moved so as to expose it and then it can be
■ Suturing is carried out Sometimes a periodon­ removed.
tal pack can be given over die raw surface
¿id removed after 2 weeks.

Hard tissue abnormalities

a) One of the most common reasons for lack of
eruption of maxillary incisors is the presence
of a supernumerary tooth. Should the tooth mon is the odontoma. It is termed composite,
be detected early (before complete root devel­
opment takes place), it may erupt on its own
after the removal. In most cases, however, due ther compound or complex.
to the patient reporting late, the eruption
 I TEXTBOOK OF PEDODONTICS

Fig. 10.9a Primary tooth impaction Fig. 10.9b Occlusal radiograph of maxilla
showing impacted primary central incisor

Fig. 10.9c Tooth is exposed after bone Fig. 10.9d Sutures placed over the incison.
removal
 SECTION 10 '. PEDIATRIC CONSIDERATIONS FOR ORAL SURGERY ^85

Fig. 10.13a Occlusal radiograph showing Fig. 10.13b Flap raised

odontome Interfering with eruption of maxillary
right central incisor

Fig. 10.13c Odontome removed

Fig. 10.13d Sutures placed Fig. 10.13e Occlusal radiograph post-*

treatment
 CS3 1 TEXTBOOK OF PEDODONTICS

It is most commonly discovered on a routine x- Acute osteomyelitis in infants

ray examination. Sometimes, it may also obstruct It usually starts two weeks after birth and is a
eruption of tooth. It is seen to: rare condition.
■ Cause no destruction of the adjacent areas
■ Be separated from the adjacent teeth by a Etiology
septum and is well encapsulated 1. Birth trauma
■ Sometimes causes divergence of the adjacent 2. Infection occurring from contaminated feed­
roots. ing bottle or unclean nipples of the mother.
3. Hematogenous infection can spread from boils
Thus, it is best enucleated and no harm is caused
or umbilicus.
to adjacent tooth/teeth. (Fig. 10.13a, b, c, d, e)

Vjl. Osteomyelitis (Fig. 10.14a, b) Microorganism commonly responsible for this

Osteomyelitis is the inflammation of the soft tis­ infection is staphylococcus aureus.
sue of the bone marrow spaces of the spongiosa
and the haversian system of the cortex. In in­ Clinical features
fants osteomyelitis occurs frequently in maxilla 1. Characterised by a sudden onset. There is a
than in the mandible, whereas the mandible is sudden edema of the palate and eyelids with
more commonly involved in adults. proptosis of the eye.
2. There is an induration and swelling of the
cheeks and abscess formation on the alveolar
mucosa.
3. Abscess is seen in the canine fossa.
4. Multiple fistulas may form.
5. Sequestra are formed from orbital margin and
outer surface of the maxilla and may affect
the development of the jaws and^ teeth.

Treatment
1. Incise and drain the abscess intraorally to
lessen toxaemia.
Fig. 10.14a Osteomyelitis of mandible treated 2. Administer broad spectrum antibiotics.
bv curettage. Pre-treatment * 3 . If sequestration has occured it should be re­
moved.
4. Good nutritious diet and fluid replacement to
be provided.

Acute osteomyelitis in children and adults

It may be localized or wide spread, resulting in
necrosis of the jaw with sequestration or even a
pathological fracture.

Etiology
1. Trauma
2. Acute dentoalveolar abscess.
Fig. 10.14b Post-treatment
 SECTION 10 : PEDIATRIC CONSIDERATIONS FOR ORAL SURGERY | fefrÀ

3. Deep periodontal pockets present all over the 4. Culture and sensitivity test, antibiotic therapy,
jaw. high protein and multivitamin diet and ad­
4. Dry socket following tooth extraction. vised bed rest
5. Infective cysts and tumors.
Chronic osteomyelitis
6. Acute facial infection and cellulitis
It is usually secondary to an acute osteomyelitis.
7' Sinusitis of maxillary sinus.
It can be primary when resistance of the host is
8. Mercurial or Bismuth stomatitis.
good and virulence of micro-organism is low. In
9. In children osteomyelitis of jaw may occur
chronic osteomyelitis symptoms are less severe,
following exanthemata measles. Diptheria,
there is dull boring pain in the jaw with the his­
chickenpox, typhoid or pertussis.
tory of chronic discharge in the oral cavity or on
the face. Sequestration is a common phenom­
Clinical features
enon in the chronic osteomyelitis where the
1. Fever may be present upto 105 F.
necrotic bone becomes separated from the liv­
2. Severe neuralgic pain.
ing bone. A localized sclerosing osteomyelitis
3. Offensive halitosis, involved tooth maybe el­
near the apex of the tooth is common in younger
evated.
age group.
4. Growth of the mandible affected resulting in
a shift of the midline.
Treatment consists of sequestrectomy (removal
5 . Swelling and unilateral numbness of the lip
m and saucerisation (removal of
of sequestrum)
and the associated cellulitis of the face. May in­
bony cavity).
volve muscle of mastication leading to trismus.
6. Multiple sinuses may be formed VIII. Apicoectomy (Fig. 10.15a, b, c)
7. Regional lymph nodes are enlarged and ten­ Apicoectomy is the root resection or root ampu­
der on palpation tation. Ifthe periapical lesion persist^following
8. Pathological fracture may occur when the conventional treatment, or there is persistent
bone is extremely weakened. postoperative discomfort that occurs after root
9. Extensive osteomyelitis of the maxilla shows canal filling, periapical curettage and
ocular symptoms, including proptosis, epi­ apicoectomy will frequently eliminate the symp-
phora, and impaired mobility of eyeball and toms.
even blindness.
Two clinical situations where apicoectomy may
Radiological picture
be considered:
1. No X-ray findings may be seen for the first
ten days.
1) A mechanical problem such as apical dis-
2. Later multiple small radiolucent patches are
charge or perforation that occurs during con­
seen in the bone due to break in the normal
ventional treatment The mechanical problem
trabecular pattern.
can lead to treatment failure. Surgical removal
3. If sequestration has occurred a radiolucent
of the untreated apical portion corrects the
margin surrounds the necrosed bone.
problem.
2) Second situation is where definitive treatment
Treatment
occurs in case of unsuccessfully treated api-
1. Incision and drainage of pus.
cal accessory canal. A simple apicoectomy can
2. Extraction of offending tooth. Curettage con­
remove apical accessory canals and failure in
traindicated at this stage.
this situation is rare.
3. Sequestrum formed should be removed.
 CE9 I TEXTBOOK OF PEDODONTICS

Fig. 10.15a Apical curettage. Pre-operative Fig. 10.15c Post-treatment showing

adiograph showing over obturation with peri­ healing lesion
apical radiolucency

Fig. 10.15b Reflection of periosteal flap and

curettage followed by retrograde filling
 SECTION 10 : PEDIATRIC CONSIDERATIONS FOR ORAL SURGERY |

Technique 6. Maintain firm pressure over the area for 10

1. After completing the root canal filling deter­ minutes after closing to avoid formation of
mine the level at which the root should be hematoma.
amputated. This level should be such as to
remove any unfilled portion of the root canal.
If periapical cyst or granuloma is present this
level should provide access to ensure its com­ Except for cases of apical perforation or peti-
plete removal. apical granuloma or cyst, the purpose of an
apicoectomy is to create an apical bevel that
2. Mucoperiosteal flap should be designed keep­ allows the clinical access to the apex for ret-
ing 3 things in mind rograde filling.
a) Incision sharply made perpendicular to
bone is important, so as to be sure that The inclination of this bevel varies, depend­
blood supply and tissue mass are adequate ing on several factors. The primary determin­
to avoid necrosis and poor healing. ing factors are anatomic k tion and the ex­
b) Flap should be large enough to provide istence of possible extra canals. Clinical vis­
a good access. ibility of the beveled apical area is directly
c) Flap should extend beyond the defective proportionate to the bevel’s inclination.
bone so that the soft tissue will be supported Beveling should be performed with a fissure
by a healthy bone when it is replaced. bur such as a #701 to create a flat, smooth
and easily visualized root surface.
3. Make an opening into the periapical bony
defect using a surgical bur or chisel. Extend Zinc free amalgam is the most commonly used
the opening in the labial plate with a bur or retrofilling material Gutta percha can also
chisel so as to obtain a good access to the de­ be used as retrofilling material wittf success.
fects. Then amputate the root at the level de­
termined with the help of the radiograph with Self-Assessment
a fissured cylindrical bur. The cyst and
granuloma should be enucleated, preferably 1. What are the common Suture materials used in
in total, using the small curets. children?
2. What are the requirements of flap design?
4. Control the hemorrhage within the defect by 3. What is a tongue-tie?
pressure, by cotton pledgets dipped in 4 . What is the treatment of Ranula?
epinephrine (adrenaline) or by crushing bleed­ 5. Why is enucleation contraindicated in Ranula?
ing points in fixe bone. 6. What are the indications for incisional biopsy?
7. What is Marsupialization?
5. Suture the mucoperiosteal flap with silk or
catgut suture material.
 10.4 Oral and Maxillofacial Injuries
in Children
Lalani Zahid, Tandon S

Introduction There is perhaps no single dental disturbance that

has a greater psychological impact on both the par­
The relative lack of exposure to alcohol-associated ents and the child than the fra cture dr loss of a child’s
motor vehicle accidents, the elasticity of a child’s anterior tooth, especially if the injury involves an
facial bones, and the anatomic protection afforded extensive loss of the tooth structure.
by the prominent calvaria account for the low inci­
dence of facial fractures in children. In reported A thorough clinical examination and proper evalu­
series of facial fractures from general hospitals in ation of the extent and nature of the facial injury is
different parts of the world, pediatric injuries (pa­ important to ensure an appropriate management.
tients 12 years of age or younger) account for 4-6% Priority should always be given to life-threatening
of the total. Below the age of 5, the incidence of and emergent procedures. The general principles
pediatric facial fractures in relation to the total is of advanced trauma life support (ATLS) as described
even lower ranging from 0.6 to 1.2 %. by the American College of Surgeons should be’fol-
lowed for resuscitation of a pediatric trauma patient.
The retnisive midface is the most protected area in Appropriate and early pre-operative consultation is
pediatric patients. Rowe estimated that fractures of essential for a good patient management. Patients
the middle third of the facial skeleton in children with a multisystem trauma and facial injuries must
comprise only 0.5% of all pediatric and adult frac­ first be assessed by a trauma surgeon with pediatric
tures in his series. experience. The trauma surgeon should then suggest
additional appropriate specialty consultations and,
Each year, almost twice as many children are (ages along with the pediatric anesthesiologist, authorizes
5 to 14) killed or injured inside as are killed or in­ surgical treatment of the patient as indicated.
jured outside automobiles. Conventional lap belts
do not properly restrain or protect pediatric patients Graduating Oral and Maxillofacial Surgeiy residents
because the anterosuperior iliac spine is not com­ in the USA when asked to define deficiencies in
pletely developed. The restraint, therefore, rides up their training often mentioned general management
onto the abdomen and chest and may itself cause of pediatric patients and specific management of
serious injuries. pediatric oral and maxillofacial surgery trauma.
Pediatric patients with injuries to the oral and fa­
Traumatic injuries of the dentoalveolar region cial structures can present to the general dentist,
among the young children are a tragic but often an pediatric dentist or oral and maxillofacial surgeons
ignored problem. Children with injuries to their an­ in their offices or in the emergency rooms of gen­
terior teeth, and their concerned parents, present a eral hospitals. This chapter is aimed to orient the
challenge for the dentist that is often unparalleled. dental surgeon, pediatric dentist and oral and
 SECTION 10 : PEDIATRIC CONSIDERATIONS FOR ORAL SURGERY [ €0®

maxillofacial surgeons to oral and maxillofacial in­

juries and their management in children.

Terminologies and Definitions

Trauma - Trauma refers to injury; damagennip№—

ment; external violence producing injury or degen­
eration.

Traumatic - Traumatic means pertaining to or oc­

curring as a result of or causing trauma.

Traumatology - Is a branch of surgery that deals

with wounds and disabilities from injuries.

Injury - Injury refers to a damage dr an insult sus­

Fig. 10.16a Soft tissue injury seen as
tained by the tissue. It may evoke dystrophic and /
a chin laceration.
or inflammatory response from the affected part.
Traumatic injury: It may be defined as a damage to
a part of the body tissue.

Fracture - A fracture can be defined as a sudden

violent breach of continuity of bone, which may be
complete or incomplete in character.

Contusion - Injury produced by blunt trauma that

results in edema and hematoma formation in the
subcutaneous tissues.

Abrasions - Injury that results from friction along a

surface, removing or ‘peeling oft’ of the superficial Fig. 10.16b Radiograph showing bone plating
layers of the skin, that results in a raw, exposed or
bleeding surface. ■ Studies have found that the chin is the most
frequently involved in case of soft tissue
Lacerations - Injury that causes a discontinuity in trauma and a scar on the chin may give an
the skin or mucosal surface. Lacerations may be sim­ indication of an injury in the past
ple, stellate, jagged, beveled or flap like.. ■ Studies have also correlated soft tissue trauma
with the extent and complexity of hard tissue
Avulsion -Loss of tissue due to trauma. injuries and found that as the severity of the
Prevalence facial fractures increased, so did the likeli­
hood of a concomitant soft tissue injury.
A. Soft tissue injuries (Fig. 10.16a, b)
■ Hunter (1992) has reported that though fe­
■ Soft tissue injuries are the most common and cial soft tissue injuries, especially minor lac­
they may or may not be associated with hard erations, contusions, abrasions and minor
tissue injury.
 I TEXTBOOK OF PEDODONTICS

bums are suffered by children often, exten­ position following the cephalo-caudal gradient
sive soft tissue injuries are rare. of growth and thus grows out of the protection
« Data from a study carried out in Manipal, of the cranium. Besides, with more outdoor
India (1999) suggests that the chin is the most games being played as well as the adventurous
frequently involved anatomical site for soft spirit acquired by the age of 6 and above, the
tissue injuries followed by the lip. Laceration prevalence of injuries in children reaches its peak
is the most frequently encountered type of in­ m this group.
jury.
C. Injuries of anterior Teeth
B. Hard tissue injuries
Several studies have been conducted by clini­
Head-Injury
cians across the world on injuries to the anterior
It is the most common cause of morbidity and
teeth and the average incidence reported in lit­
mortality in pediatric trauma patients. It has been
erature ranges from 4 to 46 % with 11 to 30% in
reported that about 40% of all automobile acci­
primary dentition and 6 to 29 % in the perma­
dents involve a head injury in children between
nent dentition. (Fig. 10.18a, b, c)
12 and 14 years of age. Therefore, children who
have sustained injuries in motor vehicle acci­
■ Age Distribution: Children in the age group
dents, fall from a height, interpersonal violence,
of 1 to 2 1/2 years sustain injuries to the pri­
trauma with ablunt instrument should be evalu­
mary dentition most frequently. This is the
ated for head injury. If histoiy, symptoms or signs
age when a child learns to toddle and is rela­
of head injury are present, these patients should
tively uncoordinated. 8 to 11 years of age in
be immediately transferred to a regional trauma
school going children shows a high prevalence
center with Neurosurgical services.
rate for these injuries in the permanent denti­
Facialfractures tion. (Table 10.6 and 7) k
Injuries to the facial skeleton are dependent on
the following factors; ■ Sex: Boys are more susceptible (o these inju­
■ Age: The average incidence reported by sev­ ries than girls, the ratio being 1.5:1. No sex
eral studies ranges from 1.5% to 8% in the predeliction has been observed in injuries to
age group of 1-14 years (Table 10.4) the primary dentition.
■ Sex: Boys are more prone to orofacial inju­
ries than girls, in a ratio of 2:1 Teeth involved
« Anatomical site: Mandible fracture is the - 37% in upper central incisors
; most frequent facial skeletal injury reported - 18% in lower central incisors
in hospitalized pediatric patients. (Table 10.5) - 6% in lower lateral incisors
(Fig. 10.17a, b, c) - 3% in upper lateral incisors

In summary, facial injuries in children are more Seasonal variation

common in boys in the age group of 6-12 years A relationship appears to exist between the
with the mandible being affected most frequently. time of the year and the prevalence of dental
Since the skeletal body ratio in the first year of injuries. Studies have shown that the fre­
life is 8:1, the skull and frontal bone are more quency of the injuries increases during the
prone to the injuries occurring during this pe­ winter months.
riod. The midface is well protected at this stage.
With age, the maxilla assumes a more protrusive
 SECTION 10 : PEDIATRIC CONSIDERATIONS FOR ORAL SURGERY |

Fig. 10.17a Mandible fracture Fig. 10.18a Fracture 11,21,22

Fig. 10.18b Fragments of fractured teeth

Fig. 10.17c Teeth in norma! occlusion after Fig. 10.18c After repair (Fragments are at­
treatment tached to the traumatized teeth)

(Courtesy Dr. V. V Subba Reddy, Principal, College of Dental Sciences, Davangere)

4
 CËE) I TEXTBOOK OF PEDODONTICS

Table 10.4: Prevalence and incidence of pediatric oral and maxillofacial injuries

Author Prevalence Age Sex

McCoy et al [1966] 6%

Rowe [1969] Less than 5% - — -----------------

Khosla and Boren [1971] 4% ----- — -

Morgan [1975] —— 6 mon.-6Years M-76.2%

F-23.8%

Fortunato et al [1982] —— 2-15 years M-70.1%

F-29.9%

Carroll et al [1987] — Upto 15 Years M: F

1.75 : 1
Tandon et al [1989] 9.14 % 1-14 years M-66.39%
F- 33.61 %

McGraw [1990] — 0-16 Years M- 59%

[12-16max] F-41%
Posnick et al [1993] — 1-12 Years M-63%
[6-12 max] F-37%
Tandon et al [1999] 8% 1-14 Years M-70%
[max 11-14] F-30%

Table 10.5: Anatomic distribution of facial fractures in the pediatric population

Author Mandibular fractures Orbital DA Mid Zygoma nose Cra­
[Year] C B A R S&P face nium
Morgan 44.4 18.9 16.7 10 10 —w ——

et al [1975] % % % % % —— —»I— — —r

Lehman 35 27 4.5 5 1.7 —•

et al [1976] % % % % %
» 1

Fortunato 28% 4% 3% 20% 10% 4B—

et al [1982]
Carroll 14.9 5.6 3.0 .75 1.8 65 .75 7.8 — —P

et al [1987] % % % % % %
Posnick 55 9 8 27 30 23 17 14 15 12
et al [1993] % % % % % % % % % %
Tandon 30 10 -- —1 —
15 10 — 25 1—

et al [1999] % % % % %

C-Condyle, B-Body, A-Alveolar, R-Ramus, S&P-Symphysis and Parasymphysis

 SECTION 10 : PEDIATRIC CONSIDERATIONS FOR ORAL SURGERY |

Table 10.6: Prevalence of injuries to the anterior teeth in the primary dentition

Country Author Year Age Prevalence

Germany Kessler 1922-37 Preschooler 4.5%

United Kingdom Schrieber 1.-950-55 1 72-2 7 10.9%
Scotland Kraig 1967 4 years 5.9%
onward
Denmark Andreason 1972 3-7 years 30.2%
Denmark Ravn 1976 1-3 years 70.0%
Iraq Yagpt 1988 1-4 years 24.4%
Mexico Sanchez 1990 4 years 72.2%
and Gracia
Nigeria Otuyemi 1996 1-5 years 30.8%
South India Tandon 1997 3-5 years 23.1%
[Manipal]
Brazil Carvalho 1998 3-5 years 18%
South Africa Hargreaves 1999 1-5 years 15%

Table 10.7: Prevalence of injuries of the anterior teeth in the.permanent dentition

Country Author Year Age Prevalence

Canada Ellis 1948 Schooler 4.2% *

United Kingdom Grundy Davies 1959 5-15 years 5.9%
1967 7-17 years 22 8
Denmark . Andreason and Ravn 1972 7-16 years 2Z3%
Dominican Republic Goday 1981 7-14 years 18.1%
Iraq and Sudan Bhagady 1981 Schooler ’ 7.7%
India Sarkar and Basu 1981 1-14 years 0.73%
Australia Burton 1985 Schooler 16.0%
South India (Manipal) Prabhu and Tandon 1989 8-14 years 13:8%
Nigeria Naqvi 1990 Schooler 1^.6%
Mexipo Sanchez and Goday 1990 11 years 37.0%
Italy Zerman 1993 6-21 years 7.3%
France Belattre 1995 6-15 years 13.6%
Jordan Hamdan 1995 10-12 years 19.2%
South Africa Hargreaves 1995 11 years 15%
Sweden Borssen 1997 1-16 years 35%
Spain Zaragosa 1998 6-12 years 5.7%
 CEID I TEXTBOOK OF PEDODONTICS

Etiology 3. Sports. During the teeny^ears, these injuries are

often related to football, baseball, basketball, ice
The records of all patients admitted to Boston Chil­ hockey, soccer and wrestling. Sometimes fight­
dren’s Hospital from 1966 to 1984 with facial frac­ ing and boxing can also be seen as the cause for
tures were reviewed by Kaban et al and revealed facial injuries.
262 cases. This did not include dento-alveolar and
sofMissue trauma. The most common etiology in 4. Battered child: A tragic cause of oral injuries in
these 262 cases was fall from a bicycle, steps, or young children is manifested in the battered child
climbing apparatus. Trauma from a blunt object syndrome, a clinical condition of children who
(baseball bat, hockey puck) and vehicular accidents have suffered serious physical abuse.
respectively, were the next most frequent sources of
facial fractures. The causes, severity and types of The incidence of various causes of injuries to the
injuries to the head and neck are quite different in teeth and the jaws ;re summarized in Tables 10.8 & 9
India from those seen in Western Europe and the
United States of America for many socio-economic Predisposing Factors
and cultural reasons. The incidence of maxillofa­
cial trauma secondary to automobile accidents in Certain factors have been identified that could pre­
India may be different from that seen in Europe or dispose a child to oral and maxillofacial injuries;
the USA for several reasons, including poor roads, 1. WHO suggests that children who are careless
lack of seat belts in vehicles, and inadequate en­ and come from broken homes are more prone to
forcement of road traffic regulations and speed lim­ injuries
its. However, injuries secondary to interpersonal 2. Children with accident-prone facial profiles are
violence and sports in the pediatric population in more susceptible to injuries. These include
India may be significantly different and possibly dentofacial deformities characterized by;
tower than in the USA. a) Increased overjet with protrusion of the up­
per incisors and insufficient lip closure.
Based on several factors described later, injury may b) Angles class II type 1 malocclusion
be limited to the teeth, soft tissues and/or hard tis­ c) Angles class I type 2 malocclusion
sues. 3. Children with cerebral palsy are a special group
within the pediatric population with a high pre­
1. Fall. Dental and maxillofacial injuries are in­ dilection to dental trauma. Their susceptibility
frequent during the first year of life, but can oc­ is due to two reasons;
cur occasionally due to fall from a stroller, bed - Many of these children are subject to abnor­
or chair. They tend to increase as a child starts mal muscle tone and function in the oral area,
to crawl, stand, or walk and are usually related producing protrusion of maxillary anterior
to lack of motor coordination. One peak inci­ teeth.
dence period for dental injuries is just before - Because of their poor skeletal and muscle co­
school age and is mainly the result of falls. ordination, they are subject to frequent falls.
4. Epileptic patients present special problems.
2. Accidents: In young children, bicycle accidents 5. Dentinogenesis imperfecta is an unusual dental
are more common, but trauma could be due to condition with increased susceptibility to trauma.
an automobile accident. In recent years, the in­ The explanation for this phenomenon could be
cidence of injuries secondary to motor vehicle decreased microhardness of dentin and abnor­
accidents [MVA] has been observed to be on the mal tapering of roots.
rise.
 SECTION 10 : PEDIATRIC CONSIDERATIONS FOR ORAL SURGERY |

Table 10.8: Etiology of orofacial injuries

Author Falls Accidents Sports Battered Altercations/

(year] related child assaults

Morgan et al [1975] 19% 60.3% 9.6% 6.4%

Fortunato et al [1982] 32.8% 47.7% 4.5% 3%

Carroll et al [1987] 42.6% 34.4% 14% ■w* 8.75%

McGraw [1990] 7% ’ 42% 8% 16.7%

Posnick et al [1993] 23% 50% 15% 4%

4

Table 10.9: Summary of the causes of injuries of anterior teeth

Causes Number of subjects Percentage

Falls 321 76.06

Fights 41 9.72

Sports 27 4»
6.10

Removing bottle caps with teeth 17 4.03

Bite on bone 5 1.66

Walked into door 3 0.71

Lifting bucket with teeth 1 0.24
422 100.00
 CS3 I TEXTBOOK OF PEDODONTICS

Mechanism of Injury 2. Resilience of the impacting object: If a tooth

is struck with a resilient or cushioned object or
The extent of soft tissue injuries to the facial area if the lip absorbs and distributes the impact, the
varies depending on the forces involved, the agent chance of a crown fracture is reduced while the
responsible for trauma, the circumstance of injury risk of luxation and alveolar fracture is increased^
and location of the injury. These injuries can vary
from minor to complex, including avulsion of por­ 3. Shape of the impacting object: sharp impact
tions of both soft tissues and underlying bony struc­ favours clean crown fractures with minimum
tures. Patients often exhibit considerable concern tooth displacement because the energy is spread
about an injury involving the facial region and every rapidly over a limited area. On the other hand,
effort must be directed toward inquiring about the blunt impact increases the area of resistance to
type of trauma. Knowledge about the mechanisms the force in the crown region and allows the
of injury7 and the vector of forces may give a clue to impact to be transmitted to the apical region,
the diagnosis. causing a luxation or root fracture.

Direct trauma 4. Direction of the impacting force: The impact

When the tooth itself is struck against a surface or on the tooth can occur at different angles, most
when an object strikes a tooth or teeth, for e.g.: often striking the tooth on the facial surface, per­
against playground, equipment, a table or chair or pendicular to the long axis of the root. Depend­
floor. This type of trauma usually involves the ante­ ing on the direction of the impacting force, the
rior dentition. type of fracture will vary. By testing the fracture
properties of enamel and dentin, it has been seen
Indirect trauma that the enamel is the weakest parallel to the
This type of injury is seen when the lower dental enamel rods and that the dentin is most easily
arch is forcefully closed against the upper, as by a fractured perpendicular to the dentinal tubules.
blow on the chin in a fight or fall. This type of
trauma favors crown or crown-root fractures in the Classification *
premolar or molar region, as well as the possibility
of jaw fractures in the condylar and/or symphysis L Oral and Maxillofacial injuries
regions. For the convenience of treatment planning, it is
better to classify the injuries in the oral and max­
Factors characterizing an impact to the teeth or illofacial region. All injuries to the face may be
jaws divided into two basic groups
* Injuries to soft tissues
L Energy of impact: This factor includes both * Injuries to bone
mass and velocity. Examples of these combina­
tions are a force of high velocity and low7 mass 1. Soft tissue facial injuries
(gun shot] or high mass and minimal velocity A. Type o f injury
(ground). Low velocity blows cause the greatest 1. Contusion with or without hematoma
damage to the supporting structures of the den­ 2. Abrasion
tition, but tooth fractures are less frequent. In 3. Accidental tattoo [numerous small foreign
contrast, high velocity impacts, result in crown particles embedded in dermis]
fractures and are usually not associated with 4. Retained foreign bodies
damage to the supporting structures. 5. Puncture
 SECTION 10 : PEDIATRIC CONSIDERATIONS FOR ORAL SURGERY |

6. Laceration 3. Lower third of face

a) Simple - Mandibular dentition
b) Beveled - Alveolar process
c) Tearing - Symphysis
d) Burst or stellate type - Corpus or body
7. Avulsion flap [undermined laceration] - Angle
8. Avulsion injury [loss of tissue] - Ascending ramus
- Condyle
B. Location of injury - Coronoid process
1. Forehead
2. Brow IL Injuries to the dentition
3. Eyelids Dental injuries seen commonly in children in­
4. Nose clude;
5. Ears a) Subluxation [loosening of teeth without dis­
6. Cheek placement]
7. Chin b) Displacement
8. Lips c) Tooth fracture
9. Intraoral
In the primary dentition, teeth are more fre­
2. Facial fractures quently displaced or luxated than they are frac­
A. Type of fracture tured. This is because the alveolar bone in the
1. Closed [simple] young child has large marrow spaces and is rela­
2. Open [compound] tively pliable. It yields to blows to the primary
3. Greenstick teeth, allowing fliese teeth to be niqved rather
4. Comminuted than holding them firmly and thus causing frac­
5. Displaced tures. In contrast, injuries in the permanent den­
6. Undisplaced tition lead more often to crown or root fractures.

B. Location of fracture CLASSIFICATION OF TRAUMATIC INJURIES TO

1. Upper face THE ANTERIOR TEETH
- Frontal bone
- Temporal bone Traumatic injuries often have medico-legal impli
*
- Frontal sinus[glabella] cations and it is therefore essential to maintain ac-
- Supraorbital cur^le documentation by using a simple and sys­
tematic method for recording the injuries. Many
2. Middle third of face classifications exist for describing injuries to the
- Nasal bones and septum teeth and supporting structures, but the majority of
- Maxillary sinuses these in general add confusion as opposed to sim­
- Orbital bones plifying issues. Factors such as etiology, anatomy,
- Zygoma and zygomatic arch pathology and therapy have been used as a basis for
- Maxilla (LeFort I, II or III) most classifications. In this chapter the most popu­
- Alveolar process lar classifications a re discussed because of their sim­
- Maxillary dentition plicity and clarity.
 I TEXTBOOK OF PEDODONTICS

Classification by Rabinowitch [1956] sification of Disease to Dentistry and Stomatology.

Rabinowitch has classified injuries to the primary Certain trauma entities were not defined and in­
teeth ip the following way cluded in the WHO system. The following classifi­
1. Fractures of the enamel or slightly into the den­ cation includes injuries to the teeth, supporting
tin ' ; Structures, gingiva and oral mucosa and is based on
2, Fractures into the dentin ' anatomical, therapeutic and prognostic considera­
3/ Fractures into the pulp tions. This classification can be applied to both the
4. Fractures of the root primary and the permanent dentition.
5. Comminuted fractures
6. Displaced teeth A. Injuries to the hard_dental tissues andpulp
L Crown Infraction N873.60 : An incomplete
^Classification by Ellis and Davey [1960] fracture[crack ] of the enamel without loss of
Ellis and Davey have succeeded in classifying all the tooth substance .
the injuries simply and clearly. It is one of the most 2. Uncomplicated crown fracture : A fracture
widely accepted methods of classification based on contained to the enamel [N873.60] or involv­
the numeric system. ing enamel and dentin, but not exposing the
pulp [N873.61] .
Class 1 Simple fracture of the crown involving 3. Complicated crown fracture N873.62: A frac­
little or no dentin. (Fig. 10.19, 20) ture involving enamel and dentin and expos­
Class 2 Extensive fracture of the crown involv- ing the pulp.
ing considerable dentin, but not the den- 4. UnciimplLcated.cro^
< tai pulp. (Fig. 10.21a) : A fracture involving enamel, dentin and ce-
Class 3 : Extensive fracture of the crown involv- mentum but not involving the pulp.
> ing considerable dentin and exposing 5. Complicatedcnojyn rootTrhcture N 873.64 :
x the dental pulp. (Fig. 10.21b) A fracture involving enamel, dentin and ce-
Class 4 :. The traumatized teeth that become non- mentum and exposing pulp . *
vital with or without a loss of crown 6. Root Fracture N873.63 : A fracture involv­
structure. ing dentin, cementum and the pulp.
Class 5 : Teeth lost as ajresult of trauma.
Class 6 Fracture of the root with or without a B. Injuries to the periodontal tissues
loss of the crown structure. l? Concussion N873.66: An injury to thetooth
Class T . Displacement of a tooth without supporting structures without abnormal loos­
fracture Of the crown or root ening or displacement of the tooth, but with
Class S : Fracture of crown en masse and it’s marked reaction to percussion
replacement 2. Subluxation N 873.66: An injury to the tooth
Class 9 : Traumatic injuries to primary teeth. supporting structures with abnormal loosen­
ing but without displacement of the tooth.
Traumatic injuries to primary teeth are considered 3. Intrusive Luxation [central dislocation]
separately from those of the permanent teeth be­ N873.67: Displacement of the tooth into the
cause of the different treatment criteria and tech­ alveolar bone. This injury is accompanied by
niques. comminution or fracture of the alveolar socket
4. Extrusive luxation [peripheral dislocation,
Classification by Andreasen [1981] partial avulsion] N873.66 : Partial displace­
This classification is based on a system adopted by ment of the tooth out of its socket.
the WHO in its application of the International Clas­
 SECTION 10 : PEDIATRIC CONSIDERATIONS FOR ORAL SURGERY |

Fig. 10.19Ellis class -1 fracture involving Fig. 10.20 Tooth restored with a composite
the maxillary right permanent incisor

Fig. 10.21aEllis class - II fracture involving Fig. 10.21b Ellis class - III fracture - pulp
the maxillary left permanent incisor. exposure involving the maxillary right perma­
nent central incisor.

Fig. 10.21c Laceration of oral mucosa Fig. 10.21d Post-treatment with sutures
I
i
I TEXTBOOK OF PEDODONTICS

5. Lateral Luxation N873.66: Displacement of Modification ofEllis classification by Me Donald,

the tooth in a direction otherjlijn^xially. This Avery and Lynch [1983]
is accompanied by comminution or fracture
of the alveolar socket. Class 1 Simple fracture of the crown involving
6. Bxafticulation [complete avulsion] N873.68 little or no dentin.
: Complete displacement of the tooth out of Class 2 Extensive fracture of the crown jcvolv-
its socket. ing considerable dentin, but not the
dental pulp.
C. Injuries of the supporting bone Class 3 : Extensive fracture of the crown with an
1. Comminution of alveolar socket [Mandible exposure of the dental pulp.
N802.20 , Maxilla 802.40]: Crushing and Class 4 : Loss of the entire crown.
compression of the alveolar socket. This con­
dition is found together with intrusive and Classification by Ulfohn [1985]
lateral luxation.. This classification is evolved from a clinical endo­
2. Fracture of the alveolar socket wall [Mandi­ dontic point of view. He classifies crown fractures
ble N802.20, Maxilla N802.40]: À fracture into three simple classes:
contained to the facial or lingual socket wall. A. Fracture of enamel
3. Fracture of the alveolar process[ Mandible B. Fracture of the crown with indirect pulp expo­
N802.20, Maxilla N802.40]: A fracture of the sure through the dentin.
alveolar process which may or may not in­ C. Fracture of the crown with direct pulp exposure.
volve the alveolar socket.
4. JFracture of the Mandible a nd Maxilla [ Man­ Classification by WHO [1993]
dible N802.21, Maxilla N802.42] : A fracture Recently, WHO has recommended Andresen’s clas­
involving the base of the mandible or maxilla sification following only injuries to hard dental tis­
and often the alveolar process [jaw fracture]. sues and periodontal tissues. *
The fracture may or may not involve the al­
veolar socket. Aims and Principles of Treatment
*

D. Injuries to gingiva or oral mucosa When treating children who have received traumatic
1. Laceration of gingiva or oral mucosa injuries, a sound psychological approach to both the
N873.69: A shallow or deep wound in the child and the parent is important, as often these
mucosa resulting from a tear and usually pro­ present a complex problem. The situation is further
duced by a sharp object. (Fig. 10.21c, d) complicated with the parents feeling guilty that they
were not watching the child or in some way hold­
2. Contusion of gingiva or oral mucosa N 902.x ing themselves responsible for the state of affairs.
6 : A bruise usually produced by an impact Anxiety regarding the prognosis and particularly
from a blunt object and not accompanied by a the appearance of the child is usually present.
break of the continuity in the mucosa, caus­
ing submucosal hemorrhage. The general principles for resuscitating pediatric
multiple trauma patients are described in the Ad­
3. Abrasion of gingiva or oral mucosa N 910.00: vanced Trauma Life Support (ATLS) Manual and
A superficial wound produced by rubbing or course of the American College of Surgeons. This
scraping of the mucosa leaving a raw bleed­ systematic approach to the traumatized adult pa­
ing surface. tient described in ATLS is also useful in caring for
 SECTION 10 : PEDIATRIC CONSIDERATIONS FOR ORAL SURGERY |

children. There are, however, differences between patients with the central nervous system impairment,
pediatric and adult patients that must be kept in management of direct tracheal injury, maintenance
mind: of adequate pulmonary toilet, and intubation when
1. Children have a larger body surface area to mass the larynx cannot be managed with endotracheal
ratio and are therefore more prone to hypother­ procedures. In urgent circumstances, venous access
mia. through the saphenous vein is a good choice. When
2. Children swallow air when they are injured or a rapid vascular access is required in a child with
frightened and therefore have gastric dilatation. circulatory collapse, intraosseous infusion directly
x This has anesthetic and aspiration implications. into the marrow cavity of the proximal tibia in chil­
3. Abdominal girth and the volume of die perito­ dren under 5 years of age and into the distal tibia in
neal cavity in children and infants are relatively children over 5 years of age is an alternative to stand­
small. Significant intra-abdominal bleeding usu­ ard intravenous cannulation during the phase of
ally leads to a change in girth. resuscitation.
4. Infants are obligate nose breathers, and their
nasal air passages are relatively narrow and eas­ Rationale for the therapy depends on a correct di­
ily obstructed. agnosis and formation of a priority list. Thus, one
5. The chest wall in children is very pliable, and should first evaluate head, cervical spine and other
major thoracic injuries may exist with few ex­ systemic injuries. If the patient has been deemed
ternal signs of trauma. stable after examination (clinical and radiographic),
6. Children may maintain normal or borderline the soft tissue injuries and the facial fractures are
blood pressure levels despite significant evaluated along with injuries to teeth.
hypovolemia, because of constriction of the vas­
cular bed. Preliminary evaluation regarding maintenance of
the airway, which may at times be hampered by pool­
American College of Surgeons guidelines on po­ ing of blood or posterior displacement of the tongue
tential cervical spine injury in all patients with head associated with a bilateral parasymphysis fracture
and neck trauma should be adhered to. Studies have in an unconscious patient Signs and symptoms sug­
shown concomitant cervical spine injuries in pa­ gestive of neurologic involvement may be present
tients with maxillofacial trauma range from 0.3 to and need to be addressed immediately;
19%. Lalani et al in a study carried out in Manipal, 1. H/O loss of consciousness
India showed that a significant number of patients 2. Altered mental status
had sustained isolated soft tissue injuries to the face 3^ Dilated and unreactive pupil
and had concomitant cervical spine trauma. 4. Blurring of vision
5. Severe headache
The establishment and maintenance of an adequate 6. Dizziness
airway is fundamental to the management of acutely 7. Drowsiness
traumatized patients. The preferred method is en­ 8. Seizures
dotracheal intubation (oral or nasal) with cervical 9. Vomiting
spine control. The size of the tube needed for a child 10. Loss of smell, taste, hearing and Zor sight
is roughly determined by the diameter of the child’s 11. Discharge from the nose and ears
external nares or fifth finger. A tracheostomy, with
its associated complications in children, is selected Glasgow coma scale cannot be applied to the
only as a last resort. Indications for tracheostomy pediatric population, but is a good guideline for a
are the need for a long term management of rapid neurological examination.
 d) I TEXTBOOK OF PEDODONTICS

CLINICAL EVALUATION ■ How did the injury occur?

The accident’s nature can yield valuable infor­
In a stable patient, the clinical evaluation should mation about the type of injury to be expected.
begin with recording the history from the parent or g.: a blow to the chin will often cause a frac­
E.
other relative who had witnessed the injury and ture of the sÿmpHysis and/or condylar region and
should be followed by a thorough systemic physical ~ crown- root fracture is more common in the
examination. Apart from the demographic details and premolar and molar region. Accident in which
the circumstances of the injury, the history is also a child has fallen with an object in mouth [ paci­
important from a medico-legal point. Accidents, fier toy] tends to dislocate the teeth in a labial
criminal assaults, serious altercations require notifi­ direction.
cation to the law enforcement authorities.
■ Treatment given elsewhere or source of refer­
Evaluation of the child with a maxillofacial injury ral? ~~ '
is often difficult and requires patience and compas­ Treatment such as immobilization, reduction or
sion on the part of the examiner. Sedation can be of reimplantation of avulsed tooth should be con­
help in some cases for adequate evaluation, but sidered.
should not be used in children with a suspected head
injuiy. Chloral hydrate or meperidine HCL, chlo­ ■ History of previous injuiy?
rpromazine and promethazine HCL may be used. Sustained repeated injuries to the teeth may in­
Extensive injuries may require general anesthesia. fluence the vitality and recuperative capacity of
tlie pulp.
History
History taking and examination leading to a diag­ Medical history
nosis are fundamental in all aspects of clinical medi­ A brief medical history at the onset is essential for
cine and dentistry. providing information about a number of disorders
such as allergic reactions to medications; epilepsy,
The following questions are directed to the parent cardiac disorders or bleeding disorders which can
or reliable respondent, to elicit a history, in pediatric influence emergent and definitive treatment. A de­
cases; tailed histoiy should be recorded after emergent care
L Personal data: Patient’s name, age, sex, address has been given and the patient is stable.
and telephone number.
2. History of the traumatic injury in detail. Clinical evaluation of soft tissue injuries

• When did the injuiy occur? ■ Proper assessment of the extent of tissue dam­
The time between the injury and treatment sig­ age is essential for the treatment of these inju­
nificantly influences the prognosis. ries. Careful atraumatic exploration is even more
H/O loss of consciousness, vomiting, seizures, important in children since these injuries have
bleeding from the ear, nose or throat and change an effect on growth and development.
in mental status after the injuiy
« Anesthesia: After a quick examination to de­
« Where the injury occurred? tect any life threatening injuries, the use of local
The place of injuiymay indicate necessityof teta­ anesthesia is recommended to thoroughly evalu­
nus and antibiotic prophylaxis. ate maxillofacial injuries without traumatizing
the child any further. All efforts to decrease the
 SECTION 10 : PEDIATRIC CONSIDERATIONS FOR ORAL SURGERY | CSÜ

pain during anesthesia should be made. Once closely every other day to detect any sign of in­
anesthesia has been obtained, detailed explora­ fection at the earliest possible time.
tion of the wound can be performed and defini­
tive treatment initiated. Clinicalevaluation ofthefractures ofthejaws and
teeth
The most common type of facial lacerations sus­
tainedby younger children [1-4 years] are small, ■ The history’ ofthe injuiy may indicate the mecha­
burst type lacerations sustained during a fall. Ex­ nism and the direction and the vector of force
ploration may sometimes reveal that these su­ applied to the face.
perficial appearing wounds may often extend ■ Bone injuiy is suggested by ecchymosis, edema,
right upto the bone. In gaping wounds the deeper or superficial contusions or abrasions over a bony
layers need to be recognized for the purpose of prominence.
suturing with absorbable sutures followed by ■ Subconjunctival hemorrhage, with periorbital
superficial ProleneÔ sutures. ecchymosis and edema suggests a fracture of the
zygoma, nasal bone or frontal bone.
Special care should be exercised in treating abra­ Ecchymosis and edema over the lower third of
sions containing dirt or foreign particles, as heal­ the face may be suggestive of a mandible frac­
ing may occur with permanent tattooing. All ture though sublingual hematoma is diagnostic
foreign bodies must be removed before initiat­ in most cases.
ing wound closure. Dirt or debris left behind will ■ Examination of the occlusion provide^ an im­
lead to tattooing. portant guideline for diagnosis of the fracture
as well as the reduction after definitive treatment.
Complex facial soft tissue injuries and those in­ Open bile or cross bite may indicate the presence
volving the facial nerve and parotid duct require of fractures. When deviation of the mandible
evaluation and treatment in the operating room. ^during opening and closing movements is seen,
condylar injuiy should be suspected.
Avulsive injuries may lead to loss of tissue. In ■ Trismus or inability to close the mouth may be
cases where there is a minimal loss of the tissue, indicative of a depressed zygomatic arch frac­
the undermining of margins to mobilize the tis­ ture.
sue for primaiy closure should be done. Severe ■ Bimanual palpation of the supraorbital, lateral,
avulsion injuries require skin grafts, local and/ and inferior oibital margins may reveal asym­
or regional flaps. metry, indicating a fracture. By grasping the
maxillary anterior teeth and applying pressure,
Bite wounds, most commonly caused by dogs and mobility of the middle third of the face is elic­
cats, are encountered quite often in the emer­ ited. If present, it is indicative of a Le fort I, II
gency room. They maybe of three types: or III fracture. Epistaxis may indicate nasal or
1. Avulsion tears septal fractures, or be a result of midfacial or
2. Punctures zygomatic complex fractures. Septal hematomas
3. Scratches. should be looked for and if present drained. Frac­
These injuries are highly susceptible to infec­ tured nasal bones may also be diagnosed by ten­
tion and require meticulous debridement and derness, irregularity, mobility and crepitus on
repair without a tight closure of anatomic lay­ palpation. Fractures of the mandible can be di­
ers. Prophylactic broad spectrum antibiotic cov­ agnosed by mobility of the fragments, sublin­
erage should be initiated pre-op and continued gual hematoma or a positive compression test.
for 7 days. These patients should be followed up
 I TEXTBOOK OF PEDODONTICS

EXAMINATION

An adequate clinical examination depends on a thor­

ough examination of the entire injured area after
cleaning all debris and blood in order to get a clear
view. It includes recording various signs and symp­
toms such as:
■ Pain
■ Crepitation
■ Limited mandibular opening/excursions
■ Step defects in bone contour
Fig. 10.22 Splinting of traumatized anterior ■ Anesthesia/Paresthesia
primary teeth
Other considerations include:
Clinical evaluation of thé injuries to the teeth 1. Recording of extraoral wounds and palpation of
Apart from the history taken to evaluate the facial the facial skeletal - as it can disclose jaw fractures.
injuries, questions pertaining to the injuries to the 2. Recording of the injuries to oral mucosa and
teeth would be: gingiva.
« Treatment given elsewhere or source of refer­ 3. Examination of tooth/teeth for the presence of
ral? fracture, pulp exposure, change in color.
Treatment such as immobilization (Fig. 10.22), 4. Recording displacement - intrusion, extrusion,
reduction or reimplantation of avulsed tooth avulsion.
should be considered. 5. Abnormalities of occlusion.
6. Mobility of teeth and alveolar fragments -
■ History of previous injury? ihtraoral palpation of the alveolar bone.
Sustained or repeated injuries to teeth may im 7. Reaction of teeth to percussion.
fluence the vitality and recuperative capacity of
the pulp. Clinical tests
^valuation of subjective/complaints and local Simple clinical tests include:
symptoms can provide a clue to the injury by ■ Radiographic evaluation
asking the following questions: This is an important tool for diagnosing and con­
firming clinical suspicion of fractures. The cor­
■ Is there a spontaneous pain from any of the teeth? relation of clinical findings with radiographic
This may indicate a damage to the supporting features goes a long way in an accurate assess­
structures. E.g. Hyperemia, extravasation of ment of fractures.
blood in the periodontal ligaments, damage to The various views used for specific particular
the pulp, etc.
regions of the facial skeleton are:
1. Waters View or occipitomental view (OMV)
■ Do the teeth react to hot, cold, sweet er sour food?
30/45° for midface, including the zygoma,
This indicates exposure of the dentin or pulp. Is
maxilla, maxillary orbital floors and nasal
there sensitivity to pressure on eating or touch?
pyramid.
This suggests occlusal disturbance, which may
2. Caldwell View - frontal sinuses, frontal bone,
be due to extrusive or lateral luxation, jaw or
anterior ethmoidal cells and zygomatic-fron­
crown-root fracture.
tal suture.
 SECTION 10 : PEDIATRIC CONSIDERATIONS FOR ORAL SURGERY | @9

3. Towne’s View - lateral oblique-mandible the upper and middle thirds of the face
(body, angle). have become more precise. CT evaluation
4. Panoramic View - condyles, alveolar segments of the maxillofacial skeleton should be
5. Orbital and nasal films are used for respec­ done with 3 mm sections in both axial
tive areas. and coronal plane. Spiral CT scans should
be done if three dimensional reco ikMtrue-
For the injuries to teeth the commonly used ra­ tion for pan-facial trauma is indicated. CT
diographs are; imaging in facial trauma is the standard
- Intra oral - Intra-oral periapical view (IOPA), of care in clinical practice in the USA
Occlusal.
b. Magnetic resonance imaging (MRI)
- Extra oral - Orthopantomogram (OPG) (Fig.
Based on the principle of the reflection of
10.23)
sound waves, MRI has added a new
- These reveals the stage of root formation and
dimension to the array of diagnostic aids
injuries affecting the root portion of the tooth
available to the clinician. It is an important
and the supporting tissue.
diagnostic tool to visualize the soft tissue
structures and does not have an important
■ Vitality test
role in a setting of maxillofacial trauma
- Heat test with gutta percha
management.
- Ethyl chloride
- Ice c. Laser doppler flowmeter
- Electric pulp tester ’v It is a non-invasive method, which was
- Carbon dioxide snow recommended to record blood flow in
human dental pulp by Gazelius et al
All these have the disadvantage that they do not (1986). The circulation in the pulp indi­
produce a reaction intensity easily and may give false cating vitality can be detected through
readings if root formation is incomplete or the tooth enamel and dentin covering the pulp and
has a temporary crown or splint. it also seems possible to distinguish
healthy teeth from the non-vital teeth. It
■ Special tests is also possible to make reproducible
recordings on the same tooth at different
1. Mechanical vitality testing
occasions. Doppler ultrasound is also a
- Fracture without pulp exposure: Cutting
very important tool in evaluation of
a test cavity without anesthesia, scratch­
potential vascular trauma to the neck in a
ing with a dental probe.
traumatized patient
- Fractures with pulp exposure: By apply­
ing a pledget of cotton soaked in saline, d. Pulse oximeter
reaction of the pulp to mechanical stimuli It is a method to measure pulpal circula­
can be elicited. tion directly and suggested by Curt Goho
- Dental probe should never be used as it (1999) to use as an alternative to the
may produce an additional injury. present electrical and thermal methods.

2. Other diagnostic tools

TREATMENT PLAN
a. CT-scan (Fig. 10.24ar b, c)
With the availability of advanced diagnos­
As in the evaluation, treatment should follow a logi­
tic aids such as CT scans and 3-D CT re­
cal course on the basis of priority.
construction. the definition of injuries to
 €E9 I TEXTBOOK OF PEDODONTICS

Fig. 10.23 Orthopantomogram showing fracture Fig. 10.24a CT Scan of mandible (axial section)
involving the left parasymphysis and right angle showing fracture of right angle of mandible
of mandible.

Fig. 10.24b CT Scan of mandible (axial sec­ Fig. 10.24c CT Scan of mandible (coronal
tion) showing fracture of left parasymphysis of section) showing fracture of the mandibular
mandible symphysis and bilateral condyles

(Courtsey Dr. James V. Johnson, DDS, MS, Chief of Service, Oral and Maxillofacial Surgery,
Ben Taub General Hospital, Houston, Texas, U.S.A)
 SECTION 10 : PEDIATRIC CONSIDERATIONS FOR ORAL SURGERY |

A. Emergent [immediate care]: hemorrhage may complicate the matter further

Primary care of a pediatric trauma patient is es­ and should be dealt with based on the etiology.
sentially the same as that in the adult. ATLS pro­ Measures like ligation of vessels, electrocameiy
cedures and guidelines are followed in evalua­ of visibly bleeding vessel should be done cau­
tion and management. IV access is gained and tiously. More important aretheIpcafwastires
fluid resuscitation initiated. Blood is sent for such as pressure packs ¿rid other hemostatic
CBC, serum electrolytes, group type and cross agents such as gelfoam, bone wax etc. After de-
matching, Airway is secured and adequate ven­ bridement mild oozing is normal and will stop
tilationassured. A quick physical examination spontaneously in an otlienvise healthy individual.
is carried out to rule out extremity, chest, ab-
dominal, head or spine trauma. Radiographic ex­ 3. Contamination
amination is done to confirm clinical diagnosis. Depending on the cause of the injury, •wonol^s .
The aim during this phase of treatment is to sta­ ’may be classified as clean, cleancmrtariiihated^
bilize the patient and identify the injuries. contaminated and dirty. A contaminated wound
needs to be thoroughly cleaned. Tetanus prophy­
TREATMENT OF SOFT TISSUE INJURIES laxis is mandatory in all wounds and antibiotic
prophylaxis may be prudent in patients with con­
Regardless of the type of injury, certain basic prin­ taminated wounds.
ciples that need to followed are:
4. Primary closure
1. Debridement The main aim of a clinician who treat? a case of
The procedure has two goals in mind: soft tissue injuries is to restore the tissues to their
» The removal of dead tissue and/or foreign pre-niorbid anatomy. Although facial tissue of­
body for the purpose of decreasing the load ten depicts gross disorientation, rriosf may^be A
on the natural healing mechanisms. closed primarily by directing suturirig açross tteÿ
■ Make the tissue environment as conducive to wound. 4
healing as possible.
« Mechanical cleansing is performed by using For this, principles;of management of sofiti^W
a scrub brush and saline or dilute betadine. must be followed and closure is accompanied
Strong antiseptic solutions are best avoided with accurate repositioning of various layers ofc
or should at least be followed by copious irri­ tissue to eliminate dead space. The repair should
gation with saline. Use of iodine and hydro­ commence with meticulous repositiohing of #-
gen peroxide will lead to death of native cells tached periosteum over exposed bone atthefirac-
and thus they should be used judiciously if ture sites To permit such an accuracy, it is ad­
necessary. Sharp instruments like the back end visable to place a few temporary skin suture at
of a scalpel blade or curette can be used for primé points at the comer of morith, the vermil­
retrieval of debris. Tire rich blood supply to ion border of lip or the distinctive curves or
the facial region generally ensures that the points ofthe laceration before the closure ofdeep
tissue will survive. layers. If the deepest portion of the wound in­
volves the oral cavity, the oral mucosa should be
2. Hemostasis closed first as this prevents oral fluids from con­
Hemostasis is important not only for maintain­ taminating the wound. Resorbable sutures are
ing adequate systemic circulation and tissue used for closing deep layers and non-resoibable
perfusion, but is also the first step in the healing sutures are used for skin closure. The skin mar­
cascade. Sometimes secondary or tertian gins should be slightly everted and skin closure
 | TEXTBOOK OF PEDODONTICS

should be tension free to get good esthetic re­ of antibiotic ointment or vaseline. Steristrips can
sults. Interrupted or subcuticular suturing tech­ be applied for the first 48 hours to support the
niques may be used, depending on the prefer­ wound. Sutures should be removed after 5 days.
ence of the surgeon.
T. Burns
Delayed primary closure Burns require particular attention in a child.
In some cases, due to contamination, soft Finkelstein et al [1992] have reported that chil­
tissue injuries are hot indicated for primary dren less than 5 years of age are particularly
closure. Delayed primary closure is also indi­ prone to injuiy. The etiology may be varied such
cated in cases where significant edema exists. as thermal [Flame and scald], chemical, electri­
In this procedure the area is debrided and an cal and radiation. Boys of all age groups are more
open dressing is given using antiseptic gauze prone to burn injuiy as compared to girls. Heath
until the infection is controlled or the swell­ et al [1976] have reported that 10 % of all cases
ing has abated. At this time the wound is with battered children involve burns.
closed in layers.
The American Burn Association injury severity
Secondary closure'. grading system has classified bums in children as:
Infected wounds are treated with secondary
closure. In these cases, regular debridement MINOR
and antibiotic therapy are continued till First and second degree burns that cover less than
wound cultures are negative and the wound 10% of body surface area in children less than 6.
clinically looks healthy. If more than five days
have elapsed between injury and treatment, MODERATE
the wound edges will begin to epitheliaze and Second degree burns that cover more than 10% to
secondary67 closure is necessary. Wound mar­ 20% of body surface area in children or third de­
gins are excised and skin undermined to per­ gree bums that cover less than 10% of body surface
mit closure of tissue in a layered fashion with­ area.
out causing tension on skin. Satisfactory re­
sults are obtained only if wound is kept moist MAJOR
and debridement of the dead tissues is per­ Second degree burns covering more than 20% of
formed daily. body surface area in children, third degree burns
that cover at least 10% of the body surface area,
5. Drains
inhalation burns or electrical burns, all burns in
Drains in a trauma setting should be placed only
infants and bums in which the patient is a poor risk
if there is a significant oozing at the end of the
due to pre-existing conditions.
surgical procedure from the wound bed below
the skin flap. This is commonly seen in large
Management
scalp lacerations which ooze for a long time and
Maintaining function of the affected tissue and pre­
the hematoma that collects below the tissues will
venting the complications of prolonged immobili­
delay healing and predispose the area to infec­
zation are the specific goals in the rehabilitation
tion. Drains should be removed within 48 hours
treatment of burns in children. Lack of proper edu­
or when 24 hour drainage is less than 25 ml.
cation of the parents can be cited as one of the ma­
6. Post-operative wound care jor causes of children suffering from burn injuries.
Soft tissue wounds in the maxillofacial region Exposed electrical terminals and cords are often
should be kept moist by application of a thin film grasped by the infant for stabilization and are
 SECTION 10 : PEDIATRIC CONSIDERATIONS FOR ORAL SURGERY |

potentially life threatening. Measures such as cap­ through the developing tooth crypts when trauma
ping the electric sockets with protection plugs and occurs. Later in childhood and adolescence, the de­
making sure that hot water does exceed 120 degrees velopment of the maxillary and other paranasal si­
F can be useful preventive measures. nuses results in areas of skeletal weakness and is a
major factor in the shift of facial bone fractures to­
TREATMENT OF FACIAL FRACTURES wards the zygomatic complex and LeFort fractures.

Let us briefly review the pediatric craniofacial The treatment of facial fractures follow the general
anatomy before delving into the management of orthopedic principles.
maxillofacial trauma in children. For the first sev­ a. Reduction
eral years of life, the cranium is relatively large, This involves restoring the pre-morbid anatomi­
with a prominent forehead that closely follows the cal continuity of the fractured fragments. It may
rapid pace of brain growth. The orbits and ocular be carried out by the following methods:
globes are also well developed early in life and rep­ - Open reduction, which involves exposure of
resent prominent features of the craniofacial skel­ the fractured fragments, direct visualization
eton. This early period of life is marked by a lack of and reduction
maxillary and ethmoid sinus development, as well - Closed reduction involves approximation of
as by limited dental development. As a result, there the fractured fragments without direct expo­
is limited vertical height and a horizontal projec­ sure.
tion to the face in infancy and in early childhood.
An important aid in reduction of facial fixtures
These factors result in a high skull-to-face ratio,
in the tooth bearing region is the dentition. The
leaving the frontal bones, brain, upper orbits, and
teeth and occlusion provide us with a good guide
eyes more exposed to trauma, whereas the lower
to achieve anatomical reduction of the underlying
facial bones are relatively protected.
bones.

During infancy and early childhood, the condylar

b. Fixation
process of the mandible is well vascularized; its neck
Fixation of the reduced fractured fragments to
is thick and short, making it a strong region of the
ensure immobilization for a period of 4-6 weeks
mandible, in contrast with its thin shape and lim­
in children and 6-8 weeks in adults is crucial in
ited strength later in childhood and adolescence.
fracture healing. Repeated trauma or movement
The mandible and maxilla grow throughout child­
of the area may lead to delayed or non-union.
hood, with a high cancellous-to-cortical bone ratio,
Various modalities of immobilization exist for
resulting in a greater elasticity in the jaws and in
fixation of facial fractures:
more greenstick and non-displaced fractures than
- Ivy loops
are seen in adulthood. In children, the periosteum
- Arch bars
is highly osteogenic, resulting in an early bony un­
- Gunning splints
ion of the fractured bone and active remodeling af­
- Lag screws and compression screws
ter healing has occurred.
- bone plates (titanium and resorbable)

During the first few years of life, the developing

Principles Of Pediatric Maxillofacial Fracture
permanent teeth are small, and the tooth-to-bone
Management By Region
ratio in the jaws is relatively low. Later, in the mixed
dentition pliase, this ratio changes. The resulting Cranial vault and Supraorbital ridge fractures
high tooth-to-bone ratio weakens the mandible in Fractures in the cranial vault and supraorbital ridge
specific locations and encourages the fracture are frequently seen in infants and children less than
 (300 1 TEXTBOOK OF PEDODONTICS

5 years of age. Thorough evaluation using CT scan would otherwise result. When the fracture compo­
of the brain and craniofacial skeleton, neurosurgi­ nents are severely comminuted, it is often prefer­
cal assessment, and opthalmologic consultation able to harvest the cranial bone graft and replace
must be obtained. A combined treatment plan with the entire unit. Depending on the extent of frontal
neurosurgery must be formulated if there is a con- sinus development and injury, the mucous mem­
" Head injury that requires surgical inter­ branes may require debridement with maintenance
vention or intra-cranial access is required for treat­ of a patent nasofrontal duct. If the posterior wall of
ment of the upper facial skeleton. Skin lacerations the frontal sinus is also fractured, neurosurgical con­
if present in the areas overlying, the fractures can sultation is needed to determine whether it is nec­
be used for access. However, in the absence ofthese essary to cranialize the sinus through an intracra­
a coronal incision is often necessary A coronal flap nial approach.
with subperiosteal dissection of the fracture area to
get a complete exposure to the injury site and sur­ LeFort I, II and III fractures
rounding normal anatomic structures is required. LeFort fractures generally occur in older children
Once fracture reduction is achieved, fixation is car­ and adolescents once aeration of the maxillary and
ried out with direct interosseous wires or ethmoid sinus cells has developed. These fractures
microplates. When bony defects are present, primary should be treated with open reduction and internal
bone grafting with cranial bone is the method of fixation (ORIF) techniques similar to those used in
choice. Subperiosteal dissection while reflecting the adults to achieve anatomic restoration. Closed re­
coronal flap must be doncjudiciously, since exces­ duction may be preferred in the very young child to
sive stripping of the periosteal tissue may hamper avoid injury to the unerupted permanent dentition.
growth. The maxillary circumvestibular incision gives an
excellent exposure to the fractures through the
Nasofrontoethmoid fractures zygomatic buttress, anterior maxillary wall, arid
Although nasofrontoethmoid fractures (NOE) are piriform nasal aperture regions, tf exploration of
seen more often in adolescents and adults, they may the orbital floors and medial wall is required, a
occur at any age and generally result from direct subciliary incision is added. *
trauma at the level of the frontonasal suture.
Again, judicious stripping of the periosteum while
Pre-operative assessment, incisions, and dissection reflecting flaps for access to the fracture site in young
for NOE fractures are similar to those for cranial patients is advocated.
vault and orbital ridge fractures. Nasal and nasopha­
ryngeal bleeding, with the upper airway obstruc­ Zygomatic complex fractures
tion and the need for early endotracheal intubation, A zygomatic complex fracture (ZMC) denotes a frac­
may be complicating factors. Internal fixation with ture through the frontozygomatic suture, zygomatic
microplates and screws and primary cranial bone buttress, infraorbital rim, and zygomatic arch: The
grafting are generally required to achieve and main­ orbital floor and lateral orbital wall are part of the
tain anatomic reduction and adequate fracture fixa­ ZMC fracture. The extent of displacement and need
tion to permit bone healing in the pre-injury loca­ for orbital exploration and reconstruction varies with
tion. every patient. A thorough evaluation using CT scans
in the axial and coronal planes or a spiral CT with
Frontal sinus development is minimal before 5 years a 3D- reconstruction and opthalmologic consulta­
of age. When the developed frontal sinus is injured, tion is the standard of care for these injuries. These
anterior table fractures should be anatomically fractures are classified according to Henderson’s
repositioned and stabilized if a contour deformity classification which makes treatment planning more
 SECTION 10 : PEDIATRIC CONSIDERATIONS FOR ORAL SURGERY I

simple. The most common physical findings of a various stages of development at different ages. In­
ZMC fracture include periorbital ecchymosis, sub­ jury to the developing tooth buds and bone may re­
conjunctival ecchymosis and anesthesia or sult not only from the trauma of the fracture but
paresthesia in the infra-orbital nerve distribution. also from rough surgical technique.
If a comminuted zygomatic arch fracture is associ-
^Sedwith a displaced ZMC fracture, a coronal inci­ Once the operator becomes familiar with the varia­
sion is frequently combined with intraoral and tions in the dentition, arch bars can be pldced-With
subciliary incisions to give a full exposure for ex­ relative certainty, even in2-year old children when
ploration, reduction, grafting and fixation. indicated. Obstacles to the use of surgical arch bars
can be overcome with circummandibular wires and
Nasal fractures a splint. When internal fixation techniques are re­
The development of the nasal septum is often con­ quired, either direct interosseous wires, microplates
sidered a major factor in midface growth. In theory, or resorbable plates and screws can be used.
trauma to this region in childhood should retard Monocortical screws should be used to avoid trauma
normal growth, resulting in midface deficiency. The to the developing teeth.
nasal area is the most frequently fractured part of
the face in children, yet extensive midface growth The general principles of treating mandibular frac­
retardation is rarely documented. tures are the same in children and adults, reduction
and stabilization of the bony fragments in their
Nasal fractures are often recognized but then ig­ preinjury pattern with the teeth in their premorbid
nored as unimportant, which may result in late de­ occlusion and maintenance of reduction until bone
formity with functional airway obstruction. The most union has occurred. Children have some flexibility
serious pitfail in treating nasal fractures is the fail­ in regard to the exact anatomic reduction of the bone
ure to recognize those extending outside the nose. because of remodelling potential and the occlusion
Adjacent fractures may include the maxilla, orbits, when the primary teeth exfoliate and the permanent
frontal sinus, or frontal bone region. teeth erupt. Minor discrepancies may be self
correcting or at least amenable to orthodontic align­
Laterally deviated greenstick fractures are most com­ ment. However, this should not be used as an ex­
mon in the pediatric population. When closed re­ cuse for inadequate treatment.
duction is carried out, completion of the fracture by
manipulation to avoid the problem of incomplete The treatment of fractures of the mandibular
reduction is preferred. A septal hematoma after na­ condyles remains controversial. Most clinicians
sal injury is more likely to occur in children than in advocate a conservative approach and few expound
adults. This examination is difficult to complete on the benefits of open rectoction and fixation. There
outpatients, but this complication must be watched are some definite indications for open reduction of
for and drainage instituted once it is identified, if condylar fractures as espoused by Kent et al. These
septal necrosis and perforation are to be prevented. include bilateral condyte fractures with displace­
ment and shortening of the ramus height, open con­
Mandibular fractures (Fig. 10.25a, b, c, d) dylar fracture, foreign body in the condylar fossa
The mandible of children presents a changing and upward displacement of the condyle into the
anatomy that affects the pattern of fractures seen. middle cranial fossa.
This fact must be appreciated if effective treatment
is to be given. Fracture patterns are affected by the The mandible is the fins! facial bone to complete
fact that the child’s mandible is filled with teeth in normal growth and development, and the condylar
head is an important growth center of the mandi-
 I TEXTBOOK OF PEDODONTICS

Fig. 10,25a Fracture of mandible Fig. 10.25b Cap-splint with circummandibular

wiring

Fig. 10.25c Associated soft tissue Fig. 10.25d Intra-oral post operative view
lesion
 SECTION 10 : PEDIATRIC CONSIDERATIONS FOR ORAL SURGERY |

ble. Injury to the condylar head prior to skeletal ■ Another area with growth potential is the nasal
maturity may lead to growth retardation, with re­ septum. Septal injuries may hamper growth or
sultant facial asymmetry and malocclusion. The the edema caused due to injurs7 to the nearby struc­
condylar growth center does not maintain a con­ tures may cause necrosis of the septal cartilage.
stantly low level of activity and experiences high This in turn may retard growth of the midface.
growth rates at specific times. Condylar iiijuiy be- _
fore the age of 3 is likely to result in a significant ~~ TREATMENT OF TRAUMATIC INJURIES TO
mandibular growth distortion but after 12 years of TEETH
age has little effect on mandibular growth. Between
these ages, a wide spectrum of effects may be seen. I. Emergency {immediate caref (Fig. 10.26)
Secondary growth distortion may occur in the adja­
cent regions after mandibular growth asymmetries.
This is commonly observed in the maxilla in the
form of occlusal canting and a shift in the skeletal
and dental hiidlines.

-It is difficult to prescribe a cookbook solution for

the treatment of condylar fractures. A detailed as­
sessment of the patient’s age, dentition, type of frac­
ture, associated injuries must be carried out prior to
drawing up a treatment plan. However, pediatric
patients with condylar fractures should be followed
up semi-annually for any evidence of developing Fig. 10.26 Band adaptation after trauma to the left
ankylosis or skeletal deformity till their facial growth maxillary permanent central incisor (immediate
is complete. care)
i) Initial contact:
Injuries requiring special considerations in chil­ Often these emergencies are communicated
dren by parents to the dentist over the telephone.
During such emergencies, the dentist should
Two facial injuries have singled out for their poten­ take the following steps
tial effect on the future growth of the craniofacial - After a brief history on the phone, the
region. patient should be asked to report im 11I€*
■ Condylar injuries are generally seen to occur due ately to the clinic or hospital if indicated.
to indirect trauma to the temporomandibular - The clinician should try to alleviate the
region. As the condyle is thought to be a sec­ anxiety of the caller.
ondary growth center, any trauma to it can re­ - If the phone call is about an avulsed tooth,
sult in growth retardation. These, especially be­ the following instructions should be given
fore 5 years of age, result from crush injuries to the caller:
- Insert the sink drain plug to avoid tooth
■ May lead to a retrognathic mandible resulting loss and rinse the tooth in tapjwater or
from ankylosis. The delayed mobilization of this saline.
fracture may also have a similar effect on the - Gently insert the tooth into the socket by
growth. Hence, early mobilization or no immo­ holding the crown and not disturbing the
bilization at all is advocated in these cases. root area.
 } TEXTBOOK OF PEDODONT1CS

- If replacement is not possible, place it age so it may be necessary to postpone radiographic

under the tongue of the patient and report examination and definitive treatment until the soft0
to the dentist immediately. tissue bruise has healed and the child has calmed
- The tooth can also be kept in milk while down. It is also important to carefully examine the
coming to the dentist. dentition for loose and cracked fragments, trauma
to opposing teeth and pulpal exposure. In the pri­
ii) Parent management mary dentition the extent of injury and the remain­
Dentoalveolar injury can appear alarming to ing expected life span of the tooth has to be corre­
the parent. A little blood mixed in the saliva lated to reach a decision.
can give the impression of copious
hemorrhage and clotting of the blood on the The treatment can be instituted as follows.
lips may suggest extensive laceration. When
a child arrives at the clinic the accompany­ I. Crown fracture
ing parent may be in a hysterical or extremely a. Fracture with pulp involvement
nervous condition and this complicates the - The treatment of the fracture with pulp
situation. A quick examination will reveal the involvement is challenging for it largely
extent of injury and the results should be com­ depends on the cooperation of the young
municated to the parents to alleviate their patient.
concern. - Radiograph is a must to see the extent of
the injury. Provided that the tooth can be
2. Intermediate treatment adequately restored, a crown fracture in a
Following a period of rest, if the fractured or dis­ primary tooth involving the pulp can be
placed tooth remains vital, then an esthetic res­ salvaged by performing pulpal therapy.
toration can be given during the growth and de­ - Pulp capping procedures are not recom­
velopment period if it requires minimum prepa ­ mended in primary teeth because of a high
ration. This will serve the purpose until a final incidence of failure. Pulpectomy using
restoration can be made. If the tooth becomes zinc oxide eugenol or witapex can be
non-vital, pulp therapy should be instituted. considered, provided three fourth of the
root is present.
3. Permanent procedures - In case of a risk of damage to the devel­
Permanent procedure like jacket crown should oping permanent teeth from periapical pa­
not be undertaken before growlh has ceased and thology and lack of cooperation in young
occlusion has been established. It is not advis­ children, extraction of the traumatized
able to consider permanent crowning until the primary tooth with pulp exposure and its
child has reached approximately 17 years of age prosthetic replacement is a valid method
by which time the development of the dentofacial of treatment. While performing the ex­
structures would be complete. traction, it is essential to remove the en­
tire tooth and ensure no damage occurs
TREATMENT OF TRAUMATIC INJURIES IN THE to the underlying tooth bud. Periodic
PRIMARY DENTITION checkups are. essential in case pulpal
therapy is instituted.
In the primary dentition it is never advisable to rely
b. Enamel and dentin fracture
on the patient’s assessment of the extent of dam­
Radiographs are mandatory to determine the full
age. Frequently the child is not cooperative at this
extent of the injury Involvement of dentin in
 SECTION 10 : PEDIATRIC CONSIDERATIONS FOR ORAL SURGERY I

a crown fracture necessitates restoration to seal - Sometimes, the tooth may undergo inter­
the exposed dentinal tubules. A layer of cal­ nal resorption, which may necessitate ex­
cium hydroxide or glass ionomer lining ce­ traction. The pulp may also become
ment may be applied as soon as possible fol­ necrotic at a later date and endodontic
lowing the trauma. This may then be covered therapy or extraction may be needed at that
by a composite restoration in order to main­ time. *
tain the integrity of the protective coating. If
much of the tooth structure is missing and a II. Rootfracture
bonded restoration is not possible, a preformed ■ This rarely occurs in the primary dentition.
poly carb oxylate, composite or other esthetic A periapical radiograph is required to deter­
crown is placed to restore esthetics and func­ mine the position of the fracture. The loca­
tion in addition to sealing the dentinal tubules. tion of the root fracture usually determines
At the scheduled 6 monthly, visits if the pulp the outcome. Fractures occurring in the api­
becomes necrotic, endodontic treatment may cal third have the best prognosis. If the coro­
be required. nal segment is stable, it is feasible to monitor
and maintain it if no symptoms occur, ft will
c) Enamel fractures usually remain vital and resorb normally.
Treatment of crown fractures in the^primary ■ Fractures in the middle third of the root usu­
dentition is in many aspects similar to that in ally result in a mobile tooth and will prob­
the permanent dentition. In cases of crown ably require extraction. Root fractures which
fractures, generally no treatment is needed. communicate with the gingival margin have
However the tooth needs to be periodically a poor prognosis and should be extracted.
evaluated by carrying out vitality tests and ra­ Extreme care should be employed while re­
diographic evaluation. moving root segments to avoid damaging the
- In cases where just a part^p£the enamel developing permanent tooth bud. Under no
has chipped off it may be treated by circumstances should an attempt be made to
smoothening any rough edges if present remove an apical portion unless it can easily
and applying fluoride to strengthen the be located with the forceps. Overzealoùs in­
surface layer. Slight recontouring of the strumentation increases the risk of damage to
incisal edge may be warranted to improve the developing tooth germs.
esthetics. As a second choice, acid etch
composites may be utilized effectively to ÏÏI. Displacement injuries
restore small or larger chip with an esthetic This is the most frequent injury to the primary
result at the time of the emergency appoint­ dentition due to the resiliency of the alveolar bone
ment. and the short roots of the teeth. These injuries
- If considerable tooth loss has taken place, may be extrusive, lateral or intrusive
an open faced stainless steel crown may displacements. For the fear of a damage to the
be used effectively The strip crown acid developing permanent teeth, some authors rec­
etch technique has proved to be very suc­ ommend the extraction of all displaced primary
cessful in a severe loss of enamel. teeth. A more conservative approach suggests
- Periodic check ups at 6 months interval that the teeth that cannot be repositioned or that
are necessary. Tahmassebi et al [1999] interfere with occlusion should probably be re­
have noted that enamel injuries are often moved. Very mobile teeth should not be retained
associated with luxative injuries and thus in young patients, as there is the danger of aspi­
the importance of regular recall. ration if the teeth become dislodged.
 <4l;l | TEXTBOOK OF PEDQDONTICS

a. Intrusion (Fig. 10.27) ■ Should the tooth not show any improvement
Radiographs are valuable for locating the in­ over 2-4 weeks, it is advisable to extract the
truded teeth and checking whether the crypt of tooth.
the permanent tooth has been damaged or dis­ • A buccal displacement of the primary tooth
placed. If the intruded tooth is found to be im­ will tip its root towards the crown of the de­
pinging on the permanent tooth bud, extraction veloping permanent incisor, damaging it if
of the tooth is indicated. Apart from this, the calcification is not complete. In these cases
treatment usually involves a “wait and watch” extraction is the treatment of choice. Severely
policy. These teeth usually re-erupt within 6 displaced teeth may also be extracted.
months. If after 6 to 12 months the tooth has not
shoW any signs of movement, then ankylosis c. Extrusion
should be suspected and extraction of the tooth ■ For the extruded tooth to have any chance of
performed. Sometimes re-eruption of the tooth surviving in the oral cavity, it should have
may be associated with swelling of the gingiva fewer forces exerted on it. This is primarily
and abscess formation along with pulpal necro­ determined by the occlusion of the patient,
sis, all of which will necessitate extraction of and any interference in occlusion by the tooth
the intruded tooth. hampers its prognosis.
If extrusion is slight, the tooth may be left
intact and periodically monitored. If extru­
sion is severe, the tooth will almost certainly
have lost its vitality and should be extracted.

d. Exarticulation (Fig. 10.28)

Fig. 10.27 Intrusion of deciduous central incisors

of maxillary arch

b. Luxation
■ If the luxation injury is slight (no interfer­
ence with occlusion) with no risk of the tooth Fig. 10.28 Avulsion of deciduous right maxillary
spontaneously coming out of the socket, it can lateral incisor
be left alone. Parents are given instructions
to feed the child with a soft diet and maintain ■ In all cases of exarticulation, every possible
meticulous oral hygiene. As the periodontium effort should be made to locate the tooth. If
heals, pressure from the tongue usually helps not located, a chest x-ray should be taken to
to reposition the palatally placed tooth. rule out the presence of the tooth in the air­
« If the tooth is luxated palatally, it can be gen­ way. Most of the clinicians do not consider
tly repositioned manually and splinted if nec- replanting primary teeth under any circum-
essary.
 SECTION 10 : PEDIATRIC CONSIDERATIONS FOR ORAL SURGERY |

stances due to the possibility of damage to the 2. Enamel and Dentin involvement
permanent tooth bud. Also, such teeth may Radiograph and vitality tests are advised to
get ankylosed causing difficulty in the nor­ determine the frill extent of the injuiy and the
mal exfoliation process. In these cases re­ proximity of file fracture to the pulp. . It is
placement prosthesis will serve the purpose believed that one square. millimeter of the
well. dentin exposes 20,00(Ho45,000 dentinal tu­
bules. Hence, any dentinal exposure requires
TREATMENT OF YOUNG PERMANENT TEETH immediate attention to avoid fiiitherdamage
to the pulp. Prognosis of the tooth depends
The treatment of young permanent teeth often on the following factors
presents the dentist with very challenging and com­ - -¿lie ampimtpf time the dentinejias been
plicated conditions. Before starting with any spe­ exposed (less than 24 hours has good prog­
cific treatment in the Cùse of these immature per­ nosis).
manent incisors, one should evaluate the following. - The remaining thickness of the dentin be­
■ The extent and duration of dental tissue damage tween tlie fractured tooth surface and pplp.
and the child’s previous dental experience - The state of development of the pulp.
■ Status of root development - A protective layer of calcium hydroxide or
glass ionomer must be applied at the earli­
Treatment of these teeth can be grouped into the est to seal tlie exposeddentinal tubules. The
following: crown form may then be restored with an
acid etch composite resin or a temporary
A. Crown Fracture drownT Regular recall is n^essaty to evalu­
ate the vitality of the pulp. Sometimes, an
1. Enamel involvement orthodontic band can be used as a tempo­
- Fractures involving the injury to the enamel rary matrix for retention of the dressing
is a very common but often an overlooked covering the exposed dentin.
problem, especially if direct illumination is - Another option is to reattach the fragment
used. They are easily visualized when the light of the tooth if it is loosely attached or
beam is directed parallel tothe vertical axis brought by the patient. After a thorough
of the tooth. This type of injury does not re­ cleaning with saline water, tlie tooth frag­
quire treatment, however due to associated ment can be reattached using composite
injuiy to the blood vessels, vitality tests should resin and bonding technique.
be performed at regular intervals.
3. Fracture with pulp involvement
- A fracture confined to the enamel only is un­ A careful clinical assessment with the help of
common. A radiograph is necessary to deter­ subjective pain symptoms and radiograph
mine the full extent of the injury. Smoothening should be made to determine the extent of
the fractured enamel and fluoride application exposure of the the pulp. ( Treatment of frac­
to strengthen the surface layer is,usually the tures with the involvement of pulp will de­
treatment of choice. As an alternative, the pend on a number of factors like:
acid etch technique may be utilized effectively - size of the exposure
to restore the smallest amount of enamel frac­ - pulp contamination depending on duration
ture with an esthetic result. of exposure and the place of injuiy
- vitality of the pulp ♦
- state of development of the root
 | TEXTBOOK OF PEDODONTICS

In case of pulpal exposures, the following Local anesthesia is administered and the tooth
procedures may be undertaken. is isolated. A conventional access is prepared
- Direct pulg capping and the amputation of the coronal pulp tissue
Pulpotomy (Apexogenesis) is accomplished using a sterile round bur in a
-_.Purpectomv slow speed handpiece, or a sterile sharp spooiF
Apexification - - exc^aWbf wiflTa sharp curette. After con­
trol of the hemorrhage, a layer of calcium hy-~
droxide is placed over the pulp stump. A com­
a. Pulp-Capping^ posite resin restoration can be placed to re­
Pulp capping or dressing of the exposed pulp store esthetics and function. After apical clo­
involves placing a hard setting calcium hy­ sure has occurred, endodontic treatment of the
droxide cemept over the pulp exposure. It is tooth should be performed and the crown form
indicated in the following scenarios: restored.
i) Exposure of less than 1 mm (minimal
exposure) c. Apexification
ii) Exposure not over 24 hours Apexification is defined as a methpdjQfrin-
iii)Minimal hemorrhage ducing apical closure by the formation of
osteocementum or a similar harQs^eurlhe
An additional factor that favours this treatment continued apical development of the root(s)
is the presence of a wide, incompletely formed of an incompletely formed tooth in which the
apex. Over the protective base restoration of pulp is no longer vital. Immature permanent
a composite resin can be placed. teeth which become nonvital have a blunder­
buss (divergent) root apex that makes canal
b. Pulpotomy (Apexogenesis) obturation by a nonsurgical approach diffi­
This involves the removal of the damaged and cult or impossible. \
inflamed pulp tissue to the level of clinically
healthy pulp followed by a calcium hydrox- - Anesthetize and isolate the tooth. Prepare
ide dressing. a conventional access and extirpate the
necrotic pulp. Instrument the canal 0.5-mm
Apexogenesis is defined as "physiological root short of the radiographic apex. Fill the canal
end development and formation”. The pro­ with calcium hydroxide or calcium
cedure is used to initiate a full apical closure. hydroxide and camphorated
This procedure is indicated in the following monochlorophenol. Seal the canal with
scenarios: zincoxide eugenol/IRM. The dressing
i) Relatively large exposure should be changed every 3 months until
ii) Patient seen within 72 hours apexification is achieved. Later the canal
iii) Moderate hemorrhage can be obturated with conventional endo­
dontic treatment.
An incisor with an open apex and incomplete
root formation is a good candidate for this d. Pulpectomy (Fig. 10.29)
procedure, because of the better recuperative This is the complete removal of the pulp. In­
potential of the young pulp and because of dications for this procedure are:
the difficulty in attempting conventional en­ i) pulp is degenerated, putrescent or of ques­
dodontic procedures. tionable vitality.
ii) pulp exposure greater than 72 hours.
 SECTION 10 : PEDIATRIC CONSIDERATIONS FOR ORAL SURGERY |

Fig. 10.29 Non-vital deciduous right maxillary*

central incisor following trauma
f requiring pulpectomy Fig. 10.30 Radiograph showing horizontal
fracture involving middle 3rd of roots of
This is the method of choice when a tooth with maxillary central incisor
a closed apex is nonvital. Anesthetize and
Different types of splints recommended are men­
isolate the tooth. Prepare a conventional ac­
tioned below:
cess and extirpate the pulp completely. Me­
I. Fixed Splint
chanically cleanse, prepare and obturate the
- Acid etch resin composite splint
canal with gutta percha and root canal sealer.
- Orthodontic brackets and wire splint
The crown form can be restored after this.
- Interdental wiring
- Arch wire and acid etch resin composite
B. Root Fractures (Fig. 10.30)
splint
Root fractures are relatively uncommon in den­
- Full arch vacuum molded acrylic splint
tal trauma. They may occur in the apical, mid­
dle or coronal third of the root. With fractures To avoid additional trauma and delay associ-
of the apical or middle third, pulp vitality may ated with the conventional splints, simpler
persist for an extended period of time. In case of methods such as acid-etch resin or reinforced
a coronal third root fracture, the proximity of with a wire are widely used which can be fab­
the gingival margin to the fracture site makes ricated in the dental surgery. Andresen (1981)
the pulp susceptible to bacterial invasion, lead­ and Jain et al (1996) have recommended a
ing to infection and necrosis. After a radio­ splint period of 2 to 3 months and radiographic
graphic and clinical assessment, these teeth are evaluation supported with vitality tests
usually subjected to digital reduction under a periodically. Recently, reinforced, woven
local anesthetic and stabilizationby splinting. Ef­ fibers embedded in composite, available in
fective splinting is an integral part of the treat­ ribton form (plasma treated polyethylene) are
ment of traumatized teeth and it should perform being used.
the following functions:
- Immobilize the loose tooth II. Removable Splint (SVED Splint)
- Hold repositioned teeth in alignment It is a removable appliance fabricated in
- Protect the damaged tissue from occlusal acrylic. It is constructed such that the acrylic
forces extends over the occiusal/ipcisal surface ofthe
tooth, thereby fixing and stabilizing it
 I TEXTBOOK OF PEDODONTICS

C. Displacement Injuries v) Exarticulation

i) Subluxation - Treatment of choice is reimplantation. This
- No active treatment is necessary if the tooth procedure requires recall on a regular ba­
is slightly mobile. sis for a period of at least three years.
- The patient is instructed to take a soft diet
a few days and to avoid pushing the Review of the injured tooth
tongue against the mobile tooth. All teeth that have received trauma should be re­
- Healing usually occurs inj_toJ weeks. viewed regularly. Review should be carried out ini­
- Tooth is splinted if marked loosening is tially after 1 month, at 3 months and then every 6
present. months for at least 2 years after the trauma. These
ii) Lateral displacement follow-up reviews should include sensitivity tests
- A tooth that has been displaced laterally and radiographs.
should be repositioned.
- Recent displacement is managed under lo­ Sequelae of dental injuries
cal anesthesia by holding to the tooth firmly
between the finger and the thumb (a piece A. Sequelae to primary teeth injuries
of gauze will improve in the grip) and a - Failure to continue eruption
gentle pressure is used to reposition. - Color change
- If the apex is locked in bone, the tooth - Infection, abscess
should be extruded slightly before it is re­ - Loss of space in the dental arch
positioned and can be splinted for 2 to 3 - Ankylosis
weeks. If alveolar fracture is associated - Injury to developing permanent tooth lead­
with it, splinting should be kept for 4 to 8 ing to enamel hypoplasia, crown dilaceration,
weeks. odontoma like malformation, sequestration of
- In delayed report by the patient a displaced the tooth germ, disturbances in eruption, etc.
tooth is commonly locked into its new po­ - Abnormal exfoliation
sition, hence, the tooth is left in the dis­ - Resorption of root
placed position.
- An acrylic removable splint is fabricated B. Sequelae to permanent teeth injuries
quickly by extending the acrylic over the - Color change
incisal surface of the tooth in question. - Infection and abscess
iii)Extrusion - Loss of space in the dental arch
- A tooth that has been extruded from its - Ankylosis
socket should be gently but firmly pushed - Resorption of the root
into its original position and splinted for - Abnormal root development
2-3 weeks.
- Regular monitoring is required by the fol­ C. Pathologic sequelae
low up visits. - Pulpal hyperemia
iv) Intrusion - Pulpal hemorrhage
- The re-eruption potential is present in - Calcific metamorphosis of the pulp
young permanent teeth, hence the tooth - Pulp necrosis
should be left for 3 months to see if it re­ - Internal resorption
erupts. - External resorption
- If it does not re-erupt orthodontic extru­ - Replacement resorption
sion is the treatment of choice.
 SECTION 10 : PEDIATRIC CONSIDERATIONS FOR ORAL SURGERY |

Table 10.10: Treatment modalities for traumatized primary incisor

Trauma present Pulp treatment Restoration

Enamel only Observation Smobthen rough edges

Note any color change Apply fluoride

Enamel and dentin only Calcium hydroxide or Glass Acid etch composite resin open
ionomer lining, note any color faced stainless steel crown,
change celluloid crown, polycarbonate
crown

Enamel, dentin and pulp Formocresol pulpotomy, Open faced stainless steel
puipectomy (if devital or crown, composite resin,
irreversible pulpitis) strip crown

Root fracture Observation, extraction, Space maintainer if required

splinting

Avulsion None Space maintainer if required ■

Displacement Observation, reposition, Immobilization

extraction Space maintainer if required

Con cussion/intrusio n Observe for color change, -

wait to re-erupt, if turns black -
non vital pulp - pulpectorny if
turns yellow calcific pulp,
. observe
 | TEXTBOOK OF PEDODONTICS

Table 10.11: Management of traumatized permanent incisor

Trauma present Pulp treatment Restoration

Enamel (Class I) Observe Smoothen rough edges and

fluoride application, acid
etch composite resin

Enamel and Dentin Calcium hydroxide liner Acid etch composite resin,
(Class II) sometimes to retain
restoration temporary crown
like open faced stainless
steel, acrylic and poly­
carbonate crown, orthodontic
band

Enamel, dentin and pulp * Open apex Temporary crown as

(class III) Direct pujp capping (rare) mentioned above
Calcium hydroxide pulpotomy
(1-2 hours duration, free of
contamination) Apexification Acid etch composite,
* Closed apex ~~ ~~ Jacket crown '
Direct pulp capping (rare) Post core crown
Pulpectomy _

Intrusion Observe, note change in color

or vitality, waitjo ¿e-erupt &

Concussion with mobility Mild - observe Relieve from occlusion

Severe - splint

Displacement Mild - observe

Severe - splint Immobilization

Avulsion Reimplant, splint for 10-14

days, observe

Root fracture * Cervical one-third Gold core with porcelain fused

Root canal to metal crown, space
Extraction maintainer, fixed prosthetic
* Middle one-third, splint appliance
* Apical one-third, splint
 SECTION 10 : PEDIATRIC CONSIDERATIONS FOR ORAL SURGERY |

PREVENTION OF DENTAL INJURIES child. Careful and timely treatment, which can only
be achieved by having an accurate diagnosis, can
One ofthe most tragic situations seen in dental prac­
offset most of the effects of the trauma. If left un­
tice is trauma to the dentition caused by accident.
treated, however they have the potential to cause
The incidence of such injuries appears to be on the
several defects in the developing teeth and jaws. The
rise. This leads to unnecessary time, effort apd ex­
poor esthetics that may result can also affect the
penditure on the part of the parents. The answer to
child psychologically resulting in a low self-esteem.
this problem is prevention. According to Welbuiy
In these circumstances as in others, prevention by
and Murray (1990), this prevention can be of a pri­
means of use of mouthguards, safety belts can go a
mary or secondary nature.
long way in avoiding this depressing situation.
Primary prevention
Self-Assessment

i) General measures and educational programs

1. Provide a brief narration on the history, clinical
■ never leave a child alone at home
evaluation and emergent care you would con­
■ always stay with the child near water
sider in a pediatric trauma patient with maxillo­
■ be sure that pools and ponds are well protected
facial injuries
« use gates at the top and bottom of stairs until
2. What is the impact of nasal and condylar inju­
a child learns how to navigate steps
ries in children ?
■ equip windows with sturdy screens and guards
3. How does fixation of facial fractures in children
« Always use seat belt in the car
differ from that in adults ?
■ awareness programs should be implemented
4. Classify injuries to the permanent teeth in a
for parents and public
pediatric patient.
ii) Early treatment of large overjet
5. What precautions are to be taken by the p^ents
iii) Provision of mouthguards in sports
in case of an avulsed tooth?
Secondary prevention 6. Why are children less prone to midfacial frac­
Prompt intervention following accidental damage tures?
to the teeth can have a secondary preventive effect 7. How does the treatment of condylar fractures
by reducing the complications of trauma. differ in children ?

Traumatic injuries in the oral and maxillofacial re­

gion are distressing both to the parent as well to the
 10.5 Commonly used Drugs in Children

Nayak AU, Tandon S

The most common clinical situations in dentistry gestions of peers and friends, emotional status, and
amenable to drug therapy in children are pain and presence of fear and anxiety.
infection. The drug control is vital to all phases of
dentistry and a thorough knowledge of the art and Origin Of Pain
science of analgesic therapy is essential for proper Most dental pain is inflammatory in origin and
patient care. hence responds well to drugs with anti-inflamma­
tory components.
Analgesics In Pediatric Dentistry
Classification of analgesics
The management of dental pain in pediatric patient
has lagged markedly behind than that in the adult Analgesics can be broadly classified into
patient resulting from misconceptions regarding the ■ Centrally acting (Narcotic) and
existence of pain sensation and its tolerance in chil­ ■ Peripheral acting (non-narcdtic) analgesics
dren.
Centrally Acting Analgesics *
Concepts About Pain In Children These are more effective against severe and/or acute
L Children have higher tolerance to pain pain, but have a greater incidence of adverse ef­
2. Pain perception is low because of biologic im­ fects. They usually are administered parenterally and
maturity are devoid of anti-inflammatory and antipyretic ef­
3. Little or no memory of a painful experience fects. Serious drug dependence and abuse liability
4. More sensitive to side-effects of analgesics has limited their use in pediatric dentistry.
5. Special risk for addition to narcotics Eg. Morphine, codeine, pethidine, methadone,
dextro propoxyphene
Pain Perception
A good understanding of pain reaction and pain Peripherally Acting Analgesics
perception is required for a proper pain manage­ These are less effective against severe pain and with
ment. Pain perception is objective and measurable, a lower incidence of adverse effects. They are usu­
with an anatomic and neurologic basis, initiated by ally administered orally and are used in a chronic
physical and chemical stimuli. Pain perception may and low grade pain. Some possess anti-inflamma­
be similar in all patients. tory and antipyretic effects. They are frequently com­
bined with other drugs. Their low drug dependence
Pain Reaction and abuse liability has increased scope in pediatric
In contrast to this, pain reaction depends upon dentistry
learned experience, ethnic background, age, sug­ Eg: Ibuprofen, Diclofenac, Nimesilide, Paracetamol
 SECTION 10 : PEDIATRIC CONSIDERATIONS FOR ORAL SURGERY |

Table 10.12: Commonly Used Analgesics In Children

DRUGS ACTION USES DOSAGE AVAILABLE CONTRA SIDE

FORMS INDICATIONS EFFECTS

IBUPR­ Inhibits pros­ Mild to 10-15 mg/kg/ Tabs 200, Bronchial Nausea,
OFEN taglandin moderate day in divided 400,600 asthma, Peptic vomiting
synthesis by pain doses and 800 mg ulcer, Hyper­ cholestatic
interfering with ■* sensitivity jaundice,
cyclo oxygenase severe renal Nephrotoxicity,
needed for disease peptic ulcer,
biosynthesis breathlessness

DICLO­ Inhibits prosta­ Moderate 1-3 mg/kg/day Tabs enteric, Hypersensi­ Dry mouth,
FENAC glandin synthesis pain in divided coated 25, tivity to other bitter taste,
by interfering with doses 50 and 75 mg NSAID’s cholestatic
cyclo oxygenase Bronchial jaundice,
needed for asthma, dysarrhythmias,
biosynthesis peptic ulcer bronchospasm,
nephrotoxicity
blood
dyscrasias

NIMES- Inhibits selectively Mild to 5 mg/kg/day Chewable/ Hypersensitivity, Allergy, gastric

ULIDE prostaglandin moderate in 203 divided dispersible imparted renal bleeding only
synthesis. pain doses tabs 100 mg function in active peptic
inhibits platelet suspension pregnancy, ulcer patients
activating factor, (60 ml) and lactation
tumor necrosis also in gel
factor, metallop­ form
rotease and
histamine release

PARAC­ Inhibits prostag­ Mild pain 14mg/kg/dose Tabs Analgesic Nausea,

ETAMOL landin synthesis 6 hourly 500 mg Nephropathy, epigastric
by inhibiting cyclo 650 mg Jaundice distress, acute
oxygenase toxicity causes
pathway hepatic failure,
Methemoglobi-
unurea

ASPIR­ Inhibits prosta­ Somatic 30-65 mg/kg Tab 75 mg Gastric and

IN glandin pain at 4 to 6 325 mg duodenal distress,
synthesis interval 350 mg ulcers. Hepatic Nausea,
and renal vomiting,
disease, bleeding tinnitus,
diathesis patient vertigo,
on anticoagulant hypersensi­
therapy, children tivity,
< 12 yrs, bronch­ breathless­
ial asthma ness
 I TEXTBOOK OF PEDODONTICS

Nocardia
Combination therapyfor pain Fusobacterium
The combination of two analgesic drugs which pro­
duce analgesia by different mechanisms (central vs Pre school age group children
peripheral) might be expected to produce additive ■ Oral flora resembles that of an adult except that
effects. This may not be true for the analgesics act­ bacteroides melanogenicus and spirochetes are
ing by the same mechanisms. uncommon

The common combinations of analgesic drugs used Principles of Antibiotic Therapy:

in our practice are: The principles of antibiotic therapy ensure that these
• Ibuprofen and paracetamol agents are employed when indicated (presence of
• Diclofenac sodium and paracetamol infection confirmed by clinical signs and symptoms
• Nimesulide and paracetamol and/or laboratory tests, and antibiotic prophylaxis
« Mefenamic acid and paracetamol in a well defined situation), and at optional usage
(proper choice, dose and duration with a minimum
Antibiotic therapy for children attendant harm to the patient).
No aspect of pharmacology is more widely misun­
derstood or improperly applied than the antibiotic Antibiotics do not cure tire patient, but function to
therapy for children. The following review should provide time for the normal host defenses, initially
improve the art and science of drug therapy in situ­ overwhelmed by microbes, to gain control and elimi­
ations of infections in children. nate the infectious process
a. Antibiotics are not a substitute for surgical drain­
The rationale for choice and use of antibiotics be­ age: the drainage of pus thus established, in­
gins with the review of likely microorganisms re­ creases the efficacy of antibiotics in a particular
sponsible for common orofacial infections. case.
Antibiotic dosages for children are similar to
Ilcyelopment Of Oral Microflora those in adults (as adjusted to bods^ weight). The
• Oral cavity is usually sterile at birth exceptions, however, are the neonates who have
■ Number of microorganisms increase following reduced gastric acid, plasma protein binding,
6 to 8 hours after birth blood flow to muscles, renal and hepatic activ­
• At 12 months of age, most children have the fol­ ity and body fat, and increased extracellular fluid
lowing microorganisms in their oral cavity compared to older infants and adults. Hence, a
lower antibiotic dosing is required in neonates.
Streptococcus
a. S.salivarius is the first oral streptococcus Dose calculation by weight
b. S. mutans and S.sanguis are not established un­ Manufacturer recommended doses are based on ex­
til teeth erupt in the oral cavity tensive trials and are usually indicated for the aver­
c. S. mutans disappears when a fidl mouth extrac­ age, healthy adult male of an average weight and
tion is done and again reanoears with dentures age. Thus age, sex, weight and chronic disease of
along with following micro-organisms the major organs of metabolism (liver) and
Staphylococcus excretions (kidney) may affect the usual safe and
Veillonella effective FDA approved dose recommendations.
Actinomyces Creatinine clearance, peak and trough and sympto­
Lactobacilli matic patient response are often used to titrate doses
for a given, therapeutic effect.
 SECTION 10: PEDIATRIC CONSIDERATIONS FOR ORAL SURGERY I

Dentists seldom treat infant, but doses for pediatric method to delay or restrict microbial resistance
patient require an adjustment downward from the would be to limit the antibiotic use to proper
usual adult dose, as determined by body surface area indication, dosages and duration of use. Following
and weight. The following two formulas are used the manufacturers instructions and / or physician’s
for calculating pediatric dosages. instructions would reduce the chances of misuse and
prolong or prevent antibiotic resistance
1. Clark’s rule:
Child’s weight in lbs Antibiotic prophylaxis
------------- --------------------- x adults dose
It is the administration of antibiotics to the patients
150
without the evidence of infection to prevent bacte­
= child’s dose
rial colonization to reduce subsequent post opera­
tive complications. Eg. Antibiotic prophylaxis is re­
1. Young’s rule:
quired in a patient with a rheumatic heart disease
Age of child
to prevent infective endocarditis. It is also required
_—-------- —------ x adult dose = child’s dose
in case of immunosuppressed patients with blood
Age + 12
dyscrasias, cancer chemotherapy and graft recipi­
Anders in 1992 ents.
Administration of the drug based on infant’s weight
is seldom appropriate, Antibiotic prophylaxis for infective endocarditis
in children is given in Table 10.13
wt pd
Dose₽ = dose• x ------- ----- Patients At-Risk From Bacteremia Induced In­
wt. ad fections are discussed in Table 10.14

Surface rule better Commonly used antibiotics in children are given

in Table 10.15
/ wt pd \0.7
Dosea = doseP x \(--------------/) Self-Assessment
\ wt. ad /
1 Which are the antibiotics commonly prescribed
in pediatric dentistry?
Dosea = dose of child 2 Which are the analgesics commonly prescribed
Dose a = dose of adult and in what dosages?
Wt. pd = weight of child 3 Write a prescription for a seven-year old child
Wtad = weight of adult who has undergone an extraction of infected
tooth.
Antibiotic resistance 4 Antibiotic prophylaxis is necessary for which of
Sooner or later, the microorganisms may develop the cases?
resistance to any antimicrobial agent (Archer 1991). 5 What are the complications associated with an­
This could be attributed either to improper use, dose tibiotic therapy?
or duration of use. Thus, the only practical
 TEXTBOOK OF PEDODONTICS

Table 10.13: Antibiotic prophylaxis for infective endocarditis in children

DRUG ORAL

AMOXICILLIN 50mg/kg 1 hour prior to procedure and 25mg/kg

6 hours after initial dose

ERYTHROMYCIN 20mg/kg 1 hour prior to procedure and 10mg/kg

(used if resistant to amoxicillin) 6 hours after initial dose

Clindamycin 10mg/kg 1 hour prior to procedure and 5 mg/kg

(used if resistant to erythromycin) 6 hours after initial dose

American Heart Association

Table 10.14: Patient’s at-risk from bacteremia induced infections

ANTIBIOTIC PROPHYLAXIS ANTIBIOTIC PROPHYLAXIS USUALLY
INDICATED NOT INDICATED
VERY HIGH RISK LOW RISK
Previous episodes of infective Mitral valve prolapse without a murmur
endocarditis
Heart valve prosthesis Coronary artery disease
Coarcation of aorta Artherosclerotic plaque
Indwelling catheter in left side of heart Previous myocardial infection
HIGH RISK CORONARY BYPASS
Rheumatic heart disease Indwelling cardiac pacemakers *
Acquired valvular heart disease .Congenital pulmonary stenosis
Congenital heart disease Six months or longer after surgery for ligated
Ventricular septal defect ductus arteriosus
Patient ductus arteriosus Autogenous vascular grafts
Tetrology of fallot Surgically closed atrial or septal defects
Complex cyanotic heart disease
Systemic pulmonary artery shunt
Indwelling catheter right side of heart
Mitral value prolapse with a murmur
INTERMEDIATE RISK
Tricuspid valve disease
Asymmetric septal hypertrophy
OTHERS AT RISK PATIENTS
Orthopedic prosthetic devices
Immunosuppression
Hemodialysis
 SECTION 10 : PEDIATRIC CONSIDERATIONS FOR ORAL SURGERY I

Table 10.15: Commonly used antibiotics in children

DRUGS ACTION DOSAGE AVAILABLE SIDE EFFECTS CONTRA­
& ROUTE FORMS & ADVERSE INDICATIONS
REACTION

AMOXI­ Interferes with Per oral-20-40 Cap 250, 500 Increased thirst, Hypersensitivity
CILLIN cell wall replica­ mg/kg/day in mg, Tab 125, nausea, vomiting to penicillin
tion of susceptible 3 divided doses 250mg powder diarrhoea, pruritis neonates
organisms, the * 8 hourly for oral susp­ urticaria, angione­
cell wall rendered ension 50mg/ml urotic edema,
osmotically and 125, bronchospasm
instable, swells & 250 mg/5ml anaphylaxis
bursts from
osmotic pressure.

AMOXI Interferes with cell Per oral 20-40 - Cap 250 mg Ciscolored tongue, Hypersensitivity
CtLLIN + wall replication of mg/kg/day .500 mg, glossitis, increased to penicillins in
CLAVUL- susceptible in 3 divided bhewtabs 125 thirst, nausea, neonates
ANATE organisms, the doses (8 hourly) 250 mg, powder vomiting, diarrhoea
POSTA- cell wall rendered for ora» suspen­ hyperkalemia,
SSIUM osmotically sion 125, 250 pruritis, urticaria,
unstable, swells rhg/5ml bronchospasm
and bursts from anaphylaxis
osmotic pressure.

AMOXI­ Interferes with cell 50-100 mg/kg Tab 250 mg & increased thrust, Hypersensitivity
CILLIN + wall replication of of combination 500 mg, cap nausea, vomiting, to penicillin
CLOXA- susceptible body weight 250 and 500 hyperkalemia,
CILLIN organisms, the daily in 3 divided • mg, powder for pruritis, urticaria,
cell wall rendered doses f oral suspension bronchospasm,
osmotically 125 and 250 anaphylaxis
unstable, swells mg/15 ml
and bursts from
osmotic pressure.

AMPICI­ Interferes with cell PO 50-100 mg/ Caps 250 mg Discolored tongue, Hypersensitivity
LLIN wall replication of kg/day in 4 and 500 mg, glossitis, rash, to penicillins
susceptible orga­ divided doses powder for oral urticaria, glomerulo
nisms, the cell (6 hourly) suspension. nephritis, pruritis
wall rendered 100 mg/ml urticaria, angioneurotic
osmotically un­ and 125,250, edema, bronchosp­
stable, swells and 500 mg / 5 ml asms, anaphylaxis,
bursts from osmoti nausea, vomiting,
pressure. diarrhoea

contd.
 I TEXTBOOK OF PEDODONTICS

DRUGS ACTION DOSAGE AVAILABLE SIDE EFFECTS CONTRA­

& ROUTE FORMS & ADVERSE INDICATIONS
REACTION

CEPHA­ Inhibits bacterial PO 50-100 mg/ Cap 250 and Candidiasis, glossitis Hypersensitivity
LEXIN cell wail synthesis, kg/day in 4 500 mg, tab nausea, vomiting to penicillin,
rendering cell wall equal doses 250 and 500mg, diarrhoea, anorexia pregnancy,
osmotically (6 hourly) oral suspension pseudomembranous infants < 1
unstable 125 and 25 mgZ colitis, nephrotoxicity, month.
5 ml and 100 urticaria, rash,
mgZml anaphylaxis

COTRIM- Sulfamethoxazole PO 8 mg/kg/ Tab 80mg (TMP) Candidiasis, Steven Hypersensitivity

OXAZO­ interferes with TMP/40mg/kg Z400mg(SMZ) Johnson syndrome, to trimethoprim
LE bacterial biosynth­ SMZ in 2 divided (double strength) anaphylaxis, SLE, and/or sulfame-
(sulfame esis of proteins by doses (12 160mgTMPZ Nausea, vomiting thoxa zole
thoxazo competitive anta­ hourly) 800mg SMZ, diarrhoea, hepatitis megaloblastic
le + gonism of PABA; suspension enterocolitis, anemia,
(SMZ) trimethoprim 40mgZ200mgZ leukopenia, agranu­ Infants < 2
trimetho blocks synthesis 5ml locytosis, renal failure months,
prim) of tetrahydrofolic pregnancy and
(TMP) acid, this combina­ lactation
tion blocks 2
consecutive syn­
thesis of essential I
nucleic acids,
proteins.
&

ERYTH­ Binds to SDS rib­ PO 30-50mg/kgZ Tabs 250 and Cadidiasis, rash Hypersensitivity
ROMY­ osomal subunits day in 4 divided 500 mg, caps urticaria, pruritis, to preexisting
CIN of susceptible doses (6 hourly) 250 mg, sus­ hypersensitivity, hepatic disease
bacteria and pension 125, nausea, vomiting,
suppresses 250 mgZ5 ml diarrhoea, hepatoto­
protein synthesis xicity, abdominal pain,
pseudomimpronous
tinnitus.

METRO­ In anaerobic micro PO 5mgZkg/ Tab 400 mg Dry mouth, furry Hypersensitivity
NIDAZ- organisms metro- TID and 800 mg tongue, bitter taste, to this drug,
~E nidozole is conver­ metallic taste, renal disease,
ted to active form leukopenia, bone- pregnancy,
by reduction of its marrow aplasia, rash, lactation, hepatic
nitro group. This urticaria, nausea, disease, alcoholic
gets bound to vomiting, diarrhoea, patients
i
DNA and prevents
l

abdominal pain, (disulfurams

nucleic acid nephrotoxicity like reaction)
formation.
 SECTION 10 : PEDIATRIC CONSIDERATIONS FOR ORAL SURGERY I

Further Suggested Reading For Section -10 17. Kaban LB, Diagnosis and treatment of fractures
of the facial bones in children. J. Oral Maxillo­
1. American College of Surgeons: Advanced facial Surgery, 51, 722-729, 1993.
Trauma Life Support Course. Chicago, Ameri­ 18. Kaban LB: Facial trauma I and II. In Kaban LB
can College of Surgeons, 1989 (ed.): Pediatric Oral & Maxillofacial Surgery,
2. Archer W.H Oral and Maxillofacial Surgery:, edition 1, WB Saunders Co., pp. 209-260,1990
Vol. Fifth edition, 1975, W.B. Saunders Co. 19. Laurence DR and Bennet PN: Clinical Pharma­
3. Baker KA, Fator PG. The management of odon­ cology. 7th edition.
togenic infections. A rationale for appropriate 20. Laura Mitchell and David A Mitchill Oxford
chemotherapy, DCNA, 38(4), 689-706, 1994. hand-book of dentistry 1991 edition
4. Baldwin D.C., An investigation of psychologi­ 21. Lewis VL et al: facial injuries associated with
cal and behavioural responses to dental extrac­ cervical fractures. Recognisation, patterns and
tion in children, JDR, Vol. 45, 1637-51, 1966 management. J Trauma, 25, 90-93,1985.
5. Braham Rl, Bogetz MS' Kimura M: 22. Manson PN: Commentary on the long term ef­
Pharmacologic patient management in pediatric fects of rigid fixation on the growing craniofa­
dentistry an update, ACDC J - Dent child. 60, cial skeleton. Journal of Craniofacial Surgery
270-299, 1993. 2:69, 1991
6. Burke FJT: Reattachment of a fractured central 23. Manson PN: Skull and midfacial injuries. In
Mustarde JC, Jackson IT (eds.): Plastic Surgery
incisor tooth fragment BD J, 170,223-225,1991.
in infancy and childhood, edition 3, Churchill
7. Carroll MJ, Hill CM, Mason DA: Facial frac­
Livingstone, NY, pp. 317-345, 1988
tures in children, BDJ 193, 23, 1987.
24. Me Gaw T. Rabom W. Grace M: Analgesics in
8. Eichenwald MD: Antimicrobial therapy in in­
pediatric dental surgery: Relative efficacy of
fants and children. Update 1976-1985, Part I and
aluminum ibuprofen suspension and ace
II, Journal of pediatrics 107 (2), 161-168, 337-
taminophen elixir. ASDC J Dent child. 53, 06-
345, 1985.
109, 1987.
9. Fortunato MA, Fielding AF, Guernsey LH: fa­
25. Meadow D et al: Oral trauma in children. J.
cial bone fractures in children. Oral surgery 53,
Peadiatr. Dent 6(4), 248-251,1984.
225-230,1982.
26. Meechan JG, Wefljury RR: Exodontia and Mi­
10. Gellin M.E., Extraction procedures for the child,
nor Oral Surgery for the Child Patient. Dental
DCNA, Vol. 17, 161-172, 1973
Update 263-270, 1993
11. Graw Me BL, Cole RR: Pediatric maxillofacial 27. Miyanaga M., Takei T., Observation of child with
trauma: Age related variation in injury. Arch multiple submerged primary teeth, JDC, W. 65 ,
Otolaryngeal Head Neck Surg, 116,41,1990. 495-8, 1998
12. Hall RK: Facial trauma in children. Austr Den­ 28. Montgomery HE, Krueger DE. Principles of anti-
tal J 19: 336-45, 1974 infective therapy, DCNA, 28(3), 423-433,1984.
13. Harding AM: Pharmacologic consideration in 29. Nainar S.M.. Profile of primary teeth with pul­
pediatric Dentistry, DCNA 38,733-754, 1994. pal involvement secondary to caries, JDC, Vol.
14. Hooley J.R. , Golden D.P. surgical extractions, 65, 1998
DCNA 38 (2), 217- 236,1994. 30. Nathan JE, West MS: Comparison of chloral
15. Hunter GT: Pediatric Maxillofacial trauma. hydrate hydroxyzine with and without meperid­
Pediatric clinic of North America, 35(6), 1127- ine for management of difficult pediatric patient.
1144, 1992. ASDC J dent. Child 54, 437-44,1987.
16. Ingle and Leij K Bakland Text book of endo­ 31. Needle man HL: Orofacial trauma in child abuse:
dontics 4th edition Types, prevalence, management and dental
 | TEXTBOOK OF PEDODONTICS

professions involvement. Pediatr. Dent. 8: 71- 37. Staves E, Tinanoff N: Decline in salivary S
80; 1986. mutans levels in children who have received
32. O’ Mullane DM: Some factors predisposing to short term antibiotic therapy. Pediatric Dentistry;
injuries-of permanent incisors in school children. 13, 176-173, 1991.
BDJ, 134, 328-332, 1973. 38. Topazian and Goldbert: Oral and Maxillofacial
33. Pallasch Clinical drug therapy in dental prac­ infections.- 3rd edition, 1994
tice 1973. 39. Thomas J Pallasch: Pharmacology for dental stu­
34. Posnick JC, Wells M and Pron GE: Pediatric dents and practitioners. 1980 edition
40. Welbery RR and Murray J J: Prevention of trauma
facial fractures evolving patterns of treatment. J
to teeth. Dent. Update, 17, 117-121, 1990.
oral maxillofacial surgeiy, 51, 836-844, 1993.
41. Welbury RR, Meechan JG: Minor Oral Surgeiy
35. Scheer B: Emergency treatment of avulsed inci­
for Children : 1. Medical Problems Influencing
sor teeth. Br. Med. J. 301, 4, 1990.
Management. Dental Update 160-166, 1993
36 . Simonsen RJ: Restoration of a fractured central
42. Zilberman et al: Effect of trauma to primary in­
incisor using original tooth fragments. J. Amer. cisors on root development of their permanent
Dent. Assoc. 105, 646-648, 1982. successors. J. Pediatric Dent. 8, 284-293, 1986.
 ^SECTION - 11,

Dental Care for the

Special Child
11.1 Introduction
Goel R, Bhat M

Dental care for special children is often neglected American Association of Pediatric Dentistry(1996)
by both parents and dentists, a sad but true fact. states, a person should be considered dentally handi­
The terms ‘special child’ or ‘disabled child’ are of­ capped if there is pain, infection or lack of func­
ten reserved for those who are having impairment tional dentition which affects the following:
that restricts or limits daily activity in some manner. a. Restricts consumption of a diet adequate to sup­
There by these handicapped children can be broadly port growth and energy needs
divided into medically compromised children and b. Delays or otherwise alters growth and develop­
developmentally disabled children. These children ment
need our attention, more so because of the fact that c. Inhibits performance of any major life activity
they are unable to take care of their basic oral health including work, learning, communication and
care needs. Despite the recognition of the role of recreation
dental profession in taking oral care for these
children, many dentists display a reluctance to accept Classification
these children as patients. This is due to many reasons
like, dentist’s lack of knowledge about the various A.Frank and Winter, (1974), have classified handi­
disabilities afflicting the children, his fear of patients cap as:
with inability to develop personal relationships and * blind or partially sighted
unfamiliarity with the procedures regarding compre­ * deaf or partiallydeaf _
hensive dental care. WHO in 1981 first started * educationally subnormal,
medical services to handicapped children. Since then,
a number of specialist pediatric dentists are willing * nraiadjusted
and qualified to provide dental health services. * physically handicapped ~
* defective of speech
Definition * senile

The World Health Organization has defined a handi­ B. Agerholm, (1975) classified handicapping con­
capped person as (one who over an appreciable pe­ ditions into intrinsic and extrinsic categories. An
riod is prevented by physical or mental conditions intrinsic handicap is one from which the person
from full participation in the normal activities of cannot be separated, while an extrinsic handi­
their age groups including those of a social, recrea? cap is one from which the person, the patient
tional, educational, and vocational nature”. can be removed, for example, social deprivation.
 I TEXTBOOK OF PEDODONTICS

C. Nowak (1976) has classified handicapping con­ made with appropriate modifications made as a
ditions into nine categories as follows: result of the nature of the handicap. In the case
1. Physically handicapped, e.g. Poliomyelitis, of mental retardation, as the patient is sometimes
scoliosis ~ unable to enter discussions regarding treatment,
2. Mentally handicapped^ e.g. Mental retarda- the accompanying relative has apart in deciding
tioiC * the eventual care required.
3. Congenital defects, e.g. Cleft palate congeni­
tal heart disease 2. The attitude of the parents towards particular
4. Convulsiye disorder. e.g. Epilepsy problems:
5. Communication disorder, e.g. Deafness, Parents have feelings of sorrow, guilt, anger and
Blindness self-pity when a child is born with handicapped
6. Systemic disorder, e.g. Hypothyroidism problems. The family has been emotionally,
Hemophilia physically and financially tied up with the pa­
7. Metabolic disorders, e.g. Juvenile diabetes tient’s medical conditions, which makes them
8. Osseous disorders, e.g. Rickets, Osteopetrosis difficult to get interested in dental needs of the
9. Malignant disorders, e.g.; Leukemia child. The attitude of the parents influence the
dental service based on two types of behaviours,
D. Considering the variations in the types of treat­ namely overprotection and underprotection. If
ment modalities for handicapped children, for it is an overprotected child, the parents bring
the convenience of management, they can be the child and ask about dental procedures,
categorized into two: whereas if it is an underprotected child the par­
1. Developmentally disabled child ents will not be bothered about the child’s oral
2. Medically compromised patients care. Informed consent must be taken prior to
starting any treatment, which may also include
Treatment factors to be considered general anesthesia or even the use of physical
restraints.
3. Attitude of the society: These children are some­
1. Understanding the condition
times not well accepted by the sotiety and this
Before planning any treatment, the dentist must
may have a psychological impact on the child’s
carefully assess and evaluate the handicap pa­
mind. This fact should be taken into considera­
tient’s dental needs and his/her ability and will­
tion during treatment.
ingness to cooperate during treatment. The
4. Attitude of the patient: The dental management
handicap patient differs from a normal patient
techniques must be carried out with tender lov­
with regard to the professional relationship be­
ing care. If the treatment provider uses harsh
tween patient and the dentist. Usually it is a words to the child, then the child will not come
three-way relationship, but in the case of handi­ to the office at all.
capped children it may involve fourth or even 5. Attitude of the dentist towards the particular con­
fifth interested parties, i.e. a headmaster or head­ dition: the dentist’s attitude must always be posi­
mistress of a residential special school. Assess­ tive, but most of the time the dentist has a nega­
ment should be achieved via a history and clini­ tive attitude due to following reasons;
cal examination. The level of communication a. Lack of education and experience on the part
and intelligence of the child should be elicited of the dentist to deal with such children
along with the relevant past medical and dental b. Fear of the patient
history. During clinical examination, an assess­ c. Feeling incompetent to treat
ment as to the ease of operating can be made. d. Inability to develop relationships
Treatment plans for handicapped patients are e. Physical repulsion
 SECTION 11 : DENTAL CARE FOR THE SPECIAL CHILD |

f. Substandard fees cerebral palsy are associated with difficulty in swal­

g. Need for special equipment and dental office lowing and the food may need to be poured. Proper
architecture. instructions for breastfeeding and weaning should
be given to decrease the chances of nursing caries.
Therefore dental care of the disabled child should
be aimed at developing an empathy in the dental Fluoride
practitioners towards these children. Systemic fluoride through the ingestion of optimally
fluoridated water should be advocated to handi­
Preventive Measures capped children. Where the level is suboptimal, fluo­
ride supplementation is required (tablets, drops,
Plaque control rinses). Regularly, scheduled professional applica­
Handicapped patients tave a poor standard of oral tion of topical fluoride should be carried out both in
hygiene along with a higher prevalence of periodon­ the fluoridated and nonfluoridated areas. Use of fluo­
tal disease. Prevention centers around systematic ride containing dentifrice and daily mouth rinses
removal of bacterial plaque. Tooth brushing and are beneficial in the handicapped children with very
flossing, the most effective plaque controlling meth­ poor oral hygiene.
ods require practice, skill, and effort. Most handi­
capped individuals may find all of these tasks daunt­ Preventive restorations
ing and are unable to achieve adequate standards of These include the application ofpit and fissure seal­
plaque control. The brushing technique for these ants, preventive resin restorations, and even stain­
children should be carried out by theparents/guard- less steel crowns (in cases of severe bruxism or in-
ians. An often recommended technique is the hori­ terproximal caries).
zontal scrub method due to its ease of performance.
Modifications of toothbrushes can be made, i.e. the Self-Assessment
grips can be modified using the patients hand to
custom design the handle, bicycle handles can be 1. Define handicapped chidlren.
fitted over the brush handle to give a better grip. 2. Classify handicapping condition as given by
Electric toothbrushes can also be used. Nowak.
3. What are tire preventive considerations in handi­
Diet capped children?
A balanced diet is essential for nutrition as well as 4. Who is an intrinsic handicap?
a part of the preventive program for the handicapped 5 . What are the factors to be considered before treat­
children. The diet may vary depending upon the ing a handicapped child?
handicapping condition present. Conditions like
 11.2 Management of Developmentally
Disabled Child
Bhat M, Tandon S,.Goel R

A. MENTAL RETARDATION: The children who Table 11.2 I.Q classification guide
are disabled due to developmental conditions and
IQ range Grade
not able to enjoy the privileges of a normal child.
Mental retardation as a general term is applied to Above 140 Very superior
persons whose intellectual development is signifi­
120-139 Superior
cantly lower than that of normal persons and whose
ability to adapt to their environment is consequently 110-119 High average
limited (McDonald 1983). Mental retardation is
90-109 Average
defined by the American Academy on mental defi­
ciency as “significantly subaverage intellectual func­ 80-89 Low average
tioning, existing concurrently with deficit in adap­ 70-79 Borderline impaired
tive behavior and manifested during the develop­
mental period.’’ Mental retardation translates an <69 Mentally retarded
intelligence quotient (I.Q.) which is calculated as:
Etiology
*

Mental age
—---------- ------- —----- x 100 Mental retardation affects more children than any
Chronological age other congenital disease. It has been attributed to
various etiologic factors (Table 11.3)
The American Association of Mental Deficiency has
recommended the following classification for men­
Dental Problems
tal retardation based on LQ.
They also present with multiple anomalies of facial
Table 11.1 Characteristics of mental retardation structures, eruption time, sequence and number,
presence of malocclusion, enamel hypoplasia. They
I.Q. Description Practical description may also show a higher prevalence of dental caries
52-68 Mild Educable in special classes and periodontal disease, because of poor oral hy­
36-51 Moderate Trainable, perform self help giene and cariogenic diet patterns.
skills, sheltered workshop
Treatment Considerations
employment
20-35 Severe Ability limited to simple
language, self help skills The dentist must first assess the child’s mental level
19 & Profound Consistent custodial care so as to gauge the level of cooperation to be ex­
below required pected and make adjustments accordingly:
 SECTION 11 : DENTAL CARE FOR THE SPECIAL CHILD |

Table 11.3: Etiological factors of mental retardation

Prenatal influences Natal influences Post-natal influences

• Maternal and fetal • Infection • Cerebral infection Eg: Meningitis

infections Eg: Rubella Cerebral trauma • Cerebral trauma
• Kernicterus Birth injuries • Poisoning ~
• Cretinism • Haemorrhage Cerebral vascular accident
• Prenatal unknown cause • Hypoxia, anoxia • Post immunization encephalopathy
• Fetal alcohol syndrome • Hypoglycemia • Malnutrition
• Genetic diseases
Eg: Down’s syndrome

■ Short attention span, restlessness, hyperactivity,

and enatic emotional behaviour characterize MR
patients undergoing dental treatment.
■ Familiarize the patient to the office, dental per­
sonnel to reduce his/her fear of the unknown
before undertaking any treatment
■ Speech must be slow and simple.
■ Only one instructidn at a time should be given
■ TSD and TLC approach in mild cases whereas
sedation in hioderate cases.
■ Carefully listen to the patient as these children
often have trouble with communication.
■ Appointments should be short and scheduled
during the early part of the day.
« Children should be nianaged wdh a blend of
kindness and firmness.
■ General anesthesia may be indicated in cases
Fig. 11.1 Chid with Down’s Syndrome
where adequate levels of cooperation cannot be
characterized by a) widely separated eye and flat
achieved or where extensive rehabilitation is re­ nasal bridge, b) Anterior open bite
quired.
■ Permanent restorations and preventive proce­ Predisposing Factors and Causes
dures with regular recalls. Advanced maternal age, uterine and placental ab­
normalities, chromosomal aberrations.
B. DOWN’S SYNDROME (Fig. 11.1a, b)
General manifestations of Down’s Syndrome
This is one of the most recognizable malformation
S/wZZ
syndromes. It may occur due to trisomy of chrom-
-a« Brachycephalic (round) skull resulting in a flat­
some 21 (95%), translocation (3%) or due to mo­
tened face and occiput
saicism (2%).
b. Presence at birth of third fontanelle. Just ante­
rior to the posterior fontanelle.
Incidence
c. Flat nasal bridges with a small maxilla.
It is found to occur as 1 in even 600 newborns.
 I TEXTBOOK OF PEDODONTICS

Eyes Tongue
a. Oblique palpebral fissures with prominent epi­ ^r^Protrusive fissured (scrotal) tongue.
canthic folds. - CircumvaUatepapillagjnay be enlarged, but fili­
b. Brushfield’s spots appear on the iris in a ring form papillae may BeaSsent.
concentric with the pupil. - Macroglossia.
c. Scanty eyelashes.
d. CataractsTsquint and nystagmus are common Lips
-^Thick, dry, fissured.
Ears
a. Dysplastic ears with abnormal pinna Occlusion
' -"^AnienoFopen bite and crossbite, class III ten­
Neck dency.
Short and broad with excess skin posteriorly - Small-maxilla,

Hands Palate
a. Broad and short (clinodactyly) with a single - Often appears high with horizontal palatal
transverse palmar crease (simian crease). shelves (omega palate).
b. Short incurved little finger. - Bifid uvula, cleft lip and palate.
c. Multiple loops on finger tips.
Eruj>tipji^i&£iE^
Muscles And-Joints - Retarded
Hypotonicity and hyper extensibility. - Early shedding of deciduous teeth

IQ Teeth i

Often severally retarded with an IQ of 25-50. - Hypodontia especially third molars and maxil-
larylateral incisors.
Associated congenital abnormalities, - Microdontia. *
a. Congenital heart lesions are found in upto 50% - Hypocalcification and hypoplastic defects.
( atrial septal defect, atrioventricular canal and - Low incidence of caries.
VSD).
b. Duodenal atresia. Periodontium
c. Atlanta axial instability. - Severe, early onset periodontal disease due to
d. Umbilical hernia. local factors like poor oral hygiene, tooth mor­
e. Multiple immunological defects affecting the phology and malocclusions and systemic factors
skin, GIT and respiratory tracts. like decreased humoral response, reduced
f. Acute lymphoblastic leukemia 20 times more chemotaxis, impaired phagocytosis, poor circu­
common in these children. lation, etc.
g. Hypothyroidism and Alzheimer’s disease.
Dental treatment
Oral manifestations..-.
■ These children (10%; are mentally retarded (mod­
Mouth .-~ erate to severe) and requireiappropriate treatment.
- Small drooping mouth ■ Incidence of cardiac disease associated with
- Open mouth posture Down syndrome is 40% and will require ad­
equate prophylaxis.
 SECTION 11 : DENTAL CARE FOR THE SPECIAL CHILD |

■ Increased incidence of leukemia and acute and Dental Treatment

chronic infections of the upper respiratory tract ■ Most accept dental care willingly, do not cause
can also alter treatment any unusual management problems
■ Children are generally affectionate and coopera­ ■ In resistant patients, analgesia, sedation or gen­
tive and present no special problems during eral anesthesia may be used.
management
■ Nitrous oxide analgesia or TSD in mildly ap­ D. CEREBRAL PALSY
prehensive patients can be used ; general
anesthesia in severe resistance to dental treat­ This is one of the most severely hand! mg con-
ment. ditions affecting childhood. Cerebral palsy is de­
■ Preventive procedures along with chlorhexidine fined as a non-progressive lesion which occurs in
mouth wash may be beneficial. thedeveloping brain before, during or after birth,
■ Pulp treatment in deciduous teeth are contrain­ leaving the child with a variety of neurological prob­
dicated in patients with cardiac problems because lems. 50% of these children die in infancy or re­
of the risk of bacteremia whereas in permanent quire institutional care. The motor deficit is fully
teeth it can be considered if an adequate apical evident only as the child develops.
seal can be obtained.
The condition manifests itself as a number of neu­
C LEARNING DISABILITY romuscular dysfunctions and involves muscle weak­
ness, stiffness, paralysis, poor balance, irregular gait,
This term does not include any learning problems and uncoordinated or involuntary movement. There
caused due to visual, hearing , motor handicap, is a loss of voluntary muscle control. One newborn
mental retardation, emotional disturbanceorenvi- in approximately 200 live births is affected.
ronmental conditions.
Etiology
Definition Any factor that causes decreased oxygenatipn to the
The term is applied to children who exhibit a disor- developing brain can lead to a damage to the brain.
der in one or moreofthe basic psychological proc- Complications of labour; or delivery, infections of
esses, involved in understanding or using spoken the brain like meningitis, encephalitis, toxemia of
or written language. pregnancy, congenital defects of the brain,
% kemicterus, heavy metal and drug poisoning, any
Incidence trauma to the head, premature bir^withjCNS
Affects 3 to 15 % of the population and is four times abnormality are the common causes.
more common in males.
Classification
I. Based on anatomical involvement
Etiology
^«-Monoplegia - involvement of one limb only
Cause remains unclear. Minimal brain injury and
Hemiplegia - involvement of one side of the
damage to CNS have been implicated. A genetic
body
predisposition can also be traced.
^e<Paraplegia - involvement of both legs only
Learning disability can be manifested in disorders
^d^uadriplegia - involvement of all the four
of thinking, listening, talking, reading, writing,
limbs
spelling or arithmetic. It includes conditions like
minimal brain dysfunction, dyslexia, developmen­ II. Based on neuromuscular involvement:
tal aphasia, etc. 1. Spasticity
2. Athetosis
 €59 I TEXTBOOK OF PEDODONTICS

3. Ataxia „ i. Frequent uncontrolled jaw movements are

4. Mixed seen that cause abrupt closing of the jaw or
severe bruxism
1. Spastic cerebral palsy
3. Ataxia
Clinical features a. Approximately in 5% of cases
a. Approximately seen in 70% of cases b. Involved muscles unable to contract com­
b. Increased motor tone resulting in stiffness and pletely
difficulty in moving limbs c. Involvement of cerebellum
c. Increased deep tendon and stretch reflexes d. Lack of balance leading to staggering gait
d. Involvement of cerebral cortex e. Visual organs may be involved
e. The foot and leg flexed and rotated resulting
in a limping gait with circumduction of the 4. Mixed
affected leg a. Approximately 10% of cases
£ Lack of control of neck muscles, trunk mus­ b. Combination of characteristics of more than
cles and intra-oral muscles one type of cerebral palsy
g. Impaired chewing and swallovying with
speech problems 5. Tremors
h. Wherein the involved muscles show hyperir­ a. Shaking of parts of the body
ritability, exaggerated contractions when b. Involvement of basal ganglia
stimulated, tense muscles
L Excessive drooling, persistent tongue thrust, 6. Rigidity
and speech impairments. a. Resistance to passive movements
b. Basal ganglia is involved. \
2. Athetosis^ c. Voluntary movements slow and stiff.
Clinical features
a. Approximately in 15% of cases Characteristic of cerebral palsy is the persistent
b. Involvement of basal ganglia neonatal reflexes, i.e. asymmetric tonic neck reflex,
c. Uncontrolled voluntary muscle contraction tonic labrynthine reflex, and the startle reflex. Along
d. Generalized delay in motor development and with these defects we can also see mental retarda­
the child may show drooling, dysphagia, tion, seizure disorders, sensory deficits and speech
speech difficulties and grimacing. disorders like dysarthria.
e. Hypertonicity of the neck musculature with
excessive movement of head leading to held Dental Problems
back head with mouth open and tongue pro­ Several conditions are more common in these chil­
truded dren than in the normal population.
f. Peri-oral muscles hypotonic with mouth
breathing, bruxism ■ Dental Caries
g. Most often not associated with convulsions Most children may have a higher caries rate than
or mental retardation. normal children. This may be due to their in­
h. Characterized by slow twisting or writhing ability to maintain good oral hygiene, to the par­
involuntary movements(athetosis) or quick ent’s tendency to overindulge them with soft and
jerky movements(choreoathetosis) and con­ cariogenic food, and to the increased prevalence
stant uncontrolled motion of involved mus­ of enamel hypoplastic defects on their teeth.
cles
 SECTION 11 : DENTAL CARE FOR THE SPECIAL CHILD |

Periodontal Disease Treatment

Occurs with a great frequency, as the patient is
unable to brush or floss adequately. Due to diffi­ ■ Thorough medical and dental history should be
culty in chewing and swallowing, children tend taken, along with consultation with the child’s
to eat soft foods that are high in carbohydrates. physician.
They may also be on phenytoin to control sei­ « Maintain a calm, friendly and professionalat-
zure activity which is a cause of some degree of mosphere, be empathetic about the child’s prob­
gingival hyperplasia. lems.
■ Many patiente can and prefer to be treated in the
Malocclusions wheelchair, which may be tipped back into the
Occurs twice as often than in the average popu­ dentist’s lap.
lation. Commonly noticed are protrusion of the ■ The patient’s head should be stabilized through­
maxillary anterior teeth, excessive overjet and out t he procedure and the back should be elevated
overbite, open bites and unilateral cross-bites, to reduce swallowing problems.
the cause being the disharmonious relationship ■^Ugeplo'sical restraints judiciously for control of
between intraoral and perioral musculature. In flailing extremities^)
spastics, class II div 2 malocclusion is observed, « The variety of mouth props and finger splints can
along with constricted maxillary and mandibu­ be used for control cfinvolimtaiyjaw movements.
lar arches. In the athetoid group, Class II div 1 ■ Avoid abrupt movements.Jights and noises to
malocclusion is seen along with a high and nar­ minimize startle reflex reactions and introduce
row palatal vault. intraoral stimuli slowly to avoid gag reflex.
■ Local anesthetic can be used with care and
Bruxism stabilization against any sudden movement by
Commonly seen in athetoid cerebral palsy re­ the child.
sulting in severe attrition, loss of vertical dimen­ « Rubber dam can be used to protect the working
sion and temporomandibular joint disorders. area from hyperactive tongue movement, al­
though floss should be attached to small objects
Trauma such as cotton rolls that can become dislodged
Due to the nature of the disorder, these children ■ Gauze shields should be used during extraction
are susceptible to trauma, especially of the max­ to avoid tooth aspiration'
illary anterior teeth. ■ Piemedication can be used to reduce hyperto­
nicity, involuntary movement and anxiety.
Children ma>7 have excessive drooling and diffi­ ■ General anesthesia can be used as a last resort if
culty in swallowing the case is not manageable chairside.
« Do permanent restorations and preventive meas­
Spastic cerebral pals}7 patients present with spas­ ures
tic tongue thrust, constricted mandibular and
maxillary arches, class II div II malocclusion E. EPILEPSY
(75%) usually with a unilateral crossbite.
The epilepsies are a group of disorders character­
Athetoid cerebral palsy patients presents with a ized by chronic, recurrent, paroxysmal changesZuL
mouth breathing, tongue protruding between the neurolgic function caused by abnormalities^ mffie
teeth and the lips, bruxism, high narrow palate electrical activity of the brain . Jsach episode of neu­
and anterior open bite. rologic dysfunction is called a seizure and the
 €ЕЭ I TEXTBOOK OF PEDODONTICS

seizure may be convulsive when accompanied by Commonly seen are the absence seizures(petit
motor manifestations or may be manifest by other mal) in children and the Primary Generalized
changes in neurologic function. Seizures tonic-clonic(grand mal) which occur
most commonly.
Etiology
Epileptic disorders can occur due to idiopathic or Absence seizures consist of:
symptomatic reasons. In the idiopathic group the ■ Sudden cessation of the ongoing conscious ac­
condition cannot be attributed to any demonstrable tivity without convulsive muscular activity or loss
lesion of the brain and are frequently of genetic ori­ of postural control
gin. In the symptomatic group, the condition is as­ ■ Brief lapses of consciousness or awareness may
sociated with the pathology' of the brain due to de­ occur
velopmental anomalies such as brain malformation, ■ Usually last for a few seconds to minutes and
injury, or disease such as fever, hypoxia, are quite inapparent
hypocalcemia. ■ Occur in children of 6 to .14 years

Classification Tonic -Clonic seizures consist of:

The earlier classification of epilepsy included petit ■ Start without warning.
mal, grand mal and psychomotor or temporal lobe ■ Heralded by a sudden loss of consciousness, a
epilepsy. The International League Against Epilepsy tonic contraction of the muscles, loss of postural
has classified epileptic seizures as follows. control, respiration arrests and the patient be­
comes cyanotic, pupils dilate, the eye ball roll
• Partial or Focal Seizures upwards or to the side, the face becomes distorted.
Simple partial seizures (with motor, sensory, au­ ■ After 10 to 30 seconds, the tonic phase is fol­
tonomic, or psychic signs) lowed by a clonic phase of several minutes du­
Complex partial seizures (psychomotor or tem­ ration wherein the .muscles ale violently con­
poral lobe seizures) tracted, with profiise salivation, perspiration, and
Secondary generalized partial seizures involuntary bladder and bowel evacuation.
■ The contractions become less violent and gradu­
• Primary Generalized Seizures ally cease.
Tonic-clonic (grand mal) ■ Child then remains stuperous and goes into a
Tonic deep sleep.
Absence (Petit mal)
Atypical absence Oral manifestations of Epilepsy
Myoclonic Injuries caused by the fit:
Atonic a. Soft tissue lacerations of tongue or buccal mu-
Infantile spasms cosa.
b. Facial fractures
■ Status Epilepticus
c. Trauma to teeth - avulsion, luxation, fractures
Tonic-clonic status
d. Subluxation of the TMJ
Absence status —‘ * T . «

Epilepsia partialis continua

Injuries due to drug therapy
• Recurrent Patterns a. Gingival hyperplasia
Sporadic b. Recurrent aphthous like ulceration
Cyclic c. Anomalous dental development like small teeth,
Reflex delayed eruption
 SECTION 11 : DENTAL CARE FOR THE SPECIAL CHILD I

d. Cervical lymphadenopathy 5. If the convulsions do not stop within a few min­

e. Secondary infections of this fibrous overgrowth utes then give diazepam ( lmg/kg) IV and slowly
when oral hygiene practices are neglected result­ up to 10 mg' ’
ing in friable and hemorrhagic tissues 6. Give oxygen
7. If condition does not improve, admit to hospital
Dental management
Dental treatment
Prevention of seizures in the dental office can be
- Appointments should be kept short.
best managed by:
- Importance of tooth brushing procedures and
1. Complete medical history should be acquired
regular dental review must be stressed.
regarding the type and frequency of seizure epi­
- If appliances are indicated for tooth movement
sodes prior to treatment.
and tooth replacement, the fixed type is preferred.
2. Reduce stress on the patients with
psychobehavioural preparations, sedation, etc.
F. DEAFNESS
Diazepam is the drug of choice because it has
anticonvulsant properties. This includes individuals who have total deafness
3. Use of dental chair ligfefis avoided. as well as the hearing impaired making them suffer
4. Avoid seizure promoting drugs, such as from varying degrees of deafness. Inevitably their
phenothiazines, IV local anesthetics. speech is affected as sounds have to be heard to be
5. Appropriate drug therapy for seizures. Earlier imitated. This reduced ability to communicate
dilantin. sodium has been used but nowadays new through speech influences adversely the psychologi­
drugs are used like vigabatrin, lamotrigine, cal development and social integration of the deaf
gabapentin and topiramate?-:----- children.
6. Due to the use of antiepileptic medication
(dilantin sodium), typical fibrous gingival hy- Etiology
^perplasia may occur Surgic^Tremovarmly^ ■ Prenatal
F necessary in certain cases and the child’s physi­ Causes like viral infections (rubella and influ­
cian can be consulted about a change in medica­ enza), ototoxic drugs, congenital syphilis, he­
tion. redity, etc.
■ Perinatal
Office management ofseizure- Causes like toxemia late in pregnancy, birth
1. If the seizure occurs in the dental chair the chair injuries, prematurity, erythroblastosis foetalis,
is lowered to a supine position. The patient is anoxia, etc.
protected from injuring himself bymovingsharp ■ Postnatal
objects away, wrapped tongue blade is placed to Causes like injuries, ototoxic drugs (streptomy­
prevent tongue biting. cin, kanamycin, aspirin), viral infections ( mea­
2. When a seizure occurs, the dentist has to pre­ sles, mumps, chicken pox, influenza, meningi­
vent the child from injuring himself. A tis, poliomyelitis).
mouthprop of rubber or plastic should be inserted
into the oral cavity to prevent tongue biting. The Dental Problems and Treatment
patient should be shifted to a place where he/she ■ Poor oral hygiene related to learning disability
cannot liarm themselves. and hypoplastic teeth can occur in hearing im­
3. Maintain a patent airway paired children?"
4. Suction may be usefill to avoid aspiration of se­ ■ During the preappointment interview, the man­
cretions, but if it is not available the head should ner of communication should be elicited along
be turned to the side. with a detailed medical history.
 I TEXTBOOK OF PEDODONT1CS

« If the parent is allowed to remain in the operatory, ■ Make physical contact reassuringly and do not
then he/she should be positioned such that the suddenly grab or move the patient without prior
child can see them (thus reducing any anxiety) notice.
s Proceed slowly in a warm and reassuring man­ ■ The dentist can make use of touch, taste and
ner, using facial expressions, smiles, gestures, smell rather than the TSD methodising strong
physical contact, and praise. tastes in small quantities as these may be rejected
« Speak directly facing the patient in a normal by the child).
tone, without using slang(as child may be lip « Prolonged immature swallowing pattern due to
reading). a reluctance to consume solid foods, poor oral
• Adjust the hearing-aid while using a handpiece hygiene related to learning disabilities, as well
as all sounds may be amplified as hypoplastic teeth have been identified as pos­
• Use the tell-show-do, positive reinforcement and sible oral manifestations in visually impaired
modelling behavior modification techniques children.
« Pretreatment sedation or even general anesthesia ■ Trauma to the anterior teeth also occurs with a
may be required for more serious behavioural higher frequency than in the normal population.
management problems. ■ Increased gingival inflammation due to inabil­
ity to visualize and remove the plaque.
G. BLINDNESS « Avoid using any signs, expressions of pity and
references to blindness as an affliction.
Blindness affects a large number of individuals ■ Oral hygiene should be explained and the child
world-wide. It is not an all or none phenomenon, guided through the procedures by the dentist
and a person is considered affected by blindness if along with the use of audiocassettes and Braille
the visual acuity does not exceed 20/200 in the bet­ pamphlets.
ter eye, with the correcting lenses, or if the visual
amity is greater than 20/200 but accompanied by a Self-Assess men«
visual field of no greater than 20 degrees.
1. Define handicapping condition.
Etiology
2. Define WHO and AAPD definition.
■ Prenatal
3. Give the classification of handicapped conditions.
Causes are optic atrophy, microphthalmus,
4. What is the parental attitudes to handicapping?
tumors, cataracts, toxoplasmosis, rubella,
5. What are the types of physical restraints used
syphylis, TB meningitis, etc.
for handicapped conditions?
« Postnatal
6. Define mental retardation.
Causes are trauma, hypertension, premature
7. WhatisI.Q?
birth, hemorrhagic disorders, leukemia, diabe­
8. Wha t are the causes of mental retardation?
tes mellitus, glaucoma, etc.
9. How do you classify mental retardation?
10. What are the oral features of a mentally retarded
Dental Problems and Treatment
‘ child?
11. Define cerebral palsy.
« Complete medical history along with the degree
12. What are the types of cerebral palsy7?
of visual impairment is ascertained prior to treat­
13. What are the oral manifestations of cerebral palsy?
ment.
14. What are the clinical features of Down’s Syn­
Describe in detail the office settings, office per­
drome?
sonnel, and treatment procedures before start­
15. What are the oral manifestations of Down’s syn­
ing anything.
drome?
 s

11.3 Management of Medically

Compromised Patients
Bhat M, Tandon S, Gœl R

A medically compromised condition is where the the heart, (tetralogy of Fallot, transposition of great
patient suffers from a certain systemic condition vessels, pulmonary stenosis, tricuspid atresia). Clini­
which puts him at a risk when regular dental treat­ cal manifestations can include cyanosis, hypoxic
ment is required. Due to this, the pedodontist has to spells, poor physical development, heart murmurs
take certain precautions so as to enable him to go and clubbing of fingers and toes.
through the treatment without complications.
Etiology of congenital heart disease (CHD)
1. HEART DISEASE ■ Etiology of CHD is usually multifactorial and
there is an apparent interaction between genetic
There are two categories of heart conditions, i.e. and environment factors.
congenital and acquired. Congenital heart defect is ■ Maternal rubella, maternal diabetes and drugs
usually due to an aberrant embryonic development during pregnancy (e.g. alcohol, phenytoin)
of a normal structure or the failure of the structure ■ Children with inborn errors of metabolism and
to progress beyond an early stage of embryonic de­ connective tissue disorders and other syndromes
velopment. Congenital heart disease can be further like down’s syndrome, williams syndrome have
classified as cardiac lesions.
■ Acyanotic
a Cyanotic ACQUIRED HEART DISEASE

Acyanotic Congenital Heart Disease

Rheumatic Fever
In this condition there is a minimum, or no cyanosis.
It can occur at any age, but is rare in infancy. Most
It consists of two different categories, the first
commonly it appears between 6 and 15 years of age.
consisting of defects that cause left-to-right shunt­
The condition can be fatal in the acute stage or can
ing of blood within the heart (atrial septal and ven­
lead to a chronic rheumatic heart disease as a result
tricular septal defects). The second category con­
of scarring of the valves.
sists of defects that cause obstruction (aortic steno­
sis, coarctation of the aorta). Clinical manifestations
The clinical symptoms: T Duckett Jones has pro­
of the first defect include congestive heart failure,
posed useful diagnostic criteria (Table 11.4)
pulmonary congestion, heart murmur, laboured
breathing and cardiomegaly
Infective bacterial endocarditis
A very serious infection characterized by microbial
Cyanotic Congenital Heart Disease
infection of the heart valves or endocardium. Two
In this condition, cyanosis is seen on minimum ex­
forms are present, the acute and subacute forms. In
ertion due to right-to-left shunting of blood within
 I TEXTBOOK OF PEDODONTICS

Table 11.4: Clinical symptoms of rheumatic fever (T. Duckett Jones)

Major manifestations Minor manifestations Supporting evidence

Carditis Fever Group A

Polyrathritis Arthralgia Streptococcus infection
Chorea Increased ESR
Erythema marginatum Previous history of RF
Subcutaneous nodules Prolonged PR interval

the acute form a fulminant disease occurs as a result line, injections of local intraoral anesthetic ex­
of infection with highly virulent microorganisms like cept intraligamentary
Staphylococcus, group A Streptococcus, and ■ Pulp therapy of the primary teeth is not recom­
Pneumococcus. The subacute variety develops in mended due to the high risk of chronic infec­
individuals who already have an existing congenital tion. Instead, extraction of the offending tooth
cardiac disease or rheumatic valvular lesions, caused and its replacement with a space maintainer is
by viridans streptococci( commonly found in the oral advocated (distal shoe space maintainer not ad­
cavity). vocated)
■ In the permanent dentition, endodontic therapy
The clinical symptoms may be undertaken after a careful evaluation and
They include low, irregular fever, with sweating, case selection (a tooth with a poor prognosis is
malaise, anorexia, weight loss and arthralgia. In­ better removed)
flammation of endocardium increases cardiac prob­ ■ Oral sedations and nitrous oxide analgesia may
lems and murmers. Transient bacteremia is an im­ be beneficial in reducing anxiety and minimiz­
portant initiating factor in subacute bacterial endo­ ing risk
carditis. ■ Orthodontic treatment under antibiotic prophy­
laxis, especially during band placement and re­
Dental problems and treatment moval
■ Prior to treatment complete medical history » In patients who are on anticoagulant therapy
should be elicited and consultation with the haematological monitoring and cessation of an­
child’s cardiologist is necessary to determine the ticoagulation therapy are important before any
child’s ability to tolerate the planned dental treat­ dental surgery is undertaken
ment, complications that can arise and antibi­ ■ Children suffering from severe, debilitating heart
otic prophylaxisfrefer to chapter on antibiotics) disease requiring extensive dental work-up
to be given should be treated in a hospital under general
■ Antibiotic prophylaxis may be recommended in anesthesia.
infective endocarditis patients for those dental
procedures likely to induce gingival bleeding like 2. LEUKEMIA
scaling, minor surgeries, incision and drainage,
Leukemias are neoplasms derived from hemato­
intraligamentary injections.
poietic cells that proliferate initially in the bone mar­
« Dental procedures that do not require prophy­
row before disseminating to the peripheral blood,
laxis include those which may not induce
spleen, lymph nodes, and ultimately other tissues.
gingival or mucosal bleeding, such as simple
These immature appearing, undifferentiated blasi
orthodontic appliances, filling above the gum
cells replace normal cells in the bone marrow.
 SECTION 11 : DENTAL CARE FOR THE SPECIAL CHILD |

Incidence ■ Gingiva is boggy; edematous, deep red and bleeds

Occurs at 13 per 100,000 people per year. Acute easily.
lymphocytic leukemia is primarily a disease of chil­ « Ulceration and pallor of oral mucosa.
dren and young adults. ■ Rapid loosening of teeth due to necrosis of peri­
odontal ligament.
Classification ■ Occasionally cranial nerve palsies, lip
Leukemia is classified according to the morphol­ paresthesia, jaw pain, gangrenous stomatitis.
ogy of the predominant abnormal white cells in the ■ Manifestations in the jaw include loss of trabecu-
bone marrow. They are further classified according lation, destruction of the crypts of developing
to the progression of the clinical cqurse as acute or teeth, loss of lamina dura, widening of periodon­
chronic. tal ligament space, and.displacement of teeth and
■ Acute Lymphocytic Leukemia tooth buds.
■ Acute Nonlymphocytic Leukemia ■ Oral changes can be attributed to anemia, granu­
- Acute Myelocytic Leukemia locytopenia and thrombocytopenia all of which
- Acute Monocytic or Myelomonocytic result from the replacement of the normal bone
Leukemia marrow elements by undifferentiated blast cells
- Erythroleukemia or direct invasion of the tissue by the leukemic
- Megakaryocytic Leukemia cells.
« Chronic Myelocytic Leukemia
- Juvenile, Philadelphia chromosome negative Dental Problems and Treatment
- Adult, Philadelphia chromosome positive ■ As infection is the primary cause of death in 80%
■ Chronic Lymphocytic Leukemia of children with leukemia followed by bleeding,
the primary aim of dental treatment should be
Etiology to prevent, control and remove oral infection,
Cause in most patients is unknown, although both inflammation and hemorrhage.
genetic and environmental factors are important. ■ Consult the child's physician prior to any treat­
They occur with increased frequency in children ment and take a complete medical history.
with syndromes like Down, Bloom, Klinefelter, etc. ■ Elective dental procedures are to be postponed
Ionizing radiation, chemicals like benzene, aromatic if the child is not in first remission unless there
hydrocarbons are some of the environmental fac­ is a nidus of infection intraorally that could be a
tors that have been implicated in causing leukemia. potential source of systemic infection.
■ Avoid prescribing drugs like aspirin that can alter
Clinical manifestations
platelet function.
Anemia, thrombocytopenia, increased WBC, neu­
■ As candidiasis is common, topical antifungals
tropenia, abnormal bone marrow aspirate, pallor,
may need to be applied.
fever, tachycardia, adenopathy, gingival bleeding
« Pain from ulcerative lesions can be relieved by
increased irritability, lethargy; persistent fever, vague
application of topical obtundents.
bone pain, hepatosplenomegaly, etc
■ Deep lesions that bleed spontaneously - apply
Oral Manifestations topical bovine thrombin.
« Seen in 29% of children ■ Pulp therapy on primary teeth is contraindicated
■ Regional lymphadenopathy and endodontic treatment on permanent teeth is
■ Gingival abnormalities, including hypertrophy not recommended.
and bleeding are more common with nonlympho­ ■ If platelets are less than 20,000/ cubic mm den­
cytic leukemia whereas petechiae and ecchy­ tal treatment should not be undertaken without
moses are more common in ALL. prophylactic platelet transfusion.
 I TEXTBOOK OF PEDODONTICS

■ If Absolute granulocyte count (AGC) is less than insulin supplementation may become necessary.
1000/cubic mm elective dental treatment should NIDDM is most common form and it represents
be delayed. between 80% to 93% of all diabetes mellitus cases.
■ Avoid mouth brushing and substitute with moist
gauze wipes with chlor hexi dine if platelet count Table 11.5 General signs and symptoms
is low
■ Managing of xerostomia through the use of sug­ Early features Late features
arless sweets, sorbitol - based gum, artificial sa­
liva and topical fluoride ■ Polyuria ■ Vomiting, nausea,
■ Polydipsia ■ Abdominal pain
3. DIABETES MELLITUS ■ Pruritis (skin, ■ Renal dysfunction
__ . . .. ---
rectum or vagina) ■ Hyperventilation
Diabetes mellitus is the most common endocrine ■ Weakness (metabolic acidosis)
disease of childhood. It is often associated with an ■ Recent weight loss ■ Dehydration
inadequate supply of insulin to meet physiologic « Constipation ■ Hypovolumia
needs of the body at the cellular level. The primary ■r Mental confusion ■ Paresthesia of the
disease manifests in two forms: ■ Acetone breath extremities
Type I or insulin- dependent diabetes mellitus ■ Dysaesthesia
(¿DDM) ■ Neuropathy
Type II or non-insulin - dependent diabetes mellitus ■ Muscle wasting
(NIDDM) ■ Shock
« Coma
Type I results from deficient insulin production
caused by the destruction of the beta cells of the Onset of symptoms may ocqur suddenly in IDDM,
islets of langerhans. It is often referred as Juvenile where as in NIDDM may produce similar signs and
onset diabetes because it often manifests in child­ symptoms except that the onset occurs relatively
hood or adolescence. The reasons for failure of the slowly, obesity is common and ketoacidosis is less
islet beta cells is unclear but it appears to be the severe. Diabetic complications are uncommon in
product of an interaction of environmental, genetic children and management of this disease at an ear­
and immunological factors. Here the beta cells are lier stage will prevent certain long term side effects
damaged when genetically predisposed individuals such as retinopathy, autonomic nerve degeneration,
are subjected to a virus, which induces a sequence hypertension, cerebrovascular, cardiovascular pe­
of destructive autoimmune responses. IDDM con­
ripheral vascular disease, renal dysfunctions, mus­
stitutes 5% to 15% of all diabetes cases, with the
cle wasting, etc.
onset often abrupt and the condition may be unsta­
ble and difficult to control.
Oral manifestation
1. Reduced salivary flowL
Type II or NIDDM was previously referred to as
2. Burning mouth/tongue
maturity - onset diabetes. It is rare in infancy, but
3. Candidiasis
the incidence rises among school - age children.
Occasionally, an adolescent may present with this 4. Altered taste
diabetes but this is uncommon and there is often a 5. Progressive periodontitis
family history. It results from impaired insulin func­ 6. Dental caries
tion rather than deficiency. Insulin production may 7. Oral neuropathies
be diminished, however, later in the disease and 8. Parotid enlargement
 SECTION 11 : DENTAL CARE FOR THE SPECIAL CHILD | <^81

9. Sialosis « Use of pulp capping and deciduous pulpotomy

10. Delayed wound healing procedures is questionable in the child with un­
11. Increased glucose content in gingival crevicular controlled diabetes? But vital pulp therapy may
fluid be preferred to a stressed extraction procedure
under local anesthesia.
Dental Problems « Non-vital tooth with evidence of infection ex-
Evidence regarding the incidence of dental caries traclion is the only choice of treatment
remains controversial It has been reported that well ■ Fixed and removable orthodontic appliance may
controlled young diabetic experiences a normal or be preferred, depending on the periodontal health
even reduced level of dental caries, which has been of the patient.
attributed to restriction of sugar and carbohydrates, ■ Prophylactic antibiotic may be recomjnended in
effective metabolic control, good oral hygiene and use of surgical procedures
regular dental review. Dietary control is often diffi­ ■ Vasoconstrictor drugs with LA to ensure pro­
cult to enforce which encourages frequent snacking, found anesthesia are advocated, but excessive
the elevated salivary glucose, decreased salivary flow adrenaline dosage is contraindicated to prevent
may be responsible for promoting dental caries in an increase in blood glucose levels and for this
the uncontrolled patient In children with poorly reason glucocorticosteroids should be avoided.
controlled diabetes, the levels of severe gingivitis
and periodontitis are higher due to decreased sali­ Medical treatment
vary flow or elevated salivary glucose in these pa­ • In case of Type I insulin is administered which
tients. The incidence of periodontitis increases is available in three forms
among diabetic subjects after puberty which has been • Short-acting, intermediate-acting, (upto 24 hrs),
suggested due to disturbed local polymorphic neu- long-acting, (up to 36 hrs). Current therapy com­
tropliil chemotaxis, combined with increased plaque, bines short and intermediate - acting agents with
and phagocytosis compromise may explain the in­ or without long-acting insulin. Insulin is admin­
creased levels of gingivitis found in children with istered at meal times and blood glucose levels
poorly controlled diabetes. are measured at least twice a day.
■ A well balanced nutritious diet based on meal
Dental Management arffifsnack structure with appropriate carbohy­
■ Dental management is aimed at implementation drates particularly high in fiber is essential
of a preventive protocol, symptomatic relief of ■ Oral hypoglycemic drugs are used to stimulate
any oral manifestations of the disease and im­ insulin production and promote its uptake in type
mediate provision of primary care II diabetes
■ Comprehensive medical history along with Strict patient compliance is essential for effec­
screening tests for diabetes are essential tive treatment in both types.
■ Dental appointments should be short, stress free,
as atraumatic as possible Management of Diabetic Emergencies
■ Early morningappointments are preferred and
the patient should eat a normal breakfast before A. Hypoglycemic attack or insulin shock
the appointment to prevent hypogfycemia It develops due to stress, insulin overdose, and
■ Conscious sedation is preferred than deep seda­ poor dietary control or glucose levels at or be­
tion but if patient has to go for general anesthesia low 40 mg/dl.
then admit him in the hospital and then insulin
regimens should be adjusted by the diabetologist. Signs and symptoms
- Mood changes, and irritability
 | TEXTBOOK OF PEDODONTICS

- Disorientation, blurred vision - Severe hypotension

- Lethargy, slurred speech - Abdominal pain and vomiting
- Strong, bounding pulse - Loss of consciousness (diabetic coma)
- Nausea and stomach ache
A diabetic (ketoacidotic) coma occurs at glucose
- Sweaty skin
levels between 300 and 600mg/dl and when
- Hunger, shaking, tingling around the mouth
ketones are present in urine and the blood pH is
- Increased gastric motility
below 7.36
- Hypothermia
- Loss of consciousness
Management of hyperglycemic reaction
(diabetic coma):
The condition develops quickly and treatment
1. maintain open airway in hospital unit
must begin rapidly In severe cases if treatment
2. Administer 100% oxygen ajong with intravenous
is delayed, seizures Can develop which may prove
fluids to prevent vascular collapse.
fatal.
3. Perform finger stick blood glucose test
4. Administer insulin under controlled conditions
Management of insulin shock
e. monitor serum electrolytes and glucose
i.
1. Administer oral carbohydrates such as orange
5. Patient recovery is usually slower than for insu­
juice, soft drinks, and candy.
lin shock.
2. If no recovery is seen within 2-5 minutes and
the patient is unconscious administer If the child is disorientated or unconscious, then
a. Intravenous dextrose (50ml in 5% concentra­ may be difficulty in differentiating betweei
tion) hypoglycemia and hyperglycemia. Under such cir
b. Intramuscular glucagqnjlmg) followed by cumstances management should be fo
intramuscular epinephrine (0.5mg of 1:1000 hypoglycemic emergency, which is a life threaten
concentration) ing condition. The small quantities of glucose ad
3. The patient usually takes 5 to 10 jninutes to ministered will not exacerbate the hyperglycemi
recover and observe closely until stable, and state in the event of an incorrect diagnosis.
give oral glucose when conscious to prevent
4. RESPIRATORY DISEASES
hypoglycemia from recurring.
4. If the patient does not respond after five min­
utes emergency procedures should be initiated Cystic fibrosis
Cystic fibrosis is a monogenetic disorder (autosome
recessive) that presents as a multisystem diseas
B. Diabetic crisis or Hyperglycemia
involving the exocrine glands-not just the pancrea
It develops when blood glucose levels rise over
(micro obstruction leading to cystic degeneration
11.1 mmol/1 ( fasting 8.0mmol./litre). It devel­
but the sweat glands as well as the glands in th
ops more slowly than hypoglycemia.
liver. It is characterized by chronic obstruction, aii
way infection, maldigestion caused by pancreati
Signs and symptoms
insufficiency, and other abnormalities of the dige;
- Weak pulse five tract. Sexual development is delayed and fai
- Rapid and deep breathing (kussmaul’s respi­ ure to thrive is observed. Defective gland secretioi
ration) cause abnormal water and electrolyte transpo
- Dry skin across the epithelial cells resulting in a chronic re
• Acetone breath piratory and GI disease. Over retention of mucoi
- Increased frequency of micturition takes place in the lungs. Occurs as lin 2000 lr
- Thirst births.
 SECTION 11 : DENTAL CARE FOR THE SPECIAL CHILD |

Oral Manifestations chial tree to a multiplicity of stimuli. It is mani­

■ Variable degree of discoloration of teeth due to fested by a widespread narrowing of the air pas­
tetracycline therapy, enamel hypoplasia. sages, and clinically by paroxysms of dyspnea,
■ Low incidence of dental caries due to frequent cough, and wheezing. It is an episodic disease
intake of antibiotics, increased pH, buffer capac­ wherein the attacks are short lived and the patient
ity7 of saliva, together with the increased levels seems to recover from them completely clinically.
of calcium and phosphorus of saliva. Approximately 10%of children are affected. In
b Changes in salivary7 viscosity7 and composition childhood, there is a 2:1 male/female preponder­
h High incidence of mouth breathing, open bite ance, which equalizes by 30 years of age.
associated with chronic nasal and sinus obstruc­
tion Etiology
« Dental development and eruption are delayed The condition is mostly allergic in etiology. Allergy
■ Oral ulceration may result from pancreatic en­ can be to foreign substances like dust, pollen, choco­
zymes being held in the oral cavity7 late, etc; respiratory infection, emotional distur­
bances, exhaustion, and a change of climate.
Dental Problems and Treatment
■ Complete medical history and consultation with Dental Problems and Treatment
the child’s physician is imperative ■ Completemedical history should be elicited (fre­
« Patients can be treated in an upright position to quency of attacks, irritating stimuli, severity of
enable the clearance of secretions. attacks, medications taken)
■ Anterior tooth discoloration can be treated with ■ Seat the patient in an upright position for dental
composite veneering or jacket crowns procedures.
■ Sedation carries the risk of respiratory depres­ ■ Treat child soon after a dose of medication is
sion and a compromised airway given, and if the child is using an inhaler it
■ General anesthesia should be considered, only should be broughtalong for the dental appoint-
if local anesthesia is not successful, with antibi­ ment in case of an attack
otic coverage when there is a significant pulmo­ ■ Sedation and general anesthesia can be given, if
nary7 involvement indicated.
■ Strict oral hygiene program and regular dental « Patients who are receiving corticosteroid therapy
care if systemic conditions are under control are at a risk from stress. Therefore the double or
■ Dietary7 advice with sugar-free liquid antibiotic triple the steroid dosage and adjust the time of
preparations. appointment to ensure that the patient is seen
shortly after medication has been administered
Medical management >-Use ofaspirin, NS AID and penicillin are con­
■ Recurrent infections are treated with antibiotics traindicated.
■ Regular physiotherapy with postural drainage of ■ Local anesthesia can also be given
chest fluids. ■ Use of nitrous oxide- oxygen sedation is most
■ Advise high-calorie diet with supplemental pan­ desirable in such patients
creatic enzymes and vitamins with their meals ■ In case of an asthmatic attack in emergency ad­
« Nasogastric intake if oral intake is not possible minister 100% oxygen with the patient in a sitting
position leaning forward and subcutaneous
5. ASTHMA administration of 0.3 ml of 1:1000 epinephrine.

Asthma is a disease of airways that is characterized

by an increased responsiveness of the tracheobron-
 1 TEXTBOOK OF PEDODONTICS

PSYCHOBEHAVIORAL
6. DISORDERS « Preoperative sedation with muscle relaxants and
nitrous oxide - oxygen analgesia can also be used
AUTISM for treatment.
Autism is a severely incapacitating disturbance of ■ Psychotherapy and family counselling for the
mental and emotional development that causes prob­ success of oral hygiene programs as well as for
lems in learning, communication and relating to establishing the patient-dentist rapport.
others. The condition manifests in the first three ■ Use of papoose boa rd or pedi-wrap may be nec­
years of life, with no known cure and occurs due to essary.
a physical disorder of the brain. ■ GA in case of extensive treatment.

Incidence 7. HAEMOTOLOGICAL DISORDERS

Occurs in approximately five in 10,000 births, be­
ing four times more common in boys. Haematological disorders may be broadly classified
into three groups;
Etiology 1. Red cell disorders
L Organic brain damage or dysfunctions 2. White cell disorders
2. Lack of environmental stimulation of psycho­ 3. Disorders of homeostasis, including platelets and
logical factors coagulation factors
3. Defective metabolic processes
1. Red cell disorders
Clinical manifestation Anemia is defined as reduction in the volume of
These children often have a poor muscle tone, poor red blood cells (haematocrit) in the packed cell vol­
co-ordination, drooling, hyperactive knee jerk, stra­ ume (PC V) or in the concentration of hemoglobin
bismus, and epilepsy. They have strict routines and in peripheral venous blood. The various types of
prefer soft and sweetened foods, thus increasing car­ anemias are as follows: *
ies susceptibility Because of poor tongue co-ordi­
nation autistic children tend to pouch food instead Iron deficiency anemia (Table 11.6) ♦
cf swallowing. They often exhibit an extreme re­
sistance ¡c being held and show tantrums and ag­ Vitamin B-12 deficiency anemia (Table 11.7)
gressive or destructive behaviour to fearful situa­
tions. Autism can be listed as extreme loneliness, Folate deficiency anemia (Table 11.8)
language disturbance, mutism, parrotlike,
repetitious speech, difficulty with the concept of yes, Pernicious anemia (Table 11.9)
confusion in the use of personal pronouns, obses­
sive desire for the maintenance of sameness, and Hemolytic anemia (Table 11.10)
eating disturbances. Mental retardation is evident
in one-half to two-thirds of autistic children and Aplastic anemia (Table 11.11)
seizure disorders become manifested, as they grow
older. Sickle - Cell Anemia
It is inherited as an autosomal recessive disorder
Management due to an abnormal hemoglobin known as
■ Phenytoin therapy may lead to gingival sequel. hemoglobin *S ’, lose their oxygen with a distortion
■ A patient and slow approach should be used. of the erythrocytes into a sickled shape occurs. The
■ Use the tell-show-do and positive reinforcement sickling phenomenon which occurs only in a re­
behaviour management techniques. duced oxygen tension, causes both a chronic
 SECTION 11 : DENTAL CARE FOR THE SPECIAL CHILD

Table 11.6: Iron deficiency anemia

Type of anemia Microcytic, hypochromic anemia

Causes 1. Associated with low serum iron, low serum ferritin

2. Found in conjugation with a prolonged bottle feeding habit
where the transition to balanced solid diet has been incomplete
and where cow's milk continues to be main dietary component
3. In teenaged girls may be associated wiih menorrhagia

Oral Manifestations Painful atrophy tongue

Decreased healing response
Pale mucosa
Angular chelitis
Gingivitis and periodontitis

Treatment Maintenance of a thorough oral hygiene

Symptomatic treatment
Supplementation as per the requirement of the patient

Table 11.7: Vitamin B-12 deficiency anemia

Type of anemia Macrocytic, anemia

Causes Unusual in children but may be associated with coeliac disease

or Crohn’s disease or in strict vegetarians with inadequate
dietary intake

Oral Manifestations Angular chelitis

Stomatitis
Pharyngitis
Severe glossitis
Glossopyrosis with difficulty in swallowing
Neurologic dysfunction

Treatment Symptomatic dental treatment

Supplementation as per the individual requirement

Table 11.8: Folate deficiency anemia

Type of anemia Macrocytic, anemia

Causes Found in patients suffering from malabsorption syndromes

including coeliac and Crohn’s disease
In renal dialysis patients, epileptic patients with phenytoin therapy
Metabolism disorders like Lesch-Nyhan syndrome
Lack of folic acid intrinsic factor

Oral manifestations Angular chelitis

Stomatitis
Pharyngitis
GIT dysfunction

Treatment Same as above

I TEXTBOOK OF PEDODONTICS

Table 11.9: Pernicious anemia

Causes Lack of Vit-B12 intrinsic factor

Oral manifestations Same as in vitamin B12 deficiency anemias

Painful glossy tongue
Beefy red coloured tongue
Apthous ulcers
Atrophy of filliform papillae
Hunter glossitis

Management Supportive therapy by blood transfusion

Treatment of infection by hydroxycobalamin 1000 mg IM
daily for 1 week followed by 100 mg once in 3 months as
maintenance dose

Table 11.10: Hemolytic anemia

Causes It results from premature destruction of red cells caused by

Intracorpuscular defects in erythrocytes congenital or
acquired
Hereditary spherocytosis
sickie cell anemia, thalassemia
Extra corpuscular factors *
infections agents, cardiac valvular prostheses,
hyper splenism, RH factor incompatibility,
chronic liver disease,

Management Splenectomy, Folic acid therapy, Prophylactic antibiotics,

Vaccination against infection, Antibiotic coverage before
dental procedures
 SECTION 11 : DENTAL CARE FOR THE SPECIAL CHILD | tifo
¡5

Table 11.11: Aplastic anemia

Causes Is the result of bone marrow dysfunction or failure in production

of erythrocytes

Causes:
Acquired:
■ Idiopathic
■ Autoimmune

Drugs:
Cytotoxic
■ Idiosyncratic
■ Infectious-hepatitis
■ Pregnancy
■ Paroxysmal Nocturnal Haemoglobinuria

Congenital / familial
■ Fanconi’s anaemia
■ Dyskeratosis congenita
■ Black fan-diamond anemia

Oral findings ■ Gingival hemorrhage

■ Mucosal pallor
■ Petechial spots
« Oral ulceration and infection
■ Neutropenia - there is a lack of resistance to infection
J

Management General management

■ Removal of cause
■ Immunosuppressive agents, e.g. androgenic steroids
■ Antibiotics
■ Bone marrow transplantation or peripheral stem cell infusion

Oral and dental management consideration should be given to:

« Hemorrhage tendency
■ Anemia
■ Increased susceptibility to infection
■ Corticosteroid therapy and anti-rejection drugs
■ Emergency dental procedures should not be performed
without physicians consult.
■ Soft tooth brushes are advised
■ Block anesthesia and pulp therapy are contraindicated
■ Topical anesthetic agents are advised for oral ulcerations
 I TEXTBOOK OF PEDODONTICS

compensated hemolytic anemia and vaso-occlusive mandatory, fluid maintenance is necessary and
crisis, resulting in pain and tissue damage caused preoperative exchange transfusions may be
by infarction. needed.
■ Use desferrioxamine mesylate by subcutaneous
Clinical features infusion and hydroxyurea may be used to raise
HbF levels and reduce the frequency and sever­
Generalfeatures ity of vaso-occlusive crisis
« Anemia due to haemolysis ■ Minimize stress, because significant stress, de­
• Aplastic crisis creases the child’s ability to oxygenate tissues
■ Impaired growth adequately.
• Skeletal deformities ■ Hepatitis precautions while treating sickle cell
disease patients
Dental
■ Empliasis on preventive dental health like brush­
» Jaw pain caused by infarction or oesteomyelitis
ing, fluorides, diet counselling and recall
« Labial anesthesia due to cranialneuropathies
« Mental nerve palsy due to vaso-occlusive crisis
THALASSAEMIA
• Susceptibility to infection
• Hypomineralisation of dentin, abrupt alteration Thalassaemia is inherited as an autosomal, reces­
of dentinogenesis, calcified bodies in pulp cham­ sive disease and is characterized by a reduced syn­
ber thesis of one or more of the a / p globin chains,
•» Hyper cementosis leading to a decreased haemoglobin production and
• Osteoporosis of the jaw due to bone marrow a hypochromic microcytic anaemia. The a
hyperplasia thalassaemias, of which there are four main subtypes
• Dense lamina dura are widely distributed in people W Asian or African
descent. The p thalassaemias affect the people of
Other
the Mediterranean area and parts of Africa, Asia
• Infarcts of the CNS, lungs, kidney, spleen
and Middle East.
• Dactylitis hand-foot syndrome
» Skin ulcers, avascular necrosis, retinopathy, he- The thalassemias are frequently referred to as ma­
p 4 ,c and splenic sequestration, hepatomegaly, jor and minor forms, distinguished by their mani­
obstructive jaundice, hematuria cerebro-vascu­ festation in either homozygous or heterozygous state.
lar accidents with resultant hemiplegia Thalassemia major is the most common.

Dental management Clinical features are:

• Use of local anesthesi i with vasoconstrictor. ■ Manifestation appears within the first year of life
« Conservative approach to dentistry. ■ Severe anemia, failure to thrive, poor appetite
« Prevention of infection by the use of postopera­ ■ Hepatosplenomegaty, folate deficiency, growth
tive antibiotics and prophylactic antibiotics be­ retardation, jaundice, recurrent ulcers
fore surgical proceedings. « Hemosiderosis due to iron overload, following
• Inhalation sedation is safe provided that 100% frequent transfusion
oxygen is administered for at least 4 to 5 min­
utes. At the end of the procedure to avoid diffu­ Oral changes
sion hypoxia airway should be maintained with, ■ Hyperplasia of the marrow; leading to expan­
NO-O2 sion of marrow cavity.
■ Where general anesthesia is unavoidable in hos­ ■ Chipmunk facies with an enlargement of the
pital, maintenance of at least 30% oxy gen is maxilla and spacing of the teeth, increased over
 SECTION 11 : DENTAL CARE FOR THE SPECIAL CHILD I

jet, protrusion of the middle third of the face, HEMOPHILIA

extreme tightness of the upper lip. Hemophilia is a heredity blood disorder character­
■ Ocular hypertelorism, epicanthal folds and ized by a deficiency of the plasma proteins needed
browning of the skin. for normal clotting.
■ Radiographic changes: ‘chicken wire’ appear­
ance of the alveolar bone, delayed pneumatisa­ The most common type of hemophilias are the
tion of the sinuses, hair-on-end appearance of hemophilia - A with a prevalence of 1:7500 males
the skull (Table 11.12)
■ Large medullary cavities, thin cortices and gen­
eralized osteoporosis
■ Pain and swelling of the parotid glands and - Hemorrhage from many sites intraorallv
atrophic candidiasis - Gingival hemorrhage may be prolonged and
massive
Dental management of p thalassaemia
- Mouth lacerations^
■ Prevention of dental disease
- Presence of mandibular pseudotumor with ra­
■ Avoidance of general anesthesia in the presence
diographic changes of tooth displacement, en­
of a chronic, severe anemia, cardiomyopathy and
largement of bony structures, delicate
endocrine problems
trabeculaes, and areas of radiolucency
■ Need for antibioi prophylaxis
- Caries and periodontal disease is high because
■ Prevention methods against HIV and hepatitis
of poor oral hygiene
DISORDERS OF HEMOSTASIS
Complications
Hemostasis is a series of events that culminates in
- Inhibitors to factor VIII may develop
the spontaneous arrest of bleeding from a damaged
- Arthritis, degenerative joint disease secondary
blood vessel. Without hemostasis, minor injuries
to recurrent bleeding
would be life-threatening and surgery would be
- Blood borne viral infections like hepatitis and
impossible. Hemostasis occurs as a function ofplate­
HIV
lets, vascular constriction, coagulation and fibrinoly­
sis. Coagulation occurs by the interaction of intrin­
Treatment Of Hemophilia - A
sic and extrinsic factors in the clotting cascade.
Some of the common coagulation defects are as the
Replacement with plasma^product containing fac­
following:
torVni.
Congenital Acquired
Minor hemorrhage - 40% level of factor VM
Haemophilia - A ■ Vitamin K deficiency
(associated with liver Severe bleeding or major surgery -an initial level of
disease)
80% to 100% followed by a maintenance level.
Hemophilia -B ■ Clotting antibodies
Vonwillebrand’s ■ Stored blood
disease transfusions In a mild to moderate hemophilia A, l-deamino-8-
Deficiency of other ■ Anticoagulant drugs D-orginine vasopressjng (DD AVP^ a synthetic ana­
clotting factors e.g., warfarin log of vasopressin (antidiuretic harmone) can be
e.g.: XI and XII used to raise factor VIII to hemostatic levels.
■ Diffuse intravascular
clotting (as in meningoco­
ccal septicaemia)
 I TEXTBOOK OF PEDODONTICS

Table 11.12: The characteristics of Hemophilia

Coagulation defects Etiology and Laboratory Clinical

transmission findings features

Hemophilia - A or - Factor VIII deficiency - Normal platelet count - Spontaneous

classical hemophilia - X -linked recessive - Normal bleeding time hemorrhage
■- 80% of hemophilias trait, males are - Normal prothrombin - Hemarthrosis with
that are seen affected, females time. pain, stiffness and
- circulating antibodies are carriers - Prolonged partial limited motion
to factor VIII thromoboplastin - Chronic
(inhibitors) develop time musculoskeletal
in 10% to 14% of - Factor VIII assay problems in repeated
patients 0% to 40% episodes or muscle
hemorrhage
- Easy bruising
- Deep hematomas
and hematuria

Hemophilia - B - Factor IX deficiency - Normal platelet count - Spontaneous

or Christmas - X-linked recessive - Normal bleeding time hemorrhage
disease trait, males are - Normal prothrombin - Hemarthrosis with
- 15% of hemophilias affected, females time pain, stiffness and
that are seen are carriers - Prolonged partial limited motion
- circulating antibodies thromboplastin time - Chronic
to factor IX (inhibitors) - Factor IX assay 0% musculoskeletal
develop in 1% to 2% to 40% problems in repea­
of patients ted episodes of
hem arthroses or
muscle hemorrhage
- Easy bruising
- Prolonged bleeding
after surgery
- Deep hematomas
and hematuria

Hemophilia C - Factor XI deficiency - Normal bleeding time Prolonged bleeding

or Plasma - Normal platelet after surgery or trauma
thromboplastin Function tests
antecedent - Normal prothrombin
- Autosomal recessive Time
inheritance - Prolonged partial
- Male and female Thromboplastin time
equally affected - Abnormal
Thromboplastin
Generation test in
severe cases
- Factor IX assay 0%
to 40%
I........................... ..
contd.
 SECTION 11 : DENTAL CARE FOR THE SPECIAL CHILD |

Coagulation defects Etiology and Laboratory Clinical

transmission findings features

Von Willebrand’s - Von Willebrand - Normal platelet - Since there is an

disease factor deficiency that count impaired primary
is found in plasma, - Prolonged Weeding platelet plug
platelets, megakar­ time formation, it leads
yocytes and endo­ - Normal prothrombin to hemorrhages
thelial cells, either time from the skin and
quantitative or - Possible prolonged the mucosa
qualitative partial thrombo­ - Easy bruising
- It also serves as a plastin time if factor - Epistaxis
carrier for the VIII less than 30% - Prolonged bleeding
coagulant part of - Decreased platelet after surgery
factor VIII in the adhesiveness and - GIT hemorrhage
plasma aggregation - Becomes
- Autosomal dominant - Quantification of milder with age
inheritance with VMF antigen, VWF
males and females activities, factor VIII
equally affected activity, ristocetin
cofactor & ristocetin
induced platelet
aggregation

Classification

Depending upon factor level hemophilia A and B are classified as:

Degree of severity % of factor VIH / IX Characteristics

available

Severe Less than 1% - Frequent bleeding episodes

occurring 2-4 times/ month
- Bleeding without a specific history
of trauma
■ - Bleeding into joints and muscles
j
Ïi - Hemarthrosis
- Musculoskeletal problems
i
i - Psuedotumors in the jaws
i - Deep hematomas and hematuria

Moderate 1-5% - Occasional spontaneous joint bleeding,

minor trauma may initiate hemorrhage
- Develops target joints with repeated
episodes of bleeding

Mild 5-35% Significant hemorrhage only after a major

insult
1 - .. , .. , ......
 | TEXTBOOK OF PEDODONTICS

Hemophiliacs with inhibitors of factor VIII, destroy ■ Use wedges and matrices for a proximal box.
factor VIII clotting activity, therefore in such cases ■ Use of 8 A or 14 A retainers are avoided but high
use prothrombin complex concentrates(PCC) or fac­ speed vacuum and saliva ejectors are used.
tor IX complex concentrates, containing factors II, ■ Use retraction cords during crown preparation
VII, IX and X which can bypass factor VIII « Antibiotic prophylaxis before extraction.
inhibitors. ■ Use of topical hemostatic agents such as bovine
thrombin, microfibrillar collagen hemostat,
Treatment of Hemophilia - B gelfoam, absorbable oxidized cellulose, cellulose
Replacement with plasma product, 40%, high in bandage, collagen, bovine collagen bone wax,
factor IX as well as with prothrombin complex con­ surgicel.
centrates (PCC). Fresh frozen plasma (FFP) is an ■ Instrumentation and filling beyond the apex
emergency alternative. should be avoided.
■ Fixed appliances preferred than removable
Treatment of Hemophilia - C ■ Arch wires should be secured wit1' elastic bands
Since there is no concentrate containing factor I, ■ Careful adaptation and cementation of bands
treatment requires the use of fresh-frozen or lyophi­ should be done but usually preformed bands and
lized plasma, along with local and topical meas­ brackets are preferred.
ures. ■ DD VP increases fibrinolytic activity and should
be used only in conjunction with an
Treatment of Von Willebrand’s Disease antifibrinolytic agent.
Treatment generally involves
■ Fresh frozen plasma or ciyoprecipitate to in­ PLATELET DISORDERS
crease the factor VIII level and improve platelet
adhesiveness. The various platelet disorders are classified in Ta­
« DDAVP may be used to achieve hemostasis ble 11.13
• Local and topical measures. £

Platelet disorders can be divided into those caused

Dental Considerations by platelet dysfunction (qualitative) and those caused
• If the patient’s apprehension is significant, se­ by inadequate numbers of platelets (quantitative).
dation or nitrous oxide-oxygen inhalation anal­ Platelets normally number between 150,000 and
gesia is considered and also using acetami­ 400.000/ cumm. of blood. Patients with counts less
nophen, propoxyphene hydrochloride, narcotic than 100.000 have a moderate disease, and those
analgesics is required. with less than 50,000 have a severe thrombocyto­
» When general anesthesia is considered, oral in­ penia, when levels drop to 30,000 to 50,000 spon­
tubation is preferred over nasal intubation, taneous bleeding occurs.
• Intramuscular injections should be avoided.
• For patients who require deep scaling, initially Idiopathic thrombocytopenic purpura
do supra gingivally and then repeat after 7-14 It is an auto-immune disorder in which there is an
days after proper healing. abnormal reduction in the normal circulating blood
« Factor replacement before frenectomy and other platelets, affecting 4 in 100,000 children per year
periodontal surgeries. with a peak incidence of upto 4 years. It may be
• Electrosurgery is done because of the possibil ity acute (seif-limiting) in 80 to 90% of cases or chronic
of continued bleeding. in 10% to 20%.
■ Small carious lesions are restored without a fac­
tor concentrate replacement.
 SECTION 11 : DENTAL CARE FOR THE SPECIAL CHILD |

Table 11.13: Various platelet disorders and their characteristics

Congenital Acquired Conditions associated with

platelet disorders

Glanzmann’s - Platelet dysfunction due to drugs - Renal failure

Syndrome eg: aspirin, and other NSAIDs, - Associated disease processes
Bernard-doulier phenytoin, cotrimoxazole eg: leukemia, aplastic anemia
Syndrome - Thrombocytopenias eg: Idiopathic - Cyanotic congenital heart disease
Wiskott-aldrich thrombocytopenic purpura,
Syndrome immune thrombocytopenia
associated with infection, eg:
infectious mononucleosis, HIV,
rubella, varicella
- Increased platelet activity, eg:
nephrotic syndrome, kawasaki’s
disease, cirrhotic liver disease

Causes ■ Hemorrhages, bullae and vesicles of mucous

There are a variety of causes of thrombocytopenia membrane often occur as a result of platelet count
both reversible and irreversible. below 20,000/ cu mm
■ No clinical bleeding or surgical hemorrhage is
Reversible causes are: expected with greater than 50,000/ cu mm of
- Drugs, transient bone marrow suppression ow­ circulating platelets
ing to cytotoxic chemotherapy. ■ Spontaneous bleeding rarely occurs, until counts
- Gold salts, indomethacin, digitoxin, quinidine, are below 10,000 to 20,000/ mm
quinine, hydrochlorothiazides, alcohol, thiazine
diuretics, all these have been implicated in de­ Oral manifestations
creased platelet production. ■ Ecchymoses and frank hemorrhages
• Profuse gingival hemorrhages
Reversible thrombocytopenia usually remit in 1 to ■ Petechiae also occur in the mucosa, and com­
2 weeks after removal of the causative agent. monly palate appear with numerous, tiny,
grouped clusters ofreddish spot only a millimeter
Irreversible causes of thrombocytopenia include or less in diameter
leukemias, lymphomas, aplastic anemia, hyper-
splenism causes sequestration of platelets, and im­ General and dental management
mune mediated (HIV). ■ Elective dental treatment should be deferred until
a platelet count is above 50,000/mm3
General Manifestation ■ Give steroids at a dose of 1 to 2 mg/kg to bring
■ Sudden onset of purpura up the platelet level
■ Bruising ■ Splenectomy
■ Conjunctival and retinal hemorrhages « Replacement therapy usually involves platelet
■ Epistaxis concentrate transfusion or whole blood transfu­
sion before oral surgical procedures, one unit of
 <¿23 I TEXTBOOK OF PEDODONTiCS

platelets usually increases a patient’s count by Causes of chronic renal failure

6000/mm3
• Improve red cell mass, supply coagulation fac­ Congenital anomalies of the kidney and the urinary
tors tract tend to produce CRF before the age of 5 years.
w Use local measures of hemostasis After 5 years glomerular and hereditary renal dis­
■ IV immune globulin 19 kg/day twice before den­ eases become more prominent (Table 11.15).
tal extraction
• Avoid blocks and extraction if possible during Clinical manifestations
acute phase Fatigue, headache, anorexia, nausea, polyuria,
« Avoid NS AID’s and aspirin 7 days preoperatively polydypsia, muscle cramps, paresthesia, facial puffi­
before any surgical procedures ness, dryness, itchiness of the skin. Advanced CRF
creates hypertension, fluid retention, anemia, aci­
Table 11.14 Laboratory findings for platelet dosis. These complications can lead to cardiac fail­
disorders ure. General appraisal of the dental patient reveals
a pale brownish complexion, growth retardation,
Test Disorders
muscle weakness and wasting. Uremic breath, the
Quantitative Qualitative skin may show areas of bruising due to altered plate­
let function.
Bleeding time Abnormal Abnormal

Capillary fragility Abnormal Abnormal Laboratory findings

Increased blood levels of phosphate, urea, po­
Platelet count Abnormal Normal
tassium
ADP and collagen Normal Abnormal Reduced blood levels of calcium and protein
Clot retraction Abnormal Variable Prolonged bleeding time and a monocytic nor­
mochromic anemia
Clotting time Normal Normal
Decreased platelet count and reduced activation
Plasma of plasma factor III
recalcification time Abnormal Variable Lowered hemogloblin and hematocrit count
PTT Normal Normal
Oral Manifestations
Thromboplastin
Oral manifestations of CRF depend on the time of
generation test Abnormal Abnormal
the onset of the disease, its duration, its severity
Thrombin time Normal Normal and the nature of underlying disease. Soft tissue
changes are more common and significant. Hard tis­
RENAL DISEASES sue changes will occur in advanced cases. For teeth
to be affected, CRF must occur during development,
Chronic renal failure (CRF) for bone growth to be altered CRF must be prolonged
Chronic renal failure can be defined as a progres- and occur during critical growth periods.
rive and irreversible decline in the total number of
functioning nephrons, with a concomitant decline Clinical and radiological oral findings are given
in the glomerular filtration rate. Renal diseases have in Table 11.16
been classified as acute, chronic, acquired or con-
|ienitaL
 SECTION 11 : DENTAL CARE FOR THE SPECIAL CHILD |

Table 11.15: Causes of chronic renal failure

Localized Obstructive Systemic

■ Proliferative ■ Upper urinary tract ■ Benign / malignant

obstruction Î hypertension
■ Membranous glomerulo ■ Hydronephrosis * Poiyartenös nodosa
nephropathy
■ Chronic pyelonephritis ■ Retroperitoneal fibrosis ■ Disseminated lupus
erythematosus
■ Tuberculous pyelonephritis « Neoplasm « Primary and secondary
amyloidoses
■ Renal calculi ■ Adenoma ■ Potassium deficiency
■ Congenital nephritis ■ Urethral stricture ■ Hyper calcemia
■ Polycystic disease ■ Urethral valves ■ Cystinosis
a Medullary cystic disease ■ Bladder neck obstruction « Oxalosis
■ Renal hypoplasia • Neurogenic bladder ■ Thrombotic thrombocytopenic
purpura
■ Renal tubular acidosis a Lead or cadmium poisoning
■ Balkan nephropathy ■ Diabetes

Table 11.16: Clinical and radiological oral findings of renal disorder

Clinical Radiographic Jaws Teeth

a Mucosal pallor « Total/partial loss of lamina dura ■ Pulpal narrowing

■ Candidiasis and ■ Demineralization of bone ■ Pulp calcifications
oral petechiae
« Extrinsic discolouration ■ Localised radiolucent lesions ■ Dentinal bridging
of teeth (brown tumors)
■ Enamel hypoplasia « Loss of distinct cortical borders : ■ Intradental -
of hard palate, sinus foramina, radiolucencies
inferior alveolar canal

■ Decreased rate of dental ■ Oral calcifications ■ Root resorption

caries
■ Tooth mobility and tooth ■ Arterial calcifications facial
loss prematurely artery, carotid artery
■ Uremic stomatitis with
oral ulcerations
■ Pain
« Peripheral giant cell
lesions
■ Intraoral hematoma with
tendency to bruise
■ Chronic marginal
gingivitis
« Uremic odour because
of high urea saliva levels
 J TEXTBOOK OF PEDODONTICS

Medical and dental treatment oral health care workers because of the pandemic
nature of the disease. The number of seropositive
1. Consultation with the patient’s physician or ne­
patients visiting the dental office is increasing and
phrologist is usually required.
an early diagnosis of the condition is of prime im­
2. Prevention of fluid and electrolyte imbalance,
portance. Infection with HIV results in profound
limitations of uremic symptoms through restric­
immunosuppression, rendering the host susceptible
tion in protein intake, correction of hypocalcemia
to the development of various opportunistic infec­
and hyperphosphatemia and the control of
tions and neoplasms. Compared with adults, the pro­
anemia and hypertension.
gression of HIV infection is more rapid and severe
3. Artificial filtration in the form of either perito­
in infants and children due to the on-going devel­
neal dialysis or hemodialysis.
opment of different organ system and an immature
4. Renal transplantation in endstage renal disease
immune system that is less resistant to infections.
5. Acute renal disease stages, elective dental treat­
The oral cavity is particularly susceptible to infec­
ment may be postponed until the condition
tion, since it harbors numerous micro-organisms
improves, only emergency care is indicated.
that thrive in conditions of immunosupression
6. When surgical procedures are considered, assess
thereby oral lesions are frequently among the first
the bleeding time.
symptoms in HIV-infected children. Early detection
7. Avoid hypertension medications.
of HIV -related oral lesions can be used to diagnose
8. Fluid/electrolvte balance should be maintained
HIV infection, elucidate progression of the disease,
by managing those oral diseases like herpetic
and provide therapeutic intervention.
stomatitis, severe caries, cellulitis that may
compromise a child’s fluid intake.
Definition
9. Careful planning of drug therapy in order to
AIDS can be defined as presence of antibodies to
avoid or modify the dosage of drugs that are ne­
HIV and presence of opportunistic infections.
phrotoxic. s
10. Managing growth retardation and malocclusions
Epidemiology
11. Precautions against transmission of serum hepa­
AIDS and HIV infection continue to spread rapidly
titis during dental treatment.
affecting an increasing number of women and chil­
12. Optimal treatment timing is 1 day after dialysis
dren worldwide. The World Health Organization
when blood is free of wastes and heparin levels
(WHO) reported that one million children were in­
are waning.
fected with HIV by the end of 1992 and estimated
13. Antibiotic prophylaxis before dental treatment is
that 10 million children will be born infected by the
to prevent bacteremia.
year 2000. With the high global prevalence of AIDS,
14. Increased need for oral prophylaxis due to in­
India is in early stages of the pandemic but the in­
crease in calculus formation.
fection is spreading at an alarming pace. In India on
15. In patients with adrenal suppression secondary
October 1987 the first seropositive infant was
to exogenous steroid administration, steroid sup­
identified with the etiology of prenatal transmis­
plementation may be given prior to general
sion. According to a report of the ministry of health
anesthesia or major dental procedures.
in 1995 on AIDS, Maharastra, Tamilnadu followed
by Delhi, Rajasthan and Manipur had more AIDS
AIDS
cases and the total AIDS cases were 1094, with
The human immuno deficiency virus infection (HIV) males 839 and females 255.
is of major interest and concern to dentists and other
Etiology and Modes of Transmission
AIDS is caused by human immuno deficiency virus
 SECTION 11 : DENTAL CARE FOR THE SPECIAL CHILD |

(HIV) a human RNA retro virus. The four recog­ C. Sexual transmission
nized human retrovirus belong to two distinct groups, 1. Infants bom to mothers who are prostitutes
the human T lymphotropic retrovirus, HTLVI and 2. Unprotected homosexual and heterosexual
HTLVIII and the human immuno deficiency viruses, intercourse which accounts for 75% of trans­
HIV - I and HIV - IL The most common cause of mission
AIDS throughout tire world is HIV -1. 3. Frequent foreign travel with sexual contacts
abroad
Popovic in 1983 made a break-through with identi­
fication of HTLV HI as the causative agent of AIDS. D. Body fluids transmission
HTLV III was isolated from patients with AIDS and HIV has been detected in various body fluids of
AIDS related complex and the antibodies specific infected persons. But only blood, semen, breast
for HTLV III were detected in nearly all HIV pa­ milk of infected HIV mother, tears, sweat, urine,
tients. vaginal or cervical secretions have been impli­
cated in transmission, whereas with saliva trans­
Modes of transmission mission has not yet been proved.

A. Parenteral transmission
Michael Glick et al (1989) have detected HIV pro-
1. Needle sharing among intravenous drug abus­
viral DNA in the dental pulp of a patient with AIDS,
ers
confirming that pulp can also be the transmitting
2. HIV - Infected patient to health care worker
medium for this disease there by alarming the den­
3. Patients with hemophilia, hematological dis­
tists to take necessary precautions in pulp manage­
eases, major surgeries, haemodialysis, requir­
ment.
ing blood transfusions.
4. Blood transfusion from donors who tested
Therefore, the dentists have a risk of transmission
negative to HIV but were in the window pe­
if there is a break in epithelium acting as a portal
riod (the time between contracting the dis­
entry for HIV either due to the needle, blade, pulp
ease and testing positive).
tissue or blood contact.
5. Tissue or organs transplant from HIV-infected
donors
Pathogenesis
6. Household contacts without established sexual
HIV attacks the immune system specifically T-
or drug related risk behaviours
lymphocytes, B-lymphocytes, monocytes,
7. Heath care worker to the patient.
promyelocytes, oligodendrocytes, capillary cells,
B. Peri-natal transmission epithelial cells, fibroblasts, etc. The first step in in­
It occurs before, during or shortly after birth fection by HIV is its binding of viral surface pro­
1. Prenatal and neonatal transfer from the HIV tein GP 120 to CD4 cell surface receptor of T4
infected mother to the baby during the 8-12 lymphocytes, which plays a leading role iñ T cells
weeks of gestation have been reported. lysis and infection. After binding, the virus foses
2. Mother infected with HIV through blood trans­ with the cell membrane of the host and enters the
fusion during or shortly after the child birth human cell. When this virus enters the human cells
3. Mother was infected during unsafe sex with releasing its RNA inside the cell, viral RNA is first
an infected partner when pregnant or during converted to a RNA-DNA hybrid by ‘reverse
breast feeding transcriptase’ present in the virus. The integrated
4. Afflicted with AIDS related illness during provirus acts as a template for the viral RNA syn­
pregnancy or breast feeding thesis and also brings about cell transformation,
5. Transmission during cesarean delivery
 I TEXTBOOK OF PEDODONTICS

massive viral budding from the cell surface, which Major signs
ultimately leads to cell death or irreversible immu­ ■ Chronic diarrhoea for more than one month
nosuppression by producing more virus and further ■ Prolonged fever for more than one month
killing of CD4 (T4) lymphocytes leading to a variety ■ Weight loss
of ÍHtüiuaodeüciency problems, opportunistic infec­
tion, malignancies and autoimmune diseases. Minor Signs
■ Oropharyngeal conditions
Some of the immunological abnormalities are: ■ Repeated cough for more than one month
« Quantitative abnormalities of T-lymphocytes ■ Generalized lymphadenopathy
• Functional abnormalities of T-lymphocytes ■ Generalized dermatitis
« Functional abnormalities of B-lymphocytes ■ Maternal HIV infection
■ Functional abnormalities of monocytes/
macrophages Typical pediatric findings (Rubenstein, 1986)
■ Serologic abnormalities ■ Pulmonary lymphoid hyperplasia
■ Reversal of CD4/CDS + T-lymphocytes ratio ■ Salivary7 gland enlargement
■ Deficient prevention of IL-2 and interferon. « Pyogenic bacterial infection such as otitis media
■ Antilymphocytic antibodies and auto antibodies ■ Developmental craniofacial features
especially antiplatelet, anticoagulant ■ Chronic recurrent diarrhoea
■ Hepatosplenomegaly
Although the immune system abnormalities are « Chronic pneumonitis
similar in pediatric and adult HIV infection, im­ ■ Failure to thrive
portant differences exist. In children, along with the ■ Progressive encephalopathy
immature immune system, the disease process has
a shorter incubation period with a more rapid and Oral and perioral findings of AIDS in children are:
fulminant disease process. In pediatric HIV infec­ 1. Fungal infection like candidiasis with different
tion, the immunological marker is abnormal B - cell types like
function (poor response to B-cell mitogens and - Angular chelitis *
polyclonal hypergammaglobulinemia), which actu­ - Hyperplastic
ally precedes T-lymphocyte decrease. These B cell 2. Bacterial infections either generalized, localised
defects predispose the infants and children to more or pyogenic
frequent and severe bacterial infections than those 3. Viral infections like
in adults. In infants there is no striking reversal of - Herpes zoster
the CD4 / CD 8 -F T-lymphocytes ratio. Decreasing - Herpes simplex
CD4 ZCD8 + T lymphocytes ratios are often initially - Hairy7 leukoplakia
due to an increase in number of suppressor CD8 + - Herpetic stomatitis
lymphocytes rather than a depletion in CD4+T- 4. Unknown etiology7 lesions
lymphocytes. 5. Parotid enlargement with xerostomia
6. Petechiae
Diagnosis 7. Apthous stomatitis
Diagnosis of pediatric AIDS is by clinical screen­ 8. Linear gingival erythema
ing and serologic confirmation. World Health Or­ 9. Cervical lymphadenopathy
ganization has defined pediatric AIDS as an infant 10. Gingival and periodontal lesions like ANUGand
or child presenting with at least a major criterion necrotizing ulcerative periodontitis
along with at least 2 minor criteria in the absence 11. Oral ulcerations
of any immunosuppression. 12. Dysmorphic craniofacial features
 SECTION 11 : DENTAL CARE FOR THE SPECIAL CHILD I

Table 11.17 Commonly used antifungal drugs

Other malignancies reported in HIV infected chil­
dren include hepatic fibrosarcoma, hepatic leiomy­ Drugs Dose
osarcoma, hepatoblastoma, acute lymphoblastic
Topical
leukemia, Hodgkin’s lymphoma and Ewing’s sar­
coma. 1. Nystatin suspen­ 1-2 mol to be applied to the
sion (100000 v/ml) affected area tds or qds.
Candidiasis
Recurrent candidiasis, which is persistent for long 2. Amphotericin 1 ml to be held in the
periods and often resistant to conventional antifun­ suspension mouth or applied to the
gal therapy, is a frequent oral manifestation in (100mg/ml) affected area after food
pediatric HIV infection/AIDS. Oral candidiasis in qds for 14 days.
HIV infected children is variable and is manifested
Older children
as pseudomembranous plaques, erythematous
patches, angular cheilitis, hyperplastic plaques. 1. Nystatin pastilles 1 pastille to be sucked

Angular cheilitis appears as fissures or cracks at (100000b/ml) qds for 7 days

the commissures of the lips. 2. Amphotericin i 1 lozenge to be dissolved
Lozenges (10mg) in the mouth for 10-15
Treatment
days
The lesions may subside or disappear with treat­
ment, but relapse is common The treatment can be 3. Clotrimazole 10 mg troches < 5 /day

either topical or systemic (Table 11.17). orally

Viral Infections: Systemic

In HIV - infection, several viruses are able to colo­ 1. Fulconazole j By mouth or IV by

nize or react, producing lesions in the mouth. These i infusion 3-6 mg/kg on
include herpes - group viruses and papillo­ : first day followed by
maviruses. 3 mg/kg daily thereafter
every 72 hrs in neonate
Herpes simplex upto 2 weeks old and
Herpes simplex is caused by herpes simplex virus I every 48 hrs in neonate
(HSV) and it recurs frequently in children with an 2-4 weeks old.
advanced HIV disease. The virus become latent in
trigeminal ganglion and any sort of stimulation to 2. Ketoconozole Orally with food, 3mg/kg

the sensory nerve may reactivate the virus along the daily with food for

sensory nerves to the mucosal or the epithelial sur­ 2-3 weeks

faces interrelated by the reactivated ganglion lead­ 3. Amphotericin B 0.25mg/kg/day IV

ing to recurrent oral herpes lesions. These lesions
in children may manifest as gingivostomatitis and rapidly to cause extensive mucocutaneous involve­
recurrent lesions are seen as vesicles on the vermil­ ment and as immunosuppression increases, an in­
lion border, which ruptures and form ulcers (cold crease in severity and frequency of r
sores or herpes labialis) on the lips or appear as orolabial lesions occurs.
clusters of small painful ulcers on the palate and
gingiva. In healthy children, HSV lesions resolve Herpes Zoster
in 10-14 days and generally require only a pallia­ Herpes zoster is caused by varicella zoster (HVZ) vi­
tive treatment. In HIV- infected children, these le­ rus due to re-activationofthe virus along the cutane­
sions are chronic, recurrent and may progress ous surface ganglion because of immunosuppn
 I TEXTBOOK OF PEDODONTICS

HVZ can produce oral ulceration in the lips and seen in HIV infected individuals may even be the
oral mucosa usually accompanied by skin lesions. first signs of HIV infections. Gingivitis in HIV
The lesions evolve during 1 -2 days to form true vesi­ infected children appear as an intensely
cles and bullae formation. Later, the bullae may be­ erythematous band that extends 2 to 3 mm apically
come bulbous, hemorrhagic, necrotic and painful from the free marginal gingiva and the attached
which lasts for up to 6 weeks in infected persons gingivae. The gingiva may be reddened, edematous,
and we can see repeated episodes of zoster infection. and show spontaneous bleeding with punctate
lesions.
Oral hairy leukoplakia
Oral hairy leukoplakia is a viral induced lesion whose NUP is characterized by a localized lesion result­
origin is the Epstien - Barr virus (EB V) which is ing in a rapid loss of supporting periodontal struc­
rarely manifested in children. Hairy leukoplakia tures and loose teeth with no pocket formation. Other
correlates with a risk of rapid progression of HIV features are soft tissue and bone necrosis, pain and
disease. It appears as a nonscrapable, white, finely bleeding.
corrugated lesion along the lateral borders of the
tongue. The distinguishing feature of HIV -G and HIV-P is
a lack of response to removal of the plaque and good
Oral warts oral hygiene maintenance.
They maybe seen in an HIV infected patient, with
human papilloma virus as the etiologic agent. Some Treatment
warts have a raised, cauliflower appearance whereas « Aggressive curettage
ethers are well circumscribed, have a flat surface, « Peridex (0.12% chlorhexidine digluconate)
and almost disappear when the mucosa is stretched. rinses three times daily
Human papilloma virus (HPV) found in the oral le­ ■ Antibiotic treatment
sions in HIV infected persons is different from the %

HPV types associated with anogenital warts. Parotid enlargement with xerostomia involving
salivary glands
*.
Treatment of viral infection The parotid glands are diffusely swollen and firm
Herpetic lesions maybe treated with systemic doses without evidence ofinflammation or tenderness with
of acyclovir ranging from 1 to 2 gm daily taken unilateral or bilateral involvement.
orally or IV in individuals with more severe oropha­
Treatment
ryngeal lesions or in those unable to swallow.
a Chronic parotid enlargement does not require
treatment
Bacterial Infection
■ Drugs like zidovudine can be given but usually
Oral lesions of bacterial origin may include myco-
the recurrence of the lesion may occur.
bacterium aviumintracellulare and Klebsiella
pneumoniae. Oral ulceration
Recurrent apthous ulcers in HIV infected persons.
HIV associated gingivitis (HIV-G) and HIV as­ They appear as a well circumscribed ulcers with an
sociated periodontitis (HIV-P) erythematous margin. The ulcers of a minor form
Linear gingival erythema (LGE) and ANUG like appear as 0.5 to 1 cm, herpetiform appear in clus­
lesion called as necrotizing ulcerative periodontitis ters of small ulcers (1-2 mm) usually on the soft
(NUP) occur frequently in HIV infected adults and palate and oropharynx, major ulcers appear as large
have been reported occasionally in HIV infected necrotic ulcers of 2-4cm which are painful and last
children. These gingival and periodontal diseases for several weeks.
 SECTION 11 : DENTAL CARE FOR THE SPECIAL CHILD |

Treatment c. Disposable needles to be used

■ Fluconomide ointment (0.5%) d. Gloves (double) should be used
■ Orabase 3-6 times/day e. Change of clothes
■ Dexamethasone 0.5 mg/ml 3. Proper sterilization

Petechiae HIV is sensitive to heat for 20 minutes but

20 -30% of HIV infected patients may develop autoclaving at 121 ° C for 15 minutes at one atmos­
thrombocytopenic purpura at any age. Oral lesions pheric pressure kills this virus or dry heating of in­
appear as small blood filled purpuric lesions. struments upto 170 ° C. At room temperature it can
survive for about 7 days. The virus can be inacti­
Causes vated by hearing lyophilized factor at 68°C for 72
■ HIV induced autoantibodies hours, liquid plasma at 60°C for 10 hrs.
■ Megakaryocyte infection Disinfectants for innate objects: Chemical disinfect­
■ Aplasia ants must not be used for needles and syringes. Be­
■ AZT therapy which may suppress the bone mar­ fore immersion of innate objects on chemical disin­
row fectant remove gross contamination on the instru­
ments like dried blood because disinfectant will not
Cervical lymphodenopathy is significantly related penetrate into these. The common disinfectants that
to a decline in CD4 + T cells and an increase in are used are:
serum IgM. ■ 0.2% sodium hypochlorite
■ Calcium hypochlorite
Prevention ■ 6% hydrogen peroxide for more thari 30 minutes
Oral and dental management of HIV infected chil­ ■ 2% glutaraldehyde and 6% hydrogen peroxide
dren requires the implementation of a preventive combination
protocol, aggressive treatment of established dental ■ sodium dichloroisocynate
infection and use of an antibiotic cover to prevent
infection. The various approaches are Disinfectant for living tissues are
1. Practising safe sex and a single partner sex ■ Povidine
2. If a pregnant lady on testing proves that the foe­ ■ 2% propranol
tus is also HIV positive, she should be allowed ■ Ethanol
to medically terminate pregnancy ■ HIV is completely inactivated by treatment for
3. Blood and blood products to be screened for any 10 minutes at room temperature with 10% house­
contamination hold bleach, 50% ethanol, 35% isopropanol,
4. Not to reuse needles 0.5% paraformaldehyde or 3% hydrogen perox­
5. Educating the populations. ide
Gloves may be autoclaved, disinfected by immers­
In dentistry, there is little scope of HIV transmis­ ing them in boiling water for 20 minutes. Alterna­
sion. Though HIV and antibodies to it have been tively overnight soaking of 1% sodium hypochlo­
isolated from saliva and blood, but no known case rite.
of HIV positive patient has been detected. There­
fore, the precautions to be taken are Global AIDS Strategy
1. proper medical history of the patient
2. barrier techniques like I. Prevent sexual transmisión of HIV by:
a. Eye protection in terms of eye glasses a. Information and education
b. Mouth mask (disposable) « Avoid multiple sex partners
 €&£) I TEXTBOOK OF PEDODONTICS

■ Educate the people about AIDS and its mode ■ Voluntary counselling, contraception and
of transmission, how they can protect them­ other fertility regulation services should be
selves and their partner by use of condoms available to women.
support services ■ Research needs to pursue the development of
■ School health education program on AIDS/ perinatal vaccines or some drugs for prevent­
STD should be developed with the help of ing perinatal HIV transmission.
teachers, or social organization.
AIDS Vaccine
b. Health and social services through A lot of research on this aspect is coming up, but
■ Early diagnosis and treatment with appropri­ still not successful because it is seen that through­
ate drugs must be made available through out the course of HIV infection the genetic make up
health personnel of virus is constantly changing from one method of
« Early diagnostic methods in women so as to transmission to the other. In addition, the genetic
prevent its transmission to children makeup of HIV vaccine varies across regions as well
» Should provide AIDS education counselling as within individuals. Therefore, different vaccines
and voluntary HIV testing will be needed to defeat the virus in different re­
■ Shake hand as a personal form of communi­ gions of the world, at least 9 sub types of HIV are
cation and to change ones behaviour about labeled, which is impossible. Therefore, an individu-
al’s best chance for protection against any infection
protection
requires a vaccine prepared from a virus that ex­
■ Use of media, newspapers, pamphlets, post­
actly matches the virus to which he/she will be ex­
ers, banners, films, advertisement etc.
posed.

c. A supportive environment to prevent sexual

Drugs used for AIDS
transmission of HIV through
Mainly antiviral drugs like K
■ A supportive public environment
a. Acyclovir 1 to 2 gm daily orally or IV
■ There should not be any legal barrier to give
b. Zidovudine (AZT) which a.ttac^s the virus
informative messages about sexual health and through the enzyme reverse transcriptase
no barrier that would hinder people from re­ c. Three other inhibitors are also in market, namely
ceiving and acting on prevention messages ■ Dideoxycytosine (ddc)
■ Dideoxyinosis (dd I)
II Prevent blood borne transmission of HIV ■ Stavudine (d4 T)
■ By use of safe blood and blood products. d. Use of protease inhibitors like
• Ensure safe blood supply by the donors. ■ Saquinavir, indinavir and ritonavir
■ Screening donated blood for HIV prior to e. Triple drug therapy combines indinavir with
transfusion and use of proper techniques. AZT and 3TC to reduce HIV copies in the plasma
« Develop cheaper and reliable HIV tests. of infected patients.
« Avoid use of unsterilized needles and needle
puncture. S elf-Assessment
■ Carefill attention to infection control proce­
dures, including proper sterilization of equip­ 1. What are the types of Hemophilia?
ment used for surgical and other invasive pro­ 2. What do you mean by X-linked recessive and
cedures. X-linked dominant?
3. What are the oral manifestations of hemophilia?
III Prevent perinatal transmission of HIV 4. What do you mean by replacement therapy?
■ Avoid child bearing by HIV infected women 5. What are antifibrinolytics?
 SECTION 11 : DENTAL CARE FOR THE SPECIAL CHILD |

6. What are the dental considerations while treat­ 9. What are the dental findings in patients suffer­
ing a hemophilic patient? ing from renal disorders?
7. What are the oral manifestations of platelet dis­ 10. When was the first seropositive infant identified
orders? in India?
8. What is the causative factor of herpes zoster? 11. How many children are expected to be affected
by HIV by the end of2000 according to W.H.O. ?
 11.4 Cleft Lip and Palate

Pramod Kumar, Tandon S

Introduction b. SECONDARY PALATE: It includes the palate

behind the incisive foramen. It develops by a
In ancient time, the cleft lip and palate deformity positional change of the palatal shelves of the
was considered to be due to the effect of evil powers maxillary process from a vertical to horizontal
or due to effect of a solar eclipse on the pregnant position and then fusion starting from incisive
woman. In many communities these afflicted child foramen progressing towards uvula. This fusion
were supposed to bring a good fortune for the fam­ takes place between 7 to 12 weeks of the intrau­
ily. In other tribes they were often removed from terine life.
the community and were left to die alone. But now
the scene has changed completely. The DEVELOPMENT OF CLEFT
multidisciplinary approach towards this problem led
to a steady improvement in its end-results. Now a A. Cleft lip : Various theories have been evolved to
cleft baby leads a happ^v life in the society without explain the development of the usual cleft lip;
much esthetic or functional deficiencies. To some ■ Failure of fusion between median nasal proc­
extent the embryogenesis of the cleft is well under­ ess and maxillary process (Dursy-His hypoth­
stood and numerous procedures from various den­ esis).
tal and surgical disciplines produce an optimal func­ ■ Failure of mesodermal migration between the
tional and aesthetic result. two layered epithelial membrane which re­
sults due to fusion between the two processes.
Embryology This eventually leads to a breakdown and cleft
formation (Fleischmann,4 Veau and Stark).
Embryologicalh the area of the lip and palate is ■ Rupture of cyst formed at the site of fusion.
divided into primary palate and secondary palate.
B. Cleft palate: At 7 weeks of intrauterine life two
a. PRIMARY PALATE: It includes the central por­ palatal shelves from maxillary process lie verti­
tion of the upper lip (philtrum), alveolus bear­ cally on either side of the tongue. Between 8 to
ing four incisors and the palate anterior to the 9 weeks of intrauterine life, tongue drops down
incisive foramen. It develops from median na­ due to growth of stomodeum and extension of
sal process and fuses with maxillary process be­ the head. Thus, palatal shelves become free and
tween 4-7 weeks of intrauterine life. Later, meso­ swing into a horizontal plane. By 12 weeks, a
dermal reinforcement of the branchial membrane complete fusion of palatal shelves in midline
takes place. By mechanism of polarization takes place. Several mechanisms have been pro­
ectoderm proliferates and create nostril, posed for development of cleft palate.
alveololabial sulcus. ■ Alterations of intrinsic palatal shelf force.
 SECTION 11 : DENTAL CARE FOR THE SPECIAL CHILD | íMjft

■ Failure of the tongue to drop down (as in Table 11.18c: Prevalence of different types of cleft
Pierre Robin Syndrome). in India
■ Non-fusion of the shelves.
Place Type of cleft with percentage
■ Fusion of the shelves with a subsequent break
down due to inadequate mesodermal migra­ CLP CP CL
tion.
Dharwad 44.3 12.8 42.9
■ Rupture of inclusion cyst formed at the site of
Delhi 68 18 14
fusion. Fusion of palatal shelves occurs one
Chennai 84.7 1.9 13.3
week late in females, exposing the female
palate longer to teratogenic influences. Hence,
the incidence of cleft palate in females is ■ With an increase in parental age there is an in­
greater than males. creased risk of producing an affected child. Birth
order has no significant relationship with the
INCIDENCE defect.
■ Incidence of cleft lip and palate increases when
The overall incidence of cleft lip and palate varies one or more close relatives are involved. (Table
from 0.5 to 3.63 per 1000 live births (Table 11.18a). 11.19).
Fog-Anderson (1942) has studied the distribution
according to the type of cleft (Table 11.18b). Table 11.19: Predicted incidence of the defect
with affected relatives
Table 11.18a: Incidence of cleft lip and palate in
Affected Predicted incidence
different races:
relatives (%) of cleft lip and
Geographic Incidence per 1000 palate
Section/Race live birth
One sibling 4.4
Negro 0.5 Two sibling 9.0
Caucasians 1.0 One sibling one parent 3.2
Japanese 2.34 Two sibling one parent ' 15.8
American 2.91
Children from a consanguis marriage (marriage be­
Table 11.18b: Incidence of different types of cleft. tween blood relatives) show an increased incidence
Type of cleft
of clefts.
incidence (Percent
of all cleft cases)
Due to the increased social acceptance of cleft pa­
Cleft lip alone 25% tients, inter related marriages (those between a nor­
Cleft palate alone 25% mal person + person with a cleft) are on the rise.
Cleft lip and palate 50% Children from these marriages have an increased risk
both of having cleft defects.

■ Male excess has been reported in combined cleft ETIOLOGY

lip and palate defects and female excess in iso­
lated cleft palate patients. ■ In spite of a vast literature available on the
■ Unilateral defects are more common than bilat­ etiology of cleft lip and palate, the etiology of
eral defects and in unilateral defects left sided this defect is yet to be understood.
preponderance has been recorded.
 I TEXTBOOK OF PEDODONTICS

• Various factors which are responsible for devel­ environmental factors results in the defect. There is
opment of cleft lip and palate are: an increasing evidence that most clefts in human
I. Genetic factors. beings appear due to multifactorial causes, i.e. due
II. Environmental factors. to combined effect of genetic influence and various
III. Gene-environment interactions. environmental factors.
/

Genetic factors (Monogenic): Cleft lip associated ASSOCIATED SYNDROMES

With cleft palate is more common in males. Cleft
palate alone is more common in female. This shows Cleft lip may be associated with the following syn­
vague influence of heredity over occurrence ofclefts. dromes -
In about one-fifth to two-fifth of these patients, a 1. Down’s Syndrome (Trisomy 21)
positive family history can be elicited. Vander 2. Wardenburg’s Syndrome (abnormalities of pig­
Woude’s syndrome where lip pits are associated with mentation of hair, iris and skin, deafness).
cleft lip and palate gives rise to Mendelian pattern 3. Vander Woude’s Syndrome (lip pits).
of autosomal recessive inheritance. In rare clefts the 4. Orofacial digital Syndrome: median cleft lip as­
heredity factor seems to be very unusual. sociated with post axial hexadactyly and bilat­
eral accessory toes is found only in Indians.
Enviromental factors: Various environmental fac­ 5. Treacher Collins Syndrome (hypoplastic
tors like fever with rashes (eg: Rubella), exposure zygoma, micrognathia, external and middle ear
to radiation, drugs, trauma and complications of defects).
pregnancy (eg : development of amniotic bands and 6. Pierre Robin Syndrome (micrognathia,
oligohydramnios) during the first trimester of preg­ glossoptosis with respiratory obstruction).
nancy can lead to development of various types of 7. Klippel Feil Syndrome (short neck with an ab­
defects. On an average attack of rubella during first normal or missing cervical vertebra)
trimester can lead to the 75% incidence of birth de­
fects like cleft. Increased incidence of cleft and CLASSIFICATION OF CLEFT LIP AND PALATE
mental retardation was noted in offsprings of preg-
There are many classification systems of cleft lip
nant women in Nagasaki and Hiroshima after atomic
and palate available, but none of them has found
explosions. Various drugs which can cause signifi­
wide clinical acceptance. Various classification sys­
cant increase in the incidence of cleft and other con­
tems can be broadly classified into two categories :
genital anomalies are thalidomide, anti-epileptic
I. Morphological classifications.
drugs (diphenyl hydantoin), hormonal pills, LSD,
II. Embiyological classifications.
quinine, antimitotic drugs. Experimental cleft lip
and palate have been produced by a deficiency of
MORPHOLOGICAL CLASSIFICATIONS
vitamin As Pantothenic acid, nicotinic acid, nitro­
gen mustard, nucleic acid antagonists, steroid and Davies and Ritchie (1922) and Veau (1931) have
ACTH .Consumption of alcohol, smoking and hy­ given morphological classification based on the site
poxic conditions in the mother are also considered and extent of the cleft (Fig. 11.2a, b, c, d). The Veau
to play an important role in development of clefts. classification is as follows.
Group I : Cleft of the soft palate only.
Gene (Polygenic) environment interactions: Many Group II : Cleft of the hard and soft palate till
cleft lip and palate cases show a slight familial ten­ the incisive foramen.
dency but do not give rise to the Mendelian pat­ Group III Complete unilateral cleft of the soft
terns of inheritance. In these cases, the interaction palate, hard palate, the alveolar ridge
between multiple genes with small defects and and the lip on one side.
 SECTION 11 : DENTAL CARE FOR THE SPECIAL CHILD I &&

Fig. 11.2a Cleft involving lip only Fig. 11.2b isolated cleft palate

Fig. 11.2c Unilateral cleft lip and palate Fig. 11.2d Bilateral cleft lip and palate

(Courtesy Dr. Shyam Bhat, Director, Cleft Up and Palate Centre,

A. B. Shetty Memorial Medical College, Mangalore.
I TEXTBOOK OF PEDODONTICS

AB C

DE F

A. Normal anatomy E. Group II complete

B. Group I unilateral (left) F. Group III unilateral
C. Group la unilateral (left) G. Group III bilatera
D. Group la bilateral

Fig. 11.3 Types of cleft lips and palates

 SECTION 11 : DENTAL CARE FOR THE SPECIAL CHILD I

Group IV : Complete cleft of the soft palate, hard Tessier (1976) has classified the rare facial clefts,
palate, the alveolar ridge and the lip the discussion of which is beyond the scope of this
on both sides. note.

EMBRYOLOGICAL CLASSIFICATIONS SYMBOLIC AND COMPUTERGRAPHIC

(Fig. 11.3) PRESENTATION (Fig. 11.4)

Kernahan and Stark (1958) and Spina (1974) have

cleft lip and palate depending on the embiyological
principles.

Kernahan and Stark classification is given below:

Group I: Cleft of the primary palate only

■ Unilateral
■ Bilateral
■ Total
■ Subtotal.

Group II: Cleft of the secondary palate only

■ Total
■ Subtotal
■ Submucous

Group III : Cleft of both primary and secondary

palate.
■ Unilateral - Total, Subtotal.
■ Median - Total, Subtotal.
■ Bilateral - Total, Subtotal. Fig. 11.4 The stripped Y classification

Spina classification is as given below Kernahan (1971) has proposed stripped Y classifi­
cation for rapid graphic presentation of the defect.
Group I: Pre-incisive foramen clefts
This was subsequently modified by Ehlsaky (1972)
■ Unilateral,
and Millard in 1976.
« Bilateral,
■ Median (cleft of the lip with or without an al­ (Rt) (Lt)
veolar cleft). Total, partial. 1,5 : Nasal .floor
2.6 : Lip
Group II : Transincisive Foramen clefts (Cleft of
3.7 : Alveolus
the lip, alveolus and palate)
■ Unilateral 4.8 : Hard palate anterior

■ Bilateral to incisive foramen.

9,10: Hard palate posterior
Group III: Post incisive foramen clefts to incisive foramen
■ Total 11 : Soft palate.
■ Partial

Group IV: Rare facial clefts In the stripped Y classification, the involved area is
shaded bv pen to graphically represent the defect
 €E0 | TEXTBOOK OF PEDODONTICS

For computers, various types of cleft can be recorded immediate area of the cleft. Due to absence of
in form of numeric codes (eg : 10 for cleft lip, 11 normal lip pressure abnormal development of
for cleft palate, 12 for cleft palate and 13 for other dento-alveolar process can occur in the vicinity
lip and palate defects). Computers can be used to of the cleft lip.
store and analyze the data regarding clefts in vari­
ous ways. III. FACIAL GROWTH FOLLOWING SURGICAL
REPAIR
FACIAL GROWTH IN CLEFT LIP AND PALATE
a) Effect of lip repair: Tight upper lip following
I. PRENATAL GROWTH: repair significantly inhibits the facial growth
in anterio-posterior direction. Increased tight­
Various forces which influence the facial growth ness in the upper part of the lip mainly inhib­
in the utero are: its the basal bone growth resulting in retru-
a) Over maxillary segment on non cleft side; sion of midface. Increased tightness in the
■ Pull of lip and cheek ^muscles lower part of the repaired lip near free border
« Tongue pressure. leads to retroclination of dentoalveolar struc­
■ Relatively unstrained nasal septum growth. tures.
b) Over maxillary segment on the cleft side;
■ Intrinsic deficiency b) Effect of palate repair: Palatal repair may in­
■ Pressure from alar base due to stretching hibit the growth of the maxilla and due to scar
of the nostril. contracture, reduction in the maxillary arch
may occur.
Due to the above mentioned forces, the deficiency
produced in the cleft lip and palate babies are:- CLINICAL FEATURES \

A. Incomplete unilateral cleft lip and palate

cases: Larger maxillary segment on noncleft The cleft babies are usually brought Jo the outpa­
side shows a severe deviation of the midline tient department with a complaint of facial deform­
away from the cleft. Smaller maxillary seg­ ity, inability to suck mother’s milk and nasal regur­
ment shows retropositioning or growth inhi­ gitation of milk. Later on, the cleft palate child de­
bition and collapse. Nose is deviated towards velops a speech defect and middle ear infection (in
normal side. Ala is flared and alar cartilage a few cases).
develop and grow in deformed matrix.
Examination of unilateral cleft lip and palate cases
B. In Bilateral cleft lip and palate cases: Pre­ reveal nose deformity (tip deviated to normal side,
maxilla tilts forward and/or shifts to one side ala on cleft side flared, nostril horizontally oriented),
due to tongue pressure. Smaller maxillary seg­ lip deformity (cleft of lip), cleft alveolus, hypoplas­
ments on either side shows similar growth tic and a collapsed maxilla on the side of the cleft
pattern as in unilateral cases. and the cleft of the palate.Bilateral cleft lip and pal­
ate cases, in addition to the features of unilateral
IL FACIAL GROWTH IN UNREPAIRED CLEFT LIP cleft on either side, reveal a protruded premaxilla,
AND PALATE CASES small prolabium, absent or short columella and a
shallow gingivolabial sulcus.
A functionally normal facial skeleton develops
in unrepaired cases except for presence of local Older cleft cases show malpositioned rotated inci­
bony defect due to intrinsic deficiency in the sors, hypoplastic teeth (especially lateral incisors
 SECTION 11 : DENTAL CARE FOR THE SPECIAL CHILD |

and canine on cleft side), and posterior cross bite, ■ Predental treatment is provided which comprises
supernumerary teeth and crowding of the dental feeding plate, pre-surgical orthopedics and help
arch. surgeon in repair by stimulating palatal bone
growth and preventing collapse of dental arches.
TOOTH DEFECTS IN CLEFT LIP AND PALATE ■ Make study records by photographs, models.
CHILDREN
3-5 months
■ Supernumerary teeth ■ Introduce the parents to dental care for the pri­
■ Congenitally missing teeth mary teeth.
■ T-cingulum ■ Alignment of the primary teeth and palatal ex­
■ Peg shaped teeth pansion to be started using a simple fixed appli­
■ Thick curved hypoplastic incisors ance like W-arch and Arnold expander.
« Normally formed lateral incisors usually absent ■ Plastic surgeon to repair the lip
and replaced by abnormally formed supernumer­ ■ Audiology/ENT surgeon first assessment
ary teeth which can erupt at birth as “natal” teeth ■ Suction myringotomy for “glue ear”
■ Gemination, fused supernumerary is frequently
present 12 months
■ Geminated conical tooth may also be present in ■ Pedodontic review. Palatal prosthetic speech
the region of lateral incisors appliance may be required to correct
■ Delayed eruption pattern of permanent teeth velopharyngeal incompetence.
■ High incidence of hypoplasia in the incisors next « Explain possible eruption abnormalities
to alveolar defects ■ Plastic surgeon to repair the palate
■ Isolated enamel developmental defects( in un­ ■ Speech pathologist’s first assessment
operated cases) ■ Review by the audiologist and ENT surgeon
« Enamel defects can also occur in deciduous cus­
pids, molars and first permanent molars 2-6 years
■ Feeding difficulties ■ Pedodontist should review facial growth and
development with regular monitoringat one-year
CLEFT LIP AND PALATE TEAM interval.
■ Preventive measures for caries like fissure seal­
The case of cleft lip and palate is undertaken by a ing, fluoride application
multidisciplinary team, usually headed by a plastic ■ Restorative care if needed
surgeon and consisting of other experts (Table 11.20). ■ Plastic surgeon to review 12 monthly
6-7 years
PROTOCOL FOR DENTAL CARE OF CLEFT LIP
« Pedodontist to review the case and continue treat­
AND PALATE IN CHILDREN
ment for mixed dentition.
■ Preventive or early orthodontic intervention with
The protocol is developed to provide a comprehen­
advice of home care, which would involve pro­
sive treatment in alliance with other experts to at­
cedures like removal ofsupemumeraiy teeth, cor­
tain optimal treatment in the cleft lip and palate
rection of crossbite.
patient.
■ Radiographic evaluation (special occlusal view)
« Orthodontic consultation.
At birth
■ Attend referral
toH I TEXTBOOK OF PEDODONTICS

Table 11.20: A Multi-disciplinary team for cleft lip and palate patients

Experts involved Role

Obstetrician Refers the child to plastic surgeon and pediatrician for expert opinion
Counselling the parents

Pediatrician or Provides medical pare

Neonatologist Refers the case to the plastic surgeon

Plastic surgeon Heads the team of cleft lip and palate case
’ Discusses the case with members of the team in the conference
held monthly or weekly
Carries out initial lip repair and palate surgery
Performs pharyngoplasty or reversionary lip and nose surgery.

Oromaxillofacial Usually comes in the picture of bone grafting

surgeon ‘ If any final orthopedic surgery is, performed at later stage.

Neurosurgeon If any Craniofacial syndrome is associated.

Pedodontist A key member who sees the baby and the parent at the time
of repair of the lip.
* Provides presurgical orthopedic treatment for the baby
Pedodontist monitors the growth and development
To maintain perfect oral health
To guide the occlusion and facial growth
Motivates the parent and the child to cooperate with the treatment.

Orthodontist Provides presurgical dental orthopedic consultation at the initial stage.

• Carries out definitive orthodontic treatment once the full permanent
dentition is erupted

Speech Pathologist Monitors the speech development to normal.

• Tests for an adequate palato-pharyngeal closure and guiding the
surgeons as to whether a pharyngeal flap may be necessary

Audiologist To test hearing in the baby, infant and the young child.
Providing essential information in hearing loss for both speech
pathologist and otolaryngologist.

Otolaryngologist Concerns with the health of nasopharyngeal tissues, including

tonsils, adenoids and middle ear structures.
Blockage of the auditory canal and gluteneous secretion (glue ear)
is very common in these cases.

Psychologist Plays an important role when the child’s family is under stress.
 SECTION 11 : DENTAL CARE FOR THE SPECIAL CHILD J

8 years MANAGEMENT OF CLEFT LIP AND PALATE

■ Combined coalescence with team members PATIENTS

■ Suitability about bone grafting

■ Dental bone assessment (OPG, wrist, lateral Cleft lip and palate is a multifaceted problem which
cephalogram) requires carefully planned team work to rehabili­
■ If needed the patient should be prepared for bone tate the patient. Treatment of this deformity starts
graft protocol at birth and continues upto adulthood. Various spe­
■ Review by the plastic surgeon, speech patholo­ cialities involved in the management are Plastic Sur­
gist and ENT surgeon. gery, Pedodontics, Orthodontics, Speech therapist,
■ Pedodontist to review early if orthodontic inter­ ENT Department, Prosthodontics, Pediatrics and
Maxillofacial surgery department.
vention is needed to relieve crowding and
retroclination of the anterior teeth.
Parent Counselling at Birth:
Parents are usually not prepared to face this prob­
9 year
lem. Sometimes, they have a feeling of guilt that
■ Combined orthodontist and pedodontist coales­
they had done something wrong during pregnancy.
cence.
They should be clearly informed that there is noth­
■ Bone graft alveolar cleft at half to one-third root ing known which definitely results in the cleft and
development of permanent cuspid. there is nothing known which they could have done
■ Review by other experts if required. earlier to prevent its occurrence. The management
plan regarding surgery, dentistry aid speech therapy
10-12 years should be explained properly. The nature and out­
■ Pedodontist to plan future treatment. come of surgery is explained and they are informed
■ Orthodontic consultation. how can they help in the outcome by co-operating
• Monitoring changing dentition and growth. during the course of treatment
■ Preventive measures with a review of dental
health Feeding Advice:
Babies with cleft palate are unable to suck mother’s
12-15 years milk because intraoral negative pressure is not pos­
■ Orthodontic treatment sible. To tackle this problem expressed mother’s
■ Pedodontic review at yearly intervals regarding milk (manually or by breast pump) is given with
other dental treatments the help of a spoon. Feeding by a large nipple with
■ Oral surgeon to assist if the orthodontist requires a large hole, catheter and syringe, nasogastric tube
■ Review by the plastic surgeon has been described but all these methods are diffi­
■ Speech pathologist to review (changing of the cult for the parents and it is difficult to maintain
pitch of voice in boys). Increase hypemasality good hygiene. Spoon feeding is easily learnt by the
parents and maintaining hygiene is much easier.
and nasal regurgitation may result as oronasal
Second problem in these babies is nasal regurgita­
fistula might open up more while orthodontic
tion of milk. This problem can be solved by raising
expansion of arches is being undertaken. This
the head end of the baby while feeding by approxi­
requires speech pathologist’s opinion before the
mately 45°. The third problem is of excessive air
initiation of orthodontic treatment.
swallowing while feeding. For this frequent burp­
ing is done during feeding.
 I TEXTBOOK OF PEDODONTICS

Cleft Lip Repair planned on the lateral side of cleft. In this method
» Timing'. At the time of birth, the lip is less well the minimal tissue is discarded and the result
developed and vermilion border is not very con­ can be modified during the surgery.
spicuous. Thus a majority of surgeons follow the
“Rule of 10” as a guide for timing of lip and Tennison Randall repair (Fig. 11.6): This method
anterior palate repair. At the time of operation gives a clear mathematical design to achieve the
the hemoglobin should be 10 gm percent, age goals of repair. A triangular flap is created on
approximately 10 weeks, weight 10 lbs (4.54 Kg) the lateral side of the cleft to fit into the triangu­
and total leukocyte count less than 10,000 per lar defect produced on the medial side of the cleft.
cubic mm (i.e. no infection). This procedure can be planned exactly after ini­
tial measurements. The result cannot be modi­
• Types of cleft lip surgery. Several types of cleft fied once the lip is cut. The scar is more promi­
lip operations have been described for unilateral nent than in other procedures.
cleft lip. The most commonly used operations
are Millard’s rotation advancement flap and Veau Repair (Fig. 11.7): It is the simplest one
Tennison-Randall Triangular flap methods.. stage straight line closure and produces satis­
Rose-Thompson straightline repair, the Skoog’s factory result in a bilateral cleft lip. In this
procedure are less frequently used. The proce­ method vermilion flap from either lateral side
dures like rectangular flap method of Hagedorn- of the cleft is brought down over the prolabium
Le Mesurier are rarely used. Bilateral cleft lip to augment the vermilion in the center of the
can be repaired in two stages by the above men­ upper lip.
tioned procedure or in a single stage by Veau III
procedure, Millards single stage procedure or Cleft Palate Repair
Black procedure.
■ Timing: Effect of the cleft palate repair on mid
« The various meth­
Basic steps in cleft lip repair: facial growth, speech and dental occlusion
ods of lip repair are aimed at lengthening the greatly influences the timing of repdir. If palate
philtral ridge on the cleft side to make the cu- repair is done after full growth of the maxilla,
pids bow horizontal and to correct the nose de­ midfacial growth retardation and dental
formity as much as possible. The lip is closed in malocclusion problems will be less, but speech
three layers - mucosa, muscle, skin. The ulti­ problem will become very severe. Early repair
mate aim of the repair is to achieve equal length leads to a better speech development but severe
of philtral ridges on either side, horizontal cu- mid facial growth retardation and dental
pid’s bow, accurate repair of muscle, skin, mu­ malocclusion. Experience of most of the surgeons
cosa without vermilion deformity, proper align­ shows that the repair.of palate between 1 - V/2
ment of white line, symmetrical nostril floor, and year of age gives the best balanced result.
finally an aesthetically acceptable scar.
■ Types of cleft palate repair:
Millard's repair (Fig. 11.5): In Millard’s repair Cleft palate is repaired by mucoperiosteal flaps.
rotation flap (a) and columella flap (c) are Cleft palate can be repaired in two ways -
planned on the medial side of the cleft. After
full thickness of the lip is cut along the marking Single Stage Repair:Single stage repair (by Von
a rotation gap is produced on the medial side Langenbeck repair and Veu Wardill Kilner V-Y
which is filled by an advancement flap (b) push back palatoplasty) at the age of Wi yea?
 SECTION 11 : DENTAL CAPE FOR THE SPECIAL CHILD |

Fig. 11.5 Millard’s Repair

Fig. 11.6 Tennison Randall Repair

(¿2

Fig. 11.7 Veau III Repair

 TEXTBOOK OF PEDODONT1CS

produces normal speech in 50 to 70 percent of d) Late mixed and early permanent dentition (from
cases but midfacial growth retardation problem 9!/? years on).
is riot solved. Cleft palate repair by a double op­ e) Permanent dentition.
posing Z-plasty of Furlow is relatively new pro­
cedure aimed at reducing the midfacial growth Pre-dental treatment
retardation problem. However more experience
is required with this procedure before reaching i) Feeding plate: Since feeding problem in cleft
any conclusion. palate babies can be easily overcome by proper
feeding advice, presurgical feeding plate is rarely
Two Stage repair: Cleft palate can be repaired required.
in two stages - ii) To help the surgeon in the repair of the cleft by
i) First Stage - Soft palate repair before 18 pushing premaxilla back or moving maxillary
months followed by obturation of the hard pal­ segments The decision regarding assisting the
ate till the second stage repair. surgeon in repair should be left to the surgeon.
ii) Second Stage - Hard palate repair at 4-5 yr. It is surgeon’s responsibility to discuss with the
This Schweckendiek tw?o stage procedure al­ dentist to get the best possible position of the
lows better midfacial growth, but the speech maxillary segment for his own technique.
results have been unacceptably poor. iii) To stimulate palatal bone growth and to restore
orofacial "functional matrix”. This can be best
Veau-Wardill-Kilnar ’V-Y’ Pushback palato­ achieved by a functional repair of the lip and
plasty (Fig 11.7): In this .method, two mucope- the palate. Presurgical Orthopedics for this is
riosteal flaps are raised from a hard palate and rarety indicated.
nasal layers are mobilized. Abnormal attachment iv) To expand or prevent the collapse of maxillary
of palatal muscles are divided from the poste­ segment. The effort at this stage to expand or
rior border of the hard palate to be sutured in prevent the collapse of the ntexillary segment to
midline to the opposite side the palatal muscles reduce the need for a later orthodontic treatment
(intravelarveloplasty). Suturing is started from has not been proved to be significantly benefi­
the anterior end of the nasal layer and progressed cial in cleft lip and palate cases (Fig. 11.8a, b, c,
towards the uvula. Muscles of the soft palate are d, e).
sutured in midline and then the oral layer is
closed starting from uvula. Primary dentition treatment (Fig. 11.9a, b, c).

Orthodontics And Maxillary Orthopaedics'. At this age, a proper alignment and/or expansion
Methods of Orthodontic intervention and their use­ of the primary dentition can be done more easily.
fulness ait different stages of dentition methods is as But, often the problems are not very severe at this
follows stage and does not require a very active or enthusi­
a) Predental treatment - prior to eruption of pri­ astic treatment. Simple form of fixed maxillary lin­
mary molars; gual appliance (i.e. either a W-arch or an Arnold
- Presurgical expander) are preferred over the removable split
- Postsurgical palatal type of appliance because of occasional co­
b) Deciduous dentition (3 to 6 years) - after full operation problems and a high relapse rate with a
eruption of primary dentition. removable appliance. In a few cases, speech patholo­
c) Early mixed dentition (7 to 9 years) - after or gists advice palatal expansion for improving speech.
during eruption of permanent maxillary incisors.
 SECTION 11 : DENTAL CARE FOR THE SPECIAL CHILD |

Fig. 11.8a Pre-operative maxillary arch showing Fig. 11.8b Appliance placed in oral cavity
bilateral cleft of primary palate

Fig. 11.8c Post-treatment expansion has

taken place

Fig. 11.8d Pre-treatment radiograph Fig. 11.8e Post-treatment radiograph,

note the expansion visible anteriorly
ÍW> I TEXTBOOK OF PEDODONTICS

Fig. 11.9a Cleft lip and palate patient requires

dental rehabilitation

Fig. 11.9b Cast showing lip and palate deformity

Fig. 11.9c Obturator in place

 SECTION 11 : DENTAL CARE FOR THE SPECIAL CHILD |

Mixed dentition treatment lems at this stage are posterior cross bite and mal-
posed permanent incisors.
Various problems which require attention at this
stage are: If orthognathic surgery is done to correct the un­
derlying skeletal imbalance, pre-operative and post­
i) Minor cross bites: may be neglected but severe operative orthodontic treatment is needed to achieve
cross bites are corrected by expansion by usual proper alignment, position and inclination of the
methods. Once correction is complete, full time teeth on their respective arches
retention is required. This is because there is no
niidpalatal suture system to fill in bone and con­ The possibility of opening of oronasal fistula due.to
solidate the expanded maxillary segments. The arch expansion resulting in increased hypeniasality
stretched scar of the previous operation can also and nasal regurgitation must be discussed before
cause the collapse of maxillary segments. Even starting orthodontic treatment.
if cross bite is corrected and retention device is
given at this stage, the possibility of a need to ROLE OF E.N.T. SPECIALIST, SPEECH
re-expand at the permanent dentition stage cannot PATHOLOGISTS AND SPEECH THERAPY
be ruled out. This is because of aggravated max­
illary hypoplasia with growth-. In cleft palate patients due to abnormal function of
eustachian tube there is an increased risk of otitis
ii) Retro inclination ofpermanent incisors and an­ media. The parents are counselled for a possible
terior cross bite: It can lead to esthetic, speech hearing loss. ENT Specialist, Audiologist and Speech
and psychological problems. To correct this usu­ specialist work together to note the middle ear prob­
ally partial banded approach is needed. Once lems and progress in Speech. Speech therapy is
alignment is corrected, a full-time retention de­ started from 6 months of age and if needed contin­
vice is needed. ued till adulthood.

iii) Crowded dentition: This may require serial ex­ Speech problems could be due to velopharyngeal
traction whereby primary cuspids are removed incompetence, oronasal fistula, severe anterior or
to treat incisor crowding and the primary molars posterior cross bite or faulty habits of the patients.
may be removed to hasten the eruption of the A proper orthodontics procedure or surgery in con­
first bicuspids. sultation with the speech pathologist may be re­
quired to correct these problems. Very rarely, pala­
iv) After alveolar bone grafting: Alveolar bone tal prosthetic speech appliance is needed to correct
grafting is done just before canine erupts. Or­ velopharyngeal incompetence..
thodontic movement of the canine may be initi­
ated 6 weeks following placement of bone graft. Abandoned Procedures
With orthodontic movement of canine enough Some of the procedures/modalities which once
space is created in the arch to allow the cuspids formed a part ofthe protocol for these patient’s, have
to erupt. been abondoned due to their demerits and these in­
clude:
Permanent dentition treatment: ■ Routine use of feeding appliance
The principles and techniques of permanent denti­ ■ Pre-surgical orthopaedics
tion treatment of cleft lip and palate cases are simi­ ■ Pre-maxillary strapping and traction
lar to those in non cleft orthodontics, except the • Use of overdenture
period of retention is invariably longer. The prob­ ■ Use of obturators in asymptomatic fistulae
 | TEXTBOOK OF PEDODONTICS

Self-Assessment 4. What is the treatment protocol for cleft lip and

palate patients?
1. Classify cleft lip and palate. 5. What is the role of pedodontist in cleft lip and
2. What are the common dental findings in cleft palate patients?
lip and palate patients before and following sur­
gery?
3. What are the different surgical techniques for
cleft lip and palate surgeries?
 11.5 Common Craniofacial Syndromes
in Children
Rao PLNG, Nautiyal Y, Tandon S

A syndrome is a group of signs and symptoms that occur together and characterize a disease. The
multiple manifestations may be related by common developmental or metabolic conditions. This poses
great challenge to the examiner to adequately diagnose and distinguish a syndrome from other pathologies.

Table 11.21 Commonly seen syndrome

SYNDROME ETIOLOGY CRANIOFACIAL FEATURES OTHER FEATURES

Albright’s 3 Unknown ■ Severe disturbance of body • Recurrent bone pain.

syndrome tissues, usually the mandible. ■ Bony asymmetry and
■ Expansion & deformity of jaws pathological fractures.
■ Eruption pattern of the teeth is ■ Cafe’-au-lait spots on skin.
disturbed. « Precocious puberty in
« Iritraoral pigmentation in some females.
cases. • Disturbance of endocrine
■ On radiograph the jaw bone system
appears as muftilocular ■ Multiple intra-muscular
radiolucencies. soft tissue myxomas.
■ The cortical bone appears
thin and expanded.

Aldrich ■ Hereditary ■ Spontaneous bleeding of ■ Thrombocytopenic purpura,

syndrome disorder gingiva and nose. eczema, petechiae of the skin.
■ Palatal petechiae. ■ Increased susceptibility to
■ Thrombocytopenic purpura and infection results in boils, otitis
eczema beginning on the face. media, bloody diarrhoea and
« Increased susceptibility to respiratory infections.
infection. ■ Occurrence of lymphoreticu-
lar malignant neoplasm.

Block- ■ Transmitted ■ Restricted to teeth and involves • Pigmentation fades in few

Sulzberger as a sex both deciduous and permanent years ending in clusters of
syndrome linked dentition. chromatophoresin upper dermis.
dominant « Delayed tooth eruption. { ■ Local generalised baldness.
trait ■ Peg or cone shaped tooth ! ■ Opthalmologic lesions
crowns. « CNS involvement
■ Congenitally missing teeth. ■ Lesions of skeletal system
• Malformed teeth.
■ Additional cusps.
 <¿23 I TEXTBOOK OF PEDODONTICS

SYNDROME ETIOLOGY CRANIOFACIAL FEATURES OTHER FEATURES

Caffey- « Unknown ■ Mandibular bone is usually ■ Changes in other bones of the

Silverman etiology affected body e.g. clavicles, scapula,
syndrome ■ Thooghtto ■ Jaw involvement manifests as ribs similar to that of jaw occur.
be embryo­ facial swelling. « Fever
nal osteo- « Soft tissue swellings are ■ Irritability
dysgenesis associated with deep muscles, ■ Pseudoparalysis
following generally in the areas of bony • Dysphagia
local defect involvement, e.g. scalp, face, ■ Pleurisy
in blood neck
supply to « Residual asymmetric deformity
the area. of the mandible.
■ Allergic ph- ■ Severe malocclusion.
' enomenon « Radiographically unilateral or
■ It could bilateral thickening and
also result sclerosis of the cortex is seen.
because bf ■ Hyperostosis lags behind
heredity. clinical swelling of soft tissues.

Crouzon’s ■ Genetic ■ Protruberant frontal region. ■ Spina bifida

syndrome & disorder « Triangular frontal defect ■ Patient may or may not be
Apert’s ■ Hypoplasia of maxilla. mentally retarded
syndrome ■ High arched palate.
(Fig. 11.10a, ■ Cleft in some cases.
b, c, d) ■ Exaggerated facial angle.
■ Mandibular prognathism
« Parrot’s beak appearance ot
the patients nose. 4
■ Associated eye changes e.g,
hypertelorism, strabismus,
blindness.

• Crouzon’s syndrome is craniofacial dysostosis occurring without syndactyly.

• Apert’s syndrome is craniofacial dysostosis occurring with syndactyly. (Fig. 11.12)

Down’s ■ Trisomy of ■ Flat face ■ Sexual underdevelopment

syndrome 21st chrom­ » Large anterior fontanelle • Cardiac abnormalities
osome ■ Open sutures « Hypermobility of joints
• Small slanting eyes with ■ Mentally retarded
epicanthal folds
« Open mouth
■ Frequent prognathism
■ Macroglossia
■ Fissured or pebbley tongue
■ High arched palate
■ Malformed teeth
« Decreased caries

contd.
 SECTION 11 : DENTAL CARE FOR THE SPECIAL CHILD |

Fig. 11.10a Apert syndrome proptosis Fig. 11.10b Anterior open bite
hypertelorism mid-face
deficiency

Fig. 11.10c O.P.G showing maxillary and Fig. 11.10d Frontal view showing
mandibular asymmetry of the face asymmetry of face
<4^1 I TEXTBOOK OF PEDODONTICS

Fig. 11.11a Hurler syndrome - Unerupted Fig. 11.11b Skeletal deformity of

teeth with thick fibrous tissue, delayed the back
eruption of lower teeth

Fig. 11.11c Lateral cephalogram showing a Fig. 11.11d Multiple radiolucencies

steep mandibular plane in mandible resembling dentigerous
CVSt
 SECTION 11 : DENTAL CARE FOR THE SPECIAL CHILD | @¡9

Fig. 11.12 Apert syndrome - Syndactyly Fig. 11.13 Pierre Robin syndrome
characterized by cleft palate, retrognathic
mandible resulting in bird facies

Fig. 11.14 Turner’s syndrome showing Fig. 11.15 Vander Woude’s syndrome
webbing of posterior neck characterized by deft lip palate and lower
lip pits
 | TEXTBOOK OF PEDODONTICS

Fig. 11.16 Beckwith Weidmann syndrome Fig. 11.17a Goldenhar syndrome

characterized by macroglossia characterized by under development
and exopthalmos of the first brachial arch

Fig. 11.17b Goldenhar syndrome Fig. 11.17c Goldenhar syndrome showing

showing macrostomia malocclusion
 11.6 Pédiatrie Prosthodontics

Tandon S, Nautiyal Y

In spite of increased awareness regarding oral health Prosthodontic Replacements

care, children may present with a badly decayed den­ Depending on the type of deformity, various forms
tition, often beyond repair and requiring extraction. of prosthodontic replacements are available and can
The only treatment of choice in such cases would be categorized into:
be to provide prosthetic replacement. 1. Complete denture construction
2. Removable partial denture construction
Prosthodontics for children is the division of art and 3. Immediate dentures
science of dentistry, which is concerned, with the 4. Overdenture
replacement of missing primary and permanent teeth 5. Obturator
by fixed or removable substitutes. 6. Intra oral appliance for infants
7. Pedodontic Implants (under trial)
How Does Tooth Loss Occur In Children?
Teeth can be lost or require replacement as a result Anatomical and Psychological Considerations in
of number of factors a Child Patient
■ caries Oral mucosa and Skin
■ trauma « Unlike adults, the denture bearing mucosa in
■ infection children are thicker and well circulated
■ congenital anomalies e.g. cleft lip and palate ■ They are therefore less prone to trauma
deformities ■ Skin changes, .e.g. giving proper dentures can
■ systemic disorders e.g. osteopetrosis compensate skin folds around the mouth in child
■ premature tooth loss patients.
■ radiation damage
Residual bone changes
■ intrinsic stains
■ Maxillary and mandibular bones are more po­
■ neoplasia
rous in children and have abundant blood sup­
ply.
Why Do We Need Pediatric Prosthodontics?
« This results in faster healing of the extraction
Replacement of teeth is required to establish:
sockets following which the prosthesis is con­
■ esthetics
structed.
■ speech
■ Growth of the dental arches requires a frequent
• mastication
change of denture
• integrity of dental arches
« health of supporting tissues Tongue and taste changes
■ prevention of undesirable habits • Loss of tooth results in placement of toa^got^
« psy chological and mental health of the patients tween the edentulous ridges.
 <3*9 I TEXTBOOK OF PEDODONTICS

■ Unlike adults inflammation of tongue or taste pediatric patients. Diagnosis and treatment plan­
buds or taste alteration is uncommon in chil­ ning involves the following aspects
dren. ■ History
• Intra oral examination
Salivary flow changes ■ Extra oral examination
■ Children have a good salivary flow and thus have ■ Radiographic examination
fewer problems during denture wear.
■ Xerostomia might be seen in certain syndromes. It varies from the adult patient by many factors like:

Psychology of patients 1. Growth - In young children the presence of teeth

■ Child may develop inferiority complex if teased is vital for the development of perioral structures
by friends and ridiculed by parents during this and proper psychology.
period.
2. Mastication - The dentures should facilitate ef­
PRE-PROSTHETIC PREPARATION fective mastication and not affect the dietary
habits & nutrition of the child.
Before proceeding with the prosthesis it is neces­
sary to carry out pre-prosthetic preparation. It com­
3. Speech - The denture should not affect the de­
prises the following procedures:
veloping articulation of speech, resonance of
« Removal of grossly decayed deciduous or per-
voice and phonetics.
j; manent teeth.
|j ■ If the decayed teeth are in restorable condition
4. Inter arch distance - In case of certain systemic
then they should be utilized fbr overdenture
disorders decreased interarch distance in the pos­
| construction. Renewal of exostosis or tori
terior region may not enable placement of teeth
yj • Treatment of bony or soft tissue lesions like cysts,
!J tumors, frenal attachments. in that particular area. Thus only the denture
base can be extended till there. *
I. ■ Vestibuloplasty or ridge augmentation for small
!i flat ridges, e.g. ectodermal dysplasia.
• Surgical correction of cleft lip and cleft palate. 5. Space management - The denture can be given

!
to the pediatric patient for space management to
■ Alveolectomy for removal of sharp bony spicules
facilitate proper eruption ofpermanent teeth. The
is carried out while taking care of the perma-
clasps of the appliances should not interfere with
| nent tooth bud.
the eruption of permanent teeth
Care should be taken during bone surgeries like,
exostosis in a young child since the maxillary and 6. Neuromuscular skills - The neuromuscular
the mandibular bone is in developing process. Com- skills in the child are not as developed as that of
! plications like damage to nerves, arteries, sutures an adult. The better the neuromuscular co-ordi­
j or growth centers may result. Alveoplasty where nation the better is the adaptation to the new
only trimming and rounding up of sharp bony mar- denture.
j : gins is required can be done at any age of a child
j patient. 7. Patient education - The child patient must un­
1 ;c derstand the need for the prosthetic replacement,
J !' Important Considerations During Prosthetic
its maintenance and the importance of good oral
Treatment Planning In Child Patients
hygiene.
} Proper diagnosis and treatment planning are im­
portant before starting any dental procedures on
 SECTION 11 : DENTAL CARE FOR THE SPECIAL CHILD I

8. Parent attitude - While treating the child pa­ 5. Secondary impression is made with zinc
tient the parent may have to be taken into more eugenol or silicon impression material and the
consideration than the patient himself The par­ master cast is poured in stone.
ents play an important role in explaining the
treatment plan to the child patient. 6. Occlusal rim is fabricated to record the jaw_re­
lationship. In case of younger children, jaw ref­
COMPLETE DENTURES (Fig. 11.18a, b, c, d) lation is difficult to record since the neuromus­
cular development completes only by 7 years of
Complete denture has been defined as a dental pros­ age.
thesis that replaces all of natural dentition and as­ « Patients of ectodermal dysplasia pose a prob­
sociated structures of the maxilla and mandible. lem since the musculature, TMJ function or
(Boucher 1982) growth maturity lags behind that of normal
children. In these cases use of soft wax rims
Technique of denture construction while recording jaw relations reduce the error.
■ Cerebral palsy patients also present problems
1. Tray selection is carried out having explained in giving a correct jaw relation. The dentist
the procedure of impression making to the child must try and achieve a good rapport with these
patient patients.
« Operant conditioning is utilized in which at ■ In osteopetrosis patients, very little interarch
first visit the patient is given upper stock tray space exists in the posterior region of thejaws.
to take home and practice placing it in mouth In these situations only upper occlusal rims
under the parent’s supervision. (Frank 1989) and soft wax is used to register centric rela­
■ In case of a small jaw, the dental mirror head tion.
can be used as a tray for the upper jaw and a
1.6mm stainless steel wire is fashioned in tray 7. Recording thejaw relations the upper and lower
form for the lower jaw to support the impres­ occlusal rims are sealed and mounted on the
sion material. pediatric articulator.
■ Semi adjustable articulator such as Dentatus
2. Impression material for the primary impression ARL could be used for the teenage patients.
is alginate. « For younger children in absence of any suit­
■ In case the child is unable to tolerate this able design of an articulator the casts must be
material, silicon based impression material can mounted in static relationship in a simple
be used because of its pleasant taste and ac­ hinge articulator.
ceptable smell. Occlusal interferences in lateral and protru­
sive positions is identified and corrected only
3. Impression making is first done for the lowerjaw when the denture is inserted in the mouth.
followed by the upper since gagging is frequently
encountered in the upper jaw. 8. Teeth selection
■ Distraction tactics used while making impres­ ■ Zero degree denture teeth are selected and
sion can often prevent gagging. arranged in a flat plane.
■ Artificial denture teeth need to be fabricated
4. Primary cast is then poured over which the spe­ if teeth are not commercially available. For
cial tray is fabricated. this impressions of deciduous typhodont teeth
are made and the teeth are casted in self-cure
acrylic.
 d«O I TEXTBOOK OF PEDODONTICS

Fig- 11.18a Induced anodontia. Teeth were Fig. 11.18b Erupting permanent first molar
extracted following rampant caries seen at the region of right maxillary
posterior arch

Fig. 11.18c Complete denture with modification Fig. 11.18d Complete dentures in mouth
to allow for permanent tooth eruption
 SECTION 11 : DENTAL CARE FOR THE SPECIAL CHILD |

• Adult teeth of the lightest and smallest size caries) or congenital absence of teeth (hereditary
can also be selected and trimmed to the re­ ectodermal dysplasia). The dentures are simulated
quired size. to resemble the deciduous dentition and thereby
provide psychological satisfaction to the patient.
9. Teeth setting of the child differs as per the age However the prosthesis needs to be replaced peri­
of the child. odically to avoid any restriction of skeletal growth.
■ In 2-5 yr old patient, all teeth aredeciduous
and primate spaces should be considered. REMOVABLE PARTIAL DENTURE
■ In 6-7 yr. old the permanent first molars are (Fig. 11.19a-c)
present, primate spaces still exist and a deep
bite is present.
■ In 7-8 yr. old the permanent incisors are
present in place of the deciduous incisor teeth.
Upper permanent laterals are half visible in
the oral cavity and primate spaces are present.
■ Between 9-10 yr. age is the “Ugly duckling
stage”: and the lower permanent canines re­
place the predecessors. First premolars replace
the first deciduous molars.
■ By 12 -13 yr all permanent teeth are present
except the third molars.

10. Denture delivery

■ The patient should be given verbal and writ­ Fig. 11.19a Child undergoing induced anodontia
ten instructions regarding denture care and due to nursing caries - pre-treatment
oral hygiene maintenance.
« Continuous wearing of denture during sleep­
ing hours may hinder the jaw growth and is
thus avoided.
« The patient is recalled after 24 hrs for any
necessary corrections in the denture base.
■ For children of 2-3 yrs of age appointments
«•S
are arranged at intervals of 6 months
■ For older children of about 5-yrs old, recall
after 3 months.
■ Complete dentures should be relieved in the
areas of erupting teeth following evaluation
on the radiographs.
■ Dentures should be periodically relined fol­
lowing adjustments made for the erupting
Fig. 11.19 (b) Pre-treatment, shy smile lacking
teeth
confidence, (c) Post-treatment, bold and beautiful
smile.
Complete dentures prove to be very useful to the
patients suffering from induced anodontia (rampant
 I TEXTBOOK OF PEDODONTICS

Removable partial denture is a partial denture that Class 6 - Bilateral mandibular anterior posterior
can be readily placed in the mouth and removed by Class 7 - One or more primary or permanent
the wearer. (Boucher 1982) In Pediatric dentistry anterior
removable denture play a major role on restoring Class 8 - Complete primary
the function, esthetics^ phonetics as well as space
maintenance. Removable dentures classified according to the type
of material by Finn (1997):
Indications
« Restoration of appearance - Esthetics ■ Maxillary dentures
■ Weak abutment teeth which cannot support a 1. Acrylic
fixed appliance 2. Acrylic with wrought wire clasps
« Closure of cleft palate and congenitally missing 3. Acrylic with cast metal framework
teeth
• Edentulous area where more than 1 mm bone ■ Mandibular dentures
over the erupting permanent teeth is present 1. Acrylic
« Correction of speech abnormalities 2. Acrylic with wrought wire clasps
« Prevention of harmful oral habits 3. Acrylic with lingual bar and wrought wire
» Restoration of masticatory efficiency clasps
• Primary or young permanent teeth lost as a re­ 4. Acrylic with cast metal clasps containing oc­
sult of trauma clusal rests
• The dentures are indicated only after the child 5. Wrought wire clasps soldered to a lingual bar
is of 8years. with acrylic saddles

Advantages Cast metal framework and clasps with acrylic sad­

• They are easier to fabricate dles in the dentures are constructed hi chrome co­
« Can be used as space maintainers balt for longer use.
■ Not very expensive £

• Easy to remodel or reline as the jaw grows Components of removable partial denture

Disadvantages: 1. Denture base

« May result in caries in the adjacent teeth 2. Clasp
« The teeth may succumb to periodontal diseases ■ maxillary denture Cast clasps
■ Untoward effects on growth and development. Wrought clasps
> Loss of alveolar bone ■ mandibular denture One piece casting
• Oral mucosal disorders. including lingual bar
" Cast clasps and lingual
Classification bar soldered together
Removable partial dentures for children have been Wrought clasps and
classified by Brauer (1964). Based on the edentu­ wrought bar soldered
lous area in the mouth, they have been grouped as together
Class 1 - Unilateral maxillary posteriors 3. Occlusal rests
Class 2 - Unilateral mandibular posteriors
Class 3 - Bilateral maxillary7 posteriors The denture base provides stability and retention to
Class 4 - Bilateral mandibular posteriors the denture. The main function of the clasps is re­
Class 5 - Bilateral maxillary anterior posterior tention. Occlusal rests are required on first perma­
 SECTION 11 : DENTAL CARE FOR THE SPECIAL CHILD |

nent molar to prevent its mesial tipping as the den­ ■ Resin jackets all ceramic and metal ceramic *
ture settles in the 2nd deciduous molar area. crowns on vital teeth.
■ All ceramic and metal ceramic crows supported
Instructions to the patient by posts and cores on non-vital teeth.
The patient is given instructions similar to those
giv^Wl^orirplete denture and shown the proce­ Restoration of single or multiple missing teeth
dure for insertion and removal of the denture.
This is accomplished by:
FIXED PARTIAL DENTURE (Fig. 11.20a, b, c) ■ Resin bonded retainers as an alternative to con­
Fixed partial denture is a tooth borne partial den­
ventional fixed partial dentures.
ture that is intended to be permanently attached to
« Pin ledge and partial veneer crown retainers
the teeth or roots that furnish support to the resto­
■ Inlay retainers
ration (Boucher 1982).
■ Full veneer crown retainers
■ Fixed partial denture pontics
Indications
■ Cantilevered prosthesis
Fixed partial dentures give excellent results where
the teeth are of relatively normal anatomy and are
well supported. It is indicated in the following con­ Over Dentures
ditions: Over denture is a complete or partial removable
1. Endodontically treated teeth denture supported by retained roots to provide sup­
2. Congenitally malformed teeth port, stability, tactile and proprioceptive sensation
3. Hypoplastic teeth to reduce ridge resorption (Boucher, 1982).
4. Fractured teeth Primary over denture can be constructed at 3 years
5. Congenitally missing teeth of age since the growth in maxillary arch anterior
6. Discoloured teeth to the intercanine line is reduced by age 3. As the
jaw grows posteriorly, the patient ‘grows out’ bf the
Contraindications dentures distally. Growth of palatal vault from the
■ In younger patients great care should be taken 5th to the 11th years should also be kept in mind
during preparation of the tooth. while constructing the denture.
■ Deciduous and young permanent teeth have a
large pulp Indications %
■ Teeth are under the partial eruption stage 1. Patients with very few teeth
■ Mobile or periodontally involved teeth 2. Teeth with a small clinical crown or short roots
■ Grossly carious teeth with a minimal tooth struc­ 3. Small dental arches with a little lip support
ture
4. Large spaces between teeth, which are difficult
If unfavourable biological response is expected due
to correct orthodontically.
to periodontal considerations, than an adequate peri­
5. Congenital malformations
odontal management e.g. crown lengthening pro­
cedures, gingivectomy, flaps, ostectomy should be
Contraindications
» carried out.
1. When other type of prosthesis can achieve supe­
rior results
Restoration of single malformed, discolored or
fractured teeth (Fig. 11.21a, b) 2. Patients with poor oral hygiene
This could be carried out by various restorative pro­ 3. Psychological factors
cedures like:
 | TEXTBOOK OF PEDODONTICS

Fig. 11.20a Tooth reduction for maxillary right Fig. 11.20b Crown built up on die with inlay
central incisor wax

Fig. 11.20c Completely fabricted crown in oral

cavity

Fig. 11.21a Hypoplastic maxillary incisors Fig. 11.21b Esthetically restored teeth
requiring prosthetic rehabilitation
 SECTION 11 : DENTAL CARE FOR THE SPECIAL CHILD |

SYNDROME ETIOLOGY CRANIOFACIAL FEATURES OTHER FEATURES

Ehler • Hereditary ■ Fragile oral mucosa ■ Hyperelasticity of skin

Dan los disorder of ■ Retarded healing of mucosa ■ Skeletal abnormalities
syndrome connective ■ Bleeding following tooth ■ Ocular lesions
tissue brushing
■ Hypermobility of TM J with
repeated dislocations
■ Altered tooth structure with
lack of normal scalloping at
DEJ_ pulp stones, extensive
periodontal destruction
■ Frontal bossing
■ Wide nasal bridge
■ Hypertelorism

Ellis Van ■ Autosomal ■ Fusion of midline portion of ■ Number of ectodermal disorders

Creveland recessive upper lip to the maxillary present with involvement
syndrome inheritance gingiva eliminating mucolateral of -nails, chondrodysplasia,
with sulcus polydactyly and heart diseases.
parental « Natal teeth
consangu­ e Prematurely erupted deciduous
inity teeth
■ Congenital absence of teeth
■ Cone shaped hypoplastic teeth
■ Supernumerary teeth

Gorlin & ■ Hereditary • Deformity arid displacement • Cutaneous abnormalities

Goltz condition of developing teeth. like - basal cell carcinoma
syndrome transmitted ■ Occurrence of odontogenic and dermal cysts.
as an auto­ keratocyst which frequently • Osseous abnormalities
somal develops into ameloblastoma e.g. rib anomalies.
dominant ■ Mandibular prognathism ■ Ophthalmologic abnormalities
trait ■ Neuralgic abnormalities
e.g. mental retardation
■ Sexual anomalies e g .
hypogonadism in males and
*
ovarian tumors

Hurlers ■ Disturbance ■ Large head ■ Progressive corneal clouding

syndrome of mucopo­ • Prominent forehead ■ Hepatomegaly <
(Fig. 11.11at lysaccharide « Saddle nose ■ Short neck an&spinal
b, c, d) metabolism ■ Wide nostrils abnormalities
« Shortening and broadening of • Claw hand \ ,
mandible with prominent gonion. • Short stature
■ Spacing of teeth « Mentally retarded
■ Localized destruction of bone. • Stiff joints
■ Gingival hyperplasia ■ Valvular heart disease
• Enlarged tongue ■ Relatively short limbs

contd.
 | TEXTBOOK OF PEDODONTICS

SYNDROME ETIOLOGY CRANIOFACIAL FEATURES OTHER FEATURES

Klinefelter « Extra X ch­ « Taurodontism ■ Relatively short limbs

syndrome romosome
in males

Marfan « Hereditary ■ High arched palate ■ Excessive length of tubular

syndrome disorder ch­ ■ Bifid uvula bones resulting in long thin
aracterized « Malocclusion extremities
by defective « Multiple odontogenic « Spidery fingers
collagen cysts of maxilla and ■ Hyperextensibility of joints and
organizat­ mandiible frequent dislocations
ion. ■ TMJ dysarthrosis ■ Kyphosis or scoliosis
■ Long narrow face a Flat foot
■ Cardiovascular complications

Pa pill on ■ Unknown ■ Severe bone destruction

Lefevre ■ Both deciduous & permanent
syndrome dentitions are involved
■ Premature exfoliation
■ Inflammatory gingival enlarge­
ment, gingival ulceration,
deep pockets.

Pierre Robin ■ Nonspecific ■ Cleft palate « Heart defects

syndrome • Micrognathia • Skeletal abnormalities
(Fig. 11.13) ■ Glossoptossis « Ocular lesion#
■ Retrognathic mandible,
resulting in bird facies &

Scherthaner ■ Unknown ■ Abnormalities of skull, teeth ■ Deformity of shoulder girdle

Marie and jaws and long bones
Sainton ■ Delayed closure of fontanelles a Partial absence or thinning
syndrome ■ High, narrow arched palate of one or both the clavicles
■ Cleft palate a Defects of vertebral column,
■ Underdeveloped maxilla pelvis, bones of digits.
■ Prolonged retention of a Anomalous muscle.
deciduous teeth and
subsequent delay in eruption
of succedaneous teeth
■ Roots of teeth are short and
thinner than usual and may be
deformed
■ Cementum is absent
• Unerupted supernumerary teeth
are present

Contd.
 SECTION 11 : DENTAL CARE FOR THE SPECIAL CHILD |

SYNDROME ETIOLOGY CRANIOFACIAL FEATURES OTHER FEATURES

Stevens ■ Unknown « Severe bullous form of ■ Bullous lesions involve skin,

Johnson erythema multiforme' eyes and genitalia apart
syndrome ■ Involves oral cavity with painful from the oral cavity.
lesions ■ Fever
■ Ulceration of lip ■ Malaise
« Photophobia

Treacher • Failure of « Macrostomia

Gollins differentia­ « High palate
syndrome tion of ■ Cleft palate
maxillary « Blind fistulas between ears
mesoderm and angles of mouth
at and after ■ Bird or fish like facies
50mm stage ■ Hypoplasia of facial bones
of embryo especially malar bones and
mandible

Turners ■ Missing X « Heart shaped facies « Congenital lymphodema

syndrome chromos­ • Prominent ears • Broad chest
(Fig. 11.14) ome ■ Webbing of posterior neck ■ Hypogonadism
■ Low posterior hairline

Van der • Hereditary ■ Association of pits of lower lip

Woudes congenital and cleft lip or cleft palate
syndrome malforma­
(Fig. 11.15) tions

Beckwith ■ Unknown ■ Macroglossià, auricular areas ■ Exophthalmos, umbilical hernia,

Weidmann hypoplasia of abdomen
syndrome ■ Musculature visceromegaly
(Fig. 11.16) (Kidney, adrenals, pancreas)
(Exophthal­ hypoglycaemia.
mos Macro-
glossia
Gigantism)

Sturge « Unknown ■ Congenital capillary ■ Hemangioma of meninges,

Webers hemangioma of face over choroid; usually unilateral
syndrome trigeminal nerve distribution
(Encephalo
trigeminal
angiomato­
sis)

Horner’s « Lesion of ■ Ptosis, Miosis, anhidrosis over

syndrome cervical Ipsilateral face enophthalmous
sympathetic
fibres (injury ■ Heterochromia iridis'

contd.
 I TEXTBOOK OF PEDODONTICS

SYNDROME ETIOLOGY CRANIOFACIAL FEATURES OTHER FEATURES

tumour
etc.)
■ Congenital
form

Osler- ■ Autosomal ■ Telengiectatic mucocutaneous ■ Lesions (vascular ectasia) in

Webers- Dominant lesions over lips, tongue, conjunctivae, palms, larynx,
Rendu inheritance nasal mucosa, face, and ears. pharynx, gastrointestinal
syndrome tract, bladder vagina,
(Hereditary bronchi, brain, liver.
hemorrhagic
telangiect­
asia)

Aniridia « Familial ■ Absence of iris, photophobia, « Glaucoma, corneal degeneration

Sporadic nystagmus, defective vision calaraits, optic nerve
(associated hypoplasia, Macular
with Wilms’ degeneration
tumour)

Goldenhar • Unknown ■ Underdevelopment of brachial

syndrome Spontane­ arch (zygoma, maxilla,
(Nemitual ous trigeminal nerve, upper part of
microsomia) mutation external ear, parotid) and
(Other name­ branchial arch 11 (temporal bone,
lateral facial external + middle ear, facial
dysplasia, nerve, muscles of facial £

otomandibulo expression)
vertebral ■ Macrostomia, skin tags from
anomaly tragus to oral commissure.
intrauterine
facial necro­
sis, first &
second bran­
chial arch
syndrome)
(Fig. 11.17a,
b, c)

Self Assessment

L In which syndrome will you find cafe-au-lait spots?

2. What is the etiology of down’s syndrome and list out the dental findings?
3. In which syndrome will you find an extremely retrognathic mandible?
4. What is Hurler’s syndrome?
5. What is Goldenhar syndrome?
 SECTION 11 : DENTAL CARE FOR THE SPECIAL CHILD |

Advantages 3. This also helps to gain confidence from child

1. It proves to be superior treatment method when patient in future
only a few teeth are remaining in the mouth. 4. Spares the patient of inconvenience and distress
Since it provides a broader distribution of func­ or inability to masticate food or ary dietary modi­
tional and parafunctional forces. fications
2. Conservation of alveolar ridges 5. Minimal change in appearance
3. Conservation of remaining abutments 6. Guides placement of teeth in their former posi­
4. Prosthesis stability is improved tions
5. Provides a better retention
Disadvantages
6. It requires a minimal palatal coverage since the
1. Need relining since bone resorption occurs fol­
prosthesis is retained by the teeth
lowing extraction
7. Better propioceptive response
2. They are replaced by a complete denture once
8. Fewer denture adjustments are required
soft tissues and bone have healed
9. It is easily modified to complete dentures

Obturators
Disadvantages
Obturator is prosthesis used to close a congenital or
1. Overdenture may be bulkier than a complete
acquired opening in the palate (Boucher 1982).
denture
Ambioise was one of the first to use artificial means
2. Increased risk of caries ifproper oral hygiene is
to close a palatal defect as early as 1500.
not maintained.

Indications
Types of Overdentures
1. Congenital oral defects, e.g. cleft lip and palate
2. Acquired oral defects of maxillary carcinomas
Overdentures have been classified based on the stage
of patients dentition and time of treatment into: Advantages
1. Immediate overdentures L Restoration of functions like mastication,
2. Transitional overdentures deglutition and speech
3. Remote overdentures 2. Restoration of esthetics
3. Improvement of psychological trauma
Conventional overdentures have been modified to 4. Preservation of remaining oral structures
utilize magnets fitted into the cavities prepared in 4. Normal development of remaining oral structures
endodontically treated teeth.
Different types of obturators
Immediate Dentures 1. Feeding obturator - used for feeding the new­
Immediate dentures are dentures constructed before born or infant with congenital maxillary defects
all the remaining teeth have been removed and in­ 2. Surgical obturator-used immediately following
serted immediately after the removal of the remain­ surgery to facilitate feeding and wound healing
ing teeth. 3. Interior obturator - maintains physiology and
esthetics during healing following surgery or
Advantages trauma
They are advantageous since: 4. Hollow obturator - is hollow to reduce bulk and
1. They avoid humiliating edentulous periods of improve retention and stability
healing. 5. Metal base obturator - is permanent and is placed
2. The denture acts as a protective splint and thus after complete healing of the wound and
decreases pain ■completion.
 <^(<> 1 TEXTBOOK OF PEDODONTICS

Fig. 11.22a Palatal fistula in anterior palate Fig. 11.22b Obturator serving the function of
missing teeth

Fig. 11.23 Obturator for soft palate

6. Palatal obturators Stage 1 (0-18 months)

* dental obturator - used for hard palate defects ■ Impression is made in a low, heat orthodontic
(Fig. 11.22a, b) compound or silicone rubber impression mate­
• speech bulb type obturator - used for soft pal­ rial using aluminum tray or soft spoon or cut
ate defects and velopharyngeal closure (Fig. down denture tray.
11.23) ■ The cast is then poured on which a custom tray
is constructed of cold-cure acrylic resin.
Obturator for cleft lip
* and palate defects ■ Functional impression is then made following
which obturator is constructed.
Management of these patients is required from the ■ The obturator can also be constructed after 1st
very beginning to meet the immediate needs of the impression with silicone impression material.
newborn The cast is poured in stone and obturator is made
with curing silicone.
 SECTION 11‘. DENTAL CARE FOR THE SPECIAL CHILD |

■ Areas of excessive pressure are identified and Nasotracheal intubation is associated with
reduced ■ trauma to the nasal septum and
■ Most of these appliance serve until 3 months of ■ Deformities of the nares.
age at which the lip closure is carried out.
The infant is an obligatory nose breather but
Stage II (18 months to 5 yr.) _ nasogastric feeding tubes obstruct the nares and
This is the age of speech development, thus there cause mucosal edema. Thus to avoid the above men­
are 3 types of prosthetic speech appliance for chil­ tioned sequelae Pedodontist can provide intraoral
dren appliance and be of great help to the Neonatologist.
1. Obturator with palatal - velar - pharyngeal por­
tion Self-Assessment
2. Base plate type, which functions to obturate the
palate and helps speech J. Why is it important to replace teeth?
3. Anterior prosthesis, which contours the upper 2. What are the various prosthodontic replacements
lip and improves anterior occlusion for children?
3. How are pediatric prosthodontic patients differ­
■ The 1st type is used as training, diagnosis and ent from adults?
temporary appliance 4. What is an important indication for a complete
■ The 2nd type is constructed when perforation denture? How do you prepare a complete den­
exists in the hard palate and growth of the child ture for a child patient?
is desired before surgical closure 5. Classify removable partial dentures?
■ The 3rd type helps to build arch form of maxilla 6. What are indications and contraindications for
and restore the function of mandible and create a fixed partial denture?
a pleasing profile 7. Explain the technique for polycarbonate crown
construction?
Stage III ( 6-10 or 11 years of age) 8. What are overdentnres and what is their advan­
If the defect is not yet corrected interim obturator is tage over complete dentures?
given to improve facial appearance. These are peri­ 9. What is an obturator? How is an obturator fabri­
odically adjusted to allow eruption of developing cated for cleft lip-palate patients?
dentition.Thus the obturator helps to restore func­ 10. What is the modification required for feeding
tion, esthetics, speech and thereby avoids psycho­ tube in infants and why is it required?
logical trauma to the patient.
Further Suggested Reading For Section -11
Intra Oral Appliance For Infants
The intraoral appliance has been developed and 1. Adcock-S, Markus-AF: Mid facial growth fol­
designed to stabilize orogastric feeding and lowing functional cleft surgery. Br - J -Oral ■
orotracheal tubes to prevent obstruction to the nares Maxillofac - Surg. 35(1): 1-5 Feb 1997.
and trauma to the palate and alveolar ridge. The 2. Anil S, Beena VT, Nari RG, Varghese BJ: De­
long-term usage of orotracheal tubes in infants has tection of HIV antibodies in saliva and its im­
been associated with plications. Indian J Dent Res W 6,95-98. Jufy-
■ air-way damage Sept 1995,
■ palatal groove formation, 3. Bardnard KM, Smallridge J: Recognizing and
■ acquired cleft palate and caring for the medically compromised child: 3
• Defective primary dentition. Haematological disorders. Dental update,
402-410 November 1993.
 I TEXTBOOK OF PEDODONTICS

4. Barr CE et ai: Recovery of infectious HIV - 1 down syndrome. Primary and secondary
from whole saliva. JADA. Vol 123: 37-45. Feb­ orofacial pathology. Journal of Dentistry for chil­
ruary 1992 dren, Vol: 57, No.8,437-441 November-Decem­
5. Barrock G: Recent advances in etched cast res­ ber 1990.
torations J.P.D. Nov 52(50 619. 1984 18. Lie-W et al: Electromyography investigation of
6. Brewer A.A. and fenton A.H.: The Over den­ masticator muscles in unilateral cleft lip and pal­
ture. DCNA 17:723-46 ate patients with anterior corset. Cleft Palate.
7. Chigurupati R, Raghavan SS, Studen-paviovich Craniofac. J. 35(5), 415-418, Sep 1998.
DA: Pediatric HIV infection and its oral mani­ 19. Nagase - T et al: The effect of muscle repair on
festations a review. Pediatric dentistry, 18:2:106- postoperative facial skeletal growth in children
113. 1996 with bilateral cleft lip and palate. Scand - J -
8. Clark DB: Dental findings in patients with Palate - Reconstr - Surg - Hand - Surg. 32(4):
chronic renal failure: An ovendew. Journal of 395-405. Dec 1998.
Canadian dental association: No. 10, 781-785. 20. Noverraz AE: Timing of hard palate closure and
1987 dental arch relationships in unilateral cleft lip
9. Devita VT, Hallman S, Rosemberg SA: AIDS and palate patients, a mixed longitudinal study.
Etiology, diagnosis, treatment and presentation. Cleft - Palate - Craniofac J, 30(4), 391-6, 1993.
4 1 edition 1997, Lippincott, Raven Publishers. 21. Parry J A, Harrison VE, Barnard KM: Recog­
10. Enemark H, Bolund S, Jorgensen I: Evolution nizing and caring for the medically compromised
of unilateral cleft lip and palate treatment, a long­ child: 1 Disorders of the cardiovascular and res­
term results. Cleft palate J, 27(4), 345-61,1990. piratory systems. Dental update: 25:325-331 Oc­
11. Erenberg A. Nowak AJ: Appliance for stabiliz­ tober 1998.
ing orogastric and orotracheal tubes in infants. 22. Patton LL, Ship JA: Treatment of patients with
Crit. Car. Med. Aug: 12(8)669-70,1984 bleeding disorders. Dental Clinics of North
12. Glick M, Trope M, Pliskin ME: Detection of HIV America: Vol 38, No. 3: 465-482 July 1994.
in the dental pulp of a patient with AIDS. JADA, 23. Ped. Dent: Handicapped definition. American
Vol. 119; 649-659 November 1989. Academy of Pediatric Dentition. 1996.
13. Harris EF, Hullings JG: Delayed dental devel­ 24. Pediatric Dentistry reference manual Vol 21,
opment in children with isolated cleft lip and No.5, Page 20, 1999-00.
palate, Arch, Oral Biol, 35(6), 469-73, 1990. 25. Precious - DS: Declaire -J: clincial observations
14. Hoyer H, Limbrock JA: Orofacial regulation of cleft lip and palate. Oral - Surg - Oral - Med -
therapy in children with down syndrome, using Oral - Pathol. 75(2), 141-51, Feb 1993.
the methods and appliances of castillo-morales. 26. Paul ST, Tandon S, Kiran M: Prosthetic reha­
Journal of Dentistry for children., Vbl.57, No. bilitation of child with induced anodontia. J.
8, 443-451 November-December 1990. Clin. Pediatr.Dent Fall. 20(l):5-8, 1995
15. ICMR Bulletin 19(1): November 1989 cited 27. Rajesh P, Venkatesan P, Narayanan V: Epidemi­
shivlal: AIDS Asia, published by IHO India April ology of cleft lip and cleft palate. J. Ind. Orthod.
1994. Soc. 33:17-20, 2000
16? Johnstone SC, Barnord KM, Harrison VE: Rec­ 28. Ramos V et. al.: Complete dentures for child with
ognizing and caring for the medically compro­ hypohidrotic ectodermal dysplasia: a clinical
mised child: 4 Children with other chronic medi­ report J.P.D. Oct.74(4) 329-31, 1995
cal conditions. Dental update /: 26; 21-26 Janu­ 29. Rees TD: The diabetic dental patient. Dental
ary-February 1999. clinics of North America Vol. 38, No. 3: 447-
17. Limbrock GT, Hoyer H, Scheying H: Regulation 463 July 1994
therapy by castillo-morales in children with
 SECTION 11 : DENTAL CARE FOR THE SPECIAL CHILD | iîifcB

30. Rosembaum CH: Treatment of disabled patients tal disabilities considerations in dental manage­
in private practice. Dental clinics of North ment.
America; Vol.28, No.l: 95-106. January 1984 35. Suji O.O. : Preparation of feeding obturators for
31. Rosenberg MB, Phero JC: Hemostasis for dental infants with cleft lip and palate: J. Clin. Pediatr.
surgery. Dental clinics of North America: Vol Dent. Spring, 211-14, 199S, 1993
39; No. 3; 649-663 July 1995. 36. Tindlund RS, Rygh P, Bœ OE: Orthopedic pro­
32. Slavkin HC:An update on HIV/ AIDS. JADA, tection of the upper jaw in cleft lip and palate
Vol. 127: 1401-1405, September 1996 patients during the deciduous and mixed denti­
33. Smahel Z: Treatment effects on facial develop­ tion periods in comparison with normal growth
ment in patients with unilateral cleft lip and pal­ and development, cleft palate - Craniofac - J,
ate. Cleftpalate -craniofac J. 31(6), 437-5,1994. 27(2), 182-94, 1993.
34. Stewart RE: Pediatric dentistry: Scientific foun­ 37. Yoshida H et al: Cephalometric analysis of max­
dations. 1982, CV Mosby company. Section two illofacial morphology in unoperated cleft palate
chapter 7: oral manifestations of systemic dis­ patients, cleft-Palate-Craniofac J, 29(5), 419-24,
eases. Section serum, chapter 56, developmen­ 1992.
 SECTION - 12

Genetics in Pediatric
Dentistry
12.1 Basic Concepts in Genetics
Dhar P K

Genetics is the study of genes at all levels from mol­ ertiesof DNA (deoxyribonucleic acid), the substance
ecules to populations. Taken alone, the observance of which most of genes are made and that is chiefly
of morphological features may not have much rel­ responsible for the transmission of inherited char­
evance, but when these features are compared among acteristic.
different generations, e.g. grandparents, parents and
siblings, they assume importance. Genotype: Numerous phenotypic traits appear to
be transmitted from one generation to the next.
Phenotype: The numerous features by which we rec­ However, the offsprings do not inherit phenotypes
ognize an organism form its phenotype. In humans from the parents; rather they inherit the ability to
e.g: height, color of skin etc. constitute its pheno­ produce these phenotypes. This ability resides in
type. Different humans differ in their color of skin, the genome (i.e; total DNA content of a cell) and is
Color of hair, shape of face etc. These are called called genotype. The genotype represents a “genetic
phenotypic differences. Inspite of the phenotypic dif­ identity card” of an organism. It is the material that
ferences among organisms, all are similar in the is transmitted from one generation to the next. The
underlying mechanisms that govern their lives. genotype is composed of several functional subunits
There is a similarity at the molecular level, for the called genes. The expression of the phenotype is
molecules they are made of are essentially alike. attributable not only to the genotype but to environ­
mental conditions as well. These environmental
The concept of phenotype also extends when we conditions, however, do not affect the genotype.. For
view something under the microscope or even the example, one of the characteristics of animals is lo­
electron microscope. The similarities or differences comotion. If an animal is caged for, say, 6 months,
in the cell membranes, fine details within nuclei, its ability to move around slows down considerably,
and cytoplasmic bodies, all make the characteristic but if it is released in its natural environment, it
phenotype of an organism. One of the most impor­ rapidly regains its locomotoiy skills. Thus, although
tant phenotypic characteristic of an organism is its the genes that keep muscles active are already in
capacity for reproduction. place but their expression can be modified by the
type of environmental exposure. Environmental
This begins with the duplication of DNA, followed alterations of the phenotype do not reflect altera­
by duplication of cell components, e.g., chromo­ tions in the genotype, but rather the response of the
somes, mitochondria, finally culminating in the cell organism to its environment. The tanning of the
division. Thus, phenotype is a relative term. It may skin is another instance that exemplifies the same
be an externally observable feature like height and concept. Various branches that form this ever ex­
color, or a^microscopically visible feature like prop- panding science of Genetics are as follows.
 SECTION 12 : GENETICS IN PEDIATRIC DENTISTRY |

1. Genetics or classical Mendelian Genetics con­ 12. Cancer genetics is the science of studying chro­
cerns itself with the study of the external fea­ mosomal and molecular basis of malignancies.
tures of the organism from parents to offsprings.
13. Clinical genetics is a discipline of correlating
2. Cytogenetics is the chromosomal study of par­ chromosomal and/or molecular information with
ents in relation to their siblings. The term is also their clinical symptoms.
used to describe the chromosomal characteris­
tics of one cell in relation to the other cells in a 14. Genetic counselling is the science of making pre­
dividing tissue. dictions about the occurrence of genetic diseases
in the family.
3. Molecular genetics is a field of study wherein
genes are investigated in relation to their chro­ 15. Gene therapy describes the transfer of a func­
mosomal ‘address’, length, composition, etc. tional normal gene into an organism to correct
its genetic defect.
4. Radiation genetics is the study of radiation ex­
posure on the structure and function of different 16. DNA chip research is a recent introduction in
chromosomes and/or nucleic acids. the field of genetics. It *
a
is highly specialized
branch which involves grafting of DNA se­
5. Pharmacogenetics is the study of the role of quences on a silicon chip for a rapid and accu­
genes in modifying the effect of drugs. rate diagnosis of a variety of diseases, e.g; breast
cancer.
6. Behavioural genetics explores the genetic basis
of normal/abnormal behaviour. 17. Bioinformatics is one of the hottest areas of ge­
netics today. This field involves expertise both
7. Reverse genetics begins with the identification in computers and molecular biology. Here,
of a mutant gene and ends up in the verification softwares are written for storage, retrieval and
of its transcript. Normally, classical genetics interpretation of information from protein, RNA
starts with the observance of mutant phenotype and DNA databases.
(i.e. identification of the protein), leading to the
identification of the gene responsible for such a COMMONLY USED GENETIC TERMINOLOGIES
phenotype.
Acentric fragment is a chromosome material lack
8. Immunogenetics deals with the hereditary and ing centromere.

molecular aspects of immunological reactions

within an organism. Acquired characteristics are the ones that
are obtained fresh by an organ­
ism.
9. Biochemical genetics involves a study of the ge­
netic mechanisms in the biochemical pathways. Acrocentric chromosome has an eccentri­

10. Population genetics is the study of factors in­ cally placed centromere.

volved in modifying gene frequencies in a given

population. Alleles are alternative forms of a gene
at the same locus on homolo­
11. Developmental genetics deals with the iden­ gous chromosomes.
tification and characterization of genes involved
in the development of organs.
 I TEXTBOOK OF PEDODONT1CS

Aneuploidy occurs when the chromosome Chromosomes are small discrete nuclear bod­
number of the cell does not ies composed of genetic
match the multiple of its hap­ material.
loid number.
Clone (in cytogenetics) is defined as
Antisense is the non-coding strand of the two cells with the same addi­
DNA tional or structurally rearranged
chromosome or three cells with
Association describes the occurrence of a the loss of the same chromo
particular allele in a group of some. In molecular biology,
patients more often than ac­ clone refers to a set of identical
counted for by chance. copies of plasmids produced
from a single recombinant plas­
Autosomes are chromosomes other than mid. In tissue culture; clone is
sex chromosomes (22 pairs in a cell line derived from a single
human cells) cell.

Banding is a technique to differentially Codon is a set of three adjacent bases

stain specific regions of a chro­ in DNA/RNA that specify an
mosome. The most commonly amino acid.
used procedures are Q-, G-, C,
R- and T- banding. Crossing over is an exchange of genetic
material between homologous
Bivalent refers to a paired homologous chromosomes during meiosis.
chromosomes in meiosis.
Culture is a terminology used to
Carrier refers to a recessive heterozy­ describe growth of cells in-vitro.
gote.
Culture medium is a solution of nutrients that
çDNA is a complimentary DNA for a meets the metabolic needs of
messenger RNA molecule. the cells in-vitro.

Cell cycle is the period from one division Dominant refers to a trait expressed in
to the next.Centromere is region heterozygotes.
within a chromosome by which
chromatids are held together. Double minutes are small acentric and paired
fragments of chromosomes.
Chiasma refers to the crossing of chro­
matid strands of homologous Enhancers are DNA elements that magnify
chromosomes during meiosis gene transcription.
as a result of meiotic recombi­
nation. Euchromatin is the DNA that actively
transcribes.
Chromatids are identical copies of a chro­
mosome produced by replica­ Eukaryotes are organisms with a nucleus
tion. and a nuclear membrane.

Chromatin is the complex mix of DNA and Exon is a coding region of a gene.
protein in the interphase cell.
 SECTION 12 : GENETICS IN PEDIATRIC DENTISTRY |

Fragile site is the most easily breakable Introns are non coding sequences that
region of a chromosome. interrupt the coding portions of
a gene
Fragile X synd. describes a condition that
occurs due to presence of frag­ In vitro denotes outside the body i.e;
ile site near the end of the long under artificial conditions.
arm of X chromosome, result­
ing in mental retardation. In vivo refers to “within the body".

Gene is an entire DNA sequence that Karyotype is an arrangemeqt of chromo

is necessary for the synthesis somes according to Interna­
of a functional polypeptide or tional Standard Cytogenetic
RNA sequence. Nomenclature Guidelines, such
that the largest chromosomes
Gene pool is the sum of all genes present are placed first and the small­
at a given locus in the popula­ est ones last.
tion.
Marker is an abnormal chromosome
Gene therapy is a technology of introducing chromosome easily identified by its peculiar
foreign genetic material into a morphology.
patient to correct his/her genetic
defect. Pedigree is a diagrammatic representa­
tion of a family history.
Genetic describes artificial production of
engineering new combinations of DNA. Penetrance is the magnitude of phenotypic
effect of a gene.
Genetic marker is a distinguishing feature that
is used to study the inheritance Phenocopy is an environmentally induced
pattern of genes in cell lines, mimic of a genetic disorder.
pedigrees or populations.
Phenotype is an observable characteristic

Genetics is the scientific study of varia­ of an individual.

tion and heredity.
Promoter is a DNA sequence that signals

Genome refers to a complete set of genes RNA polymerase to initiate tran­

characteristic of a species. scription.

Heterozygotes are combinations of one domi­ Recessive trait is the one that is expressed
nant and one recessive aBele. only in homozygous

Homologous chromosomes are exactly Restriction are enzymes which cleave DNA
similar in size, shape and Enzymes at specific .sites.
genetic composition.
Reverse is an enzyme that can make
transcriptase a complementary DNA from an
Idiogram is the graphic representation of
a karyotype. It is based on the RNA molecule.

size of the chromosomes as

measured on a scale.
 I TEXTBOOK OF PEDODONTIGS

Satellite DNA is highly repetitive short DNA end, chromosomes would have fused with each other
sequence that is not transcribed forming a large single mass of chromatin, as found
into RNA. in bacteria. Chromatin is a complex of DNA, his­
tone and nonhistone proteins that exist in both con­
SexJimited trait is expressed only in one
densed (heterochromatin) and decondensed (euchro-
gender.
matin) forms. In contrast to heterochromatin,
Sexiinked inheritance occurs when a gene euchromatin mostly comprises of active genes. Het­
is carried with a sex chromo­ erochromatin is present as reversible (e.g.; X-chro-
some. mosome) or fixed forms (e.g.; distal Y chromosome).
Chromatin is attached to the nuclear scaffold or ma­
Transcription is a process of formation of trix that extends throughout the nucleus and attaches
complementary RNA from a to cytoskeleton at the nuclear envelope.
DNA sequence
Ultra Microscopic Configuration (Fig. 12.2)
Translation is a formation of polypeptide
from a mRNA sequence.
A nucleic acid consists of a chemically linked se­
quence of nucleotides. Each nucleotide is made up
Wild type refers to the most frequent
form of a normal allele. of a nitrogen base, a deoxyribose sugar and a phos­
phate group. The term “acid” is suffixed to DNA
X-linked are the genes carried on because its nucleotides are esters of phosphoric acid.
X chromosomes. The coiling of DNA strands is helical like a circu­
lar staircase that always retains the same cylindri­
STRUCTURE OF A CHROMOSOME: BASIC CON­ cal diameter and width of steps. DNA undergoes
CEPTS plectonemic coiling - i.e. the one that involves for­
mation of a wider groove (22 Angstroms across)
Chromosomes are the genetic elements of and a narrow groove (12 Angstroms across^). These
eukaryotes. grooves are used for binding of histones and non­
histone proteins. The DNA double helical model
IJght Microscopic Framework (Fig. 12.1a, b) discovered by Watson and Crick was right handed
(B type). However, later other types of DNA: A, C,
They are visible in the light microscope during mi­ D, E and Z forms were discovered. Except Z-DNA
tosis and meiosis and can be conveniently studied all other types arc right handed i.e. the turns run
at 1000 times magnification under a microscope. clockwise looking along the helical axis. In a chro­
The karyotype - a collective term for arranging chro­ mosome DNA molecule is tightly linked with basic
mosomes on the basis of their size, centromeric po­ protein molecules called histones. Instead of two
sition and banding pattern is species-specific. The bases, DNA can also be formed from only two ni­
normal chromosome number in a human diploid trogen bases i.e. pure A:T DNA or pure G:C DNA.
œil is 46. Usually a chromosome consists of two But in real practice the human DNA is composed
arms with an intervening non-staining gap called of four nitrogen bases for two reasons: (1) a poly
centromere. The upper shorter arm is called “p arm” AT or poly GC DNA would enforce structural re­
and the lower longer arm is called ”q arm”. strictions on the folding of DNA and (2) such a DNA
Telomeres close the ends of the chromosomes and would code for less than 20 amino acids, (necessary
snake it insensitive to the presence of neighbouring for our survival). If DNA is exclusively composed
Chromosomes. In absence of a well-defined telomeric of A-T pairs only 4 different amino acids would be
 SECTION 12 : GENETICS IN PEDIATRIC DENTISTRY |

Fig. 12.1a Structure of chromosome at metaphase stage

800-1200 nm
Chromosome
Packing ratio = 5,000 to
10,000
Average size = 40 nm
= 152 milion
base pairs
Acitve DNA = 1.2 nm (3%)

Narrow groove
0.34 nm —

Wide groove

DNA turns
1.8 times
Core histone

146 Base pairs

Linker histone Solenoid

60 Base pairs (25-30 nm da)

Nucleosome

Fig. 12.1b DNA coils to form chromosome

 <^> | TEXTBOOK OF PEDODONTICS

o o

Metacentric Submetacentric Acrocentric

Fig, 12.2 Three types of human chromosomes.

synthesized during translation. Similarly, in case of Types of Genes

poly GT-DNA, a maximum of seven amino acids
would be biosynthesized by the cell, both of which Antioncogene (or tumor suppressor) is involved in
are incompatible with our survival. controlling cellular growth; inactivation of which
leads to cancer. Housekeeping gs. We expressed in
What is a Gene? all cells because it encodes protein needed for basic
A gene is a combination of DNA segments that to­ functioning. Leaky gs. are ones in which a switch
gether constitute an expressible unit, leading to the in the sequence of bases results in the production of
formation of one or more RNA molecules. The com­ a mutant protein that has only partial enzymatic
ponents of a gene include: activity. Lethal gs. either kill the organism or per­
1. the transcribed region (the transcription unit), & mit its survival only under special conditions.
2. the regulatory sequences that flank the transcrip­ Luxury gs. are transcribed in abundance in particu­
tion unit. lar cell type e.g; ovalbumin gene in eggs. Mimic gs.
refer to different genes producing the same effect.
No single definition is, however, entirely satisfac­
Oncogene is a gene found in the chromosomes of
tory or appropriate for every class of gene. Genes
tumor cells whose activation is associated with the
range in length from several hundred base pairs to
conversion of normal cells into cancer cells. Over­
more than 2 million base pairs of DNA, and are
lapping gs. extend over and partly cover the
made of alternating pattern of exons and introns.
neighbouring genes. Proto-oncogene is a normal
Exons are segments of a gene that reach cytoplasm
gene that with slight alteration by mutation or other
as a part of functional and mature RNA (mRNA,
mechanism becomes an oncogene.Recessive g. con­
tRNA or rRNA). Introns are parts of a gene that,
trols a recessive character. Regulatory g. synthe­
when transcribed into RNA (mRNA, tRNA or
sizes repressor which switches off the activity of
rRNA) are spliced out during the maturation proc­
structural genes. Silent gs. are mutant forms of gene
ess of the latter.
 SECTION 12 : GENETICS IN PEDIATRIC DENTISTRY |

having no detectable phenotypic effect. Tissue spe­ OTHER FORMS OF HUMAN DNA
cific gs. are active only in a particular cell or time
in development. In addition to a single and double helical DNA, tri­
ple and tetra helical forms have also been found in
What is a Telomere? human cells. DNA rich in guanine bases can adopt
Telomeres are the only regions of a chromosome a tetra-helical form. Researchers are currently ex­
that comprise .a single helical DNA present as hair­ ploring whether converting a stretch of double heli­
pin-like structure. The inability of telomeric DNA cal DNA into a triple helical form might be a new
to replicate is due to the physical constraints im­ strategy for treating viral diseases, such as AIDS,
posed by the process of replication itself. During cancer, etc. In fact, some new companies like Triplex
replication, the ‘leading’ daughter strand copies it­ Pharmaceuticals (Texas, U.S.A), as well as the al­
self completely, while the lagging strand reaches ready established ones, like Ciba-Giegy, have at­
very close to the ends but cannot go beyond. Such a tached top priorities to 3s DNA research.
situation arises, because there is no room ahead for
binding the templates as well as synthesizing com­ It is believed that when life started mitochondria
plementary DNA downstream. Because of the par­ and chloroplast existed in bacterial forms. Later
tial replication, shortening of telomere occurs in during the process of evolution these prokaryotic
normal cells However, in cancer cells the trunca­ forms chose symbiotic relation with the animal and
tion of telomeric DNA is prevented by an enzyme plant cells respectively. Since prokaryotic DNA is
telomerase”. Telomeres may also serve as “mitotic “inironless” we find the mitochondrial and
clocks” i.e; its length can indicate the number of chloroplast DNA is free of noncoding sequences.
divisions undergone by the cell. Gene expression is
repressed near telomeres, apparently because the
genes get buried when DNA folds to become a chro­ Self-Assessment
mosome.
1. Why is DNA an acid?
What are repetitive DNA sequences? 2. Why is DNA composed of 4 nitrogenous bases
DNA sequences occurring many times in eukaryotic instead of only 2?
DNA are called repetitive DNA sequences. Genome 3. Why are grooves necessary for DNA?
of higher organisms can be divided into unique se­ 4. Does the direction of coiling change the features
quences, moderately repetitive and highly repeti­ of DNA?
tive regions. Unique sequences and highly repeti­ 5. Why is telomeric DNA single stranded?
tive sequences are often found in constitutive het­ 6. Why is mitochondrial DNA without introns?
erochromatin, suggesting a purely structural role. 7. What is the role of 97% ofjunk DNA?
Moderately repetitive DNA contains families of dif­
ferent sequence eleiuents e.g.: LINE and Alu fami­
lies.
 12.2 Chromosomal Abnor malities

Dhar PK, Tandon S, Paul U

All human diseases can be considered to result from of prophase or prometaphase chromosomes are
an interaction between an individual’s unique ge­ called microdeletion syndromes.
netic make-up and the environment. The environ­
mental problems can be physical (X- rays and ul­ STRUCTURAL CHROMOSOMAL

traviolet rays), chemical (toxic affluents released by ABNORMALITIES (Fig. 12.3A, B)

factories), gaseous (harmful gases discharged from
refineries, smelters etc). In certain conditions, the They can be produced by any one of the following
abnormal genetic component expresses itself so four mechanisms.
strongly that there is no need for special external
insults to spoil it further. The anomalous genotype a. Deletion: Breaking away of a portion of a chro­
runs in the family with a statistically predictable mosome. When a chromosome suffers two ter­
accuracy. Such diseases are termed as genetic dis­ minal deletions followed by the fusion of bro­
eases. Some genetic diseases appear veiy early, when ken ends, a ring chromosome is formed.
they are called congenital (or birth associated) or £

alternatively they may take decades to “pull the pin b. Inversion: The broken part reattaches itself in
out of grenade”. Genetic disorders arise from either reverse orientation.
structural or numerical change in the
chromosome(s) or gene(s) of autosomes or sex chro­ c. Translocation: Two chromosomes break and ex­
mosomes. Chromosomal disorders are generally change their broken segments in reciprocal
severe in nature because they mostly involve huge translocations. Robertsonian translocations in­
segments of DNA which contain many genes. More volve two acrocentric chromosomes that fuse
the number of genes affected, the greater is the se­ near the centromeric region with a subsequent
verity of disorder. loss of short arms.

Mutations of a single base in a gene or a stretch of d. Duplication: An over-representation of a specific

base pairs (even thousands of them) are not micro­ chromosomal region(s).
scopically visible to the cytogeneticists. In fact, for
a normal chromosome to be detectably disturbed, a e. Transverse centromeric division: Instead of di­
lengthy segment of DNA (equal to 10 million base viding longitudinally, centromere divides in
pairs) must be deleted, duplicated or translocated. transverse plane forming an isochromosome.
Syndromes warranting a high resolution analysis Thus, there is a duplication of one arm and loss
of another.
 SECTION 12 : GENETICS IN PEDIATRIC DENTISTRY I

It can occur because of the failure of cytokinesis

at the time of cell division and a multiple ga­
metic fertilization.

Aneuploid/polyploid cell can arise due to:

1. Non-disjunctiorL i.e. both the chromatids go to­
wards one pole. Non-disjunction produces one
monosomic and one trisomic cell.
2. Anaphase lag, i.e. a slow anaphase movement
of chromosomes. One chromosome fails to be
incorporated within the nucleus of the daughter
cell. The result of anaphase lag is one mono­
somic cell and one normal diploid cell.
3. Multiple gametic fertilization: Dispermy i.e; fu­
sion of two sperms with a single ova, results in a
zygote that is triploid.

What is a Syndrome? (Fig. 12.4)

A syndrome represents^ collection of symptoms and
signs caused by a particular genetic makeup. Clini­
cal diagnosis of a chromosomal disorder is based
on features which, when taken alone, have no par­
ticular diagnostic value. Some of the symptoms like
short stature, low IQ, mental retardation or aggres­
siveness may be commonly present in the popula­
tion, It is only when a combination of these features
are present, can we suspect a syndrome (Fig. 12:5a,
b, c). For details refer to section 11.
Fig. 12.3A Abnormal metaphase plates
showing a) ring chromosome
GENETIC BASIS OF DENTAL DISORDERS

12.3B Abnormal metaphase plates showing

a) double minutes, b) dicentrics. Early investigations confirmed genetic basis tp three
most common dental problems; malocclusion, peri­
NUMERICAL CHROMOSOMAL odontal disease and dental caries in dentistry, but
ABNORMALITIES research findings have had little impact on clinical
practice.The complexicity of multiple aetiolopcal
a. Aneuploidy: The diploid chromosome number factors and technical difficulties encountered have
of a cell is not an exact multiple of its haploid shown limited progress in this direction. Hie criti­
number (e.g; 45, 47 in human cells). It occurs cal questions like how many genes are involved in
because of non-disjünction of chromosomes, i.e; imparting effects on dental tissues and where these
chromosomes fail to separate at anaphase and genes are located, are yet to be answered. In this
are transferred together to one pole.
b. Polyploidy: Chromosome count exceeds the dipr lighted for dental disorders.
loid number and is also an exact multiple of its
haploid number (e.g; 69,92, etc., in human cells). Bit
 | TEXTBOOK OF PEDODONTICS

CHROMOSOMAL ABNORMALITIES

Numerical Structural

Aneuploidy Polyploidy

Monosomy Triploidy

Tetraploidy

Embryo usualy
aborts

Klinefelter

Fig. 12.4 Chromosomal abnormalities and associated diseases.

 SECTION 12 : GENETICS IN PEDIATRIC DENTISTRY |

Round cranium Mental retardation

Epicanthic folds
Hypertelorism

Dysplastic ears
Small mouth
Simian crease

Short nose, upturned nares

Short broad Abundant neck skin

hands
Protruding wrinkled tongue

Congenital heart defects

Intestinal stenosis
- Megacolon

Umbilical hernia

Acute lymphoblastic Hypotonia

leukemia
Libido wpakly
manifested

Short and stockly feet

Gap between 1st &

2nd toe

Fig. 12.5a Clinical features of Down’s syndrome.

&
 4 TEXTBOOK OF PEDODONTICS

Short stature

Low posterior hairline

Auditory defects

Webbed neck

Broad chest

Coarctation of aorta
Small breasts

Widely spaced nipples

Amenorrhea Cubitus valgus

Streak ovaries, infertility

Hypoplastic nails

Pubic hair sparse

External genitalia £
Pigmented nevi
underdeveloped

Fig. 12.5b Clinical features of Turner’s syndrome

 SECTION 12 : GENETICS IN PEDIATRIC DENTISTRY |

Normal intelligence or Mild mental

Fig. 12.5c Clinical features of Klinefelter syndrome

 TEXTBOOK OF PEDODONTICS

Short stature

Low posterior hairline

Auditory defects

Webbed neck

Broad chest

Coarctation of aorta
Small breasts

Widely spaced nipples

Amenorrhea Cubitus valgus

Streak ovaries, infertility

Hypoplastic nails

Pubic hair sparse

External genitalia
Pigmented nevi
underdeveloped

Fig. 12.5b Clinical features of Turner’s syndrome

 SECTION 12 : GENETICS IN PEDIATRIC DENTISTRY |

Normal intelligence or Mild mental

Low plasma testosterone

Tall, slim, enunchoid stature Weak facial hair

Coarse voice

Osteoporosis

Gynecomastia

Feminized habitus

Hypogonadism

Fig. 12.5c Clinical features of Klinefelter syndrome

 <•£0 I TEXTBOOK OF PEDODONTICS

Occlusal variation centromeric region of the Y chromosome.

Dental occlusion reflects the interplay between a Amelogenin is one of the major matrix proteins,
number of factors including tooth size, arch size secreted by ameloblasts and it is thought to direct
and shape, the number and arrangement of teeth, the growth of hydroxyapatite crystals. It appears
size and relationship of the jaws, and also the influ­ that mutation of the human amelogenin gene is as­
ences of the soft tissues including lips, cheeks and sociated with some X linked types of amelogenesis
tongue. The term malocclusion is generally used to imperfecta.
refer to variations from normal occlusal develop­
ment, and although in some instances it is possible Although most genetic studies of craniofacial growth
to specify the cause of a particular malocclusion, and morphology have concentrated on osseous struc­
for example, genetic syndromes, embryological de­ tures, the functional matrix concept proposes that
fects or trauma, most malocclusions represent vari­ the morphology of the craniofacial skeleton is de­
ations from normal development for which there is termined by the surrounding soft tissues. A rela­
no apparent cause. With so many factors involved tionship has been demonstrated between the mor­
in the development of occlusion it is little wonder phology of craniofacial features and the amount of
that most examples of malocclusion display multi­ muscular activity but little is known about the ge­
factorial inheritance with both genetic and environ­ netic basis to variation in soft tissue structure or
mental influences contributory to phenotyping vari­ function. In this regard the finding of significant
ability. genetic variance in masseter muscle electrical ac­
tivity and morphology in recent twin studies is of
Many workers have suggested that racial admix­ considerable interest.
ture increases the occurrence of malocclusion. Link­
age studies in humans have been mainly restricted Periodontal problems
to studies of the sex chromosomes and have clari­ Currently, the periodontal diseases are considered
fied the roles of X and Y chromosomes on craniofa­ as a group of related, but vastly different, inflam­
cial morphology. The X chromosome appears to matory diseases affecting the supporting structures
mainly regulate enamel thickness. On the other of the periodontium. These diseases range in sever­
hand Y chromosome seems to affect both enamel ity from gingivitis which is largely a reversible con­
and dentin. The X and Y chromosome are also seen dition if the causative agents are removed and con­
to influence craniofacial growth and development. trolled, to the very aggressive forms of early onset
Cephalometric analysis of a sample of 47, XXY periodontitis which manifest in several forms all of
males indicates pronounced facial prognathism in which demonstrate early and rapid destruction of
the Klinefelter males, especially in the mandible. the periodontium and can be extremly difficult to
Studies of 45, X females indicates a retrognathic manage. Although this disease will not develop in
face, with short mandible and flattened cranial base the absence of plaque it is apparent that plaque alone
angle. It is suggested that the X chromosome may is not sufficient to lead to the disease. For example,
alter morphology of the cranial base by affecting there are many instances where individuals may
growth at the synchondroses, that is cartilaginous have significant plaque and calculus deposits yet
joints and it also has a direct effect on mandibular manifest little overt evidence of the disease.
shape. Human dental enamel amelogenin gene is
located on both the X and Y chromosome although This converse holds true also in that some individu­
the gene on the X chromosome is predominant Us­ als appear to have very minimal plaque and calcu­
ing molecular genetic techniques, the amelogenin lus deposits yet manifest significant periodontal
gene has been localized to the distal portion of the destruction.
short arm of the X chromosome and to the peri-
 SECTION 12 : GENETICS IN PEDIATRIC DENTISTRY |

Genetic risk factors may be studied by establishing Other intrinsic and extrinsic environmental fac­
an association between the disease and inherited tis­ tors of possible genetic association
sue markers. In an infectious disease such as peri­ Apart from the above considerations with respect
odontal disease, the association between the HLA to genetics and periodontal diseases, numerous other
antigens and various forms of the disease has been modifying and predisposing factors influence the
of interest with several studies reporting the inci­ manifestation of the various periodontal diseases.
dence of Class I and II HLA antigens in patients Modifying factors are defined as any condition that
with early onset periodontal disease. alters the way in which the host might respond to
bacterial challenge, while predisposing factors are
DNA Probes those conditions that enhance the accumulation of
DNA probe identifies species-specific sequences of dental plaque or hinder its efficient removal, sev­
nucleic acid that make up DNA, thereby permitting eral have a genetic component.
identification of organisms.
Both normal and abnormal variation in tooth crown
The technique is based on the concept that DNA is and root form can have a significant impact on the
a double helix consisting of two complementary accumulation of dental plaque and thus on the mani­
strands of paired bases. When the double strand is festation of periodontal disease.
split the separation occurs between the base pairs.
If renatured they bind again. The genetic basis of abnormalities of enamel and
dentin are considered in the presence of enamel
To prepare the probe, specific pathogens used as anomalies, surface roughness which may lead to
marker organisms are lysed to removed their DNA. inadequate plaque removal. Poor appearance of the
Their double helix is denatured, creating single hard and soft tissues may lead to further problems
strands that are individually labeled with a radio of poor motivation for maintenance of adequate oral
active isotope. Subsequently, when a plaque sam­
hygiene.
ple is sent for analysis it undergoes lysis and dena­
turation single strands are chemically treated, at­
In the case of cemental anomalies, such as
tached to a special filter paper and then exposed to
cementopathia or cemental tears there is the poten­
the DNA library. The DNA library includes probes
tial for inadequate attachment of the periodontal
for A. Actinomycetem comitans, P. gingivalis, B.
ligament fibers and subsequent compromised bio­
intermedins, C.rectus, E.corrodens, F.nucleatumand
logical function.
T. denticola.
Systemic disease like diabetes and rheumatoid ar­
DNA probe identifies species-specific sequences of
thritis are examples of diseases which have a ge­
nucleic acid that make up DNA, thereby permitting
netic component and may have enhanced periodon­
identification of organisms.
tal breakdown as a secondary feature.

Drawbacks
In these cases the role of genetics is of modifying
1. These assays are available for only a few putative
the host response such that upon significant bacte-
pathogens.
2. DNA probes also do not provide any information cellular responses cannot function adequately These
about the antibiotic sensitivities of the infecting examples of genetic influences on the i
bacteria. tion of periodontal diseases further serve ■yy

light the multifactorial, nature of the

 | TEXTBOOK OF PEDODONTICS

The major clinical implications of studying the role Type III (the brandywine type);
of the host genome in the various periodontal dis­ Clinical studies have shown that dentinogenesis
eases lie in leading to a better understanding of the imperfecta type II and type III could occur in the
variability in disease manifestation as well as being same family. Dentinal dysplasia is another auto­
of some diagnostic value. By recognizing that some somal dominant form of inherited defects of den­
forms of periodontal disease may have a strong ge­ tin. (For details refer section 3)
netic component it has become necessary to iden­
tity those individuals and subsequently screen their Dental caries: Evidence from experimental caries
immediate relatives for signs of developing prob­ in rats suggests that there is an approximately 50
lems. In addition, by recognizing that some forms percent genetic contribution to the development of
of periodontal disease may form part of a syndromic caries. Yu et al in 1988 found an association be­
condition early recognition of those signs can aid tween caries experience and the proline rich pro­
in the identification of such individuals. teins present in saliva of infected patients. The in­
heritance of proline rich proteins follows an auto­
Gene replacement therapy for both the host and somal dominant mode but no linkage analysis stud­
parasite, genome is a rapidly growing research area. ies have yet been carried out to investigate this fur­
The implications for this kind of research are excit­ ther.
ing and warrant close attention in the years to come.
The issue of genetics in a common human disease The investigations reviewed in this chapter provides
such as periodontal diseases is very significant and us with a solid foundation of knowledge about the
involves aspects of disease aetiology, susceptibility; influence of genetic factors on disorders of cranio­
manifestation and management. facial growth, the oral supporting tissues and the
dental hard tissues. Therefore with the significant
Recently it has been observed that inserting a ben­ advances in human genetics which are taking place
eficial gene into blood immune cells taken from HIV now, we should soon be able to screen those indi­
infected patients can block the AIDS Virus from viduals at risk and implement preventive measures
replicating in these cells. Blocking replication does to provide protection from disease onset.
not eliminate the virus but prevents activation, the
process by which it changes from a dominant infec­ Biomimetic materials:
tion to an active one. This therapy is being tried for Genetically engineered materials are in the trial
the patient’s suffering from HIV infections. which may mimic the nature of tooth substance and
help to regenerate the dental tissue. Recently
Dental hard tissues: Amelogenesis imperfecta can BRAX-I gene has been isolated, which is found to
be inherited as an autosomal dominant trait, or in be responsible for the control of enamel growth. It
autosomal recessive or X linked forms. X linked is developed in gel form, which is applied onto the
disorders are characterized by an absence of male cavitated tooth surface. This helps in regrowth of
to male transmission by virtue of the fact that males enamel, filling up the decayed portion of tooth.
who are affected must pass on their Y chromosotne
to their sons. Dentinogenesis impertecta was first Self-Assessment
identified as a disorder distinct from amelogenesis
imperfecta. Shields in 1967 classified dentinogen­ 1. Why are chromosomal disorders generally se­
esis imperfecta into Type I (with osteogenesis im­ vere in nature?
perfecta), Type II (without osteogenesis imperfecta) 2. What is submicroscopic chromosomal abnormal­
ity and microdeletion syndromes?
 SECTION 12 : GENETICS IN PEDIATRIC DENTISTRY |

3. Why do we find X-chromosomal disorders more 7. What is DNA probe?

frequently than autosomal disorders? 8. Is there any genetic contribution to the develop­
4. Till now no Y linked disorder has been reported. ment of caries?
Why? 9. What do you understand with Biomimetic mate­
5. Which disease gene has been identified in Down rials?
syndromes? 10. What is the scope of gene replacement therapj
6. Describe any four mechanisms by which struc­ in dentistry?
tural chromosomal aberration can arise.
 12.3 Single Gene Disorders
i

Dhar PK

Introduction or sex linked inheritance. In reality, genes are never

dominant or recessive. It is only their protein prod­
Human genetics deals with the variations between ucts that produce clinical patterns called as "domi­
humans. These variations are, in part, reflections nant” or "recessive”. There are approximately 1200
of differences that exist at the DNA level. Varia­ single gene disorders and account for more than 5%
tions that influence gene function are usually re­ of all hospital admissions. Single gene disorders can
ferred to as mutations. Other variations that do not be classified into autosomal and sex chromosome
affect health or functioning of an organism are called linked disorders.
polymorphisms. Mutations_may arise in somatic cells
or germ cells, but only germ cell changes are herit­ AUTOSOMAL DISORDERS
able. The ever on-going gene 'experiments of na­
ture’ have resulted in a wide variety of mutant phe­ Autosomal dominant disorders arise due to defect
notypes, which might have remained unknown in in at least one gene out of a pair of genes on
lab conditions. Disorders caused by the transmis­ autosomes. (Fig. 12.6) (Table 12.1)
sion of a single mutant gene show either autosomal

Table 12.1 Distinguishing features of autosomal dominant condition

Features
■ Disease usually appears in each generation.
■ Delayed age of onset
« Vertically transmitted
■ Mostly involve structural proteins
■ Variability in clinical expression
■ Affected individual has an affected parent
■ Male and female siblings are equally affected
• Capability of transmission is the same in both the affected parents
■ Most patients are heterozygotes for the mutant allele
■ Each child of an affected parent is at 50% risk of inheriting the abnormal gene

Potential confounding factor.

In absence of male-to-male transmission, an autosomal dominant trait cannot be
distinguished from an X-linked dominant inheritance.

Examples:
Osteogenesis imperfecta, mesiodens, Hypocalcified type I. Hereditary Dentinogenesis
imperfecta, Dentin dysplasia (Radicular type), Apert’s syndrome
 SECTION 12 : GENETICS IN PEDIATRIC DENTISTRY |

à à i ¿¿¿ ¿à ¿Oià

Fig. 12.6 Autosomal dominant inheritance

Fig. 12.7 Autosomal Recessive inheritance

 CS) I TEXTBOOK OF PEDODONTICS

Autosomal recessive disorders occur when both the aborted resulting in significant increase of affected
genes on autosomes are affected. Since two abnor­ females in the population. Another reason for a
mal genes are required for obtaining a given clinical higher abundance of the affected females is the lack
phenotype their incidence is low compared to auto­ of male-to-male transmission.
somal dominant disorders. (Fig. 12.7) (Table 12.2)
X linked dominant disorder arises from an affected
Table 12.2 Distinguishing features of autosomal re­ heterozygote female. (Fig. 12.8) (Table 12.3)
cessive condition
Table 12.3 Distinguishing features of X-linked domi­
Features nant condition
■ The illness usually appears suddenly in the
family Features:
• Males and females are equally affected ■ Both sexes are affected, but males are more
a Less variable in clinical expression severely affected
« Early age of onset ■ Complete absence of father to son
■ Consanguinity greatly increases the rate of transmission
Incidence «‘ All daughters of affected father are affected.
• Most of the offsprings are normal in the « Affected heterozygous females equally
family transmit the trait to male and female
« An affected offspring may or may not have siblings
an affected parent « Female to female transmission observed
■ Affected homozygotes have more uniform due to excessive abortions of male fetuses
clinical symptoms ■ Affected females have a deficiency of live­
• Mostly results in defective enzymes born sons

Potential confounding factor Potential confounding factor;

Multiple cases may not occur especially in Strong resemblance with autosomal dominant
small families condition. However, excess affected females and
lack of male to male transmission confirms the
Examples X-linked dominant pattern
Dentin dysplasia (Coronal type), Hereditary
Amelogenesis imperfecta (Hypocalcified type II), Examples:
Hypophosphatasia, Hurler’s syndrome Xg blood group, Vitamin D resistant rickets, Oral
facial digital syndrome (type I), Melnick-Needles
syndrome
X-LINKED DISORDERS
X linked recessive disorder arise in female reces­
X-linked disorders arise due to the defect of the sive homozygotes or less frequently male
gene(s) located in X-chromosome. Since a female hemizygotes. (Fig. 12.9) (Table 12.4)
has two X-chromosomes, she maybe dominant (het­
erozygous) or recessive (homozygous) for the mu­ SEX LIMITED AND SEX INFLUENCED
tant gene. However, males with only one X PHENOTYPES
(hemizygous), display a full impact of the syndrome
regardless of how the mutant gene presents itself in Male limited sexual precocity is an autosomal dis­
females. Due to severity7 of the X-linked disorder in order that is manifested by the development of ado­
males, the affected male fetuses are frequently lescence in males at about 4 years of age. Females
 SECTION 12 : GENETICS IN PEDIATRIC DENTISTRY

Fig. 12.8 X-linked dominant inheritance

Fig. 12.9 X-linked recessive inheritance

 <S> I TEXTBOOK OF PEDODONTICS

Autosomal recessive disorders occur when both the aborted resulting in significant increase of affected
genes on autosomes are affected. Since two abnor­ females in the population. Another reason for a
mal genes are required for obtaining a given clinical higher abundance of the affected females is the lack
phenotype their incidence is low compared to auto­ of male-to-male transmission.
somal dominant disorders. (Fig. 12.7) (Table 12.2)
X linked dominant disorder arises from an affected
Table 12.2 Distinguishing features of autosomal re­ heterozygote female. (Fig. 12.8) (Table 12.3)
cessive condition
Table 12.3 Distinguishing features of X-linked domi­
Features nant condition
■ The illness usually appears suddenly in the
family Features:
« Males and females are equally affected ■ Both sexes are affected, but males are more
■ Less variable in clinical expression severely affected
» Early age of onset ■ Complete absence of father to son
■ Consanguinity greatly increases the rate of transmission
incidence ■ ’ All daughters of affected father are affected.
» Most of the offsprings are normal in the ■ Affected heterozygous females equally
family transmit the trait to male and female
« An affected offspring may or may not have siblings
an affected parent ■ Female to female transmission observed
■ Affected homozygotes have more uniform due to excessive abortions of male fetuses
clinical symptoms ■ Affected females have a deficiency of live­
• Mostly results in defective enzymes born sons

Potential confounding factor Potential confounding factor:

Multiple cases may not occur especially in Strong resemblance with autosomal dominant
small families condition. However, excess affected females and
lack of male to male transmission confirms the
Examples X-linked dominant pattern
Dentin dysplasia (Coronal type), Hereditary
Amelogenesis imperfecta (Hypocalcified type II), Examples:
Hypophosphatasia, Hurler’s syndrome Xg blood group, Vitamin D resistant rickets, Oral
facial digital syndrome (type I), Melnick-Needles
syndrome
X4JNKED DISORDERS
X linked recessive disorder arise in female reces­
X-linked disorders arise due to the defect of the sive homozygotes or less frequently male
gene(s) located in X-chroniosome. Since a female hemizygotes. (Fig. 12.9) (Table 12.4)
has two X-chromosomes, she maybe dominant (het­
erozygous) or recessive (homozygous) for the mu­ SEX LIMITED AND SEX INFLUENCED
tant gene. However, males with only one X PHENOTYPES
(hemizygous), display a full impact of the syndrome
regardless of how the mutant gene presents itself in Male limited sexual precocity is an autosomal dis­
females. Due to severity of the X-linked disorder in order that is manifested by the development of ado­
males, the affected male fetuses are frequently lescence in males at about 4 years of age. Females
 SECTION 12 : GENETICS IN PEDIATRIC DENTISTRY

Fig. 12.8 X-iinked dominant inheritance

Fig. 12.9 X-linked recessive inheritance

 I TEXTBOOK OF PEDODONT1CS

are unaffected but can transmit this disease to their mosome, the possibility of a Y linked genetic disor­
sons. Ar ther example is male pattern baldness. It der is ruled out. Human traits like hairy ears and
appears to be transmitted as an autosomal domi- webbed toes which were earlier thought to have Y
linked transmission have now been linked to "modi­
Table 12.4 Distinguishing features of X-linked re­
fied"' autosomal inheritance.
cessive condition

MULTIFACTORIAL DISEASES
Features:
■ Males are mostly affected
• Affected males are related through carrier The term multifactorial inheritance refers to the
females participation of more than one gene in determining
■ Complete absence of male-to-male a particular phenotype. The number of genes im­
transmission plicated is often unknown. Two or more mutant
» Affected males transmit the defective gene genes in combination with environment cause mul­
only to daughters tifactorial disorders. Because environmental com­
• The disease may appear to skip a generation ponent plays an important role in these diseases,
• An affected female equally transmits the the term polygenic inheritance is misleading. A per­
defective gene to her children son who inherits the "right'" combination of these
• Female carrier has a 25% chance of "wrong” genes passes beyond the threshold of risk
having an affected son at which the environmental component determines
a Capability of transmission is the same in both the severity of the disease. The rate of recurrence of
the affected parents the disorder is the same for all first degree rela­
a Most patients are heterozygotes for the
tives. As the degree of relation becomes more dis­
mutant allele tant, the likelihood of a relative inheriting the same
a Each child of an affected parent is at
combination of genes becomes less. Since the pre­
50% risk of inheriting the abnormal gene
cise number of genes responsible forpolygenic traits
is unknown, the risk of inheritance for a relative to
Potential confounding factor
contact the same disease is difficult to calculate.
Consanguinity may increase the frequency of
such conditions making them resemble X-linked
Examples: Essential hypertension, coronary heart
dominant conditions
disease, diabetes mellitus, peptic ulcer disease,
schizophrenia, cleft lip and palate, spina bifida
Examples
Deuchenne muscular dystrophy, Becker muscu­
lar dystrophy, Lesch-Nyhan disease, Hemophilia GENOMIC IMPRINTING

A and B, Fabry Disease, Hereditary Amelogen-

esis imperfecta (Hypoplastic Hypomature type) We generally believe that the parental origin of a
mutant gene is irrelevant to the expression of the
phenotype. However, this principle has been proved
nant trait, but requires a testosterone level achieved
wrong. Whole chromosomes, specific chromosomal
only in males. In fact, female carriers show thin­
regions or even single genes may be inactivated by
ning of hair, especially if they are given testoster­
some inexplicable way during formation of a zy­
one exogenously. An example of sex-influenced phe­
gote. The most clear example of genomic imprint­
notype is hemochi matosis, i.e., massive deposition
ing in humans comes from the study oFtwb clini­
of iron in the liver. The disease is most common in
cally distinct disorders - the Angelman and Prader
males. Females appear to be protected by tfcir men­ Willi syndromes. In both the cases, chromosome 15
strual loss. The human Y-chromosome carries lit­ region ql l-q 13 is affected. The DNA analysis has
tle DNA apart from the testis determining factor shown that in the former, deletion arises on mater­
(TDF). Since no other gene is present on Y-chro- nally derived chromosome 15, whereas in Prader-
 SECTION 12 : GENETICS IN PEDIATRIC DENTISTRY | €EB
Willi syndrome it arises on the paternally derived fusion protein. The latent oncogenic potential
chromosome 15. of abl gets activated resulting in CML.

TRINUCLEOTIDE REPEATS Burkitt’s Lymphoma

Tumors arise in undifferentiated B lymphocytes.
This is a recently recognized type of mutation that Primary event: Reciprocal translocation between
involves the expansion of nucleotide triplets like 8q24 and 14q32.
CTG and CGG. Expansions of unstable trinucle­
Mechanism
otide repeats have been associated so far with a
« Chromosome 8 (region q24) houses c-myc gene
number of different genetic diseases including frag­
■ Chromosome 14 region q32) houses IgH (Im­
ile X, myotonic dystrophy (DM) and Huntington
munoglobulin) gene
disease.
■ Translocation between these two regions results
HUMAN CANCERS RESULTING FROM GENE
in fusion of c-myc and IgH.
MODIFICATIONS ■ Inherent property of IgH: High transcription rate
■ Effect on c-myc transcription: Amplified 2-10
Acquisition of genetic alteration is a fundamental times
process in the development of cancer. Mechanisms ■ End result: Lymph node cancer (Burkitt’s lym­
by which such alterations are generated vary con­ phoma)
siderably. Conversion of a normal cell to malignant
cell is driven by genes, and therefore understand­ Retinoblastoma
ing of the pathways that lead to such harmful con­
sequences can prove extremely useful in success­ Tumors arise in the retina of the eye.Deletion of
fully treating cancer patients. Human cancers have chromosome 13 region ql4 that houses RB gene.
been linked both to the presence of oncogenes and Mechanism
also to be absence of tumor suppressor genes. It is ■ Normal RB function : To check cell
incorrect to use the word “antioncogene” because growth in G1
"antioncogene” would imply that its sole function and S
is to suppress oncogenenic effect. In reality, how­ ■ Overexpression of RB : Obstructs cell
ever, such genes have many important roles in the growth
normal cellular metabolism. Thus, the term “tumor ■ Deleted AB (both copies) : Uncontrolled
suppressor gene” is more appropriate. proliferation of
cells
Chronic Myeloid leukemia ■ End result : Eye cancer
First consistent chromosome aberration reported in
any cancer.
Discovered by : Peter C Novel and DA Hungerford Self Assessment
in 1960.
Primary event: Reciprocal exchange between 9q34 1. Why is autosomal recessive disease less frequent
and 22qll. than autosomal dominant disease?
2. Why do we come across more females affected
Mechanism with X - linked disorders than males?
■ Chromosome 9 (region q34) houses c-abl gene 4. Why are Y-linked (holandric) genetic disorders
■ Chromosome 22 (region q 11) houses bcr gene very rare in occurrence?
■ Translocation results in fusion of Exons of bcr 5 . Describe any one mechanism of malignant trans­
and abl genes unite to synthesize Bcr-Abl formation due to oncogenes. Is it appropriate?
 12.4 Genetic Counselling

Dhar PK, Tandon S

Introduction POCEDURES FOR PRENATAL DIAGNOSIS

(Fig. 12.10)
Genetic counselling is a communication process in
which individuals seeking advice are provided with 1. Visualization of fetus
all thé scientific information to enable them in mak­ Ultrasonography: With this technique it is now
ing a decision about current or future pregnancies. possible to visualize embryo as early as 5 1/2 to
Although the proportion of people who need it, is 6 weeks of pregnancy and cardiac activity is de­
relatively small but those who need it, need it badly. tectable at 7-8 weeks. Ultrasonography has now
The personal decisions involved are difficult, become a routine procedure for verification of
whether to marry; whether to have children or adopt viable embryo, determination of gestational age,
one instead of risking a further pregnancy. When­ diagnosis of multiple gestations, determination
ever there is a genetic problem the family members of placental and fetal positions, diagnosis of fe­
want to know: 'What is the exact problem’, 'Why tal anomalies, detection of uterine malformations
did it happen’ and Will it happen again’? The di­ and a guide for passage of instruments for inva­
agnostic information helps answer the first two ques­ sive procedures.
tions. Risk assessment aims to answer the third ques­
Radiography: Although mineralization of fetal
tion. Many studies in the recent yrears have shown skeleton at 11 weeks of gestation is adequate to
that roughly 30%-40% of deaths in the pediatric pennit radiographic examination, this procedure
age group happen in children with genetic disor­ has been discarded due to safety reasons.
ders. Genetic diseases are almost always serious and
mostly incurable. Thus, prevention of this group of Fetoscopy: It has been employed for cannula­
diseases assume paramount importance. A tion of umbilical vessels and for blood sampling,
transfusion and fetal tissue biopsies.
counsellor must have a fully confirmed diagnosis of
the patient, an accurate family history and the mode
2. Analysis of fetal tissue
of inheritance of the disorder so that a precise risk
of recurrence can be estimated. Prenatal diagnosis
Amniocentesis (Optimum time: 16-18 weeks of
is offered to couples who are at high risk for pro­
gestation) Under strict aseptic conditions and
ducing a child with a congenital disorder and also
local anesthesia, 20-30 ml of fluid is aspirated.
when the couple is willing to abort a severely af­
In less than 0.1% of patients amnionitis (inflam­
fected fetus. mation of amniotic membrane) occurs. Amni-
 SECTION 12 : GENETICS IN PEDIATRIC DENTISTRY |

Fig. 12.10 Freedom! You’re 9 months away

otic fluid leakage and vaginal bleeding occur in mosome analysis, immediately after sampling,
l% women but is of no significance. About 90% or alternately after 24 hours of incubation in a
of all amniocentesis are performed for cytoge­ tissue culture medium. Direct analysis has the
netic analysis. The rest 10% is used for biochemi­ great advantage of permitting a fetal chromo­
cal investigation. The fibroblast like cells ob­ some analysis within 24-48 hours. Because the
tained at amniocentesis can be cultured in a va­ analysis is not dependent on the cell division in
riety of tissue culture media enriched with fetal culture, direct chromosome preparations are not
bovine serum for 1-3 weeks permitting accumu­ likely to be affected by contamination with ma­
lation of sufficient dividing cells for karyotyping. ternal cells, in which mitotic cells are infre­
A minimum of 15 cells are examined and the quently observed.
modal chromosome number is established. Sex
determination of fetus is 99% accurate by this Fetal and Maternal Blood Analysis: Isolation
method. and analysis of fetal cells in maternal blood is
an attractive method of non-invasive prenatal di­
Chorionic villus sampling (optimal time 9-12 agnosis. Data show that fetal cells are present in
weeks) The Chorion frondosum contains the maternal blood even as early as 33 days of ges­
mitotically active villus cells and is, therefore, tation. However, fetal cells may even persist from
the area to be biopsied. At 9-12 weeks of gesta­ previous pregnancies also. Flow cytometric test
tional age villi float freely within the intervil­ of maternal blood with anti-gamma globinMAb
lous space and are attached only loosely to the (monoclonal antibody to gamma chain of
underlying decidua, which explains why aspira­ hemoglobin molecule) is highly specific for ex­
tion sampling at the stage is usually only mini­ amining fetal cells irrespective of its gender be­
mally traumatic. In CVS sampling 10-25 mg of cause the amount of gamma hemoglobin chain
chorionic villi is collected. Because the langer- produced per cell is significantly higher in the
hans cells of the cytotrophoblast are in dividing fetus in comparison to that of adults. This
phase, it is possible to perform a “direct” chro­ cedure greatly reduces the total hr
 | TEXTBOOK OF PEDODONTICS

candidate fetal cells to be sorted by increasing tation diagnosis, first and second trimester abortions
fetal cell purity in the test sample. The smaller are avoided. The couples can decide whether to at­
number of cells present on the slide reduces the tempt a pregnancy instead of aborting the fetus at a
time and reagents spent on hybridization experi­ later stage, thus offering minimal risk to the mother.
ments. With the development of cell sorting However, the major problem with this technique at
methodology it has become possible to sort present is low pregnancy success rate. A number of
leukocytes obtained from maternal blood and strategies developed to design optimal procedures
prepare a fraction which is relatively “enriched” for the preimplantation diagnosis of genetic defects
in fetal cells. However, since the maternal cells are:
still predominate, the results to prepare fetal
karyotypes from these samples have not been Polar Body biopsy'. The chromatin of polar body is
encouraging. Furthermore, it is also possible that virtually the “mirror image” of the chromatin of the
fetal cells from previous gestations may persist oocyte. Since the first polar body does not contrib­
and complicate the analysis. It has been estimated ute to the development of the embryo it can be re­
that a 20 ml sample of maternal blood contains moved with minimal adverse effects on the oocyte.
0-20 fetal cells (i.e; 1 fetal cell per 1 million
maternal cells). To utilize these rare cells for a Multicell biopsy. Prior to the late 8-cell stage, 1-3
prenatal diagnosis of chromosome abnormali­ blastomeres of the pre-embryo are dissociated with
ties, enrichment techniques are being improvised pipetting after boring a small hole in -ona pelluc-
to make it a standard non-invasive procedure. ida, that heals rapidly afterwards.

Fetal Liver Biopsy: A variety of enzymes of in­ Blastocyst biopsy. From trophoblast (which later
termediary metabolism are expressed only in the forms placenta) of the blastocyst a number of cells
liver. The prenatal diagnosis of disorders asso­ can be safely removed for analysis without adversely
ciated with abnormalities of these enzymes can­ affecting the fetus.
not be accomplished by enzyme assay of amni­
otic fluid or chorionic villi cells. Thus, fetal liver BASIC INFORMATION REQUIRED FOR
GENETIC
*
biopsy is useful in conditions like Type I Glyco­ COUNSELLING
gen Storage disease etc.
A genetic counsellor must have:
Fetal Skin Biopsy: This approach is used only 1. Precise and fully confirmed diagnosis of the dis­
in those disorders where skin is involved e.g; ease
Epidermolytic hyperkeratosis. Definitive prenatal 2. Accurate pedigree of the family
diagnosis requires that the histological appear­ 3. Knowledge of the mode of inheritance of the
ance of the skin be pathognomonic at 20 weeks condition
of gestation.
INDICATIONS FOR PRENATAL DIAGNOSIS
PREIMPLANTATION DIAGNOSIS
1. Advanced maternal age (e.g; Down syndrome)
In this procedure, 1 or 2 cells are removed from 2. Previous child with chromosome aberration
cleavage stage embryos from the patients. The af­ 3. Intrauterine growth delay
fected embryos are identified by using molecular 4. Biochemical disorder
genetic techniques. Subsequently, healthy embryos 5. Congenital anomaly
are re-implanted in the uterine cavity enabling fur­ 6. Previous history of Neural tube defect in the
ther development till full term. By doing preimplan­ family
*
 SECTION 12: GENETICS IN PEDIATRIC DENTISTRY |

7. Structural anomalies found on the ultrasonog­

Genetic condition Risk of reccuren ce
raphy
8. Person with mental retardation or developmen­ (%)
tal delay (e.g. fragile X syndrome) Infertility 10
9. Couples with a history of recurrent miscarriages Spontaneous abortion 12.5
Perinatal death 1.0
How to identify a genetic disease?
Congenital abnormality 3.3
Mental retardation 5-20
Step 1
Translocation (21/22) *
10-15
Trisomy 21 1
1. Build up the pedigree tree "bbttom-up”, starting
with the index case and ending up with grand­ Anencephaly 5

parents, cousins, uncles, aunts, etc. Congenital heart disease 1-10

2. Ask the inotlier of the patient about her siblings, Diabetes mellitus 1-6

children, parents and all the immediate blood­ Spina bifida 5

relatives that she can remember from her side or Cleft palate 2-15.
from her groom’s side. Cleft lip and/or palate 4-10
3. Fill in the appropriate pedigree symbols to indi­
* The range indicates the risk of recurrence in “nor­
cate normal/carrier, affected individuals, still
mal parents with an affected child" to “Effected par-
births, spontaneous abortuses, twins, consan­
ents with an affected child".
guinity, unknown gender etc.

Step 2 Step 4

Analyse the pedigree chart (see chapter? and 3) and The decision making:
determine the mode of inheritance. » Allow the patient or his family members to de­
cide on continuation or termination of pregnancy.
The negative family history should not be. consid­ ■ Counselling should be supportive. Gene nutri­
ered a conclusive evidence against the presence of ent interaction is currently being established by
a heritable condition. A majority ofindividuals who Shaw et al (1998). A population based case con­
have a genetic disease will not have a “positive trol study by them has shown that Transforming
family history”. Lack of other affected persons in Growth Factor alpha (TGFa) genotype, material
the family is common and does not by any means multivitamin have a positive co-relation to risk
rule out the presence ofa genetic disease. Thé pres­ of cleft lip palate or cleft palate.
ence of consanguinity does not prove recessive in­ « Conditions with Mendelian inheritance usually
heritance, it merely makes it more likely. have high risks of recurrence.
■ Support your conclusion with chromosomal and/
Step 3 or molecular data wherever possible.
« Autosoma l dominant condition: 50% risk to the
Calculate risks of recurrence. The perception of what offspring of affected parent
constitutes high’ or ‘low’ depends on the investi­ « Autosomal recessive condition: 25% risk to the
gator. The "risk” figure has two components (i) the offspring of carrier parents
probability of occurrence of the disease, and (ii) the • X-linked recessive condition: 50% risk to sib*
burden of the disease. The table below shows risk lings (males affected, females usually carriers)
factors for commonly prevalent disorders.
 <<££} I TEXTBOOK OF PEDODONTICS

■ On observing a structural chromosomal anomaly 2. What is the earliest time for detecting fetal cells
in the patient, check the parent’s chromosomes. in maternal samples?
• Duplication or deletion of chromosome can re­ 3. How long do fetal cells persist after delivery?
sult in a congenital malformation and/or mental 4. Which cell separation technique is optimal in
retardation. maternal blood analysis?
5. Instead of highly expensive cell sorting proce­
Self-Assessment dures, can we culture the fetal cells selectively
in vitro?
1. What is the rationale behind using anti-gamma 6. What is the main advantage of a preimplantation
globin antibody to distinguish fetal from adult diagnosis over a prenatal diagnosis?
cells?
 12.5 Human Gene Therapy

DharPK

Introduction HUMAN DISEASE CANDIDATES

It was in 1979, Richard Mulligan, a 25 year old Gene therapy should be beneficial primarily for the
graduate student at Stanford University (USA) per­ replacement of a defective or missing enzyme or
formed an unprecedented feat of scientific ingenu­ protein that must function inside the cell that makes
ity. He made a molecular truck out of a deadly vi­ it, or of a deficient circulating protein whose level
ms. Normally, viruses are vehicles for their own does not need to be exactly regulated (e.g; factor
genes. But with the molecular trickery, Mulligan VIII). Early attempts at gene therapy will almost
pulled out the genes that allow the virus to replicate certainly be done with genes for enzymes that have
a simple "always-on” type of regulation e.g; ADA
and replaced the 'empty space’ with rabbit’s
(adenosine deaminase), whose deficiency causes a
hemoglobin genes. After assembling a fleet of his
severe combined immunodeficiency disease.
viral trucks, all loaded with the rabbit hemoglobin
gene, he gently layered'them over monkey kidney
DELIVERY (Table 12.5)
cells growing in-vitro. These kidney cells under­
went an astonishing transformation and churned out
Gene transfer in vivo has been performed by vari­
chains of hemoglobin molecules. This marked the ous routes, that include intra peritonial, intra ve­
beginning of the science of Gene Therapy. nous, intra arterial, intra hepatic, intra muscular
and intra tracheal. The nature of the gene to be in­
After a successful demonstration of gene transfer corporated depends on the type of disorder that is
in vitro, the stage was set for in vivo experiments. being treated and may be directed by a more com­
The first genetic "cure” reported in a mammal was plete understanding of the molecular basis of dis­
in a genetically dwarf strain of mice called "little”. eases. A number of viral and non-viral methods ex­
The equivalent human disease is pituitary dwarf­ ist for delivering the gene into the cells. The nonviral
ism. Hammer et al (1984) succeeded in inserting a transfer includes chemical or physical methods e.g;
rat growth hormone gene into the cells of these mice transfection by calcium phosphate precipitation,
in such a way that the gene was expressed at a high electroporation, microinjection, liposomal transfer
level. The deficiency in growth hormone was cor­ or receptor mediated delivery. In the viral methods
rected, and the animals grew rapidly, but the gene retroviruses, adenoviruses, adeno-associatedviruses,
was not controlled appropriately and gigantism re­ herpes virus and vaccinia virus are the most com
sulted - namely, mouse one-and-a-halftimes as large mon. At this moment scientists do not have a STlli
as a normal animal of its kind. cient technical knowledge to deliver the entire
along with its associated regulatory elements into a
 <ÉE0 I TEXTBOOK OF PEDODONTICS

Table 12.5 Viral delivery systems, their benefits and drawbacks

Viral gene delivery Benefits Drawbacks

Retroviruses ■ 100% transduction is possible « Most of the retroviral cell specific

■ A variety of host ranges can be receptors have not been identified
infected « Dependent on induction of cell
« Infection doesn’t lead to cell lysis division
■ Precise integration of transferred ■ purification of viral particles may
. genes into cellular DNA is possible lead to loss of infectivity
« Not 100% safe

Adenoviruses ■ Minor pathogen in humans • May lead to cell lysis

■ Not associated with malignancies « Integration with host DNA,
■ Can infect non-dividing cells somewhat inefficient
■ Virus particles are relatively stable ■ *May evoke immune reaction
and can be transported at high titers ■ Target cell dependent
■ Very large DNA sequences can be replication in-vivo
transferred into the cells

Adenoassociated
Viruses • Stable, integrates into non-dividing ■ Less efficient and less precise
«. ■

cells than retroviruses

■ Viral genomes with slight deletions
or rearrangements or both are
often observed K
■ May preferentially integrate with
a region of #19 linked to chronic
B Cell leukemia I *

Herpes S virus - • Ideal for treating nervous system ■ Difficult to generate stocks of
tumors replication - deficient
recombinant virus
■ Even replication incompetent
virus may kills the cells

Vaccinia virus ■ Can hfect all cell types ■ Infection with a wild type virus
may lead to cell death.
■ Individuals previously immunized
against vaccinia may mount a
significant immune response
against these engineered viral
particles.

contd.
 SECTION 12 : GENETICS IN PEDIATRIC DENTISTRY I G®

Non viral gene delivery methods Description of.the technique

NON TARGETED GENE DELIVERY

Direct injection of DNA May save gene from cytoplasmic enzyme degradation.
Effective in some immunization strategies

Electroporation Forms a temporary nanometer sized cell membrane

pores through which DNA can pass into the cell

Calcium phosphate Precipitation Safe and simple procedure

Liposomes DNA coated with synthetic cationic lipid can be

introduced into the cells by fusion.

TARGETED GENE DELIVERY -

Ligand DNA conjugate It is a combination of plasmid DNA and specific

polypeptide ligand complexes.

cell. But in future, one might use only selected por­ precision maybe achieved if one could place a tis­
tions of a retrovirus in order to construct a delivery sue - specific coat on a retroviral particle that would
and integration system that would place one copy direct the virus into the target cell, along with a
of the vector DNA into the target cells’s genome. tissue specific (and possibly even a developmental-
Expression in such a system would be controlled by time-period specific) enhancer in the construct it­
the exogenous gene’s own genomic regulatory sig­ self.
nals.
SAFETY (Fig. 12.11)
EXPRESSION
Although retroviruses have many advantages for
The second criterion for evaluating a human gene gene transfer, they also have disadvantages. One
therapy protocol is that there should be an appro­ problem is that they can rearrange their own struc­
priate expression of the new gene in the target cells. ture as well as exchange sequences with other
Even when a delivery system can transport a for­ retroviruses. A viral integration site that disrupts
eign gene into the DNA of correct cell, it is difficult an important host gene or its regulatory sequence
to make the integrated DNA function. “Normal” would definitely be detrimental. In addition, if an
expression of exogenous genes is an exception rather organism is already infected with some virus, the
than a rule. One of the biggest challenges in the Seemingly “harmless” transferred virus may com­
gene transfer experiments is to enhance and main­ bine with the endogenous virus to form a poten­
tain the level of expression. One key element may tially harmful recombinant structure. Investigators
be enhancers. These are 50-100 base pairs long se­ at NIH (U.S.A) have described three monkeys who
quences that increase the expression of the adjacent developed malignant T cells lymphomas after a bone
gene 10-100 times. Some enhancers' may even be martow transplantation and gene transfer with a
tissue specific. With a tissue specific enhancer it helper virus contaminated retroviral vector prepa­
may not be necessary to develop a/cell specific de­ ration. This finding strongly reaffirms the
livery system. The DNA could be integrated into sity for clinical protocols to use helper virus free
all cells but only be expressed significantly in that vector preparations as is required for all approved
tissue in which the enhancer is active. Even more protocols. The calcium phosphate procedure for
 <2© I TEXTBOOK OF PEDODONTICS

patients who do not yet exist, and at what point do

we cross the line into "playing God”? There is also
considerable concern about using gene transfer to
insert genes into humans for the purposes of en­
hancement i.e., to try to "improve” desired charac­
teristics. The area is further clouded by the problem
of: How to say that a given gene is being used for
treatment (or for preventing disease) or for "en­
hancement”? Enhancement involves the engineer­
ing of the somatic cells (and eventually germ cells)
in ways not related to treating a disease. The re­
search on enhancement is currently highly ill-
favored because of far reaching ethical implications.
For example, a company may require its workers to
be genetically engineered to work in a toxic envi­
ronment instead of cleaning up the environment!!

CONCLUSION

At the moment, gene therapy provides only a short

term cure that must be repeated every few months
because the cells cartying the transplanted genes
die and must be replenished. Thus, the word "gene
therapy” is actually a misnoi^er as it only-bring
about a temporary suppression of the symptoms,
instead of completely curing the patient of the dis­
ease. The safety of the procedure is sfill the major
issue. Patients affected from a deficiency of the en­
zymes HPRT, PNP or ADA are the most likely can­
Fig. 12.11 Safety from harmful viral particles
didates for gene therapy. Gene therapy will have a
major influence on the health care of our popula­
transferring an exogenous DNA, does not represent tion only when vectors are developed that can safely
a health risk and therefore, primate studies do not and efficiently be injected directly into patients.
appear to be necessaiy. Vectors will have to be engineered to target specific
cell types, insert their genetic information into a
ETHICS safe site in the genome and be regulated by normal
physiological signals. Technologically it is the most
Considerable controversy exists on the ethical as­ advanced branch of life sciences till today. In future
pect of germline gene therapy. Genetic manipula­ it may be used as an adjunct to standard therapeutic
tion of the germ cells could produce damage in fu­ procedures rather than an independent and self suf­
ture generations, Besides medical arguments, there ficient treatment system. Although the medical po­
are a number of philosophical, ethical, and theo­ tential is bright, the possibility for misuse of ge­
logical concerns. For instance, do infants have the netic engineering technology looms large, so soci­
right to inherit the unmanipulated genome, does the ety must ensure that gene therapy is used only for
concept of informed consent have any validity for the treatment of genetic diseases.
 SECTION 12 : GENETICS IN PEDIATRIC DENTISTRY I tEtfr

S^lf-Assessment 3. How important is the chromosome location for

delivering the foreign genes?
1. Is it right to use the word 'Gene therapy1? 4. How much impact will gene therapy have on
2. Can we transfer genes with their control elements medical practice in future ?
as a single unit through the vectors? 5. Is gene therapy an ultimate medicine?
 12.6 Latest Advances in Genetics

Dhar PK

Genetics is an ever expanding branch of science that 3. DNA vaccines are more stable and resistant to
will have a major impact on the future health care temperature fluctuations. Thus they can be eas­
system. For the last few years, many phenomenal ily stored and transported.
discoveries have been made that have changed the 4. Antigens retain their native form thus improv­
entire scenario of revolutionary. Among a myriad ing processing and presentation to the immune
of discoveries, three are most noteworthy: DNA system.
vaccination, Biochips and Mammalian cloning. 5. Due to prolonged antigen expression, the number
of effective doses can be substantially reduced.
DNA VACCINATION
However, few unsolved issues still remain.
In the area of vaccine technology the first revolu­ 1. Inspite of its universal acceptance, vaccination
tion took place when Edward Jenner immunized is not always an overwhelming success for
humans from small pox. The second revolution many reasons e.g. in case of Hepatitis B virus.
recently occurred as molecular biologists made 2. It is veiy necessaiy to understand the mecha­
vaccines out of DNA ! nisms by which DNA induce * immune response.
3. There is as yet no way to trash excess plasmid
DNA vaccination represents a radical change in that fails to find a way inside the cell.
the way antigens are delivered. A direct injection 4. There is a possibility of plasmid disrupting a vital
of plasmid DNA encoding an antigenic protein DNA sequence in the host cell as the process of
enables expression of the protein intracellularly. plasmid integration is totally random.
This leads to surprisingly strong responses, in­
volving both humoral and cellular branches of Future prospects
the immune system.
How can one go upon improving this technology?
DNA vaccination is performed by directly injecting One approach is to minimize the possible risks as­
the plasmid DNA encoding an antigenic protein, sociated with introducing DNA into the cells i.e. to
intramuscularly or intradermally. The amount of begin with only minimal amount of plasmid should
protein produced by the cell lead to strong immune be injected. In order to reduce the effective dose of
responses. There are many advantages of using DNA a DNA vaccine, technological improvements must
vaccines. be made. In addition to intramuscular and intrave­
1. They can be easily manufactured at an indus­ nous routes, other modes of gene transfer should
trial scale. also be explored, e g. topical application, intra-ab-
2. Different DNA vaccines can be combined and dominal route or by using inhalers. From what has
delivered in one shot. been achieved till now, it appears that DNA imniu-
 SECTION 12 : GENETICS IN PEDIATRIC DENTISTRY |

nization is on its way to make substantial inroads are benefiting from the use of DNA microarray tech­
into molecular medicine. nology: DNA array technology has applications in
various fields of human importance.
BIOCHIPS
1. Drug discovery: Pharniacogenomics
What is a DNA Chip? It can help answer questions like: Why some
drugs work better in some patients than in oth­
A DNA chip is an array of DNA sequences embed­ ers? Why some drugs may even be highly toxic
ded in a gel that layers over a silicon surface. It to certain patients? The goal of pharmaco-
provides a medium for matching the known and un­ genomics is to find correlations between thera­
known DNA samples based on base-pairing rules peutic responses to drugs and the genetic pro­
and automating the process of identifying the un­ files of the patients.
knowns. An array of experiment can be created by
hand or make use of robotics to deposit the sample. 2. Toxicological research: Toxicogenomics
A DNA chip is more commonly referred to as DNA Toxicogenomics is the hybridization of func­
array. In general, arrays are described as tional genomics and molecular toxicology: The
macroarrays or microarrays, the difference being the goal of toxicogenomics is to find correlations
size of the sample spots. Macroarrays contain sam­ between toxic responses to toxicants and changes
ple spot sizes of about 300 microns or larger and in the genetic profiles of the objects exposed to
can be easily imaged by existing gel and blot scan­ such toxicants.
ners. The sample spot sizes in microarray are typi­
cally less than 200 microns in diameter and these Gene chips permit analysis of thousands of genes
arrays usually contain thousands of spots. simultaneously. At present, such chips are avail­
Microarrays require specialized robotics and able only from a single company, Afiymetrix of
imaging equipment that generally are not commer­ Santa Clara, California, USA. Off the shelf ver­
cially available as a complete system. sions of Afiy metrix chips cost $2,500. Custom­
ized chips containing DNA from specific organ­
Wo formats of Gene Chips isms or tissues can take months to make and cost
as much as $12,000 each and each chip is dis­
Format I: probe DNA is immobilized to a solid sur­ posable. Gene chip technology depends on pho­
face such as a glass using robot spotting and ex­ tolithography, a process that requires a shining
posed to a set of targets either separately or in a ultraviolet‘light through a series of stencil-like
mixture. This method, “traditionally” called DNA masks onto a glass chip resulting in the synthe­
microarray, is widely considered as developed at sis of tens of thousands of DNA molecules of
Stanford University. interest. But making these chips and their masks,
each customized to dissect a specific problem in
Format II: an array of oligonucleotide or peptide
genomic analysis, is a clumsy, time-consuming
nucleic acid (PNA) probes is synthesized either in
and expensive process. Sometimes, as many as
situ (on-chip) or by conventional synthesis followed
100 masks are required to make a single chip
by on-chip immobilization. The array is exposed to
that has as many as 500,000 tiny, DNA-laden
a labeled sample DNA, hybridized, and complemen­
compartments. In addition to their immense
tary sequences are determined.
practical applications in diagnostic human pa­
The microarray (DNA chip) technology is having a thology, gene chips have also been used to study
significant impact on genomics study. Many fields, the aging process in mice.
including drug discovery and toxicological research
 <iij> | TEXTBOOK OF PEDODONTICS

HUMAN CLONING!! Algae, fungi, and such simple plants as club mosses
can reproduce asexually as well as sexually and can
What is cloning? be cloned. Higher plants usually reproduce sexu­
ally and form seeds. However, many—if not all—
A clone is a group of genetically identical cells. For higher plants can also reproduce asexually through
example, tumors are clones of cells inside an or­ a process called vegetative propagation, and so they
ganism because they consist of many replicas of one can form clones. Plant clones are useful for meas­
mutated cell. Another type of clone occurs inside a uring the effects of various environmental factors
cell. Such a clone is made up of groups of identical or chemical compounds on genetically identical
structures that contain genetic material, such as plants. Breeders use cloning to collect plants with
mitochondria and chloroplasts. Some of these struc­ certain desired traits. Farmers and gardeners raise
tures, called plasmids, are found in some bacteria apples, potatoes, and roses by means of clones.
and yeasts. Techniques of genetic engineering en­
The storv of Dollv
*•
able scientists to combine an animal or plant gene
with a bacterial or yeast plasmid. By cloning such a
In the summer of 1995, the birth of two lambs at
plasmid, geneticists can produce many identical
Roslin Institute in Scotland, heralded what many
copies of the gene.
scientists believe will be a period of revolutionary
opportunities in biolog}' and medicine. Megan and
The term clone also refers to a group of organisms
Morag, both carried to term by a surrogate mother,
that are genetically identical. Most such clones re­
were not produced from the union of a sperm and
sult from asexual reproduction, a process in which an egg. Rather their genetic material came from
a new organism develop from only one parent. Ex­ cultured cells originally derived from a nine-day-
cept for rare spontaneous mutations, asexually re­ old embryo. That made Megan and Morag genetic
produced organisms have the same genetic compo-- copies, or clones, of the embryo.
sition as their parent. Thus, all the offspring of a
single parent form a clone. After the birth of Megan and Morag, the work on
Dolly began. Researchers from Roslin Institute un­
Single-celled organisms, such as bacteria, protozoa, der Ian Wilmut, tested fetal fibroblasts (common
and yeast, usually reproduce asexually. Clones of cells found in connective tissue) and cells taken from
these organisms are useful in research. For exam­ the udder of an ewe tha t wa s three and half months
ple, various drugs and other compounds can be pregnant. They selected a pregnant adult because
tested on bacterial clones. All the test bacteria have mammary cells grow vigorously at this stage of preg­
the same genetic makeup. Therefore, any differences nancy, indicating that they might do well in cul­
in effectiveness among the different compounds re­ ture. Moreover, they have stable chromosomes, sug­
sult from the compounds themselves and not from gesting that they retain all their genetic informa­
the bacteria. tion. The successful cloning of Dolly from the mam-
maty derived culture and of other lambs from the
Many plants reproduce by vegetative propagation, cultured fibroblasts showed that the Roslin proto­
col was robust and repeatable.
a form of natural cloning. Plants that develop from
runners or underground stems are the clones of the
All the cloned offsprings in these experiments
plants that send out the runners and stems. Gar­
looked like a breed of sheep that donated the origi­
deners use such techniques as cuttage, grafting, and
nating nucleus, rather than like their surrogate
mound layering to produce clones of favored plants.
mothers or the egg donors. Genetic tests proved
 SECTION 12 : GENETICS IN PEDIATRIC DENTISTRY |

beyond doubt that Dolly was indeed a clone of an ■ The perpetuation of endangered species.
adult. It is most likely that she was derived from a ■ The production of offspring by i nfertile couples.
fully differentiated mamniaiy cell, although it is ■ The production of offspring free of a potentially
impossible to be certain because the culture also disease-causing genetic flaw carried by one mem­
contained some less differentiated cells found in ber of a couple; the individual without the de­
small numbers of mammary glands. Other labora­ fect could be cloned.
tories have since used an essentially similar tech­
nique to create healthy clones of cattle and mice Is it possible to clone humans?
from cultured cells, including ones from nonpreg­
nant animals. Probably yes, and in the very near future. But a great
deal more research and development of the nuclear
How to clone? transfer techniques used to clone Dolly is needed.
And it must be improved and perfected for use on
Cloning is based on nuclear transfer, the same tech­ human embiyos. Sheep embryos have some special
nique scientists have used for some years to copy characteristics that make cloning them much easier
animals from embryonic cells. Nuclear transfer in­ than cloning human embryos. Cloning an adult
volves the use of two cells. sheep was extremely difficult to do; over 270 at­
tempts were needed before Dolly was bom. Many
The recipient cell is normally an unfertilized egg
fetal lambs did not survive the early stages of de­
taken from an animal soon after ovlulation. Such
velopment. Those lambs that were carried to term
eggs are poised to begin developing once they are
were born with health problems, including mab
appropriately stimulated. The donor cells is the one
formed kidneys, and all but Dolly subsequently died.
to be copied. A researcher working under a high
Since the birth of Dolly, the first cloned mammal,
power microscope holds the recipient egg cell by
several other experiments performed on mice and
suction on the one end of a fine pipette and uses an
cows, for instance, have shown that cloning is pos­
extremely fine micropipette to suck out the chro­
sible. Korean scientists have also claimed that they
mosomes (at this stage a distinct nucleus is not
have succeeded in cloning a human cell.
formed). Then, typically, the donor cell, complete
with its nucleus, is fused with the recipient egg.
However, there lies a gap between the demonstra­
Some fused cells start to develop like a normal em-
tion that human cloning is possible and the actual
bryo and produce offspring if implanted into the
practice. Many steps are necessary7 to successfully
uterus of surrogate mother.
clone a human being, starting with the proper gene
transfer which must be carried out without a dam­
Practical applications of cloning
age to the gene (any damage would lead to embry o
■ The mass production of animals engineered to defects and miscarriage). For this reason, extensive
carry human genes for the production of certain research should be done in order to define the best
proteins that could be used as drugs; the pro­ cloning process and scientists expect to offer posi­
teins would be extracted from the animals milk tive answers in a very near future.
and used to treat human diseases.
■ The mass production of animals with genetically Valient Ventura Ltd. “World’s FIRST HUMAN
modified organs that could be safely transplanted CLONING Company”
into humans.
« The mass production of livestock that have been RAEL — the founder of a religious organization
genetically modified to possess certain desirable called the RAELIAN MOVEMENT which claims
traits. that life on earth was created scientifically in
 I TEXTBOOK OF PEDODONTICS

laboratories by extraterrestrials whose name Benefits of human cloning

(Elohim) is found in the Hebrew Bible and was Cloning would enable infertile couples to have chil­
mistranslated by the word "God”. He claims that dren of their own.
Jesus resurrection was, in fact, a cloning performed 1. Cloning would give couples who are at risk of
by the Elohim. Rael has set up a company named producing a child with a genetic defect the
VALIANT VENTURE LTD which offers a service chance to produce a healthy child.
called “CLONAID” to provide assistance to would 2. Cloning could shed light on how genes work and
be parents willing to have a child cloned from one lead to the discovery of new treatments for ge­
of them This service offers a opportunity to par­ netic diseases.
ents with fertility problems or homosexual couples 3. A ban on cloning may be unconstitutional. It
to have a child cloned from one of them. would deprive people of the right to reproduce
CLONAID’s Scientific Director, the French scien­ and restrict the freedom of scientists.
tist Dr. Brigitte Boisselier sees no, ethical problems 4. A clone would not really be a duplicate, because
with the procedure. Moreover, it’s now common to environmental factors would mould him or her
see the dead parent father a baby through the proc­ into a unique individual.
ess of frozen sperm implantation. 5. Objections to cloning are similar to objections
raised against previous scientific achievements,
The company charges $200,000 US for its cloning for example, heart transplants and test-tube ba­
services. It also offers a service called bies, that later came to be widely accepted.
“INSURACLONE” which, for a $50,000 fee pro­
vides a safe storage of cells sampled from a living Dangers of human cloning
child or from a beloved person in order to create a 1. Cloning might lead to the creation of genetically
done if the child dies of an incurable disease or engineered groups of people for specific pur­
through an accident. In the case of a genetic dis­ poses, such as warfare or slavery
ease, the cells are preserved until science can ge­ 2. Cloning might lead to an attempt to improve the
netically repair it before recreating the child (or an human race according to an arbitrary standard.
adult). 3. Cloning could result in the introduction of addi­
tional defects in the human gene pool.
The next step will be to directly clone an adult per­ 4. Cloning is unsafe. There are too many unknown
son without having to go through the growth proc­ factors that could adversely affect the offspring.
ess and to transfer memory and personality in this 5. Doctors might use clones as sources of organs
person. It will be like waking up after death in a for organ transplants.
brand new body just like after a good night sleep!”
Self-Assessment
CLONAID says it will soon develop technology to
enable humans to carry a personal Genetic Repair 1. What is DNA vaccination?
Kit. It will also offer a new service: the cloning of 2. How is DNA vaccination different from routine
pets to wealthy individuals who wish to see their vaccination procedures?
lost pet be brought back to life. This service will 3. Is DNA immunization procedure safe?
also be offered to the owners of racing horses, a 4. What is a biochip?
very promising market given the outrageous prices 5. What will be the impact of DNA array technol­
paid for champions. CLONAID will be ready to start ogy on the future health care system?
its animal cloning operation in a very short time 6. Is it possible to clone humans?
since no legislation restricts animal cloning as op­ 7. What is the mechanism of cloning technology?
posed to the cloning of human beings.
 SECTION 12 : GENETICS IN PEDIATRIC DENTISTRY |

Further Suggested Reading For Section - 12 15. McKusick V. Mendel ian Inheritance in man/
Johns Hopkins Press. (1999) (It is the best re­
1. Beaud AL et al. Gene transfer and gene therapy. source for obtaining information on human ge­
Alan R Liss. NY., 1989 netic disorders. The latest edition (1999) con­
2. Borsani G et al.A practical guide to orientyour- tains complete details of 10,000 genetic disor­
self in the labyrinth of genome databases. Hum ders. It can be accessed online at: http://
Mol Genet 7.1641-8, 1998 www.ncbi.nlm.nih.gov
3. Capecchi MR. Altering the genome by homolo­ 16. Ramsay A J, Leong KH, Ramshaw I A. DNA vac­
gous recombination. Science 244.1288-92, 1989 cination against virus infection and enhancement
4. Debouck C, Goodfellow PN. DNA microarrays of antiviral immunity following consecutive im­
in drug discovery and development. Nat Genet munization with DNA and viral vectors.
21:1 Suppl 43-50,1999 Immunol Cell Biol..75.382-8, 1997
5. Emery AE, Rimoin DL. Principles and Practice 17. Ramsay G. DNA chips: state-of-the art. Nat
of Medical Genetics (2 volumes). 2” edition. Biotechnol.. 16.40-4,1998
Churchill Livingstone, 1995 18. Robinson A, Linden MG. Clinical genetics hand­
6. Fomsgaard A . HIV-1 DNA vaccines. Immunol book. 2nd edition. Blackwell scientific, 1993
Lett. .65.127-31, 1999 19. Schena M et aLMicroarrays: biotechnology’s
7. Friedman T. Progress towards human gene discovery platform for functional genomics.
therapy. Science 244. 1275-81, 1989 Trends Biotechnol. 16.301-6, 1998
8. Giese M. DNA-antiviral vaccines: new devel­ 20. StLóuis D, Verma IM. An alternative approach
opments and approaches - a review. Virus Genes to somatic cell gene therapy. PNAS,- USA.
17.219-32, 1998 85.3150-3154, 1988
9. Hanania EG et al. Recent advances in the appli­ 21. Tai war GP, Diwan M, Razvi F, Malhotra R. The
cation of gene therapy to human disease. Ameri­ impact of new technologies on vaccines. Natl
can J of Medicine 99, 537-552, 1995 Med J India. 12.274-80, 1999
10. Harper PS. Practical genetic counseling. John 22. Trounson A, Pera M. Potential benefits of cell
Wright and Sons. 3rd edition, 1988 cloning for human medicine. Reprod Fértil Dev
11. Hoffman SL, Doolan DL, Sedegah M et al. To­ 10.121-5,1998
ward clinical trials of DNA vaccines against 23. Ward BE et al. Rapid prenatal diagnosis of chro­
malaria. Immunol Cell Biol..75.376-81,1997 mosomal aneuploidies by fluorescence in situ
12. Khan J et al. DNA microarray technology: the hybridization - clinical experience with 4500
anticipated impact on the study of human dis-, specimens. Am J Hum Genet. 52.854-865,1993
ease. Biochim Biophys Acta.25.Ml7-28,1999 24. Webster RG. Potential advantages of DNA im­
13. Lee D J, Corr M, Carson DA. Control of immune munization for influenza epidemic and pandemic
responses by gene immunization., Ann planning. Clin Infect Dis 28.225-9, 1999
Med..30.460-8, 1998 25. Wilmut I. Viable offspring derived from fetal and
14. Lo Y et al. Culture of fetal erythroid cells from adult mammalian cells. Nature. 385.810 812,
maternal peripheral blood. Lancet 344.264-265, 1997
1994
 SECTION - 13

Soft Tissue Oral Lesions

iii Children
13.1 Periodontal Diseases
Sudha P, Nayak A U

Introduction and chronic periodontitis in adults. These factors

may be susceptible to modification.
The gingiva forms an important part of the peri­
odontium, the supporting structure of the tooth. In Features of normal periodontium in children (Fig.
the maintenance of the tooth in the oral cavity, the 13.1a, b, c)
health of the periodontium as a whole is of para­
mount importance. The oral mucosa is the lining which separates the
interior of the oral cavity from the complex under­
The prevalence of gingivitis in children has been lying organs. It serves to protect these organs and
reported to be as high as 99%. The gingivitis oc­ to receive and transmit stimuli from the environ­
curring in the primary dentition tends to remain ment. t
confined to the marginal gingiva for reasons yet un­
explained. Advanced alveolar bone destruction in Gingiva
children, especially when associated with the pri­ It is a masticatory type of oral mucous
* membrane
mary dentition, appears to be quite uncommon. The that forms the covering of the teeth. It is divided
shorter life span of the deciduous teeth may be the into three zones for descriptive purposes.
reason why little attention is paid to periodontitis
in children. Also the rate of periodontal destruction Marginal gingiva
in children may be much slower to cause a substan­ The marginal gingiva includes the gingival crevice
tial loss of attachment within the life span of de­ or the sulcus and a free gingival margin. The free
ciduous teeth. gingival margin is thicker and rounder around the
primary teeth than in the permanent teeth, due to
The control of gingivitis in young children by its the morphological characteristics such as the cervi­
early detection, treatment, and prevention may be a cal bulge and the underlying constriction at the
'realistic approach to the reduction of the prevalence cemeritogingival junction, in contrast to the knife
and severity of periodontal diseases in adults. The edge margin seen in permanent dentition.
assumption that periodontal disease has its etiology
as gingivitis in children awaits a complete under­ Att ached gingiva
standing of the natural history of these periodontal The attached gingiva is continuous with the mar­
diseases. However, even if inception of chronic peri­ ginal gingiva. It is firm and resilient and tightly
odontitis is found to occur in children, common fac­ bound to the underlying periosteum of the alveolar
tors may be associated with gingivitis in children bone. In children, it appears less dense and redder
Wiä a
LS
i
%

SECTION 13 : SOFT TISSUE ORAL LESIONS IN CHILDREN

Fig. 13.1a Normal gingiva of 3% year old child

Papillary gingiva

Marginal gingiva

Attached gingiva

Alveolar mucosa

Fig. 13.1b Zones of the gingiva.

Deciduous
Teeth

Permanent
Teeth

Fig. 13.1c Morphology of interdental papilla in deciduous and permanent teeth

 | TEXTBOOK OF PEDODONTICS

than in adults due to less keratinised epithelium with The so-called probing depth of a clinically normal
its greater vascularity. The attached gingiva is more gingival sulcus in humans is 2 to 3mm. The sulcus
flaccid because of lesser connective tissue density depth around the primary teeth is comparatively
and its texture is less stippled . The two unique char­ greater than that found around the permanent teeth.
acteristics of the attached gingiva in children arc The mean values range from 1.4mm to 2.1mm.
the interdental clefts and the retrocuspid papilla
The interdental clefts are normal anatomic features Gingival fluid (sulcular fluid)
found in the interradicular zones underlying the The gingival sulcus contains a fluid that seeps into
saddle areas. The retrocuspid papilla is found ap­ it from the gingival connective tissue through the
thin sulcular wall. The gingival fluid is believed to
proximately 1mm below the free gingival groove
(1) cleans material from the sulcus, (2) contain
on the attached gingiva lingual to the mandibular
plasma proteins that may improve adhesion of the
canine. It occurs in 85% of children and apparently
epithelium to the tooth, (3) possess antimicrobial
decreases with age.
properties, and (4) exert antibody activity in defense
of the gingiva.
Interdental gingiva
The interdental gingiva occupies the gingival em­ Correlation of the normal clinical and micro­
brasure, which is the interproximal space beneath scopic features
the area of tooth contact. The interdental gingiva
can be pyramidal or have a *
coF shape in the adult Colour
dentition which is more susceptible to infection. The colour of the attached and marginal gingiva is
generally described as coral pink and is produced
In the primary dentition, interdental spacing is com­ by the vascular supply, the thickness and degree of
mon. Hence, saddle areas are present resulting in a keratinization of the epithelium, and the presence
well keratinized interdental surface. This may be of pigment-containing cells. Melanin pigmentation
tile reason for lower prevalence of periodontal le­ in the oral cavity is prominent in blacks. Gingival
sions in children because these areas are less vul­ pigmentation occurs as a difiiised, deep purplish dis­
nerable to development and progression of the in­ coloration or as irregularly shaped brown and light
flammatory processes. brown patches.

Alveolar mucosa Contour

The thin epithelium and an absence of keratin makes The contour or shape of the gingiva varies consid­
the alveolar mucosa redder than the pink gingiva. erably and depends upon the shape of the teeth and
Iflhis tissue has abundance of elastic fibers and is their alignment in the arch, the location and size of
readily movable. Its width increases with age and the area of proximal contact, and the dimensions of
the facial and lingual gingival embrasures.
eruption of teeth.

Shape
Cringival sulcus
The shape of the interdental gingiva is governed by
The gingival sulcus is the shallow crevice or space
the contour of the proximal tooth surfaces and the
around the tooth bounded by the surface of the tooth
location and shape of gingival embrasures. The
gin one side, and the epithelium lining the free mar-,
height of the interdental gingiva varies with the lo­
■grin of the gingiva on the other. The clinical deter-
cation of the proximal contact. Interdental clefting
mination of the depth of the gingival sulcus is an is a common feature in the primary dentition.
Important diagnostic parameter.
 SECTION 13 : SOFT TISSUE ORAL LESIONS IN CHILDREN |

Consistency feature of healthy gingiva, and reduction or loss of

Around the primary dentition, the marginal and the stippling is a common sign of gingival disease.
attached gingiva in children is very7 flaccid and re­ When the gingiva is restored to health following
tractable, The diminished rigidity and increased treatment, the stippled appearance returns.
retractability of the marginal gingiva around the
primary teeth have several causes. Position
1. Immature connective tissue composition: The The position of gingiva refers to thé level at which
collagen bundles are less differentiated and more the gingival margin is attached to the tooth. When
hydrated; its polypeptide chains are not as tightly the tooth erupts into the oral cavity, the margin and
crosslinked. Also, there is a lower ratio of col­ sulcus are at the tip of the crown; as eruption
lagen to ground substance in the connective tis­ progresses, they are seen closer to the root. During
sue, making it less rigid. this eruption process, as the junctional epithelium,
2. Immature gingival fibres system: The. gingival oral epithelium are reduced, enamel epithelium un­
fibre system, particularly the circular and groups dergo extensive alterations and remodeling, while
A and B fibres are incompletely differentiated at the same time maintaining the shallow
in their arrangement, leading to a less organ­ physiologic depth of the sulcus. Without this
ized state. remodeling of the epithelium, an abnormal anatomic
3. Increased vascularisation: Increased flow dur­ relationship between the gingiva and the tooth
ing this dynamic period of gingival metabolism would result
promotes tissue hydration and fluid transfer into
the sulcus. Inherent in the concept is the distinction between
the anatomic crown (the portion of the tooth cov­
Surface texture ered by enamel) and anatomic root (the portion of
The gingiva presents a textured surface like that of the tooth covered by cementum) and the clinical
an orange peel and is referred to as being stippled. crown and clinical root The clinical crown is the
Stippling is best viewed by drying the gingiva. The part of the tooth has been denuded of its gingiva
attached gingiva is stippled; the marginal gingiva and projects into the oral cavity; the clinical root is
is not. The central portion of the interdental papil­ that portion of the tooth covered by periodontal tis­
lae is usually stippled, but the marginal borders are sue.
smooth. The pattern and extent of stippling vary
from person to person and in different areas of the Periodontal ligament
same mouth. Stippling varies with age. It is absent The periodontal ligament is the connective tissue
in infancy, appears in some children at about 5 years structuré that surrounds the root and connects it with
of age, increases until adulthood, and frequently the bone. It is continuous with the connective tis *
begins to disappear in old age. sue of the gingiva andcommunicqtes with the mar­
row spaces through vascular channels in the bone.
Microscopically, stippling is produced by alternate
rounded protuberances and depressions in the Cementum
gingival surface. The papillary layer of the con­ Cementum is the calcified mesenchymal tissue that.
nective tissue projects into the elevations, and both forms the outer covering of the anatomic root
the elevated and the depressed areas are covered by
stratified squamous epithelium. The degree of Normal microscopic features
keratinization and the prominence of stippling ap­ There are two main forms of root cementum: acel­
pear to be related. Stippling is a form of adaptive lular (primaiy) and cellular (secondary). Both con­
specialization or reinforcement for function. It is a sist of a calcified inteifibrillar matrix and collagen
 (S3 I TEXTBOOK OF PEDODONTICS

fibrils. Primary cementum is the first to be formed superimposed on the underlying chronic changes.
and covers approximately the cervical two-thirds of Gingival color change and swelling appear to be
the root; it does not contain cells and is therefore more common expressions of gingivitis in children
referred to as acellular. This cementum is formed than are bleeding and increased pocket depth. The
before the tooth reaches the occlusal plane. Cemen­ characteristics of gingivitis in preschoolers can be
tum formed after the tooth reaches the occlusal plane summarized as follows:
is more irregular and usually contains cells in in­ 1. Children experience gingivitis in varying
dividual spaces (lacunae) that communicate with amounts,
each other through a system of anastomosing ca- 2. Gingivitis does not appear to have any irrevers­
naliculi. This cementum is called cellular cemen­ ible effects on the primary periodontium,
tum or secondary cementum. 3. Gingivitis in children is largely reversible,
4. The severity of gingivitis in children is less than
The alveolar process compared with that in adults with similar levels
The alveolar process is the bone that forms and sup­ of the plaque.
ports, the tooth sockets (alveoli). It forms when the
tooth erupts in order to provide the osseous attach­ Etiology
ment to the forming periodontal ligament; it disap­ Chronic inflammatory gingival enlargement is
pears gradually when the tooth is lost. caused by a prolonged exposure to the dental plaque.
Factors that favour plaque accumulation and reten­
GINGIVAL DISEASES IN CHILDHOOD tion include poor oral hygiene, abnormal relation­
ships of the adjacent teeth and opposing teeth, lack
The effects of periodontal disease observed in adults of tooth function, cervical cavities, overhanging
have their inception earlier in life. Gingival dis­ margins of dental restorations, improperly contoured
ease in the child may progress to jeopardize the peri­ dental restorations or pontics, impaction, irritation
odontium of the adult. from clasps or saddle areas of removable prosthe-
ses, nasal obstruction, orthodontic therapy involv­
The developing dentition and certain systemic meta­ ing repositioning of the teeth, and habits such as
bolic patterns are peculiar to childhood. There are mouth breathing and pressing the tongue against
also gingival and periodontal disturbances that oc­ the gingiva.
cur more frequently in childhood and are therefore
identified with this period. Clinical features
Chronic inflammatory gingival enlargement in chil­
Chronic inflammatory enlargement dren is usually limited to marginal and papillary
Periodontal diseases are present in almost all per­ gingiva. Chronic inflammatory gingival enlarge­
sons with natural teeth. From an early age gingivi­ ment originates as a slight ballooning of the inter­
tis increases in its severity to peak at the onset of dental papilla and/or the marginal gingiva. In the
puberty. Gingival enlargement may result from early stages it produces a life preserver-like bulge
chronic or acute inflammatory changes. The former around the involved teeth. This bulge increases in
is by far the more common cause. size until it covers part of the crowns. This is be­
cause of the rolled marginal gingiva seen in chil­
Chronic marginal gingivitis is the most prevalent dren. The enlargement is generally papillary or
type of gingival change in childhood. The gingiva marginal and may be localized or generalized. It
exhibits all the changes in color, size, consistency, progresses slowly and painlessly unless it is com­
and surface texture characteristic of chronic inflam­ plicated by acute infection or trauma.
mation. A fiery red surface discoloration is often
 SECTION 13 : SOFT TISSUE ORAL LESIONS IN CHILDREN |

Treatment Histology
Treatment of gingivitis is accomplished through oral The gingival abscess consists of a purulent focus in
prophylaxis. Sound oral hygiene practices are to the connective tissue surrounded by a diffuse infil­
be followed to prevent its recurrence. When oral tration of the polymorphonuclear leukocytes’s,
hygiene is suspended in humans, gingivitis devel­ edematous tissue, and vascular engorgement. The
opsjn 15-21 days. surface epithelium has varying degrees of intra and
extracellular edema, invasion by leukocytes, and
Prognosis ulceration.
Periodontal disease in adults has its origin in child­
Treatment
hood has been claimed by many researches. This is
The gingival abscess is a lesion of the marginal or
supported by the hypothesis that periodontitis is a
interdental gingiva, usually produced by an im­
progressive process and epidemiologically speak­
pacted foreign object. It is treated as follows.
ing, there appears to be a transition from childhood
gingivitis to adult periodontitis. But no cause and
Under topical anesthesia, the fluctuant area of the
effect relation relationship has been demonstrated
lesion in incised with a Bard-Parker blade, and the
yet in humans. Rarely gingivitis progresses to peri­ incision is gently widened to permit drainage. The
odontitis in prepubertal children. area is cleansed with warm water and covered with
a gauze pad. After bleeding stops, the patient is
Acute inflammatory enlargement dismissed for 24 hours and instructed to rinse every
2 hours with a glassful of warm water.
Gingival abscess
A gingival abscess is a localized, painful, rapidly When the patient returns after 24 hours, the lesion
expanding lesion that is usually of sudden onset. It is generally reduced in size and symptom free. A
is generally limited to the marginal gingiva or in­ topical anesthetic is applied, and the area is scaled.
terdental papilla. In its early stages it appears as a If the residual size of the lesion is too great, it is
red swelling with a smooth, shiny surface. Within removed surgically.
24 to 48 hours, the lesion usually becomes fluctu-
ant and pointed, with a surface orifice from which Acute necrotismg ulceratice gingivitis
a purulent exudate may be expressed. The adjacent
teeth are often sensitive to percussion. If permitted Acute nercotizing ulcerative gingivitis (ANUG) has
to progress, the lesion generally ruptures spontane­ been defined as an acute recurring gingival infec­
ously. tion of complex etiology, characterized by necrosis
of the tips of the gingival papillae, spontaneous
Etiology bleeding, and pain. Several names have been as­
signed to it such as Trench mouth. Acute ulcerative
Acute inflammatory gingival enlargement results
gingivitis, Vincent’s stomatitis, Vincent’s angina,
from bacteria carried deep into the tissues when a
Plant-Vincent’s stomatitis, Fusospirocheatal gin­
foreign substance such as a toothbrush bristle, a
givitis, Necrotic gingivitis, Putrid stomatitis.
piece of apple core, or a lobster shell fragment is
forcefully embedded into the gingiva. The lesion is
Etiology
confined to the gingiva and should not be confused
The precise etiology of acute necrotizing ulcerative
with periodontal or lateral abscesses. gingivitis is not known, but a great increase in fusi­
form bacilli and spirochetes is seen in sn»arsfr5^|>
 I TEXTBOOK OF PEDODONTICS

the lesions and clinical signs of this disease have Primary diagnostic Secondary diagnostic

been attributed to this increase in Fusospirocheatal signs signs

complexes and other bacilli.

1. Gingival bleeding 1. Pseudomembrane

Both humoral and cellular immune responses have 2. Pain 2. Fetid mouth odor
3. Interdental ulceration 3. Bad taste
been described in the tissues during the develop-
and necrosis especially in the
.ment of acute necrotising ulcerative gingivitis al­
mandibular anteriors
though the precise immunopathogenesis is still not
4. Elevated temperature 5. Wooden sensation
clear.
with resultant blunting of the teeth
and cratering of gingiva
Local predisposing factors
Various local factors include erupting teeth, inad­
Extraoral and systemic symptoms
equate restoration margins, calculus accumulation,
Patients are usually ambulatory and have a mini­
open contacts, occlusal trauma, poor oral hygiene,
mum of systemic complications. Local lymphad­
pre-existing gingivitis, and smoking, of which the
enopathy and a slight elevation in temperature are
last three seem to be the most commonly prevalent. common features of the mild and moderate stages
of the disease. In severe cases there are marked
Systemic predisposing factors systemic complications such as high fever, increased
Reports have related ANUG to periods of psychic pulse rate, leukocytosis, loss of appetite, and gen­
conflicts, emotional stress in college students, stress eral lassitude. Systemic reactions are more severe
of drug addiction and certain personality types. in children. Insomnia, constipation, gastrointestinal
Other general predisposing factors include: disorders, headache, and mental depression some­
A. Nutritional deficiency: times accompany the condition.
Several researchers have found that individual
deficiency in vitamin B complex, vitamin C com­ In very rare cases, severe sequelae such as, noma
plex are predisposed to development of acute or gangrenous stomatitis, fusospirocheatal menin­
necrotizing ulcerative gingivitis gitis and peritonitis, pulmonary infections, toxemia,
and fatal brain abscess may occur. There may be an
B. Debilitating diseases: elevation in temperature to 103° F or 104° F, with
Frequently the acute necrotizing ulcerative gin­ general malaise being common.
givitis occurs in disease states which involve de­
pression in numbers or function of leukocytes Clinical course
such as blood dyscrasias, malnutrition, Down’s The clinical course is indefinite. If untreated, ANUG
syndrome, Chediak-Higashi syndrome, diabetes, may result in progressive destruction of the peri­
odontium and denudation of the roots, accompanied
AIDS.
by an increase in the severity of toxic systemic com­
plications. It often undergoes a diminution in se­
Clinical features
verity, leading to a subacute stage with varying de­
The 3 criteria sufficient for a reliable diagnosis
grees of clinical symptoms. The disease may sub­
are 1) acute necrosis and ulceration of interproxi-
side spontaneously without treatment. Such patients
nial papillae, 2) pain, and 3) bleeding.
generally have a history of repeated remissions and
exacerbations. Recurrence of the condition in pre­
The presence of pseudomembrane is not an essen­ viously treated patients is also frequent.
tial diagnostic sign. Thus:
 SECTION 13 : SOFT TISSUE ORAL LESIONS IN CHILDREN | Cfrtfr

Treatment of acute necrotizing ulcerative gingi­

vitis
The treatment of ANUG consists of the following
phases
1. Local: Alleviation of the acute inflammation plus
treatment of the chronic disease either underly­
ing the acute involvement or elsewhere in the
oral cavity.
2. Systemic:
a. Supportive treatment: Alleviation of gener­
alized toxic symptoms, such as fever and ma­
laise.
b. Etiotropic treatment: The correction of sys­ Fig. 13.2 Acute herpetic gingivo-stomatitis.
temic conditions that contribute to the initia­
tion or progress of the gingival changes. Clinical features
Tire primary infection usually occurs in a child un­
Antibiotics are administered systemically only in der 5 years of age who has had no contact with the
patients with toxic systemic complications or local HSV-1 and who therefore has no neutralizing anti­
adenopathy. They are not recommended in ANUG bodies. It is believed that 99% of all primary infec­
patients who do not have these complications. The tions are of the subclinical type. The infection may
antibiotic of choice is penicillin. Patients who are also occur in susceptible adults who may not have
allergic to penicillin should be given erythromycin. had the primary infection.
Metronidazole may also be used.
A prodrome consisting of focal itching, burning,
Supportive systemic treatment or tingling sensations on the lips may precede her­
In addition to systemic antibiotics, supportive treat­ pes labialis the duration of which ranges from 1-2
ment consists of copious fluid consumption and days to 7 days. This may be preceded by stress,
administration of analgesics for relief of pain. Bed exhaustion, strain, oral traiima, menstruation, GI
rest is necessary for patients with toxic systemic upset, pharyngitis, sinusitis, fever, myalgia.
complications such as high fever, malaise, anorexia,
and general debility. In such cases nutritional re­ Tire condition frequently occurs during and imme­
quirements also need to be kept in mind. diately after an episode of such febrile diseases as
Herpetic gingivostomatitis (Fig. 13.2): pneumonia, meningitis, influenza and typhoid.
The herpes simplex virus (HSV) is probably more Acute herpetic gingivostomatitis often occurs in the
widely distributed and more constantly present in early stage of infectious mononucleosis.
the man than any other virus. The virus has adapted
itself to its human host a nd has achieved a highly Oral signs
successful parasitism, for over 60% of people are The condition appears as a diffuse, erythematous,
infected with this virus and remain carriers through­ shiny involvement of the gingiva and the adjacent
out life. oral mucosa, with varying degrees of oedema and
gingival bleeding. In its initial stage, it is charac­
Two types of HSV have been seen to commonly in­ terized by the presence of discrete, spherical yel­
fect humans: HSV-1 causing infections in the up­ low, white or greyish liquid-filled vesicles. The ul­
per part of the body, and HSV-2 causing infections cers may be observed on any area of the mucous
in the lower part of the body. membrane, including the buccal and labial mucosa,
 | TEXTBOOK OF PEDODONTICS

tongue, sub-lingual mucosa, hard and soft palate, uamative gingivitis, Aphthous stomatitis (Canker­
pharynx, and tonsillar areas. Large ulcerated lesions score), Erythema multiforme, Stevens- Johnson syn­
may occasionally be observed on the palate or drome
gingival tissues or in the region of the mucobuccal
fold. Treatment
Trea tment of acute heretic gingivostomatitis in chil­
Oral symptoms dren, which runs a course of 10 to 14 days, should
The disease is accompanied by generalized "sore­ be directed toward the relief of the acute symptoms
ness” of the oral cavity, which interferes with eat­ so that fluid and nutritional intake can be main­
ing and drinking. The ruptured vesicles are tiie fo­ tained.
cal sites of pain and are particularly sensitive to
touch, thermal changes, foods such as condiments Application of a mild topical anaesthetic, such as
and fruit juices, and other foods of acid content, dyclonine hydrochloride (0.5%) (Dyclone), before
and the action of coarse foods. In infants, the dis­ mealtime will temporarily relieve the pain and al­
ease is marked by irritability and refusal to take food. low the child to take a soft diet. Another topical
anaesthetic, lidocaine (Xylocaine Viscous), can be
Bxtraoral and systemic signs and symptoms
prescribed for the child who can hold 1 teaspoonful
Herpetic involvement of the lips or face (herpes
of the. anesthetic in the mouth for 2 to 3 .minutes
labia lis/'cold sore"), with vesicles and surface scab
and then expectorate the solution. A mixture of equal
formation, may accompany the intraoral disease.
parts of diphenhydramine (Benadryl) elixir and
Cervical adenitis, fever as high as 101 to 1O5°F(38.3
Kaopectate can also be used.
to 40.6° C), and generalized malaise are common.
The symptoms of the disease develop suddenly and
An antihistaminic drug will often make the child
include malaise, irritability and headache.
more comfortable and may produce drowsiness,
diagnosis which will encourage rest. Acyclovir 5% ointment
The diagnosis is usually established from the pa­ (Zovirax), a medication recommended for the treat­
tient’s history and the clinical findings. Material ment of primary genital herpes and for RHL in
may be obtained from the lesions and submitted to immunocompromised patients, has been found to be
the laboratory for confirmatory tests. useful in otherwise healthy patients as well. The
« Tzanck smear is a rapid, fairly sensitive and in­ use of the iodoxuridine (Herplex and Stoxil) how­
expensive diagnostic method. ever, remains controversial.
« The isolation of the virus can be done in tissue
Prognosis
culture or in the chorioallantoic membrane of
With a high incidence of infection and no effective
the chick embiyo. Degenerative cellular changes
treatment or prophylaxis, patients are concerned
preventable by antibody to herpes simplex con­
regarding infection, since recent reports have asso­
stitute a positive finding.
ciated HSV-2 with cervical cancer. At the present
■ Antibody titers are useful in the diagnosis of pri­
time, treatment can only palliate the pain and dis­
mary infections only as in reinfections there is a
comfort of the patient. It is the task of physicians
little change in the antibody liter.
to help prevent new infections by advising individu­
■ Stained sections of the vesicles of acute herpetic
als how long an active infection may be potentially
gingivostomatitis reveal eosinophilic intranu­
contagious to another person.
clear inclusion bodies tn the peripheral cells.
Drug induced gingival hyperplasia
Differential diagnosis includes acute necrotizing Phenytoin-induced gingival hyperplasia (PGH) has
ulcerative gingivitis, Bullous lichen planus. Desq­ been recognized as a distinct pathological entity for
 SECTION 13 : SOFT TISSUE ORAL LESIONS IN CHILDREN |

more than 40 years and is a common side effect of present, the gingiva appears pink and firm and does
phenytoin treatment. not bleed easily upon probing. More frequently,
however, inflammation superimposes and a com­
Early research showed an increase in the number of bined type of inflammatory enlargement ensues.
fibroblast in patients receiving Dilantin; thus the
condition was termed dilantin hyperplasia. Now As the interdental lobulations grow, clefting be­
the term phenytoin induced gingival overgrowth comes apparent at the midline of the tooth. With
(PIGO) is preferred time the lobulations coalesce at the midline, form­
ing pseudopockets and covering more of the crow n
Prevalence tooth. The epithelial level usually remains constant.
Increasing severity of degree of PGH is associated In some cases, the entire occlusal surface of the teeth
with: becomes covered. These lesions may remain purely
a) Decreasing age; b) Decreasing weight in all sub­ fibrotic in nature or be combined with a noti
groups c) Increasing dose of phenyotin per unit body inflammatory component.
weight d) Increasing trough serum phenytoin lev­
els; e) Increasing serum vitamin B12 levels g) De­ Treatment
creasing degree of oral hygiene. Unfortunately, no cure exists and treatment is often
symptomatic in nature. Antihistamines, topical
Etiology corticosteriods, ascorbic acid, folic acid supple­
The etiology of the condition has not been well de­ ments, topical antibiotics, and alkaline mouthwashes
fined. Several mechanisms have been implicated but have been used with a limited success and are con­
not fully substantiated, including a) disturbance in sidered to be ineffective. Conservative periodontal
adrenocortical function resulting in an exaggerated measures include a vigorous gingival massage cou­
response to tissue injuiy, b) direct action of pheny­ pled with efficient tooth brushing and gum
toin on fibroblasts and c) local response to meta­ stimulators. When surgical measures are indicated,
bolic products of phenytoin in saliva. The etiology the drug trea tment plan of the physician managing
of phenyotin hyperplasia is now felt to be multifac­ the epilepsy should be discussed and the date of sur­
torial. gery postponed if the physician is planning to dis­
continue the phenytoin.
Phenytoin associated gingival overgrowth is related
to the efficiency of oral hygiene and, thus to the Specific surgical approaches for PIGO include gin *
amount of plaque, and inadequate amounts of anti­ givectomy with periodontal knives, laser or elec­
microbial factors in oral cavity could contribute to trosurgery; and internal bevel flap surgery. The use
greater plaque accumulation. of periodontal knives allows the tissue to heal more
quickly, but more operative and postoperative!
Clinical features ing occurs. Also it requires more time and patient
PIGO, when it does develop, begins to appear as cooperation. Electrosuigery is less time consuming,
early as 2 to 3 weeks after initiation of phenytoin decreases blood loss, improves visibility, and allows
therapy and peaks at 18 to 24 months. The initial superior control for areas of limited access is self­
clinical appearance is a painless enlargement of the sterilizing and does not always require periodontal
interproximal gingiva. The buccal and anterior seg­ packs. Disadvantages include its contraindication
ments are more affected than the lingual and poste­ in cardiac pacemakers, unpleasant odour, delayed
rior segments. The affected areas are isolated at healing and potential for error in application |
first but can become more generalized later. Un­ results in an undesired bone or tissue loss. gO
less a secondary infection or inflammation is
i iîÏÏg» I TEXTBOOK OF PEDODONTICS
Í

Other drugs which cause the gingival enlargement usual gingival response to the dental plaque, and a
are nefidipine and cyclosporine. corresponding modification of the usual clinical fea­
tures of chronic gingivitis occurs. The specific man­
Combined enlargement
Combined enlargement results when gingival hy­ ner in which the clinical picture of the conditioned
perplasia is complicated by secondary inflammatoiy gingival enlargement differs from that of chronic
changes. Gingival hyperplasia produces conditions gingivitis depends on the nature of the modifying
favorable for the accumulation of the plaque and systemic influence. Local irritation is necessary for
materia alba by accentuating the depth of the the initiation of this type of enlargement. However,
gingival sulcus, by deflecting the normal excursive the plaque does not solely determine the nature of
pathways of food. The secondary inflammatory the clinical features. There are three types of con­
changes increase the size of the pre-existing gingival ditioned gingival enlargements: hormonal, nutri­
hyperplasia and produce a combined gingival en­ tional, or allergic. Nonspecific conditioned enlarge­
largement. In many instances secondary inflamma­ ment is also seen. (Fig. 13.3)
tion obscures the features of the pre-existent nonin­
flammatory hyperplasia to the extent that the entire Leukemia (Fig. 13.6)
lesion appears to be inflammatory. Leukemia is a disease characterized by the progres­
sive overproduction of white blood cells, which usu­
Conditioned enlargement ally appear in the circulating blood in an immature
Conditioned enlargement occurs when the systemic form.
condition of the patient exaggerates or distorts the

Table 13.1: Conditioned gingival enlargement features and treatment

Enlargement Clinical features Treatment plan v

i
Hormonal ■ Gingival enlargement is found in the ■ Removing all sources of irritation, »
e.g. Pubertal circumpubertal period. and controlling the plaque by means
gingivitis ■ It occurs in both male and female of scaling and curettage.
' (Fig. 13.4a, adolescents and appears in areas « Surgical removal may be required
b) of local irritation. in severe cases. The problem in these
■ Hormonal changes are reported to patients is recurrence due to
have a direct effect on the periodontal poor oral hygiene.
tissue metabolism by increasing the
permeability of the vascular system.
■ The microbiota may also react
* specifically to the increased availa­
bility of hormones in the oral fluids.
■ The size of gingival enlargement far
exceeds, that usually seen in
. association with comparable local
. factors.
■ After puberty, the enlargement
undergoes a spontaneous reduction
but does not disappear unit local
irritants are removed.

contd.
 SECTION 13 : SOFT TISSUE ORAL LESIONS IN CHILDREN |

Enlargement Clinical features Treatment plan

Nutritional « Gingiva is bluish red, soft, and friable ■ Treatment includes ingestion of
e.g. Scurvy and has a smooth, shiny surface. Vitamin C tablets and diet rich in
« Spontaneous or hemorrhage on Vitamin C like citrus fruits.
slight provocation, and surface ■ Treatment of gingivitis includes oral
necrosis with pseudomembrane ~~ prophylaxis and later on
formation maintenance of oral hygiene.
« In infants the enlarged tissue may
cover the clinical crowns of the teeth
« Typical foul breath of persons with
fusospirochetal stomatitis is present
« Swelling of the periodontal
membranes may occur, followed by
loss of bone and loosening of the
teeth, which eventually exfoliate.
■ Sometimes, ulceration and necrosis
of the papillae as infection becomes
superimposed upon the susceptible
tissues.
■ The deciduous and permanent tooth
germs of scorbutic infants have
shown small cysts and a minute
hemorrhage in some specimens.

Non specific « The lesion varies from a discrete « Treatment consists of removal of
enlargement spherical, tumor-like mass with a lesions plus the elimination of
eg. Granulo­ pedunculated attachment to a irritating local factors. The
ma pyogeni- flattened, keloid-like enlargement recurrence rateis about 15%. *
cum) with a broad base. r*
(Fig. 13.5) ■ It is bright red or purple and either
friable or firm, depending on its
duration, in the majority of cases it
presents with surface ulceration
and purulent exudation.
■ The lesion tends to involve
spontaneously to become a
fibroepithelial papilloma or persists
relatively unchanged for years.

Allergic eg. ■ The use of drugs may evoke an ■ The stoppage of the drug generally
Plasma cell allergic response manifested as an reverses this condition.
gingivitis inflammatory reaction. • Anti-alergic drugs »may also help
■ May be associated with generalized
allergic response.
 TEXTBOOK OF PEDODONTICS

Fig. 13.3 Idiopathic gingival hyperplasia Fig. 13.4a Localised pubertal

enlargement of gingiva involving
a lower left central incisor

Fig. 13.4b Generalised pubertal enlargement Fig. 13.5 Pyogenic granuloma

Fig. 13.6 Maxillary arch showing leukemic

enlargement of the soft tissue
 SECTION 13 : SOFT TISSUE ORAL LESIONS IN CHILDREN |

Oral manifestations Bleeding and clotting times and platelet count of

Oral lesions occur in both acute and chronic forms the patient should be checked and the hematologist
of all types of leukemia; myeloid, lymphoid and consulted before periodontal treatment is instituted.
monocytic. These manifestations are far more com
mon, however, in the acute stage of the disease and After the acute symptoms subside, attention is di­
are most common in monocytic leukemia: rected to correction of the gingival enlargement. The
rationale is to remove the irritating factors to con­
These primary clinical manifestations of the dis­ trol the inflammatory component of the enlarge­
ease may consist of gingivitis, gingival hyperpla­ ment.
sia, hemorrhage, petechiae and ulceration of the
mucosa. The enlargement is treated by scaling and curettage
■ True leukemic enlargement occurs commonly in carried but in stages under topical anesthesia. The
acute leukemia, but may also be seen in suba­ initial treatment consistsof gently removing all loose
cute leukemia. It seldom occurs in chronic accumulations with cotton pellets, superficial scal­
leukemia. , ing, and instructing the patient in oral hygiene for
■ Leukemic enlargement may be diffused or mar­ plaque control
ginal, localized or generalized. It may appear Antibiotics are administered systemically, the
as a diffused enlargement of the gingival mu­ evening before and for 48 hours after each treat­
cosa, an oversized extension of the marginal ment to reduce the risk of infection.
gingiva, or a discrete túmor-like interproximal
mass. The gingiva is generally bluish red and Treatment and prevention of the acute gingivitis may
has a shiny surface cyanotic, with a rounding reduce morbidity of these patients. But bleeding
and tenseness of the gingival margin, then it tendency necessitates the use of methods alterna­
increases in size, most often in the interdental tive to toothbrushing.
papilla and covering partially the crowns of the
teeth. The gingival hyperplasia, which may be Gingival cyst
one of the most constant features of the disease Gingival cysts of microscopic proportions are com­
mon, but they seldom reach a clinically significant
except in edentulous patients, is usually gener­
alized and varies in severity. size. When they do, they appear as localized en­
■ Gingival hemorrhage is a common finding in largements that may involve the marginal ami at­
leukemic patients, even in absence of clinically tached gingiva. They occur in the mandibular ca­
detectable gingivitis. The gingival hemorrhage, nine and premolar areas, most often on the lingual
which commonly occurs, is due to ulceration of surface. They are painless, but with expansion they
the sulcus epithelium and necrosis of underly­ may cause erosion of the surface of the alveolar bone.
ing tissue. The cysts develop from odontogenic epithelium or
from surface or sulcular epithelium traumatically
Treatment implanted in area. Removal is followed by unevent­
The most common form of leukemia in children, ful recovery.
acute lymphocytic leukemia, once almost always
fatal within a few months, now has a prolonged re­ PERIODONTITIS IN CHILDREN

mission and probable cure rate approaching 50 per Juvenile periodontitis

cent. This area of treatment ischanging so rapidly JP is relatively an uncommon form of severe peri­
with the introduction of new drugs and new tech­
odontal disease belonging to a group termed as an
niques.
early onset aggressive periodontal disease.
 CËE) I TEXTBOOK OF PEDODONTICS

Described by Wannenmacher (1938) as a localized A hereditary component has been hypothesized be­
disease of the supporting tissues of the teeth in teen­ cause there is a clear familiar aggregation of juve­
agers, 3 different types of diseases have been delin­ nile periodontitis. Because of higher prevalence in
eated such as a) chronic slowly progressive, b) fairly females than in males, a genetic basis has been sug­
generalized, and c) an acute progressive and more gested and numerous family reports consistent with
general. genetic transmission have been published.

IP can be classified as (1) those occurring in other­ Studies have demonstrated the presence of poly
wise healthy individuals and (2) those associated morphonuclear leukocytes with diminished chemo­
with a variety of diseases of other systems. The term tactic and phagocytic responses. An accepted model
localized is used with reference to the first group, of destruction in juvenile periodontitis is given in
although some cases may show a generalized in­ Fig. 13.7.
volvement. Cases of the second type are termed
generalized juvenile periodontitis, because the whole Clinical features
dentition is usually involved. ■ Initially losses of attachment and alveolar bone
are seen around the permanent incisors and first
Etiology molars, but with much individual variation and
The etiology of juvenile periodontitis is still not differing combinations of involved teeth. The
completely clarified. attack sequence appears to follow eruption chro­
nology. The most striking feature is lack of clini­
There is general agreement that the disease always cal inflammation despite the presence of deep
comprises an element of infection, and recent re­ pockets.
search tends to lend support to the hypothesis of ■ The disease starts as a localized form in the first
specific infection molars and or incisors, and develops, if not

Fig. 13.7: Accepted model of destruction in juvenile periodontitis.

 SECTION 13 : SOFT TISSUE ORAL LESIONS IN CHILDREN I

treated, to the generalized form of the same dis­ Radiographic findings

ease, which resembles an adult periodontitis. Vertical loss of alveolar bone around the first mo­
■ Distribution of lesions in the mouth is charac­ lars and incisors in otherwise healthy teenagers is
teristic and as yet unexplained. The classic dis­ taken to be a diagnostic sign of classic juvenile peri­
tribution is in the region of the first molars and odontitis. Roentgenographic findings include “ an
incisors teeth, the least destruction in the cus­ arc-shapedloss of alveolar bone extending from the
pid-premolar area. Three types of bone loss lo­ distal surface of the second premolar to the mesial
calization have been defined. (1) First molar surface of the second molar”. The alveolar bone in
and/or incisors; (2) first molars, incisors and these patients develops normally with tooth erup­
some additional teeth (total of less than 14 teeth) ; tion and only it undergoes resorptive changes.
and (3) generalized involvement. There is an
increase in the number of affected teeth with Microbiology
advancing age. Frequently bilaterally symmetri­ Lesion of periodontosis is characterized by a rather
cal patterns of bone losses occur. distinct microbial population of rod-shaped organ­
isms located predominantly at the base of the de­
Advanced bone loss in the primary dentition does fect. Gram-negative anaerobe, Actinobacillus
exist, and has been reported but without the dis­ actinomycetemcomitans appears to be primarily
tinctive localization. associated with the disease. The presence of a re­
■ Premature and excessive mobility of the maxil­ cently discovered genus termed Capnocytophagia,
lary and mandibular primary incisors and first has been associated with the progression of peri­
primary molars is seen. odontosis lesions.
■ Regional lymphadenopathy as a clinical finding
in about the third of the JP patients examined.. Immunology
■ Clinically there is a small amount of plaque, Defective production or function of circulating
forming a thin film on the tooth and rarely min­ neutrophils is often associated with an increased
eralizing to become calculus. The most com­ frequency and severity of bacterial infections.
mon initial symptoms are the mobility and mi­ J

gration of the first molars and the incisors. Differential diagnosis

■ Classically, one sees a distolabial migration of Conditions that could contribute to alveolar bone
the maxillary incisors, with diastema formation. loss in the primary dentition and premature loss of
Along with anterior tooth migration, an appar­ primary teeth: Hypophosphatasia, Papillon Lefevre
ent increase in the size of the clinical crown, syndrome, Histiocytosis X, neutropenia and cyclic
accumulation of plaque and calculus, and clini­ neutropenia.
cal inflammation also appear.
■ The disease progresses rapidly. The rate ofbone Treatment
loss is 3-4 times more than in typical periodon­ ■ A variety of treatment approaches to JP have been
titis. In affected persons the bone loss progresses reported, including induction of tooth eruption
until teeth are treated, extracted or exfoliated. by occlusal adjustment or passive eruption, root
■ As the disease progresses, other symptoms may resection. Subgingival irrigation with iodine and
arise. Denuded root surfaces become sensitive hydrogen peroxide has also been proposed
to thermal and tactile stimuli. Deep, dull, radi­ ■ Augmentation of scaling and root planing with< yyy.|
ating pain may occur with mastication and is surgical therapy has also been showntobcel-
probably due to irritation of the supporting struc­ fective in controlling the progression gBJP le-yg||gy
tures by mobile teeth and impacted food. Peri­ sions. either with or without.a^tol^^fO^S^^fOBfr
odontal abscesses may form at this stage.
 <?EE> | TEXTBOOK OF PEDODONTICS

cline. These different regimes have also been rate genetically transmitted trait, suggesting a
shown to markedly decrease, or eliminate, A. multigenic etiology for Papillon Lefevre syndrome.
actinomycetemcomitans from periodontal le­
sions. Clinical features
« The rationale for antibiotic coverage is based The signs and symptoms of the Papillon-Lefevre
upon the concept that JP is an infection of bac­ syndrome include the following triad: a) hyperk­
terial etiology and its use has appeared to en­ eratosis palmer-plantar; b) precocious periodontal
hance osseous repair in JP patients. Tetracycline destruction with loss or both dentitions, and c) ec­
is considered the drug of choice, since it has been topic intracranial calcifications (not a constant find­
shown to be effective against A.actinomy­ ing).
cetemcomitans and achieves a gingival fluid
level 2 to 10 times greater than the blood serum. a. Skin lesions: The skin lesions, usually start be­
tween the first and fourth year after birth and
Papillon Lefevre syndrome consist principally of well demarcated, hyperk-
In 1924 Papillon and Lefevre first described a syn­ eratotic lesions of the palms and soles bilater­
drome characterized by hyperkeratosis of the palms ally. The hyperkeratosis is usually progressive
and soles combined with a precocious periodontal and becomes dry and scaly, often with deep, pain­
destruction and shedding of the deciduous and per­ ful fissures in winter.
manent dentitions.
b. Dental signs and symptoms: The deciduous
Etiology dentition is normal in development and age of
The etiology of this syndrome is not clearly under­ eruption. But many cases have been reported
stood. Papillon and Lefevre thought it to be an en- where the deciduous dentition is affected. As
docrinopathy and suggested the possibility of vita­ soon as the last deciduous toQth has erupted, sev­
min A deficiency. They suggested that gingival epi­ eral features are seen: swollen gingiva, migra­
thelium may be abnormal as a result of defective tion and mobility of teeth, periodontal pockets,
local vitamin A metabolism. fetor-ex-oris and exfoliation in a rallier painless
sequence. By 3 J/2 to 4 l/2 years all of the decidu­
Recently, two new aspects of PLS have been dis­ ous teeth are lost. With loss of the deciduous
covered teeth, inflammation regresses and the gingiva
1. Deep subgingival fiord associated with PLS peri­ resume a normal appearance. Some of the fea­
odontitis is composed of great numbers of mo­ tures resemble juvenile periodontitis.
tile, Gram- negative anaerobic rods, including
The eruption of the permanent teeth is enhanced
Bacteroides gingivalis and Capnocytophaga, as
and may even be completed by 5 years of age
well as of a large number of spirochetes,
(except the third molars). The disease progresses
2. Some PLS patients have exhibited either a cel­
then recycles, and by ages 13 to 14 usually all of
lular immune defect with a decreased PHA
the erupted permanent teeth are exfoliated. In
stimulation of lymphocytes or a deficient chemo­
most cases, the third molars undergo the same
taxis and phagocytic function of neutrophilic
changes. The tooth extraction sites heal unevent­
granulocytes.
fully. Extracted teeth generally show a few hard
and soft deposits.
It is now generally accepted that the condition is
due to the homozygosity of autosomal recessive c. Ectopic intracranial calcifications: of the ten­
genes. Dermatological lesions similar to those seen torium, falx cerebri and choroid plexus often
in Papillon Lefevre syndrome are found as a sepa­ form the third sign.
 SECTION 13 : SOFT TISSUE ORAL LESIONS IN CHILDREN | ÎfrÀi

■ A marked predisposition for infections has Clinical features

been noted and also a low blood hemoglobin The disease occurs in severe and mild forms, and at
has also been reported. least three types are recognized. The infantile type
■ Intraoral radiographs show a severe horizon­ first appears between birth and 6 months of age.
tal alveolar bone loss almost immediately af­ The childhood type appears between the ages of 6
ter the last deciduous tooth erupts. The al­ and 14 months, and the adult type manifests during
veolar process and basal bone resorb beyond childhood and radiographically osseous radiolucen-
the apices of the roots. Unerupted teeth tend cies are seen.
to assume abnormal positions. Incomplete
root formation has been noted The disease is characterized by abnormal minerali­
zation of bone and dental tissues and is usually
Differential diagnosis manifested by premature exfoliation of the primary
Clinically similar lesions involving both tlie decidu­ teeth. Approximately 75% of patients with this dis­
ous and permanent dentitions may be seen in im­ order experience premature exfoliation of the pri­
mune deficiency states such as acatalasia, Chédiak mary teeth, which is frequently the first clinical
Higashi syndrome and neutropenia. symptom of the disease. In almost all cases of
hypophosphatasia the deciduous teeth are affected.
Treatment Only the deciduous incisors and sometimes the ca­
Before the advent of retinoids, antibiotic therapy nines are affected and the permanent teeth are usu­
was advised, but not much success was achieved. ally normal.
Vitamin A metabolites (Retinoids) are involved in
the regulation of growth and differentiation of the Diagnosis
epithelial cells. They are known to have a profound Reference ranges for alkaline phosphatase are also
effect on the keratinization by decreasing tire total age-related, children and adolescents having higher
keratin content ofthe kératinocytes. Thus, they have circulating alkaline phosphatase activity than adults.
been used and found to have a positive effect Consequently, alkaline phosphate levels can only
be interpreted against the appropriate reference
Prognosis range for the method used for measurement and the
Despite some evidence of an increased susceptibil­ age of the patient
ity to general infection in the Papillon Lefevre syn­
drome, no metabolic or immunological deficiency A diagnosis of hypophosphatasia can usually be
has been detected and life expectancy is normal. made with confidence in subjects with a consistent
clinical history and physical findings in whom se^
Hypophosphatasia
rum ALP activity is low.
Hypophosphatasia is a rather rare genetic disease
manifested by bone pain with spontaneous fractures,
Treatment
rickets-like bone lesions during childhood which are
A wide variety of treatments for hypophosphatasia
resistant to treatment with vitamin D, and prema­
have been attempted but without a proven success.
ture loss of the deciduous teeth.
Oral phosphate supplements have been attempted
Etiology with a limited success and intravenous infusions of
Hypophosphatasia is a familial disorder of the in­ plasma from patients with Paget’s disease and
born error of metabolism. There is a strong evi­ hyperphosphatemia was also of no clinical benefit.
dence that most cases of the disease result from an
autosomal recessive trait, although in other instances
dominant inheritance is indicated.
 I TEXTBOOK OF PEDODONTICS

Histiocytosis X Clinical features

The langerhans cell histiocytosis are associated with These patients have periodic symptoms including
a tumor-like proliferation but there is insufficient skin lesions and ear infections. Mucous membrane
evidence to consider them as truly neoplastic.There ulcerations, severe stomatitis and a profound neu­
is a general consensus to believe that they are reac­ tropenia are reported to develop over recurrent pe­
tive disorders in which the proliferation of Langer­ riods of 14 to 24 days (average 21). These neutro­
hans cells results from disturbances in penic conditions are usually accompanied by or
iminunoregulation. slightly preceded by a monocytosis. Normal cycling
patterns of approximately 21 days may not be seen,
In the past these diseases were referred to as histio­ but in some cyclic neutropenic patients, cycles may
have become progressively shorter with periods of
cytosis X and were subdivided into three variants:
neutrophil elevation.
Eosinophilic granuloma, Hand-Schuller-Christian
disease, and Letterer-Siwe disease. But many in­
The attached, papillary and marginal gingiva are
vestigations have confirmed that they are separate
enlarged, edematous and erythematous and bleed
entities.
easily on a gentle provocation. There is an extreme
inflammation with proliferation of the marginal
The etiology and pathogenesis of the diseases re­ gingiva accompanied by a cleft formation, recession;
main elusive. The proliferating cell in all the three antibiotics are ineffective and bone resorption
variants is Langerhans cell ofmarrow origin, which progresses rapidly to the apex of the teeth. During
is normally found in the epidermis. These cells stem the neutropenic stage, periodontal disease and de­
form a proliferative reticuloendothelial disturbance struction occurs and during the non-neutropenic
rather than an enzymatic deficiency involving lipid stage oral health returns. Overall, the destruction
catabolism necessitating their separation from true exceeds repair and alveolar bonb loss contributes to
lipid storage diseases. an early exfoliation of teeth.

Histiocytosis X is not considered to have a genetic Diagnosis

tackground. The oral manifestations of Histiocyto­ The absence of neutropenia on an hematological ex­
sis X are ulcerative necrotizing lesions of the amination cannot completely exclude the possibil­
gingiva, root exposure, increased mobility of teeth, ity of it being present since the analysis may have
halitosis, osteolytic areas of alveolar bone in the ra­ been completed during a non-neutropenic cycle of
diographic examination giving the appearance of the disease. The absence of any history of oral in­
“floating teeth”. flammation or periodic states of acute
symptomology, however, tends to exclude cyclic
Cyclic neutropenia neutropenia.
Several forms of neutropenia associated with peri­
Prognosis
odontal disease have been described. The cyclic va­
Prognosis, both medically and dentally is not en­
riety appears to be the type most frequently encoun­
couraging. The patients are at a risk of an over­
tered in the dental literature. The disappearance of
whelming and fatal bacterial infection during the
neutrophils occurs periodically, approximately every
severe neutropenia cycles.
3 weeks. After 5 to 8 days, the neutrophils begin to
reappear. It is inherited as an autosomal recessive
disorder.
 SECTION 13 : SOFT TISSUE ORAL LESIONS IN CHILDREN J GE}

Prepubertal periodontitis (Fig. 13.8) A. Extremely acute inflammation is present, with

proliferation of the gingiva.
B. There is a veiy rapid destruction of the alveolar
bone and gingiva.
C. Profound functional defects of peripheral blood
neutrophils and monocytes are seen; neutrophils
are absent from the gingival tissue.
D. Peripheral blood white-cell count is markedly
elevated.
E. Otitis media and skin and upper respiratory in­
fections are frequent findings.
F. Periodontitis may be refractory to antibiotic
therapy.
Fig. 13.8 Pre pubertal periodontitis seen with G. All primary teeth are affected; the permanent
maxillary posterior teeth dentition may or may not be affected.

Etiology Localized form:

Existing evidence indicates that prepubertal peri­ A. Only some teeth are affected; pattern of involve­
odontitis tends to occur in families, and that it is ment yet not determined.
considerably more common in females than in B. Gingival tissues may exhibit little or no inflam­
males. These observations suggest that the defect mation.
is based on an X-linked pattern of inheritance. The C. Destruction is not as rapid as in the generalized
defect might have been acquired and might have form.
resulted from a inhibition of chemotaxis derived D. Functional defects are present in either
from the periodontal bacteria. neutrophils or monocytes, but not both.
E. Recurrent otitis media is not a frequent finding
The mechanism underlying the chemotaxi defects and usually there is no history of frequent infec­
in children with localized periodontitis remains tions.
obscure. F. The disease is amenable to treatment by curet­
tage and antibiotic therapy.
Clinical features
The pattern of the disease is variable. The exact Diagnosis
time of onset has not been established. The evi­ Analysis of the pocket flora, assessment of blood
dence indicates that the disease being around the leukocyte chemotaxis and serum antibodies, com­
age of 4 years or before, but it may not be diagnosed bined with measurement of the senim and urinary
until 7 to 9 years. biochemical markers for hypophosphatasia may pro­
vide a definitive diagnosis of the condition, as well
One trait that children with localized and general­ as clarify the relationship between the two diseases.
ized prepubertal periodontitis appear to hold in com­
mon is defective peripheral blood leukocyte func­ Treatment
tion, defects in neutrophil or monocyte function, or Curettage, antibiotic therapy, and improved oral
in both cell ty pes, as determined by in vitro and in hygiene arrest the progression of localized prepu­
vivo assessment of chemotaxis or phagocytosis. Thus
bertal periodontitis.
m generalized form -
 | TEXTBOOK OF PEDODONTICS

Palmer et al (1996) concluded that tetracycline is an On the basis of cases described to date, it appears
important adjunct for a successful treatment of the that prepubertal periodontitis may be followed ei­
early onset periodontitis, particularly for the non- ther by a completely normal permanent dentition,
surgical management cases. or by periodontitis of the permanent first molars and
incisors, or by a generalized severe periodontitis of
The periodontal status has been reported to improve the permanent teeth.
remarkably after transfusion with granulocytes from Self-Assessment
normal donors.
1. What type of oral mucosa is the gingiva?
2. List out the key differences between the gingiva
Success in resolving the inflammation by combin­
of the adult and the child.
ing extraction of the hopeless molars with an ag­
3. What are the types of gingival enlargement seen?
gressive plaque control, can be obtained.
4. What are the characteristics features of Juvenile
periodontitis?
Prognosis
5. Which drugs cause a gingival enlargement?
The final outcome of the generalized prepubertal
6. What is hypophosphatasia?
periodontitis is not known. The presence of prepu­ 7. What is cyclic neutropenia?
bertal periodontitis may or may not be a harbinger 8. When does a stippling start to appear? What is
of periodontitis of the permanent dentition. the histological picture causing it?
 13.2 Commonly seen other Oral Lesions

Rao PLNG, MohanM

Introduction affected. Tumours may arise from other tissue

components e.g. lipoma, papilloma, lymphangi-
The oral cavity has the propensity to develop a va­ oma etc. Excision biopsy is advocated.
riety of lesions. In some cases these lesions may be
exclusive to the oral cavity, whereas in others they Malignant: Usually a squamous cell carcinoma;
may present as the initial manifestation of a more very rare in children, seen in older individuals
complex systemic problem. The dental professional especially those who follow outdoor occupation.
may be the first to encounter these lesions. Hence, The lower lip is involved in 90% of the cases.
it is mandatory to possess a thorough knowledge of
these diseases in order to diagnose them at the ear­ Malignant lip tumours can arise from benign tu­
liest, and render the necessary treatment. They mours of the lip (e g. carcinoma from salivary
should also be in a position to make an appropriate gland tumours, liposarcoma, etc.) - mucocele.
referral to the concerned consultants.
Treatment Surgical excision+chemotherapy +
1. THE LIP radiotherapy.

a. Submucous Cyst c. Mucocele (Fig. 13.9)

Caused by an obstruction to the duct of mucous Mucocele or mucous retention cyst is a lesion of
gland. Painless swelling, increases in size gradu­ traumatic origin. It arises as a result of obstruc­
ally. Usually the lower lip is commonly affected. tion of the minor salivary gland ducts as a result
Covered by pink mucous membrane. May be blu­ of trauma. In children, it is usually associated
ish or gray in colour due to the presence of mu­ with lip biting. It commonly occurs on the lower
cous. lip. It may be superficial or deep. The superfi­
cial lesion appears as an elevated well, circum­
Treatment: Complete excision either under lo­ scribed vesicle with a bluish hue. The cystic con­
cal anesthesia (for older children) or general tents consist of a thick mucinous material.
anesthesia (for infants or large cysts.) is the treat­ Treatment involves an excision of the cyst
ment of choice. Marsupialization is an alterna­
tive treatment. d. Haemangioma (Fig. 13.10)
Developmental malformation of blood vessels
b. Neoplasms of the lip where there is a proliferation of the sametissues
Benign: Commonly arises from the salivary e. hamartoma. Not a true tumpur?i^^^^gj
i.
glands. Slow growing firm tumour is usually a capillary, venous (cavernous) or arterial \ptep-
plemorphic adenoma. The upper lip is commonly form) haemangioma. Most of tlie haemangiomas
 <*Ei> I TEXTBOOK-OF PEDODONTICS

resolve spontaneously with age. If they do not 3. TONGUE

disappear, only then they need to be treated. It
occurs most commonly on the lips, tongue, buccal a. Lingual thyroid
mucosa and palate. Thyroid swelling present at the base of the
tongue. May be the only thyroid tissue present.
Capillary: Salmon patch, port wine stain, strawberry Can cause dysphagia, impairment of speech, res­
angioma. Salmon patch and strawberry angioma piratory obstruction or hemorrhage.
disappears with age, whereas port-wine stain is per­
manent. Treatment may be by giving thyroxin, which re­
duces the size of the gland. Radio-iodine abla­
tion can be done. Surgical excision is another
Venous: Multiple venous channels present, may be
mode of treatment.
associated with other tissues (e.g. naevolipoma).
Treatment includes, injection of sclerosing agents,
b. Fissured tongue
use of lasers or surgical excision.
Characterized by an increase in number, depth
and width of fissures seen with an increased fre­
Arterial: Type of congenital arteriovenous fistula,
quency in the mentally retarded population like
may pulsate and is called a cirsoid aneurysm. Treat­ Down’s syndrome, associated with other syn­
ment is ligation of feeding vessels with or without drome such as Melkersons Rosenthal Syndrome.
excision. Therapeutic embolization can also be con­ Most likely to be associate with chronic trauma
sidered. and vitamin deficiencies.

2. FLOOR OF THE MOUTH c. Microglossia

It is a rare anomaly, whiqh is caused due to a
a. Ranula (Fig. 13.11) small or rudimentary tongue. It is usually seen
Extravasation cysts of damaged sublingual gland. in hypoglossia - hypodactylia syndrome.
Bluish swelling seen in the floor of the mouth.
It may extend into the neck behind the posterior d. Macroglossia
border of mylohyoid; so-called plunging ranula . Is more common than microglossia. It is most of
On examination the swelling is cystic and bril­ the time associated with cretinism Down’s syn­
liantly transilluminant. It may undergo infection drome (relative macroglossia) and the tumour
or burst open. Treatment is a complete excision. of the tongue.
Partial excision with marsupialization is advo­
cated if the cyst is very large. e. Haemangioma
Developmental malformation of blood vessels i.e.
hamartoma is not a true tumour. It may be cap­
b. Sublingual dermoid
illary venous (cavernous) or arterial (plexiform)
It is formed due to inclusion of the ectoderm
haemangioma. Most of the haemangiomas re­
during fusion in the midline, in the floor of the
solve spontaneously with age. If they do not dis­
mouth, and is a type of congenital sequestration
appear, only then they need to be treated.
dermoid. May be a midline or rarely a lateral in
location. Presents as a painless swelling under
Capillary7: Salmon patch, port wine stain, strawberry7
the tongue which is usually firm or cystic. It is
angioma. Salmon patch and strawberry angioma
not transilluminant. Treatment is excision. disappear with age, whereas port-wine stain is per­
manent.
 SECTION 13 : SOFT TISSUE ORAL LESIONS IN CHILDREN | @39

Fig. 13.9 Mucocele seen on the lower lip Fig. 13.10 Haemangioma

Fig. 13.11 Ranula on the floor of the mouth

Fig. 13.12 Lymphangioma on the dorsal Fig. 13.13 Tongue Tie - Ankylo-glossia
surface of the tongue
 I TEXTBOOK OF PEDODONTICS

Venous: Multiple venous channels present, may be i. Rega fede disease

associated with other tissues (e.g. naevolipoma). Early eruption of teeth (natal or neonatal teeth)
Treatment includes injection of sclerosing agents, has been reported to cause ulceration on the ven­
lise of lasers or surgical excision. tral surface of the tongue, caused by the tooth’s
sharp edge. These can present with mild to se­
Arterial^ Type of congenital arteriovenous fistula, vere ulcerations and can sometimes seriously
may pulsate and is called a cirsoid aneurysm. Treat­ interfere with the infant’s feeding and suckling,
ment is ligation of feeding vessels with or without which may in turn affect nutrition.
excision. Therapeutic embolization can also be
considered. Over the years, this lesion has paraded under a
variety of names.
£ Lymphangioma (Fig. 13.12) ■ Caradarelli [1857] has first described this ul­
Localized congenital anomaly of lymphatic ves­ ceration in the sublingual area, leading to ‘exi-
sels. May be capillary or cavernous lymphangi­ tus lethalis’.
oma. ■ The histological appearance was described by
Riga[1881] and Fede(1890] and has hence
Capillary lymphangioma: Small lesions on the been commonly termed as the Riga-Fede dis­
skin, usually vesicles. ease.
■ Several other proposed names are:
Cavernous lymphangioma: Masses of lymphatic - Riga’s disease
cysts sometimes in neck or axilla where it is - Sublingual growth in infants
called a cystic hygroma. Can affect the lips or - Sublingual ulcer
tongue causing macrocheilia or macroglossia. - Sublingual granuloma
Excision either total or subtotal is the treatment - Reparative lesion of the tongue.
of choice. Malignancy is extremely rare. ■ Elzaz[1983] has proposed the name ‘trau­
matic ulcerative granuloma with stromal eosi­
g. Geographic tongue: It is also called as benign nophilia’ [TUGSE]. According to him, the ul­
migratory glossitis with an unknown etiology. It ceration is followed by ingress of microorgan­
consists of multiple desquamated areas of isms, toxins or foreign protein into the con­
filliform papillae of the tongue. These lesions of nective tissue. These substances, in a predis­
desquamation may be there for a short duration posed individual would cause an exaggerated
and then heal. They appear on another location mast cell -eosinophil reaction.
and hence called migratory lesions.
Treatment plan
Tongue tie (Fig. 13.13) A variety of treatment modalities have been tried
Frenulum linguae is shortened and thickened. out over the ages.
On attempting to protrude the tongue there is an a) Early treatment was directed towards excision
eversion of the lateral margins with a heaping- of the lesion. Often diagnosis constituted a
up in the^middle. The tongue cannot be pro­ problem and the disappearance of the lesion
truded completely. was associated with weaning.
b) Once the etiology of the lesion was deter­
It may be asymptomatic, but can cause difficulty mined, treatment has been targeted towards
in speaking. Treatment is division^ close to the removal of the cause rather than the lesion.
tongue. The raw area may be closed with a fine Treatment also depends on the prognosis of
catgut. the tooth.
 SECTION 13 : SOFT TISSUE ORAL LESIONS IN CHILDREN |

- If the tooth is of the ‘ mature ' variety where 4. BUCCAL MUCOSA

the root is sufficient to retain the tooth in

the oral cavity, efforts should be made to a. Fordyces granules
save it. This can be thieved by: It is not a disease but rather a developmental
1. Smootheuing the incisal edge disturbance characterized by inclusions of seba­
2. Placement of a smooth and rounded ceous glands in the oral cavity more commonly
composite. on the buccal mucosa opposite the first molar.
A small lesion can generally heal with these They are not seen in infants but appear in chil­
measures. dren after the age of 3 years andincrease during .
c) In cases of large lesions, these may not suf­ puberty.
fice and wound healing is delayed. Also ‘im­
mature teeth’ with little or no root pose the b. Frictional keratosis
danger of being aspirated. In such cases, ex­ Caused by a prolonged mild irritation by a sharp
traction of the offending tooth should be car­ tooth, removable appliances, cheek biting. The
lesion initially appears pale and translucent and
ried out. The necessity of vitamin K supple­
later progresses on to become dense, white and
mentation in an infant should be evaluated.
rough. \
Treatment is tb remove the irritating factor.
j. Rhabdomyosarcoma (Fig. 13.14)
Malignancy arising from embryonic mesen­
c. Aphthous ulcers (Fig. 13.16)
chyme which forms skeletal muscle. May present
May be minor, major or herpetiform aphthous
as an asymptomatic mass or with general fea­
ulcers.
tures like fever, anorexia, weight loss etc. Symp­
Minor ulcers are less than 0.5cm with a yellow
toms, signs depend on the site.
base and a red margin. They can appear in crops
and are painful They heal within 10-14 days.
Diagnosis is by clinical exam, C.T. scan. Some­
Major aphthous ulcers are larger, deeper and take
times M.R.I. is useful. Open biopsy will be
longer to heal. They sometimes heal with scar­
diagnostic, if done. Types of rhabdomyosarcoma
ring.
are embryonal, alveolar pleomorphic, undiffer­ Herpetiform ulcers are of 1 -2mm diameter, mul­
entiated and undetermined. tiple. Inspite of their name, they are not caused
by herpes simplex virus.
Treatment is primarily a wide surgical excision
followed by chemotherapy and if required radio­
therapy. Orbital and superficial head and neck
tumours have a better prognosis.
Hamartoma cheek
k. Papilloma (Fig. 13.15a, b) im.H
May occur on the floor of the mouth, tongue and consisting of a tumour like overgrowth inwhich
cheek. May be multiple or single. They have a
cauliflower surface. They may be sessile or hazardly with an excess of one or more compo­
pedunculaed. They are mostly benign. Compli­ nents. It literally means ‘fault’ or ‘misfire’.
cations include ulceration and rarely a malig­ Hamartomas are usually benign, but with age
nant transformation. may turn malignant. They may bevascular
Treatment is excision.
 TEXTBOOK OF PEDODONTICS

Fig. 13.14 Rhabdomyosarcoma Fig. 13.15a Papillary growth on the lateral

surface of the tongue

Fig. 13.15b Papillary growth on the cheek

Fig. 13.16 Apthous ulcer Fig. 13.17 Herpetic lesion involving the corner
involving cheek mucosa of the mouth
 SECTION 13 ; SOFT. TISSUE ORAL LESIONS IN CHILDREN |

Treatment is complete excision. This may be Clinical features

difficult in some cases, as they do not have a ■ Ulcers affecting the posterior mouth
well formed capsule. ■ Fever, malaise, irritability, anorexia, vomit­
ing
e. Naevus
Nevi are plaques or dome shaped nodules Oc­ Incidence -
curring in the oral cavity. They usually appear • Uncommon outbreaks are seen among young
in childhood and attain a certain size and per­ children
sist through adolescence and adulthood. They
are commonly st i in the palate, facial mucosa, Management
lips or tongue. The basic types of the nevi are: • Clinical diagnosis
• Junction nevi ■ Serology (theoretically) is confirmatory
Compound nevi ■ Symptomatic treatment (see herpes simplex)
• Intramucosal nevi
• Blue nevi c. Chickenpox (varicella)
• Spindle cell nevi ■ Herpes varicella - zoster (VZV)

5. VIRAL LESIONS (Fig. 13.17) Clinicalfeatures

■ Ulcers: Indistinguished from HSV, but no as­
a. Herpetic stomatitis sociated gingivitis
■ Herpes simplex virus (HSV), usually type 1 • Rash: mainly face and trunk: papules then
vesicles, pustules and scabs, in crops
Clinicalfeatures: ■ Cervical lymphadenitis
9 Incubation period 4 to 7 days ■ Fever
« Primary infection: « Malaise, irritability, anorexia
Multiple mouth ulcers
Diffuse gingivitis Incidence
Cervical lymphadenitis • Common
Fever
Malaise, irritability and anorexia Management
■ Diagnosis is clinical
Incidence: ■ Rising antibody titer is confirmatory
« Common in poor areas, and children ■ Symptomatic care: Immunoglobulin or
acyclovir in immunocompromised individu­
Management als.
• Clinical diagnosis usually
« Viral culture, immunodetection or electron d. Herpes Zoster (‘shingles’)
microscopy occasionally Varicella - zoster virus (VZV), latent in the sen­
« A rising titer of antibodies is confirmatory ary ganglion. Reactivated by, for example, im­
■ Soft diet and adequate fluid intake munosuppression
■ Antipyretics / analgesics (paracetamol elixir)
• Local antiseptics (chlorhexidine) Clinicalfeatures
a Unilateral pain, rash and oral vesicles,thçn
b. Herpangina ulcets
• Coxsackie viruses or ECHO viruses
 I TEXTBOOK OF PEDODONTICS

Incidence Diagnosis and Management

■ Mainly affects elderly or immuno-compro- The diagnosis is usually clinical, but a Gram
mised smear (for hyphae) or oral rinse may help. Dif-
ferentiation from lichen planus is the main prob­
Management lem, although very occasionally Koplik or
■ Clinical diagnosis Fordyce’s spots confuse the clinical picture. It is
■ Analgesics important to determine and treat any predispos­
■ Acyclovir ing cause.

e. Koplik’s spots (Rubeola) Antifungals such as nystatin oral suspension or

It is one of the initial oral manifestations of the pastilles, amphotericin lozenges, miconazole gel
rubeola viral infection (measles), which is an or tables or fluconazole tables are indicated.
acute contagious disease seen in children. It ap­ Chlorhexidine also has some antifungal activ­
pears as a bluish white irregular lesion sur­ ity.
rounded by a red margin, usually present on the
buccal mucosa which disappears within four to 7. BACTERIAL LESIONS (Fig. 13.18)
five days. The systemic disease presents with I

malaise, fever, coughing, etc.

6. FUNGAL LESIONS

a. Thrush (Acute Pseudomembranous Candidosis)

The term Thrush’ is used for the white fleck ap­
pearance of acute candidosis.

Aetiology
Thrush is rare in healthy patients. It may be seen
in healthy neonates, however, where the oral
microflora is disturbed by antibiotics,
corticosteroids or xerostomia. Oropharyngeal
thrush occasionally complicates the use of corti­
costeroid inhalers. Immune defects, especially
HIV infection, immunosuppressive treatment,
Fig. 13.18 Tuberculous lesion.
leukaemias and lymphomas, cancer and diabe­
tes and lymphomas, cancer and diabetes predis­
a. Strawberry Tongue (Scarlet fever)
pose to thrush.
This is the classic oral finding of scarlet fever,
which is a white coated tongue with red,
Clinical Features
hyperemic, edematous, fungiform papillae. Scar­
Thrush presents as white or creamy plaques that
let fever is an acute infection caused by group A
can be wiped off to leave a red base. Lesions
beta hemolytic streptococci. It manifests with fe­
occur mostly in the upper buccal vestibule
ver, headache, tonsillitis and rashes. Other oral
posteriorly and the soft palate.
signs include congested palatal mucosa.
 SECTION 13 : SOFT TISSUE ORAL LESIONS IN CHILDREN |

b. Tubercular lesion
The tubercular sinus usually arises from tuber­
culous lymphadenitis. Common in the cervical
region. Can occur due to tubercular osteomyeli­
tis also. Stages of development include lymphad­
enitis, periadenitis, cold abscess, collar stud ab­
scess, sinus formatibu. The patient who has en­
larged lymph nodes presents with a discharging
sinus. The discharge contains caseating material.

Treatment is excision’of the sinus and lymph

nodes along with a complete antitubercular drug
therapy. Fig. 13.19b Mulberry molars.

Tubercular lesions of the oral cavity are rela­ maxilla, saddle nose and mulberry molars (Fig.
tively uncommon. The lesion may occur at any 13.19a, b). The pathognomonic feature of the
site on the oral mucous membrane, however the disease is the Hutchinson’s triad, which includes
tongue, palate and lips are commonly affected. hypoplasia of die incisor and molar teeth, eighth
The lesion is an irregular ulcer and is very pain­ nerve deafness and interstitial keratitis.
ful.
d. Noma
c. Syphilitic lesion (congenital) It is a rapidly spreading gangrene of the oral
Syphilis is a disease caused by Treponema tissues chiefly seen in children. It occurs more
pallidum, a motile spirochete. It may be acquired commonly in the undernourished and debilitated
or congenital. children. It begins as a gingival ulcer spreading
onto the surroimding tissues of the jaws, lips,
Congenital syphilis is transmitted to the infant and cheeks. The skin becomes inflamed,
from the infected mother. They manifest a great odematous and necrotic, leading to sloughing of
variety of lesions, including frontal bossing, short large masses of the tissue.

Treatment involves managing the undernour­

ished condition and administration of antibiot­
ics.

e. Pyogenic granuloma
(Refer to periodontal lesions)

INTRA AND EXTRA ORAL SWELLING

Ludwigs angina
Bilateral involvement of the sublingual, submen-
tal and submandibular region. It is usual||^^j|| ||
Fig. 13.19a Congenital syphillis. to streptococcal infection. Features are due to
Notched incisor. both cervical and intrabuccal signs.
' ” .• ... .*■
 I TEXTBOOK OF PEDODONTICS

extends below the deep fascia of the neck and 9. PAROTID LESIONS
can cause glottic edema. This can cause death.
a. Sialadenitis:
Treatment is high doses of antibiotics. If it per­ May be acute or chronic.
sists an incision should be made in the sub­ Acute sialadenits may be viral or bacterial,
mandibular region under local anesthesia and mainly affects the parotid glands. Treatment is
deep fascia opened and pus drained. usually antipyretics and analgesics with antibi­
otics if bacterial infection is present. It usually
k Epulis (Fig. 13.20) resolves in 2-3 weeks.
It is a pink, pedunculated, submucosal mass. Rarely in the parotid gland an abscess may oc­
Usually arises from the anterior maxillary al­ cur which requires drainage.
veolar ridge. • It can present with feeding diffi­
culties. Breathing problems are rare. More com­ b. Chronic sialadenitis
mon in females. Most common cause of the inflammation of the
Treatment is local excision. salivary glands in children. Recurrent episodes
of infection can result in acinar destruction and
sialectasis. It maybe obstructive or non-obstruc-
tive. Obstruction may be due to stenosis, stric­
ture or stones.

Initial treatment is conservative with local heat,

analgesics and antibiotics. In obstructive causes
marsupialization of the duct may be required.
In refractory cases, excision of the gland is re­
quired.

c. Parotid fistula
Usually, due to injury fistula from the divided
gland substance heal by themselves, duct fistu­
las need to be explored. Pre-op sialogram is im­
portant. Repair of the of cut ends without tension
should be done. If it is not possible, a local cheek
Fig. 13.20 Epulis. mucosal flap or venous grafts can be used to
c. Cellulitis reconstruct the duct.
It is the diffused inflammation of the soft tissue
which tends to spread through tissue spaces and d. Mumps
facial planes. The spread of infection is due to Mumps is an acute contagious viral infection
the breakdown of hyaluronic acid, intercellular which is characterized by swelling of the parotid
cementing substance and fibrin. Cellulitis of the glands. Symptoms include a firm swelling of the
face and neck commonly occurs due to dental salivary glands accompanied by pain on chew­
infections. Features include a painful, firm swell­ ing food. General symptoms include fever,/head-
ing of the soft tissues. Lymphadenitis is usually ache and earache. Rarely, the submandibular and
present. Treatment involves administration of the sub maxillary glands may also be involved.
antibiotics and removal of the cause of infec­
tion.
 SECTION 13 : SOFT TISSUE ORAL LESIONS IN CHILDREN |

10. JAW CYSTS Self-Assessment

Refer to section 10
1. What is the etiology of ranula? Where is it usu­
11. JAW LESIONS ally found?
2. What is sialadenitis?
a. Cherubism 3. In which condition would you fimdKoplik’s
This is a disease affecting the jaws and it mani­ spots?
fests in early childhood, at three or four years. 4. What are the spaces involved in Ludwigs An­
The child has a chubby appearance due to the gina?
symmetric swelling of the jaws. There is a pre­ 5. Which virus causes Herpes Zoster?
mature shedding of the deciduous teeth along 6. What is ‘Thrush’?
with missing permanent teeth or delayed erup­
tion of the ones present. This bone disease may Further Suggested Reading For Section -13
regress as the child approaches puberty.
1. Albander JM, Juvenile periodontitis : Pattern of
b. Osteomyelitis (Refer to section 10) progression and relationship to clinical periodon­
tal parameters, Oral Epi. 21(4), 185-9,1993.
c. Tumors of the jaws (Fig. 13.21) 2. Andlin SA Bodin L: Dimensional alteration of
the gingivae related to changes of facial / lin­
gual tooth position in permanent anterior teeth
of children. A 2 yr longitudinal study. J. Clin -
Periodontal. 20(3), 219-24,1993.
3. Bimstein E: Periodontal health and disease in
children and adolescents. Pediar - Clin - North -
Am - 38(5), 1183-207, 1991.
4. Bimsten E, Eidelman E: Longitudinal changes
in width of attached gingivae in children. Ped,
dent (10), 22-24,1988.
5. Clinical Pediatric dentistry protocols: Gingival
and periodontal diseases: 3 edition. 38-44,
1995.
6. Daley T, Wysocki G. New developments in se¿
lected cysts of the jaws. J of Canadian dental
Association. 63(7)^26-531,1997
7. Jarrett M. Herpes simplex infection. Arch
Fig. 13.21 Mandibular tumour in a 7 year Dermatol 119: 99-103,1983
old child. 8. Logen RB et al: Periodontal disease in healthy
children 2 clinical reports, Ped. Dent 6,41-45,
Tumors of the jaws are of great clinical signifi­
1984.
cance. They may often be the result of metasta­
9. Membelli A et al: Microbial changes associated
sis. From primary sites located elsewhere in the
with the development of puberty7 gingivitis J peri­
body. The mandible is more commonly affected
odontal Pes. 25(6). 331-8, 1990.
than the maxilla. They may occur primarily
within the jaws itself.
 tfîÏÏTîl | TEXTBOOK OF PEDODONTICS

10. Miller CS, Redding SW: Diagnosis and'man­ and Other Causes of Sore Mouth Part III. Den­
agement of orofacial herpes simplex virus in­ tal Update March 73-80, 1999
fection. Dent Clin North AM. 36: 879-895,1992 14. Scully C, Porter S: Orofacial Disease: Update
11. Ramberg PW, Linghe J, Gaffar A - Plaque and for the Dental Clinical Tear:3. White Lesions.
gingivitis in the deciduous and permanent den­ DentaLUpdate? April 123-129, 1999
tition. J. Clin Periodontal. 21(7), 490-6, 1997. 15. Scully C. Oral infections in the immuno-com-
12. Scully C, Epstein J, Porter S et al: Viruses and promised patient. Br Dental J. 172: 401-407,
chronic disorders involving the human oral 1992
mucosa. Oral Surg Oral Med Oral pathol, -72: 16. Scully C. Orofacial herpes simplex virus infec­
537-544, J 991 tions: Current concepts on the epidemiology,
13. Scully C, Porter S: Orofacial Disease: Update pathogenesis and treatment and disorders in
for the Dental Clinical Team: 2. Ulcers, Erosions which the virus may be implicated. Oral Surg
Oral Med Oral Pathol. 68: 701-710, 1989
 SECTION - 14

Essential Research Methodology,

Epidemiology and Biostatistics
14.1 Research Methodology
Nair SK

Introduction RESEARCH METHODOLOGY

In order to provide the best care to patients and the The basic steps involved in a research process are:
community, apart from instruments and infrastruc­ 1. Identification of the research problem
ture the health care professionals must be thorough Identification of the research problem is an im­
with the critical appraisal of latest scientific litera­ portant step in any research. The research prob­
ture. They must be life-long learners. It is required lem should be relevant, interesting, feasible,
to develop skills in selecting salient articles, under­ ethical and novel (RIFEN). The inspiration
standing study methodology and to apply these find­ for such problems can be obtained from critical
ings to their own patients. However, doctors who reading of published articles, systematic obser­
rely on scientific literature are confronted with many vation of patients, treatment modalities and its
limitations. Primarily the published conclusions outcomes. Discussion with expert members
need not be valid and, secondly study design and working in a particular area of research could
statistical methods may be twisted to the extent that also contribute substantially to the identification
the findings deviate substantially from the truth. of a RIFEN research problem.
Many important research questions may not be an­
swered or answered questions may be irrelevant for 2. Literature review
the population with which you are concerned about. Once a RIFEN problem has been identified, the
For example, study results based on western popu­ next step is to collect relevant literature. The lit­
lation can not generalize to Indian population with erature search has to be targeted to know
out doing a critical review. Further, the health care i. How far the same or similar research prob­
professionals must sharpen theirability to carry out lem has been studied previously
independent research work, with the hope that it. To understand the limitations in those stud­
through out their career they contribute scientific ies
knowledge which will be used to improve the health iii. To critically assess the required modifications
status of the needy. Truthfully to achieve these goals, which would shed some new knowledge.
a learner should essentially gain knowledge in the
basics of Research Methodology, Epidemiology and The relevant literature can be obtained from printed
Biostatistics. This chapter deals with these concepts publications like text books, journals and other pe­
from the point of view of requirement of a graduate riodicals. Now electronic media like medline,
student in health sciences. medilars, internet etc. are of great help to identify
and accumulate the relevant literature.
 | TEXTBOOK OF PEDODONTICS

3. Protocol preparation quotes must be referenced. In a nutshell, introduc­

Once sufficient and critical knowledge about the tion should justify the relevance and significance
relevant literature concerning the formulated of doing this particular research.
problem is acquired, the investigator can pro­
ceed to prepare a protocol. Protocol is a basic Objectives
document which explains all the guidelines to This is a very brief section where the objectives aim­
be followed during the study. The basic struc­ ing to be achieved by doing this study have to be
ture of the protocol is as follows. stated. In writing the objectives the determining
i) Title and investigators. rule is that it should be RIFEN and one should be
ii) Introduction. able to achieve it with in a reasonable time. The
iii) Objectives. statements should be simple, clear, specific and
iv) Materials and methods. measurable. It would be better to avoid composite
v) Ethical considerations objectives, and if needed such objectives should be
vi) Limitations broken into two or more simple objectives. Then
vii) References. number of objectives also has to be limited.
viii) Appendices.
Materials and methods
Title and investigator This is the most important part of the research which
Title should be very short but informative. It should guarantees the validity and acceptability of the re­
convey the main objectives, population to be stud­ sults. In this section, one has to explain the materi­
ied and if possible the study design. However, one als which will be used for the study. This consists
should avoid usage of superfluous words. The best of chemicals, instruments and other materials in­
way to orient oneself towards writing a good title is cluding details of manufacturers names and ad­
to critically go through titles of published articles dresses. Methodology section should be explained
of reputed journals. Example of a good title is in sufficient detail in such a way that, if required,
“Prevalence of dental caries among preschool chil­ the study could be replicated by other investigators.
dren in Udupi district, Karnataka: A cross sectional Methodology starts with a description of the study
survey”. Followed by the title, list of names of all design, followed by briefing of the target popula­
investigators with their academic degree and affili­ tion. Then explain the size of the sample and the
ation has to be given. sampling method. For sample size calculation there
are various statistical methods available, which are
Introduction decided depending on the study design, outcome
The purpose of introduction in a research protocol variables, and availability of the resources. It is
is to provide a logical and scientific justification for mandatory to specify the inclusion and exclusion
the study. To achieve this, one has to describe pre­ criteria. List the variables to be measured including
cisely the magnitude and quantum of knowledge units of measurement. Define all terms that may be
available regarding the problem. Further, identify interpreted differently by different people. Stand­
the gaps and controversies in the existing knowl­ ard references should be given wherever needed.
edge and justify the relevance of the present study Outcome attribute being measured should be defined
in enhancing the existing knowledge and improv­ without ambiguity. The instrument or questionnaire,
ing treatment modalities. A substantial contribution which will be used to measure these variables also
of writing this part can be obtained from literature should be specified properly. In case of using an
review7. However, the introduction should be as brief instrument or a questionnaire developed by others,
as possible. One need not have to summarize every provide reference. In such a situation it is better to
known fact, but every fact which one provide the knowledge about the validity and
 SECTION 14 : ESSENTIAL RESEARCH METHODOLOGY, EPIDEMIOLOGY AND BIOSTATISTICS |

reliability of the instrument. Another important as­ 3. The effect of confounders which may not be able
pect to be stated in methodology is the duration of to adjust.
the study. A brief check list of points to be explained 4. Selection bias and measurement biases, which
in methodology is as follows are likely to creep in
a. Study design 5. Internal validity and external validity.
b. Target population 6. Limitations anticipating in analysis
c. Sample size and sampling method
d. Inclusion/Exclusion criteria At the end, it would be ideal to explain the steps
c. Study period which will be taken by the investigator to minimize
f. Study variables, outcome measures and unit of these limitations.
measurement
g. Definition of all terms and variables and their References
classification All statement of facts quoted in the protocol must
h. Methodology of data collection be duly referenced. The most accepted style of writ­
i. Method of analysis including the computer pack­ ing references is the '"Vancouver style” which is
ages and statistical methods which will be used. otherwise known as the " uniform requirements for
It would be appropriate *if one could divide the manuscript submitted to biomedical journals”. This
methodology into various sub-heading as ex­ sty le was set forth by the International Committee
plained above and then elaborate each one of of Medical Journal Editors (ICMJE) which has been
them. accepted by more than 400 International medical
Journals. The salient features of the style are,
Ethical consideration 1. Number the references consequently in the order
Another area, which is gaining veiy much impor­ in which they are mentioned in the document.
tance presently, is the ethical consideration of the 2 . The titles of the journals should be abbreviated
study Nqw, it is very particular that the study should according to the style used in the Index Medicos.
be cleared by the Ethical Committee of the institu­ 3. The references accepted but not yet published
tion. Whenever required, the letter concerning this must be cited as “in press” and submitted, but
clearance should be attached to the protocol. The not yet accepted should be cited as “unpublished
important point in ethical consideration is that the observations”
benefits of the study should outweigh the risks. To 4. List all authors, but if the number exceeds six,
establish this, it is better to summarize potential give six followed by et al.
benefits and risks. Wherever required subjects of
privacy and confidentiality should be protected. Appendices
Similarly, the informed consent should be obtained The following items should be attached with the
from the subject. protocol as appendices.
1. Letters of approval (if required)
Limitations
No study can be completely perfect, especially in a 3. Informed consent (if required) form
limited time frame with limited resources. It is very 4. Time task chart
unlikely to have a perfect design. Hence, the best 5. Budget
way is to have an honest discussion about limita­
The protocol has to be subjected to a critical review
tions which can creep into the study in terms of
of the research committee and in the final draft of
1. Flaws in study design
the protocol their suggestions has to be
2. Limitations in sampling methods and the size
incorporated.
of the sample
 I TEXTBOOK OF ’EDODONTICS

4. Conducting study as per the protocol In the case of a thesis, the certificate is usually writ­
Once the approved final draft of the protocol has ten and signed by the supervisor and otherwise writ­
been made the next step will be to conduct the ten and signed by the investigators. There should
study as per the protocol. As far as possible, be a clear statement in the certificate^about the
there should not be any violation, of the proto­ validity, originality and authenticity of the study.
col. However, if there is some unavoidable de­
viation to the protocol, it should be brought to The investigators must acknowledge the individu­
the knowledge of research and ethical commit­ als who provided technical assistance, administra­
tee and remedial measures should be taken. tors who provided facilities and resources, funding
agencies, agencies who provided materials and sub­
5, Preparation of report
jects involved in the research.
Once the study is completed, the report has to
be prepared in a scientific format. The overall
The results section is a new entrant in the final re­
structure of the report may be similar to proto­
port and this is the section for presenting your data.
col with addition of few more sections. The gen­
Here, you present your results in a logical sequence
eral report format be:
with the help of tables, graphs, figures and photo­
1. Title
2. Names of Investigators
graphs. Among the tables, graphs and photographs,
3. Certificate about the originality of the study critically decide which is the most appropriate form
4. Acknowledgements to present a particular result. All presentations
5. Content should be properly titled. Avoid non-technical
6. Introduction terms.
7. Aims and objectives
8. Literature review From the summary, a quick reader should under­
9. Materials and methods stand the methodology as well asXhe results obtained
10. Results and conclusions of the study.
11. Discussion £

12. Summary and conclusion The specific recommendations based on your study,
13. Limitations which could be used to improve the health status of
14. Recommendations the people, health care sendees and health policy
15. References should be brought out in recommendations. All these
16. Appendices recommendations must be intended from your study.
In this section, if warranted, one can recommend
The general guidelines for the title, name of inves­ further studies to improve the present knowledge.
tigators, introduction, aims and objectives, litera­
ture review, materials and methods, limitations, ref­ S elf-Assessment
erences and appendices will be the same as explained
in the protocol. However, introduction and materi­
1. What is RIFEN?
als method sections should be written in the past
2. What do you understand with basic structure of
tense. Further statements like “protocol was ap
the protocol?
proved by the institute ethical committee”,
3. What is ethical consideration of a research pro­
“informed consent was obtained from the subjects”,
etc. should be included in methodology according posal?
to the merits of the requirement. Similarly addi­ 4. What is Vancouver style for references to be writ­
tional limitations occurred during the study should ten?
also be mentioned in the limitations section. 5. What are the guidlines for preparing a scientific
protocol?
 14.2 Epidemiology and Biostatistics

NairSK

Epidemiology is the study of the distribution and from the entire population to compare disease fre­
determinants of health related states or events in quencies between different groups during the same
specified populations and the application of this period of time or in the same population at different
study to control the health problems. The specific points of time. In a cross-sectional survey the sta­
objectives of epidemiology are i) to identify the tus of an individual with respect to die presence or
etiology or the cause of a disease and the risk fac­ absence of both exposure and disease is assessed at
tors, ii) to determine the magnitude of the disease, the same point in time. Descriptive studies provide
iii) to study the natural history of the disease, and valuable information, especially clues about possi­
i v) to establish preventive and therapeutic measures ble risk factors. However, to establish these asso­
to control the health problems. Commonly used ciations further analytical studies have to be car­
designs for epidemiological investigations are ex­ ried out.
plained briefly in this section. For a detailed un­
derstanding of these designs, the readers are advised Analytical epidemiology: In analytical epidemiol­
to refer the suggested readings. ogy, a group of individuals are systematically ob­
served to find out that the risk of disease is different
Epidemiological studies are broadly classified into for individuals who are exposed and not exposed to
two types, i) Descriptive epidemiology, and ii) Ana­ a factor. The analytical designs are further divided
lytical epidemiology. into two viz. Observational and intervention stud­
ies The main observational studies are a) case r
Descriptive epidemiology control studies, and b) cohort studies.
Descriptive epidemiology is concerned with describ­
ing the general characteristics of the distribution of In a case-control study, a group of patients with a
a disease in terms of person, place and time. Per­ disease and another control group of individuals
son means demographic factors like which age group without the disease are selected. The proportion of
the disease is more common, sex-wise distribution, exposure of interest in each group are calculated
religion-wise distribution, distribution of disease and compared. In contrary, in a cohort study, sub­
according to occupation and similar factors. Place jects without a disease are selected and classified
refers to the geographical variation, including re­ on the basis of exposed or not exposed to a particu­
gional variations, variations among countries and lar risk factor. Then these subjects arefbllowed-up
within countries characteristics of the disease in over a specified period of time to determine the oc­
terms of time included studies regarding seasonal currence of the disease in both the groups. These
variations and periodic variation. The major de­ disease frequencies in both the groups are compared
scriptive studies are correlational studies and cross to establish the possible association of the disease
sectional surveys. The correlational studies use data with the risk factor.
 <^3 I TEXTBOOK OF PEDODONTICS

Case control studies are relatively quick and less scientific investigations are limited to a sample. The
expensive. This design is well suited for studying process of selecting a representative small group of
rare diseases. In case control design one cqn study the total study population is called sampling. The
multiple risk factors simultaneously for a single dis­ reasons of studying samples as an alternative method
ease. However by this design one can not measure of studying the total population are:
incidence of the disease and it is not efficient for 1. Sampling reduces demands on resources such
rare exposures. Case-control design is more prone as finance, manpower, material, and time.
for various types of biases as compared to other de­ 2. Sampling may be the only feasible way.
signs. 3. In many situations sample may give a better ac­
curacy, since in small groups non-sampling er­
In cohort study design one can measure the inci­ rors and non-response biases can be kept to a
dence of the disease and can study even multiple minimum.
effect of a single exposure. Biases can be reduced 4. Ethical consideration may not allow to study the
and rare exposures can be studied effectively. How­ whole population.
ever cohort studies are more time consuming and
expensive. It is not efficient for the evaluation of
There are two types of sampling: Probability sam­
rare diseases. Validity also can be very much af­
pling or random sampling and Non-probability sam­
fected by losses to follow up.
pling.

Another type of analytical epidemiological design

Probability sampling
is the intervention trials. The main distinguishing
This is the method of selecting a sample by giving
characteristics of an intervention trial from the co­
all members of the population same chance of
hort design is that in the former the investigators
selection or same probability of selection. The ma­
themselves allocate the exposure where as in later
jor advantages of probability sampling are:
it is a natural exposure. The major advantage of
a) Every member in the population gets.a known
this design is that here the treatment can be allo­
probability of being included in the sample.
cated at random in a sufficiently large sample and
hence the results will be more valid. However these b) The sample is drawn by same method of ran­
trials are more expensive and very difficult to con­ dom selection, which is consistent with these
duct. probabilities.
c) These probabilities are taken into account in the
BIOSTATISTICS calculation of estimates from the sample.

One of the important and essential tools required Important probability sampling methods are sim­
for carrying out research in health sciences is bi­ ple random sampling, stratified random sampling,
ostatistics. From the beginning till the end of the
systematic random sampling, cluster sampling and
study statistical methods are applied. However, to
multistage sampling.
discuss all those methods is beyond the scope of
this section. Very commonly used methods are
Simple random sampling
briefed here. It is advised to go through suggested
This is the method of selecting a sample of size ‘n’
reading for further details.
from a population of size 'N’ by giving all possible
Sampling samples equal probability ofselection. In this proc­
ess all members of the population get an equal
For any research it is very difficult and unwise to chance of being included in the sample.
Study the whole group or population. Generally
 SECTION 14 : ESSENTIAL RESEARCH METHODOLOGY, EPIDEMIOLOGY AND BIOSTATISTICS | <%>C>

In simple random sampling, since every unit in the a hidden periodicity in the frame or population co­
population has equal chance of being included in incides with that of the selection.
the sample, representativeness of the sample is en­
sured and is subject only to a sampling error. In Cluster sampling
this sampling scheme calculation of estimates are In cluster sampling method, the population is first
easy However, if the sampling unit is small and divided into clusters of homogeneous units. A sam­
the populationis large, this method may be imprac­ ple of clusters is then selected and all the units or a
ticable because of the difficulty and expense of con­ predetermined number of units in the selected clus­
structing or updating the sampling frame. Another ters will be studied. This method of sampling cuts
drawback of this sampling scheme is minority sub­ down the cost of data collection and it is adminis­
groups of interest in the population may not be tratively more convenient method. However, the
present in the sample in sufficient numbers for study. sampling error is comparatively more in this sam­
pling scheme. Cluster sampling methods are popu­
Stratified random sampling larly used for evaluation of vaccination coverage.
In this sampling method the total population is first
divided into homogeneous subgroups or strata ac­ Multistage sampling
cording to a characteristics of interest. A simple As the name implies, this sampling is done at vari­
random sample is selected from each stratum using ous stages until the final sampling unit is reached.
the same sampling fraction. Pool all these small This method is more applicable when the popula­
samples which gives the required sample. By this tion is very large and spread out in a very large geo­
method, every unit in a stratum has the same chance graphical area. For example, in a country-wide sam­
of selection and an adequate representation of mi­ pling, at the first stage a sample of states is selected,
nority subgroups of interest can be ensured by strati­ at second stage from each state a sample of districts
fication. Further sampling error is minimum for are selected and proceeding like this only at the last
stratified random sampling. However, this sampling stage an exact population is examined. This sam­
method is more expensive and preparing sampling pling method also cuts down the cost, but increases
frame for the entire population stratum-wise is very the sampling error.
difficult.
Non-probability sampling
Systematic sampling
This is the procedure of selecting a sample from a
This is a relatively simple sampling method which
population without the use of probability or fan­
can be applied where sampling frame is available
dom method. The various non-probability sampling
in some order. In this sampling method, firstly sam­
methods are convenience sampling, quota sampling
pling fraction is calculated by dividing total popu­
and judgement sampling. These methods are not
lation by required sample size.
advised usually for scientific studies.
i.
e. sampling fraction,
N Averages and Dispersion
K = ——
n Once the data is collected property in quantitative
terms, the next step is to summarize it for deriving
Then in the list, from the first K units one unit is a meaningful conclusion. This is mainly achieved
randomly selected. Let it be rtil unit. Then r+K, through calculating two measures, namely averages
r+2K, r+(n-l)K units are selected which form the and dispersion. Average gives an idea about the lo­
sample. This is a very convenient method and sam­ cation of the data whereas dispersion explains the
ple will be evenly spread over the entire reference variation within the data.
population. However, the sample may be biased, if
 ! TEXTBOOK OF PEDODONTICS

The main measures of average are arithmetic mean, To calculate the median, first arrange the values in
median and mode. These measures are also known order of their magnitudes.
as measures of central tendency or location, since
they measure the central location of the data. e,
i. 2, 3, 4, 5, 5, 5, 5, 6, 7, 8

Arithmetic mean: Let the data contain ‘n’ numbers Here the middle value is 5 and hence 5 is the me­
x1tz, x„........... ., x ,then the arithmetic mean is, dian. The most frequently occurring value in the
above data set is 5 and hence mode is also 5.
A.M. = Sum of Xj/n
Once a good measure of average is obtained the next
inquiry will be to get a measure which represent
Arithmetic mean is very simple to calculate, very
the overall distribution of data around the calcu­
rigid measurement and depends on the whole data
lated average. Such a measure is called dispersion.
points. However extreme values influences the
These measures are also known as measures of vari­
arithmetic mean which is considered as a demerit
ation. Important and most popularly used meas­
of it. Another demerit of the arithmetic mean is it
ures of dispersion are range and standard deviation.
can not be computed even if a single observation is
missing. It is most suitable for summarizing a con­ Range
tinuous type of data, measured with a consistent Range of a data is the interval between the lowest
scale. and the highest value in that data. For the data in
the previous example range is 2-8. It is very easy to
Median calculate. In fact, by observation one can locate the
Another equally important measure of average is range. However it is very much affected by extreme
median. This is the middle most observation ob­ values and hence not considered as a good measure
tained after arranging the whole data values in or­ of dispersion.
der of magnitude. Median is very simple to calcu­
late and the extreme values do not affect much on Standard deviation *
median. It can be computed even if few values are The most widely used mea sure of dispersion is stand­
missing. ard deviation. This is a very consistent measure

Mode X (x-AM) (x-AM)2

Mode is that value in the data set, which is most
2 2-5 = -3 9
frequently occurring. Like median, mode is also not
affected by extreme values. However, for the same 3 3-5 = -2 4
data there can be more than one mode and some time 4 4-5 = -1 i
no mode also.
5 5-5 = 0 0

Example: The ages of 10 children attended the 5 5-5 = 0 0

Pediatric dentistry clinic are: 5 5-5 = 0 0
5 5-5 = 0 0
5, 3, 7, 5, 6, 4, 5, 2, 5,7,8
6 6-5 = 1 1
5 + 3 + 7 +.......... + 8 7 7-5 = 2 4
Arithmetic mean =------- —-------7-—--— = 5 8 8-5 = 3 9
10
Sum 0 28
 SECTION 14 : ESSENTIAL RESEARCH METHODOLOGY, EPIDEMIOLOGY AND BIOSTATISTICS |

and calculated based on all observations. The cal­ Thus, normal distribution helps one to describe the
culation of standard deviation for the previous set data completely. Otherwise, if we know that the dis­
of data is as follows. tribution of a particular data follows normal, then
with mean and standard deviation one can com­
Standard deviation = / pletely describe the data. This signifies the impor­
\l N tance of mean, standard deviation and normal dis­
tribution in medical literature. Even if the data di­
=
J 10 rectly does not follows normal distribution, there
are mathematical transformations available which
convert the data to follow normal distribution.
= 1.67

Tests of significance
Among all the measures of averages and dispersion,
There are situation arises where the summarized
arithmetic mean and standard deviation are the two
data for various groups are required to be compared.
extensively used measures for summarization of
These comparisons are mainly aimed to find out
health science data. The justification for applica­
any significance difference between two or more
tions of these measures can further understand from
groups. The. statistical procedures used for these
the theory of Normal Distribution.
comparisons are called tests of significance. The test
procedures developed with the assumption of stand­
Normal Distribution
ard probability distributions are known as paramet­
After a proper summarization. one looks about any
ric tests and the procedures developed without this
pattern that exists in the data. If so, we try to ap­
assumption are known as non-parametric tests. Few
proximate this pattern with known statistical or
commonly used parametric tests are student’s t-test,
probability distributions. One such commonly used
normal test and analysis of variance. Mann-whitney
distribution for approximating the data pattern is
u-test, Wilcoxon test are two important non-para­
normal distribution. This is also known as Gaussian
metric tests. Detailed description of these test can
law, after the name of famous mathematician C.F.
be obtained from the suggested reading.
Gauss. The popular use of normal distribution in
medical science is due to a few interesting proper­
Self-Assessment
ties, which this distribution possesses.

1. What do you understand by epidemiology?

Properties of Normal distribution:
2. What are case control and cohort studies?
1. The Normal curve is bell shaped
3. What is sampling?
2. It is symmetric about the mean
4. What is cluster sampling?
3. For a normal distribution mean, median and
5. What do you understand with multi-stage sam­
mode coincides
pling?
4. If the data follows normal distribution, then the
6. What is the formula for deriving the standard
interval
deviation?
Mean ± Standard deviation contains approxi­
mately 68% of the data.
Further Suggested Reading For Section -14
Mean ± 2 Standard deviation contains approxi­
mately 95% of the data.
1. International Committee of Medical Journal edi­
Mean ± 3 Standard deviation contains almost
tors. Uniform requirements for manuscript sub­
100% of data.
mitted to biomedical Journals. N Engl
336: 309-15, 1997
 CEEfcl TEXTBOOK OF PEDODONTICS

2. Lwanga SK, Cho-Yook Tye, editors. Teaching 4. Leon Gordis. Epidemiology. Philadelphia:
Health Statistics, Geneva: World health organi­ Saunders, 1996
zation, 1999. 5. Hennekens CH, Buring JE. Epidemiology in
3. Daniel WW. Biostatistics: A Foundation for Medicine. Boston: little Brown.
Analysis in the Health Sciences, 2n edition New
York: John Wiley & sons, 1987.
 SECTION - 15

Forensic Pedodontics
15.1 Introduction
Rao NG, Rao N, Dhar P

Introduction evidences by scientifically examining the objects

or substances that are involved in the crime.
Forensic dentistry is one of the most rapidly devel­ ■ Forensic odontology: is defined as the branch
oping branch of forensic medicine and forensic sci­ of the dentistry which, in the interest of the law,
ence. This is mainly due to the immense importance deals with the proper handling and examination
of dental evidence in the identification of victims of of dental evidence and the proper evaluation and
mass disaster, abuse or organized crimes. A com­ presentation of such evidence (Kieser Neilson
prehensive understanding of this science is abso­ 1981).
lutely necessary for the pedodontists as they are of­ ■ The expert: is a specialist who places his par­
ten the first one to deal with children. They can ticular professional expertise at the disposal of
play a valuable role by helping the forensic experts those requesting his assistance, but leaves the
in identifying the affected victim or criminal and legal conclusions that may be drawn from his
thereby contribute significantly in supporting and results to the coroner judge.
strengthening families to enable them to care for
children more adequately and the society to develop Historical Perspective
sensitivity and skills for respectful and healthy per­
sonal relationship. Thus, a Pedodontist can play a Forensic dentistry, though a relatively new area of
vital role in protecting the human rights of chil­ forensic science, has a long history that starts from
dren. 2500 B.C, when the first evidence was found in the
pyramid at Giza, Egypt, in a skull with a gold wire
This chapter is an attempt to highlight the strategic holding two molar teeth. In 45-70 A.D, at Rome;
position of a dentist in forensic odontology and ap­ the dental findings being used as evidence first time
plication of this science in pediatric group of our in forensic manner where the king Nero had killed
society. his mother who was identified by two maxillary
canine teeth. Nero’s mistress Sabina had Nero kill
Definitions his first wife and identified her by a discoloured
tooth. Similarly in 1477, the body of Charles the
■ Forensic medicine: is defined as the branch of
Bold was identified on the basis of several missing
medicine wherein the knowledge of medicine is
anterior teeth. In 1850, at Boston the first trial df
applied to the knowledge of law in order to de­
hanging of Dr. John Webster was ended
rive justice. (Rao 2000)
dental evidence. In 1897, at Paris the very
■ Forensic science: is a study of physical infor­
bum incidence at Bazaar de Charite
mation connected with crimes or collection of
 <ÎÜ> I TEXTBOOK OF PEDODONTICS

125 Parisian were attending the ball was published 3. Research

as the first text of a mass disaster on forensic den­ a) Academic training courses - final year dental
tistry, Most of the bodies were identified by a prac­ (BDS) and second year medical(MBBS) stu­
titioner, Dr. Amedo along with two forensic den­ dents.
tists. In 1967, a 14 year old girl, Linda Peacock had b) Post graduate training (MD/PhD-Forensic
the bite mark along with other evidence which led Medicine)
to the conviction of a young man. Thus, it can be
seen that dental evidences are of paramount impor­ THE ROLE OF PEDODONTIST
tance in this science. With the growing international
travel and association risk, the recognition has come Perhaps the most significant role is to create aware­
to forensic dentistty internationally. ness of this specialty in the society. Like any other
forensic odontologist, a pediatric dentist can apply
In India, this science of dentistiy is dealt as a part his knowledge of dentistry effectively in the follow­
of forensic medicine.However there is a strong need ing areas -
for its inclusion as a compulsory subject in the cur­
ricula of all the dental schools in India. A dental 1. Child abuse/neglect
graduate should be able to apply this knowledge in In the recent time with introduction of Child Pro­
relation to law and justice administration for the tection Act and increased trends towards mod­
society. ern life style, both child abuse and neglect are
on the verge of increase in the countries of tra­
Major Fields of Forensic Odontology ditional values like India. Therefore, the den­
tist who handles children is required by law in
1. Civil - Non criminal virtually all jurisdictions to report cases of child
abuse and neglect. A conscious effort should be
a) Identification of an individual remains, where made to eradicate completely this highly crimi­
death is not due to any suspicious circum­ nal activity in the society.
stances. This covers the majority of the work
expert carry out. 2. Mass disaster
b) Mass disasters-identification of victims of ho­ With the complete reform of interstate and in­
tel fires, aircraft and other transport accidents. ternational travel, accidents are high and caus­
c) Cranio-facial superimposition for identifica­ ing most of the disasters worldwide. In the analy­
tion sis of these incidences where children often be­
come victims,the task of identification is very
2. Criminal complicated. The vast numbers of victims who
are burnt, decomposed and mutilated can be over­
a) Identification of persons from their denti­ whelming. Therefore, these cases can be
tion or teeth systemically examined and identified skillfully
■ Living person by the dentist as the previous records show that
■ Dead person when trained experts are utilized, the identifi­
b) Dealing with bite marks identification cation rates are high and accurate.
■ Foodstuff
■ On the assailant 3. Accidental and Non-accidental oral trauma:
■ The victim Another area is which the dentist can play an
important role is in the examination of children
w ho have sustained accidental and non-acciden-
 SECTION 15 : FORENSIC PEDODONTICS | <%Eb

tai trauma involving orofacial structures via ac­ 7. Lip print identification
cident, negligence, malpractice or child abuse. The role of the skin as a repository and marker
In such cases, a detailed and accurate examina­ of evidence is evaluated in identification of vic­
tion supported with tests, radiographs and pho­ tims and suspects (lip prints, finger prints, fin­
tographs will be required by the inquiring agency ger nail) and it is found that no two individuals
as often these cases are challenged in the couft. have the same pattern of the skin on the lip. Thus,
the application of Cheiloscopy is being devel­
4. Dental fraud oped in identification by use of lip-prints.
Dental fraud is an another emerging area of liti­
gation. With the introduction of consumer’s pro­ 8. Poisoning
tection act, the dentist is required to examine Various metallic poisonings may have manifes­
patients carefully and records are to be main­ tations in the oral cavity. They are most com­
tained properly to defend himself if needed. Also monly a ssociated with a metallic taste and a non­
records are to determine whether a treatment paid specific ulcerative gingivitis, accompanied by
for by a third party has actually been performed varying amounts of pigmentation. With child
or not. labour still a menace in certain parts of the coun-
tiy, an alert pedodontist may come across cases
5. Age determination of chronic metal poisoning and should be able
In routine identification, determination of age to diagnose it by the clinical signs and symp­
of the unknown human remains in various stages toms, coupled with the history.
of decomposition or recognition of the accused
person who is suspected in the crime is vital. 9. Dental records
Since the tooth is the only tissue that can resist Teeth are unique in individuality, resistant to de­
the highest temperature and other decomposi­ struction and their records can be maintained
tion changes, age determination with the help well along with noting of developmental varia­
of human dentition or their bite marks have tions and appliances delivered if any to children.
proved to be of great importance. A pedodontist Thus, routine findings of the patients preserved
may also be a significant asset to this field in in the form of their odontograms are often used
identification. successfully for their identification.
I

6. Bite marks evidence Self-Assessment

The bite marks investigation is equally impor­
1. When wa~s the first forensic evidence found?
tant and interesting for the dentist dealing with
In which country first time dental findings was
pediatric patients. Until recent times the bite
reported as forensic evidence?
marks produced by the suspect (usually in as­
3. Define forensic odontology.
sault cases of sexually abused child) were looked
What are the major fields of forensic odontol­
upon by the other investigators as bruises. How­
ogy?
ever, through constant education, these marks r
What is the role of paediatric dentist in forensic
have been recognized for what they are, bites. 1•
dental science?
 15.2 Child Abuse

Tandon S, Rao NG

Child abuse has existed since the dawn of history. quently multiple and involve mainly the head,
Religious sacrifice and abandonment of children are soft tissue, the long bones, and the thoracic cage
frequently referred to in Greek and Roman mytholo - and that cannot be unequivocally explained
gies as well as in the Bible. Infanticide has been (Selwyn 1985).
practiced in practice as a form of birth control, and » Neglected child: is one who shows evidence of
the abuse of child labor in the nineteenth century in physical or mental health primarily due to fail­
Britain is well documented and has been reviewed ure on the part of the parent or ca retakers tb pro-
elsewhere. It is only in recent times that the chang­ xide^deqiiat el vfor the child’s needs.
ing social values have led to the identification of ■ Persecuted chi Id: i s one who shows evidence of
child abuse as a widespread medico-social problem mental ill-health caused by a deliberate inflic-
nationally and internationally. tion of physical or psychological injury that is
often continuous in nature.
The present chapter is aimed to update various as­
pect of child abuse and neglect such as diagnosis, Type of child abuse t
treatment, prevention and legal consideration, as
.»^Physical abuse 31.8%
the dentist is in a strategic position to recognize
»Educational abuse 26.3%
abused and neglected children. While detection of
■ Emotional abuse 23.3%
dental-care neglect is an obvious responsibility for
.-»• Sexual abuse 6.8%
the dental clinician, types of child abuse may also
» Failure to thrive 4.0%
be noticed in the patients visiting dental clinic.
ji International drugging or
Therefore, the dentist should not only diagnose these •' — '—•-irjoii- tju -.-rary mib

poisoning
.. — -
not specified
problems, but must also report, treat and prevent
■ Munchausen syndrome
further complications.
by proxy not specified

Definitions
Types of child neglect

■ (Child abuse: is defined as the non-accidental Neglect is an act of omission or the failure to pro­
physical injury, minimal or fatal, inflictedupon vide food, shelter, clothing, health care, safety need,
children by persons caring for them (Selwyn et dental care and supervision. ‘These may be broadly
al 1985)7 categorized into the following four types:
■ It is an overt act of commission of a care taker­ ■ Emotional neglect 27.8%
physical, emotional or sexual. Health care neglect
■ Battered baby: is a child who shows clinical or including dental neglect 8.7%
radiographic evidence of lesions that are fre­ ■ Physical neglect 7.8%
 SECTION 15 : FORENSIC PEDODONTICS |

Table 15.1: Probable factors responsible in child abuse

Stresses Ego weaknesses Vectors

■ Youthful parenthood Character disorders: ■ Stresses created by child

■ Unwanted or unplanned ■ Impulsive-aggressive ■ Specific individual
parenthood ■ Rigid-exacting psychodynamics
■ k°w soc<o~economic ■ Immaturity, passive ■ Collusion or facilitation by
status & related variables dependency or inadequacy partner
such as crowded and Depressive disorder « Culture bound disciplinary
inadequate housing Psychic disorders practice and beliefs
■ Social isolation Alcoholism ■ Relative absence of other need,
■ Long parenthood Non-specific ego defects satisfaction, frustrating
■ Partner discord ■ Low self esteem objects (social isolation)
■ Responsibiiitiesand ■ Inability to empathize
frustration of parenthood " 1° hust
■ Altered physical or
physiological status
■ Child itself (for example
infantile colic)

■ Choffin et al (1966) reported depression as a ■ AJleged self-inflicted history

strong risk factor for physical abuse which in ■ Delay in seeking medical care
turn was strongly related with the onset of sub­
stance abuse. Examining child abuse/neglect
■ Some instances of child abuse fall within a “gray
zone’* between the pure accident and negligent The dentist and his staff should be educated to get a
homicide, due to possible subconscious desires visual impression of the child as he enters the re­
of the mother or guardian to injure the infant. ception room. The practitioner should note whether .
However, the repetition of non-fatal injuries the child and parent or guardian has an appropriate
should alert the attending clinicians that some interaction. After evaluating the history in cases
instances of accident proneness in children may of suspected cases of child abuse/neglect, the ex­
be a sub-liminal form of child abuse. amination for such children should be incorporated
with a routine dental checkup.
Recording of child abuse/neglecthistory
Common sites to be observed and examined £
I
Each dental practitioner should develop an exami­
nation protocol to aid in screening and reporting of « Many abused or neglected children due to fear
suspected cases of child abuse and neglect. The may appear overly vigilant or display a ^frozen
following histories are diagnostic or extremely sus­ watchfulness ' staring constantly. There are no
picious in evaluating non-accidental trauma: spontaneous smiles and almost no eye contact.
■ Eye witness history ■ The dentist should observe the child for lack^of
• Unexplained history cleanliness, for small stature with pi 7-

• Implausible history and for evidence of lualnutritioBg

 <r/«y> | TEXTBOOK OF PEDODONTICS

of malnutrition include a posture of fatigue with ■ Body surfaces that are covered should be exam­
rounded shoulders, flat chest, a protuberant ab­ ined by lifting up the clothes to the limit they
domen and thinning of hair. The face is pale, allow. Inner things, arm pits must be checked.
muddy anddacks luster. The only area that are not in the purview of the
■ Overdressed children should also be noted, long dentist are the genitalia and buttocks. However,
steeveFand high~necked shirts or blouses dur­ the patients taken to the operating room for sur­
ing hot summer months may be worn to cover gery can be examined if suspicion arises.
signs of physical abuse._
« Face.neck shoujdj^e examined for periorbital Parent consultation
ecchymbsis, sclera hemorrhage,^ptosis, deviated
nasal septum, cigarette burn marks and hand slap Once the suspicion is confirmed, the parent should
marks^ be informed that an injury has been noticed. The
» Corners of the mouth are reported (McNees 1975 parental explanation of the cause of the injury should
et al) with binding marks from a gag tied in be understood fully by the dentist. If the findings
place for hours to force the feed. and explanation are not compatible, or if suspicion
■ Sometimes, a spoon or fork applied with enough still exists: the dentist is mandated by law to con­
force or determination, which may result in frac­ tact the appropriate CA/CM authority. The dentist
tured anterior teeth or torn frenum. should contact suitable child protective agency en­
■ While moving the child up in the dental chair in suring himself that parent will not result in the den­
a supine position or lifting up motion if result tist altering the decision.
pain, trauma is to be suspected; Then belt marks,
electric cord marks, bite marks, bruises or frac­
ture of ribs or clavicles should be suspected and
dentist should confirm by checking them which
can be performed in short time. The dentist,’
however, must train himself to be vigilant.

Definitive CM/CA examination

As the head and neck being most often involved in
abuse casesTdentist is in a unique position to iden­
tify child abuse in routine examination. The de­
finitive CM/CA examination requires a keen ob­
servation and detailed documentation when suspi­
cion exists. A systemic approach should be followed
and to protect the examiner legally, the dental as­
sistant should be present in the room and aware of
th^ dentist’s suspicion, to verify and record the find­
ings. Following areas should be examined care­
fully:
■ Detailed examination and palpation of the skull
looking for subgaleal hematomas and cephalo-
matomas (manifested as soft tender circum­
scribed areas of scalp). Time in days
• Positive sign of any battle like laceration, scare, Colour changes in a bruise during healing
(see table 15.2)
bruises.
 SECTION 15 : FORENSIC PEDODONTICS | <h№>

Table 15.2: Colour changes during healing of a bruise

Time Sign |

0-2 days Swollen, tender

0-5 days Red; blue, purple

5-7 days Green

7-10 days Yellow

10-14 days (or longer) Brown

2-4 weeks Cleared

Human Hand marks

Fig. 15.1 Bizarre-shaped bruises on buttocks
Hand marks are prevalent in almost 22% of the cases
and can leave various kinds of bruises.
■ Grab marks or finger-tip bruises: Most common ■ The wide assortment of i nstrument used to abuse
are grab marks or squeeze marks, oval shaped children suggest that the caretaker who looses
bruises that resemble finger tips. The most com­ temper grab whatever object is handy. (Fig. 15.2,
mon site is the upper arm or * shoulder. Lower 15.3)
extremities are common until the child learns to ■ Circumferential tie marks on ankle or wrist can
walk. Sometime squeezing of the cheek leave a be caused when the child is restrained. (Fig. 15.4)
thumb or two-three finger mark bruise. ■ Circumferential cuts are due to narrow rope or
■ Often linear grab marks occur due to the pres­ cord.
sure of the entire finger when capillaries at the ■ A frictional bum or rope bum may result due to
a piece or strap of sheeting is used to restrain,
edge of the injury are stretched enough to rupture.
presenting a large blister that encircles the ex­
■ In slap marks to the cheek, 2 or 3 parallel linear
tremity. (Fig. 15,5)
bruises at a finger width spacing will be seen to
■ Gagging abrasion due to restraining the crying
run through a more diffuse bruise
or yelling of children.
■ Crescent shaped bruising facing each other as a
result of pinch, primarily due to finger nail.
Table 15.3 Facial injuries prevalence in physical
Strap marks child abuse
■ Strap marks are 1-2 inches wide, sharp border
rectangular bruises of various length, sometimes
Site Percentage
covering a curved body surface.
■ Often, lash marks are narrow, straight edged Scalp 79
bruises or scratches caused by a thrashing with
a tree branch. Neck 59

■ Loop marks are secondary to being struck with Forehead 52

a doubled over lamp cord or a rope commonly
Cheek 49
breaking the skin and loop shaped scars because
of the force of distal-end. Lower jaw 48

Bizarre marks (Fig. 15.1) Upper lip 45

■ Bizarre-shaped bruises with borders are nearly
(Cameron et al 1986)
always infected when a blunt instrument is used
resulting a welt or a bruise.
 I TEXTBOOK OF PEDODONTICS

Fig. 15.2 Beating on hand for stealing Fig. 15.3 Fracture of femur

Fig. 15.4 Circumferential tie marks on Fig. 15.5 Burns due to pouring of hot water to
both ankles stop bed-wetting habit
 SECTION 15 : FORENSIC PEDODONTICS |

Facial injuries includes: (in order of decreasing Injuries of dentition include (Table 15.4)
frequency) (Tablé 15.3)
■ Contusions and ecchymosis ■ Traumatized or avulsed teeth’indication of blunt
■ Abrasions and laceration trauma or pattern injury from instrument
■ Burns ■ Discolored teeth indicating repeated trauma
■ l Bone fractures
■ Bite marks
Self-Assessment
Table 15.4 Dental injuries prevalence in physical
abuse 1. Define child abuse.
2. What do you understand with persecuted child?
Site Percentage 3. How many types of child abuse and neglect are
common.
Fractured teeth 32
4. How many probable factors of ego weaknesses
Oral ulceration 14 are responsible for child abuse?
5. What colour will be seen in a 7-10 days old
Fracture of maxilla/mandible 11
1 bruise?
(Malcez, 1979)
 15.3 Bite Marks

Tandon S, Rao NG

Bite marks are produced in flesh, foodstuffs or a

number of other materials by teeth and the surround­
ing soft tissue. Whilst it is true that the marks are
usually produced entirely by the teeth in foodstuffs
and non-living materials, the marks in human body
is often contributed to by pressure from the lips and
the tongue as well as from the teeth themselves.
Dental evidence has become increasingly important
in the investigation of noil-accidental injuries to
children. Most often bites are reported to be inflicted
in female children of age group 11-15 years, while
most of the male victims were in the age group of
4-10 years. The most common area to be bitten in
children were head, neck, limbs and trunk. Female
victims were most commonly on breast, arms and
legs; while the arms and shoulders were most often Fig. 15.6 Bite mark on the back

affected in the males. Bite marks on the cheeks,

arms, shoulders are mostly in response to crying, Definitions
while on buttocks and genitalia are intended as pun­ Since the aim of the bite mark identification is to
ishment for soiling. Bite marks in older children identify the teeth which inflicted the bite mark,
may be less punitive in nature, rather they are more Jacobsen and Keiser-Nielsen (1981) stressed the
likely to be related to physical or sexual importance to the dental experts to be able to dis­
abuse.(Whittaker D;K, 1989) tinguish between the following terminologies related
to bite marks.
Although bites (Fig. 15.6) and biting have been ■ Bite: is to tear or seize with the teeth
around as long as animals with teeth have inhab­ ■ Bite mark: a mark caused by teeth alone or in
ited the earth, the science of bite marks is compara­ combination with other oral parts or consists of
tively new and potentially valuable. Bite marks in­ teeth marks produced by the antagonist teeth can
vestigations have involved bites from both human be as two opposing arch marks.
and animal bites. ■ Tooth mark: produced by two or more teeth
■ Arch mark: Four or five marks of adjacent teeth
must be present before a mark can be identified
as a human arch mark.
 SECTION 15 : FORENSIC PEDODONTICS | fZ®

Table 15.5: Classification of bite marks depending on biting agent, material bitten
and degree of biting

I. Depending on biting agent II. Depending on material bitten

□

Human Animals Mechanical Skin Perishable Non-perishable

■ Children ■ Mammals ■ Full denture ■ Human items ■ Unanimated
■ Adults ■ Reptiles ■ Saw blade ■ Animal « Food objects such
■ Fish tooth marks items like as pipes,
■ Bicycle chain cheese, pens, pencils
and others like apple etc.
electric cord (Fig.
marks, belt 15.7a,b)
marks etc.

ill. Depending on degree of biting

Definite bite marks Amorous bite marks Aggressive bite marks

Tooth pressure marks are These marks, made in amorous These marks may show
formed when a direct circumstances, tend to be made evidence of scraping, tearing
application of pressure by slowly with absence of movement and avulsion of the tissue.
the biting edges has caused between the teeth and the tissue. This usually involves the
the tissue damage. Other Lower teeth marks are formed when ears, nose or nippies. Such
marks may be caused by teeth are pressed into tissue with a bites may be difficult to
tongue pressing tissues gradually increasing pressure. By interpret
between the necks of the contrast, marks of the upper teeth
teeth. form a series of arches where the
tissues is sucked into the mouth
and pressed against the back of
the teeth with the tongue

Fig.15.7a Bite marks on chewing-gum Fig.15.7b Bite marks on cake

(perishable item) (perishable item)

(Courtesy Dr. Kenneth Brown, Director Forensic Odontology, The University of Adelaide, South
 I TEXTBOOK OF PEDODONTICS

Classification of bite marks ■ These marks are usually inflicted by anterior

teeth
Bite marks are basically classified according to ■ May appear as scratches or abrasions
causative agent (aetioligical factors) and material ■ If scratches, they might indicate a peculiarity
bitten (Cameron and Sims 1973 -and Me Donald of the incisal edges and assist in identifica­
1974) and degree of biting (Whittaker et al 1989) tion
(Table 15.5) respectively.
Factors affecting bite mark injuries
Mechanism of bite marks:
Various mechanisms and factors involved in bite ■ Inherent skin factor
marks production are discussed at this juncture Loose skin at the site of injuiy (eg., around the
briefly. eye) will bruise more easily and extensively in
the area where excess of subcutaneous fat is
Bite Mechanisms present compared to the skin supported fibrous
A. Tooth pressure tissue with a good muscular tone.
■ Marks caused by a direct application of the
incisal edges of the anterior teeth or occlusal ■ Age
surfaces of the posterior teeth. Infants and old people tend to bruise more eas­
« The marks will depend on the force applied, ily and severely. Infants, because they have a
the duration of force applied and the degree more delicate, loosely attached skin and pres­
of movement between the tissue and teeth. ence of subcutaneous fat. Old people, because
• A pale area represents incisal edges and bruis­ of decreasing elasticity of the skin and lost sub­
ing represents the margin of the incisal edge. cutaneous fat.
■ Shape of the mark may be useful in the iden­
tification of the specific tooth. ■ Sex
• Tooth mark pattern as an attack’ or ‘defen­ Females tend to bruise more easily Than males
sive’ bite mark is seen most commonly in the and also bite mark bruising persists longer in
Battered Child Syndrome. females because of more subcutaneous fat and
delicate skin.
B. Tongue pressure
« Tooth pressure is caused when the material is
■ Time
taken into the mouth and pressed by the
The duration of bite mark is dependent on the
tongue against the teeth or palatal rugae.
force applied and the extent of tissue damage.
• This can leave a distinctive mark due to the
Tooth marks that do not break the skin last from
mechanism of suckling, a combination of
several minutes to 24 hours. In cases where skin
sucking and tongue thrusting.
■ Bite marks of sadistic origin exhibit a central is broken, the border or edges will last for sev­
ecchymotic or a 'suck mark’ radiating linear eral days, depending on the thickness of the tis­
abrasion pattern surrounding the central area sue. Thinner area retain the mark longer.
and resembling a sunburst. These are mostly
found in sexually oriented assaults. ■ Vascularity
The intensity of discoloration may depend on
C. Tooth scrape vascularity of the area. Bruises will occur and
■ May be caused by teeth scraping across the last on a more vascular area like face than in
surface of the skin
 SECTION 15 : FORENSIC PEDODONTtCS |

the site which is less vascular like bite on hand tion, lividly, embalming, decomposition or
or foot. change in position. Then, the following meth­
ods may be used for a detailed evaluation.
Characteristics of human bite mark for identi­ a. Photography
fication b. Salivary swabbing
c. Impressions
■ Human bite mark characteristics include an el­ d. Tissue sample
liptical or ovoid pattern containing tooth and
arch marks. 3. Collection of evidence from suspect
■ Simplest form of a bite mark consists of tooth Before collecting evidence from the suspect^ the
marks produced by antagonistic teeth. dentist should ascertain that the necessary search
■ An arch mark may indicate the presence of 4 to warrant court order or legal consent has been
5 teeth marks reflecting the shape of their in­ obtained, and should make a copy of this docu­
cisal or occlusal surfaces. ment as part of his/her records.
■ Other significant findings to identify a bite mark
to give the identify of the suspect are Recent advances for collecting evidences
- Presence or absence of each tooth
- Peculiar shape of each tooth ■ Xeroradiography: With this radiography, there
- Mesio distal dimensions is an advantage of seeing through tissue dam­
- Arch form and size ages that may not be seen with photographic
- Relationship between the upper and the lower techniques.
jaws « Transillumination: This is particularly success­
- Any unusual features, such as rotation, frac­ ful in enhancing low light energy images pro­
tured teeth, supernumerary teeth, microdontia duced by an intra-dental injection of chemically
diastema, etc. luminescent liquids.
■ Videotape analysis: With this advanced compu­
Bite mark analysis terized technique, it is easy to analyze a trans­
parency, as the eye can focus on certain aspects
The guidelines for bite marks analysis are given by of densify display as die levels of densify are sepa­
American Board of Forensic Odontology (ABFO) rated or broken down. This video and computer
and careful use of these helps in enhancing the qual­ analysis, such as color discrimination, provide
ify of the investigation and conclusions. The col­ a more definitive data, both quantitative and
lection of evidence regarding the bite marks falls in qualitative.
following categories. ■ Superimposition technique: It is a technique
whereby an image of the bite marks inflicted on
1. Description of the bite marks the deceased child is directly compared with bite
• Demographic data marks obtained from the suspect for identifica­
■ Location of bite marks tion.
■ Shape ■ Scanning microscopy: Which helps in demon­
• Colour strating three dimensional characteristics in a.
■ Type of injury bite mark for example, depth of the bite mark.
■ DNA fingerprinting: DNA fingerprinting ha?
2, Collection of evidence from victim been developed since the 1980s as a molecular
It should be determined first whether the bite tool for the genetic specification of ag in^^^^p
mark has been affected by washing, contamina­ It has been found immensely usefill ig
 I TEXTBOOK OF PEDODONTICS

court decisions requiring identifications with a between the right and left sides and between the
high precision. upper and lower lips. Lip prints on drinking glasses,
facial tissues, magazines and undergarments have
The DNA testing is based upon the occurrence been used as evidences in actual court cases also.
of a family of DNA sequences that are randomly The science of examining the lip prints is called
repeated and dispersed throughout the genome. Cheiloscopy. (Fig. 15.8a, b)
These short repeatable sequences are called
minisatellites. Each person has a unique
minisatellite composition and by making use of
DNA fingerprinting technique this individual­
specific variation can be detected. The immense
importance of DNA fingerprinting was demon­
strated for the first time by Jeffreys and his col­
leagues in 1985, by using a minisatellite probe
chosen of a human myoglobin gene. The prob­
ability that any two individuals share the same
minisatellite sequence is 3 x IO11. If we use two
probes (for two distinct different minisatellite re­
gions), the probability further reduces to 5 X10'19.
Researchers have identified 20 such loci that are Fig. 15.8a Lip prints - Male
unique to an individual, thus increasing the di­
agnostic power of this technique enormously
However, the most common practice is to use 4-
5 probes simultaneously, thus increasing the di­
agnostic accuracy of this technique to 99.99%.
The technique can even be applied on a drop of
blood, a hair follicle or a loose scraping from
the skin of the victim. For forensic tests, gener­
ally the DNA of the second exon of the human
leukocyte antigen (HLA)-DQ-a is used most
commonly. The test that is widely used is
Amplitypez HLA-DQ-alpha Forensic kit, mar­
keted by Perkin-Elmer company. This procedure
has an accuracy of 98-99% but a newer proce­ Fig. 15.8b Lip prints - Female
dure, the Poly-Marker Test (PM), is supposed to (Courtesy Dr. Ratnakar Das former HOD Forensic
have up to 99.7% precision. Medicine, KMC, Manipal)

LIP PRINTS (Cheiloscopy) Legal aspects

Lip prints have been used as an identification aid Increased recognition of abuse/neglect has brought
in much the same manner as fingerprints. It is also rapid changes within the arms of the legal system
analogous to a bite mark analysis. Of the many dif­ and medical, dental and social services. Among
ferent types of lip prints, vertical, branched, inter­ the most important developments are impressions
sected and reticular patterns are most commonly of new legal duties on medical and dental profes­
found. Minor differences have also been observed sionals and the growing impacts of these profes-
 SECTION 15 : FORENSIC PEDODÓNTICS }

ions on the legally presented child abuse and den- may be helpful in the case, including physical
d neglect cases. evidence and comments obtained from question­
ing or interviewing.
Jasic knowledge of the legal aspects and practices ■ To remain objective toward all parties
ertaining to child protection is paramount. A den- ■ To treat any dental injuries
ist should be well versed with the current legal sys- ■ To establish and maintain a professional thera­
mi for child protection. A separate doctrine, par- peutic relationship with the family
nts patriae1, is also important in understanding laws ■ To hold the child whose life is in danger and
eveloped to protect children. Dental professionals transfer the child to a hospital or a physician for
hould know the definitions proposed of child abuse/ proper care.
eglect and existing related laws under the Draft
iodel Child Protection Act 1977, to protect him- Levels of prevention of child abuse/neglect
*lf and apply it correctly in child abuse/neglect
A pedodontist can contribute towards the preven­
ases. Dentists should strictly follow the don’t do1
tion of this criminal act by understanding various
r 'do always’ principles.
issues related to child abuse and applying them at
different level:
ertpin principles one has to remember in forensic
edodontics are:
Should always be fully aware of legal standards A. Primary level
•r'

of care and legal responsibilities The dentist can follow those approaches that are
Should keep legibly written, accurate case applicable to a population in general, without
records targeting a particular high risk group.
Records should be made in the presence of the ■ At this stage greater attention needs to be
patient given directed at screening children at a
Additions or corrections should never be made higher risk of mal-treatment
to alter the original records. However if correc­ « Greater use should be made of routine child
tions are inevitable, may be done and duly health supervisoiy visit to explore psychologi­
signed. cal issues.
Should keep update knowledge ■ Parents at risk for abusing their children are
Diagnostic tools like radiographs should always frequently very needy themselves, and being
be used preoperatively and post operatively nurturantto their children is difficult. Theie-
Avoid diagnosis and recommending treatment fore, they should be screened and counseled.
on phone ■ Comprehensive evaluation of child’s and
Should always be in consultation with legal/ family’s situation should be done assisted by
medicolegal expert to review insurance policies social worker and mental health professional.
or any financial, legal matter.
B. Secondary level
revention of child abuse - Rote of pedodontist » Secondary prevention concerns efforts di­
rected to those who are known or thought to
lgeneral, the dentist’s role who handles child pa­
be at a specially high risk for child abuse
ints in identifying and preventing child abuse/ne-
neglect
ect as follows:
■ It is important that pedodontists
To observe arid examine any suspicious evidence
his limitations and assume
that can be ascertained in the office
To record according to the law, any evidence that
 GQ I TEXTBOOK OF PEDODONTICS

Table 15.6: Sex identification

Distinguishing feature Male specific variations Female specific variations

Size of the mandible Large and broad Small and less broad

Mandibular angle Large, rough outer surface Small, smooth outer surface

Frontal angle Small Large

Palate Large and broad, U shaped Small, parabola like

Occipital condyle Large Small

Teeth Large, lower 1st molar, Small, more often 4-cusped

more often 5-cusped

parenting capabilities and family functioning organs of the victims, or their secondary sexual char­
thereby enabling them to a more adequate care acteristics. However, in mutilated bodies the essen­
for their children and avoid possible maltreat­ tial evidence for identifying the sex may be absent.
ment. Thus, we must look for alternative ways to recog­
nize the gender of the person in question. One of
C. Tertiarv level
the most reliable ways to identify the sex, is by look­
This level of prevention refer to interventions
ing for the sex chromosome. Another, less reliable
after the condition is already identified and it is
but most commonly used methodology is the iden­
really synonymous with the treatment. It is still
tification of Barf body in buccal smear. However, it
considered prevention because the goal is to pre­
is also possible to attempt sex identification with
vent a recurrence of the condition or the poten­
reliable accuracy, by a careful examination of the
tial negative sequelae.
teeth of the victims, as shown in the Table 15.6
■ This treatment of abused child depends on the
accurate identification of abuse and neglect. £

■ The pedodontist should ensure that child is

Self-Assessment
referred to a designated child protection
agency and the child’s situation is further
1. Define bjte, tooth and arch marks.
\ evaluated.
2. Classify bite marks based on aetiological factors.
« He should not make the report and disengage,
3. What is amorous bite mark?
as he often has valuable information which
4. What are the factors which affect bite mark in­
might help in treatment, monitoring the situ­
juries?
ation and facilitating the work of the child
5. What is Cheiloscopy?
protection agency.

DETERMINATION OF GENDER (Table 15.6)

Identification of sex, whether male or female can

easily be determined by examining the sexual
 15.4 Dental Age Assessment

Rao N, Tandon S

The determination of age plays a significant role months in the utero and is completed during the
within forensic science, not only in identification fourth year when the roots ofthe second primary
of bodies but also in connection with crimes and molar teeth are usually fully formed. The meth­
accidents. When the subjects have undergone ods used are:
changes so extensively that the characteristics yield
no information, the teeth are often the only means ■ Gravimetric method
of identification. In order to present as broad a pic­ In the foetus, or infant where teeth are not
ture as possible of this subject, some of the tech­ present in the mouth, any evidence of dental
niques that are in current use will be reviewed and development is concealed within the jaws. A
evaluated. To understand it more clearly, the age gravimetric observation can be made on the
determination can be considered in two periods. mineral content of foetal and infantile teeth
■ The developmental period which begins in the and relationship between the square roots of
utero and ends when dentition has reached ma­ the weights of the ashed teeth and the known
turity. age of the subject can be determined. This
■ The post developmental period which extends method appears to be a reliable method as the
from the time of dental maturation to termina­ variation in the rate of tooth development
tion of life. during this period is minimal:
(Third molars’s development has been consid­
ered in some of the studies for age assessment, « Histologic approach
but disregarded because of the extreme variabil­ In order to understand the rationale of this
ity in their time of emergence. Extensive re­ technique, a knowledge of the pattern of den­
search is needed in this direction). tine formation is necessary. Development of
the hard tissues of a tooth is a rhythmic proc­
In children, the determination of age is considered ess with the formation of successive layers of
during the first developmental period from the utero tissues. Evidence for this is to be found in
till the dentition matures. Methods that are used the incremental lines that can be observed mi­
can be applied to two separate timings as human croscopically in undercalcified sections of the
dentition is of two types. enamel and dentin. In primary teeth, wheBi
hard tissue formation begins prenatally and
I. THE DEVELOPMENTAL PERIOD is completed postnatally, the neonatal accen­
tuated incremental lines can sometimes be
A. Methods applicable during first stage seen, which is believed to reflect
First stage of development is when calcification in metabolism occurring during neonatalpe-
of primary dentition begins as early as three riod. This usually represents
 CTI | TEXTBOOK OF PEDODONTICS

days of retarded development. The presence Above mentioned methods can also be used dur­
of such lines confirms that infant had survived ing this stage for assessment of age but most com­
the first three to four weeks of life. It is re­ monly used method is visual supported with ra­
ported that deciduous dentin is produced at diographs. Gleiser and Hunt (1955) consider
the rate of four microns per day (Shour 1946) the degree of calcification of a tooth is a more
and it was suggested (Miles 1963) that meaningful indication of dental maturation than
mea suring the thickness of the dentin on the the time of its clinical emergence. The
pulpal side of the neonatal line can provide an evannescent (short time appearance) and elusive
indication of age. There are certain reserva­ nature of tooth emergence makes this factor of
tion about the use of this technique as the little value, when considered by itself, in the as­
neonatal line is not always readily discernible. sessment of age.

■ Visual and radiographic method In recent times, the following two methods have
As these two are regarded complementary to been most commonly in use for the estimation of
each other, these two methods are usually age:
applied together for age determination Visual
examination provides the information regard­ ■ Demerjian et al (1973) formulated a new method
ing the number of teeth that are present in of age by reference to the radiological appear­
the dental arches and the dentition to which ances of the seven teeth on the left side of the
they belong. Most of the chronological ta­ mandible. The maturity scoring system was
bles are the modifications of the findings of based on 2928 panoramic radiographs of 3 - 17
Logan and Kronfeld (1933) available to cor­ years old French Canadian children. Since the
relate the tooth development with age. authors stated that the system depended on the
population considered, this method was applied
The shortcoming of depending solely on this in South Kanara children b^r Serene and Tandon
visual observation is that the entire primary (1997). Unfortunately, the method was not ap­
dentition is usually functional by the begin­ plicable in Indian children in South Kanara.
ning of the third year and no significant
changes can be seen in the dental arches un­ ■ Mornstad et al (1994) estimated the age with
til the seventh year when the first permanent the aid of tooth development by a new method
molars emerge. Thus, visual examination of based on objective measurements, such as crown
the primary dentition could only provide in­ height, apex width and root length. A multiple
formation that would enable the professional regression model was used to demonstrate a lin­
state the age between 2 and 6 years. Radio­ ear relationship between some of these distances
graph would reveal the resorption of the roots and age.
of the primary teeth. (Fig. 15.9)
■ Based on the number of teeth erupted into the
B. Methods applicable during second stage oral cavity, Tounsend and Hammel (1999) have
This stage refers to calcification of the perma­ proposed a method. However, the variance in
nent teeth which begins during the first six tooth eruption limits the applicability of such
months after birth in the case of the incisors and methods to the population. Besides the number
canines, and ends with the completion of the of teeth enipted being a discontinuous variable,
roots of the second molars at about fifteen years. accurate age estimation can be done only during
Emergence of the teeth into the oral ca vity oc­ particular period of growth.
curs between the first and thirteenth years.
 SECTION 15: FORENSIC PEDODONTICS I fiR

MOLARS BICUSPIDS CANINES INCISORS

Fig. 15.9 Developmental stages of the permanent dentition

 frihit | TEXTBOOK OF PEDODONTICS

II. POST DEVELOPMENTAL PERIOD Further Suggested Reading For Section - 15

1. Alexander RC: "Current and emerging concepts

The physiological age changes occurring in teeth
in child abuse". Compo Ther. 1(12), 72-736,
during post natal period provide the principal clues 1995.
to the age of an individual. Teeth exposed to nu­ 2. American Board of Forensic Odontology7 Inc:"
merous environmental factors related to habit, cul­ Guide Lines for Bite Mark Analysis"’. JADA,
tural background, diet and superimposed pathology 112: 383-326, 1926.
may modify age changes seen in the crowns. 3. Askley KFIdentification of children in a mass
disaster by estimation of dental age”, Bri Dent
Gustafson (1950) introduced a multifactorial histo­ J, 129, 167-169, 1970.
logic approach to the determination of age and ad­ 4. Beckstead JW, Rawton RD and Gites WS: "Re­
vised an arbitrary scale of points. Many others have view of bite mark evidence”. JADA 99: 69-74,
suggested to record the secondary7 dentinformation, 1979.
transparency in root formation from the apex ap­ 5. Boys Jan: "Substances abuse and child abuse.
pears to be directly related to chronologic age and Impact of addiction on the child.” Pediatric Clin­
least affected by environmental factors. ics of North America. 37(4), 881-901, 1990.
6. Casamassmo Paul S: "Child sexual abuse and
Zander and Huzeler (1958) have measured the thick­ pediatric dentist”. Pediatric Dentistiy. 8(1); 102-
ness of the cementum covering the roots of the ex­ 105, 1926.
tracted teeth and suggested that this thickness of 7. Committee on Child Abuse and Neglect: Ameri­
the cementum can also be used to relate to the age. can Academy of pediatrics. Pediatrics. 87(2),
257-260, 1991.
8. Demirjin A, Goldtein H, Tanner JM; “The new
Any method which attempts to quantify age changes
system of dental age assessment”. Human Biol­
by the allocation of points from an arbitrary scale
ogy. 45 (2), 211-227, 1973.
should be questioned and careful and intelligent
9. Greenspan John S, Sueibba James: Oral mani­
evaluation of all the evidence is essential while as­
festations of HIV infection. Oral Siirg Oral Med.
sessing post developmental period.
Oral Pathol; 73: 142-144, 1992.
10. Gustafson G, Koch G: "Age estimation up to 16
years of age based on dental development”.
Self-Assessment
Odont Revy, 25, 297-306, 1974.
11. Gustafson G, Odent D, Malmo: “Age
1 ’ What is the importance of age determination in
determinations. On teeth”. The Journal of the
forensic pedodontics? American Dental Association. 41, 45-51, 1950.
2. What is the role of pedodontics in prevention of
12. Hymel KP, Jennc: “Child sexual abuse”. Del Med
child abuse? -J, 69(8), 415-429, 1997.
3. What is DNA fingerprinting?
13. Jacobson JR and Keisen - Neilsen S: “Bite mark
4. Which chromosomal loci are frequently used in
lesion-human skin” - Forensic Sci-Int, 18: 41-
DNA fingerprinting technique?
55, 1981.
5. What are the indications of Gravimetric method? 14. Jessee SA: “Oral manifestations of child abuse
6. What is the basis of age determination method and neglect”. Am-Fam-Physician, 52(6), 1829-
suggested by Tounsend and Hammel?
1834, 1995.
 SECTION 15 : FORENSIC PEDODONTICS {

!5.Koshy Serene, Tandon Shobha: “Dental age as­ students - a plot study”. Journal of Pediatric Den­
sessment the applicability of demirjian, method tistry, 22(1), 23-27, 1997.
in south Indian children ". Forensic Science In­ 26. Thomas JD: “Adjuactive use of scanning elec­
ternational, 94, 73-85, 1998. tron microscope study in bite mark analysis. A
16. Levin LJ: “Bite mark evidenced Dental Clinics three dimensional child abuse study” J. Foren­
of North America. 21(1), 145-150, 1971. sic Sci, 31(3), 1126-1134, 1986.
17. Luntz LL: “History of forensic dentistry”, 27. Tsuchihashi Y: “Studies on personal identifica­
DCNA, 21, 7-17, 1977. tion by means of lip prints”. Forensic Sci: 3(3),
18. McDonald: “Bite mark recognition and inspec­ 233-48, 1974.
tion” J. Forensic Sci Soc. 14: 229, 1974. 28. Tsushihashi Y: “Studies on personal identifiica-
19. Miles AEW: “Dentition in the estimation of age’, tionby means’of lip prints”. Forensc. Sci. 3,232-
J Dent Res, 42,255-263, 1963. 248, 1974.
2().01eske J, Minnetor A, Cooper R: “Immune de­ 29. Veingood GM, Diclemaie RJ: “Child sexual, HIV
ficiency syndrome in children”. JAMA, 249: sexual risk and gender relations of African -
2345-2349, 1983. American Women”. Am-J-Preu-Med, 13(5),
21. Reymond AC: “Bitemark”, Cited in Australian 380-384, 1997.
Lecture Series, University of Adelaide, 1995 - 30. Young EA, Abelsar JL, Curtis GL, Nessee RM:
1996. “Childhood adversity and vulnerability to mood
22. Rothwell BR: “Bite mark in forensic dentistry - and anxiety disorders”. Depress Anxiety 5(2);
A review of legal, scientific issues”. J AD A 126: 66-72, 1997.
223-232, 1995. 31 .Rao NG 4 Textbook of Forensic Medicine and
23. Stikas Peter: “Does the dentist has an ethical duty Toxicology’ led, JP Brothers Medical Publish­
to report child abuse”. The JADA, 127,521-523, ers (P) Ltd: 78,2000.
1996. 32. Whittaker DK, Marson JK, in Paedritic Foren­
24. Suzuki K, Tsushihashi Y: “Two criminal cases sic Medicine and Pathology, Champman and
of lip prints”. Acta Crim Jpn, 41: 61-64, 1975. Hall Medical, London, 100-130,1989.
25. Tavras Athanasias L, Pai Lori: “Child abuse at­
titudes and perception of health professional
 Appendix

1. CLINICAL DIAGNOSIS OF OPACITIES OF ENAMEL

Characteristics Milder Form of Non Fluoride Incipient Dental

Fluorosis Enamel Caries
Opacities

1. AREA Usually on or near the tips Usually centered in Usually seen on smooth
AFFECTED of cusps or incisal edges smooth surface, may surface near cervical
‘snow cap’ phenomenon affect entire crown margin or contact area
at proximal surface

2. SHAPE OF Resembles line shading in Often round or oval Usually circumscribed

LESIONS pencil sketch; lines follow covered with plaque
incremental lines or
perikymata forming
irregular caps

3. DEMARCA­ Shades off imperceptibly Clearly differentiated Visible only on drying

TION into surrounding normal from adjacent normal the surface
enamel, glazed appearance enamel, may be seen
etched
A*
4. COLOUR Slightly more opaque than Usually pigmented at Do not present at the
enamel, paper white, may time of eruption, often time of eruption appears
have frosted appearance, creamy-yellow to dark as white, opaque
does not show stain at reddish orange frosted appearance
time of eruption

5. TEETH Most frequent teeth that Frequent on labial Any tooth may be
AFFECTED calcify slowly cuspid, surfaces of lower affected depending
bicuspid, second and third incisors may occur upon the local
molars, rare on lower single. Usually one attack of acid.
incisors, usually seen 6 or to three teeth Both the dentitions
8 homologous teeth affected, common get affected
extremely rare in primary in deciduous teeth
teeth

6. DETECTION Often invisible under strong Seen most easily Seen under fiber
light, most easily detected under strong light optic light at an angle
by line of sight tangential on line of sight, to the tooth surface
to tooth. perpendicular to
Distinguished after cleaning tooth surface
the tooth
 APPENDIX I

2. CAUSES OF TOOTH DISCOLOURATION

A. INTRINSIC STAINS
Generalized staining of single or complete dentition

Color Etiology Features

White Fluorotic/non-fluorotic Usually on permanent dentition.

Red/brown Congenital porphyria All teeth affected.

Opalescent teeth Dentinogenesis imperfecta All teeth uniformly affected, maybe

[blue/brown] associated with osteogenesis
imperfecta.

Green /blue Hyperbilirubinaemia Seen in children with end stage

liver disease and premature infants.

Yellow /brown Amelogenesis imperfecta Both dentitions are affected.

to dark yellow

Grey/brown Non-vitality Usually post trauma.

Localized staining on one or several teeth

Grey/black Amalgam staining Leakage of old amalgam restoration

causing discolouration around the
restoration.

Pink Internal resorption Post trauma or seen prior to

exfoliation of primary teeth.

White Developmental defect Subsurface decalcification in

* permanent teeth, post trauma,
infection.

Yellow/brown Developmental defect Usually post trauma or infection.

Chronological staining of dentition

Bright yellow Tetracycline Un oxidised fluorophore seen in

newly erupted teeth.

Yellow/grey Tetracycline Erupted teeth; oxidized fluorophore

brown [UV light] color also depends on the
type of tetracycline.

B. EXTRINSIC STAINS
Black Silver fluoride treatment ferrous Iron supplementation
sulphate

Brown Chromogenic bacteria Arrested caries

Yellow Bile pigments from gingival Billiary atresia and jaundice

crevicular fluid

Green Chromogenic bacteria Usually cervical and gingival area

 1 TEXTBOOK OF PEDODONTICS

3. CAUSES OF INTRA-ORAL BLEEDING

1 Local causes II. Systemic causes

a) Post - extraction bleeding a) Structural malformations

b) Traumatic i) Hereditary disorders of connective tissue
i) Iatrogenic Ehler’s - Danlos syndrome
Cotton roll injury Osteogenesis imperfecta
Denture injury Pseudoxanthoma elasticum
Surgery ii) Acquired disorders of connective tissue
ii) Self inflicted Corticosteroid purpura
Decubitis ulcer Senile purpura
Factitial injury Cachectic purpura
Pathomimia mucosae oris b) Infections
Morsicatio labiorum i) Bacterial
Morsicatio bucarum Septicemia
c) Gingivitis (inflammation) Typhoid
d) Local infections Scarlet fever
e) Physical Diphtheria
Calculus Tuberculosis
Food Endocarditis
f) Chemical Leptospirosis
a) Ulcer ii) Viral
Small pox
b) Structural malformations Influenza \
Hereditary hemorrhage Measles
telangiectasia AIDS
Hemangioma iii) Protozoal
Malaria
c) Tumours Toxoplasmosis
Benign iv) Rickettsial
Malignant v) Fungal
c) Autoimmune:
i) Allergic purpura
ii) Drug induced vascular purpura
iii) Purpura fulminans

d) Deficiency state
Vit C. deficiency
i) Disorders of WBC
Infectious mononucleiosis
Leukemia
ii) Disorders of RBC
Polycythemia
iii) Disorders of platelets
Purpura
Thrombocytosis

contd.
 APPENDIX | '21

4
iv) Disorders of clotting factors
Hemophilia
Von WiHibrand’s disease
Afibrinogenemia
Parahemophilia
e) Disorders of blood vessels
Lingual varicosity
Friable vessel wall
f) Miscellaneous
Kaposis sarcoma
Snake venom
Hemochromatosis

4. ENDOCRINE GROWTH AXIS

CEREBRAL CORTEX i

Sends stimulus

HYPOTHALAMUS

Releases

Cesation of GHRF to maintain balance

GROWTH HORMONE RELEASING FACTOR
(GHRF)

Acts on
SOMATOSTATIN
■1
ANTERIOR PITUITARY

Releases
PANCREASE
GROWTH HORMONE
£

Goes to
EXCESS OF GROWTH HORMONE
LIVER

Liberates
FEED BACK MECHANISM
SOMATOMEDIN

GROWTH OF BONE
AND
OTHER TISSUES
 tíif^ I TEXTBOOK OF PEDODONTICS

5. COMPARISON OF NORMAL DIAGNOSTIC VALUES

Newborn Infancy Childhood Older Ages

___________________________ HEMATOLOGY & RETICULOENDOTHELIAL SYSTEMS

Hematocrit 42-63% 30 - 40% 31 - 43% M : 42 - 52 £

F : 37 - 47

Hemoglobin (g/dl) 14 - 20 10-15 11 - 16 M: 14- 18

F : 12 - 16

RBC(x 10 /cu.mm.) 4.4 - 5.8 3.8 - 5.5 3.8 — 5.5 M: 4.7-6.1

F : 4.2 - 5.4

Leukocyte count 9-13 6- 17 4.8 - 10.8

(x 10 3 per cu. mm.)

Platelets 100 - 290 200' -450 150-450

(x 10 3 per cu. Mm.)

ESR (mm per hr.) 0-2 3 -13 3 - 13 M: 1 - 15

F : 1 - 20

Bleeding time (Ivy) 1-8 min 1-6 min

Lee - White clotting 5-8 min

time (test tube at room
temperate)

Prothrombin time <17 sec. 11-14 sec.

Partial thromboplastin <90 sec 24 - 40 sec.

time

Serum iron (mg/dl) 100- - 250 40-100 50-120 M: 60-150

F : 50-130

Serum iron binding 50 -160 100 - 400 M : 250 - 400

capacity( mg/dl) F : 150-450

Fibrinogen (mg/dl) 125 - 300 150 - 450

SERUM ELECTROLYTES

Sodium (mEq/L) 134 - 144 139-146 138 - 145 135 - 148

Potassium (mEq/L) 3.7-5 4.1 - 5.3 3.4 - 4.7 3.5 - 5.3

Calcium (mEq/L) 5.9-10.7 9-11 8.8 - 10.8 86 - 10.4

NORMAL VALUES OF RENAL FUNCTION

Serum creatinine (mg/dl) 0.6 - 1:2 0.2 - 0.4 0.3 - 0.7 0.5-1

Serum urea nitrogen (mg/dl) 21 - 40 5- 18 7-18

TESTS OF LIVER AND GIT FUNCTION

Total serum protein (g/dl) 4.6 - 7.4 6.1 -6.7 6 - 8

Serum albumin (g/dl) 3.6 - 5.4 4.4 -5.3 3.5-4.7

 APPENDIX )

6а. CHRONOLOGY OF PERMANENT AND DECIDUOUS DENTITION

Tooth Hard tissue Amount of Enamel Eruption Root

Formation enamel completed completed
begins formed at birth

Deciduous
dentition
Maxillary
Central incisor 4 mo in utero Five sixths 134 mo 734 mo 114 yrs
Lateral incisor 414 mo in utero Two-thirds 234 mo 9 mo 2 yrs
Cuspid 5 mo in utero One-third 9 mo 18 mo 3% yrs
First molar 5 mo in utero Cusps united 6 mo 14 mo 214 yrs
Second molar 6 mo in utero Cusp tips still 11 mo 24 mo 3 yrs
isolated

Mandibular
Central incisor 414 mo in utero Three-fifiths 214 mo 6 mo 114 yrs
Lateral incisor 434 mo in utero Three-fifths 3 mo 7 mo 114 yrs
Cuspid 5 mo in utero One-third 9 mo 16 mo 314 yrs
First molar 5 mo in utero Cusps united 534 mo 12 mo 214 yrs
Second molar 6 mo in utero Cusps tips still 10 mo 20 mo 3 yrs
isolated

Permanent
dentition

Maxillary
Central incisor 3-4 mo 4-5 yrs 7-8 yrs 10 yrs
Lateral incisor 10-12 mo 4-5 yrs 8-9 yrs 11 yrs
Cuspid 4-5 mo 6-7 yrs 11r12 yrs 13-15 yrs
First bicuspid 134 - 1% yrs 5-6 yrs 10-1T yrs 12-13 yrs
Second bicuspid 2-214 yrs 6-7 yrs 10-12 yrs 12-14 yrs
First molar At birth Sometimes trace 214 - 3 yrs 6-7 yrs 9-10 yrs
Second molar 2% - 3 yrs 7-8 yrs *13
12 yrs 14-16 yrs
Third molar 7-9 yr 12-16 yrs 17-21 yrs 18-25 yrs

Mandibular
Central incisor 3-4 mo 4-5 yrs 6-7 yrs 9 yrs
Lateral incisor 3-4 mo 4-5 yrs 7-8 yrs 10 yrs
Cuspid 4-5 mo 6-7 yrs 9-10 yrs 12-14 yrs
First bicuspid 1% - 2 yrs 5-6 yrs 10-12 yrs 12-13 yrs
Second bicuspid 2% - 234 yrs 6-7 yrs 11-12 yrs 13-14 yrs
First molar At birth Sometimes trace 214 - 3 yrs 6-7 yrs 9-10 yrs
Second molar 234 - 3 yrs 7-8 yrs 11-13 yrs 14-15 yrs
Third molar 8-10 yrs 12-16 yrs 17-21 yrs 18-25 yrs

(Logan and Kronfeld, 1933) contd.

CËB I TEXTBOOK OF PEDODONTICS

6b. CHRONOLOGY OF DECIDUOUS DENTITION

Tooth Hard tissue Amount of Enamel Eruption Root

Formation enamel completed (+ ISD) completed
begins (in utero) formed at birth months yr

Deciduous
Dentition
Maxillary
Centrai incisor 14 (13-16) wk Five-sixths V/2 mo 10 (8-12) 114
Lateral incisor 16 (14 2/3-16% wk Two-thirds 214 mo 11 (9-13) 2
Canine 17 (15-18) wk One-third 9 mo 19 (16-22) 3%
First molar 15% (14% -17) wk Cusps united; 6 mo 16 (13-19) 214
occlusal comp- boys
letely calcified (14-18)
plus a half to girls
three-fourths
crown height
Second molar 19 (16-23%) wk Cusps united; 11 mo 29 (25-33) 3
occlusal incom­
pletely calcified;
calcified tissue
covers a fifth
to a fourth
*
crown height X

Mandibular
Central incisor 14 (13-16) wk Three-fifths 214 mo 8 (6-10) 114'
Lateral incisor 16 (14 2/3) wk Three-fifths 3 mo 13 (10-16) 114
Canine 16 (16-) wk One-third 9 mo 20 (17-23). 37
First molar 15% (14% -17) wk Cusps united; 514 mo 16 (14-18) 2%
occlusal comp­
letely calcified
Second molar 18 (17-19%) wk Cusps ypited; 10 mo 27 (23-31) 3
occlusal incom­ boys
pletely calcified (24-30)
girls

(Lunt and Law, 1974)

 APPENDIX |

7. COMMON ABNORMALITIES OF DECIDUOUS DENTITION

Abnormality Etiology Treatment

1. Protrusive maxillary Habits Habit awareness

incisor Thumb sucking Reminder appliance
Lip biting Habit breaking appliance
Tongue thrusting Myofunctional therapy

2. Retracted maxillary Inherited growth pattern Tongue blade

incisor (anterior Imitation biting habits Inclined plane
cross bite) Difficult teething during Removal of incisal interference
deciduous molar eruption

3. Posterior cross bite Pressure habits Maxillary expansion

Digit sucking Occlusal grinding to remove
Mouth breathing interferences
Complete overclosure of Acrylic biteplane
mandibular arch

4. Open bite Oral habits Habit breaking appliance

Self correction may occur

5. Deep over bites Premature loss of deciduous Acrylic bite plane

molars Partial dentures

Common abnormalities of the mixed dentition

1. Protrusive maxillary Thumb sucking Patient motivation

permanent incisors Mouth breathing Reminder therapy
Tongue thrusting Orthodontic correction
Myofunctional therapy for
Lips

2. Retracted maxillary. Inherited growth pattern Tongue blade

incisors (anterior Retained maxillary deciduous Inclined plane
cross bite) incisors Upper lingual arch
Lack of space with springs
Trimming or extraction of
cuspids to create space

3. Open-bite Tongue thrusting Mechanotherapy

Thumb sucking

4. Crowding Tooth size arch length Space analysis

discrepancy Habit correction
Habits Proximal stripping
Serial extraction
Orthodontic treatment
 | TEXTBOOK OF PEDODONTICS

8. COMPARISON OF PSYCHOLOGICAL THEORIES

AGE MAHLER FREUD PIAGET ERIC ERICKSON

0-1 ■ Normal autistic a Oral phase ■ Sensorymotor • Basic trust vs basic

phase (birth to 1 yr.) = phase (birth to mistrust (birth to 1 yr.)
« Normal symbolic 2yrs)
phase
■ Sub-phase of
separation
individuastion
phase:
1st sub-phase -
differentiation
(5-10 months)

u
1 -2 ■ 2nd sub-phase­ ■ Anal phase ■ Autonomy vs shame &
practicing (10 - (1 to 3 yrs) doubt (1-3 yrs)
16 months)
■ 3rd subphase-
rapproachmet
(16- 24 months)

u a
2-3 ■ 4th sub-phase a Preoperational
consolidation & phase (2 to
object constancy. 7 yrs)
(2 to 3 yrs)

a
3-5 - ■ Phallic - ■ Initiative vs guilt (3 -
Oedipal phase 5 yrs)
(3 - 5yrs)

a
5-6 • Latency period —
(5/6 to 11/12
yrs)

u
6-11 - ■ Concrete ■ Industry vs inferiority
operational (6-11 yrs)
phase (7-
11 yrs)

11 + - « Genital phase ■ Formal phase ■ Identity vs role

from 11-12 yrs (11 yrs through confusion (11 yrs
and beyond) adolescence) through end of
adolescence)
 APPENDIX 1

9. STAGES OF NURSING-BOTTLE CARIES

Stages Average Age Clinical appearance

1. Initial 10-20 months Maxillary anterior teeth: opaque-white demineralization

cervical/interproxim al

2. Damaged 16-24 months Maxillary anterior teeth: yellow-brown discoloration

Cervical/interproximal, superficial defects
* #54, #64:
fist stage

3. Deep lesions 20-36 months Maxillary anterior teeth: marked enamel defects; pulpal
irritations. #54, # 64: second stage, # 74, #84; first stage

4. Traumatic 30-48 months Maxillary anterior teeth: loss of large enamel/dentin parts,
crown fractures, #54, #64: third stage. #74, #84: second
stage

10. COMPARISON OF CONVENTIONAL AND RECENT MODELS OF CARIES MANAGEMENT

/
20th Century Conventional Model 21st Century Recent Model

Develop treatment plan at first visit Provisional diagnosis and risk assessment

Assume that all lesions are active Determine caries activity over time

Restore lesions in inner half of enamel Remineralize noncavitated enamel lesions

Restore all lesions in dentin Restore only cavitated lesions

Assume that fillings control disease Reduce infection risk; restore if necessary

When in doubt, intervene surgically When in doubt, seal, repair, or remineralize

 TEXTBOOK OF PEDODONTICS

11. TREATMENT PROTOCOL FOR NURSING CARIES

I. PREVENTIVE

HOME CARE BY PARENTS:

« Elimination of cariogenic substrate
■ Substitution with tooth friendly food
« Discouraging bottle feeding at night
■ Fall asleep pacifiers should abandon
■ Gumpad cleaning during infancy period
« ‘Well baby' examination within 6 months of eruption of the first tooth
■ Digital or baby tooth brushing
■ Initiating mouth rinsing habit after consuming any solid or drinks
■ Regular visit to dental clinic once in six months

PROFESSIONAL CARE BY DENTIST:

• Educating parents regarding importance of deciduous teeth
■ Diet counseling with the parent preferably involving child paediatrician
■ Dental health education to parents regarding gum pads cleaning, tooth brushing,
frequent mouth rinsing
■ Advocating fluoride supplementation if bio availability of fluoride is deficient and
child is of high caries risk
■ Advocating fluoride containing dentifrices once a day only after four years of age
■ Applying fluoride varnish topically
« Application of fissure sealants in first and second primary molars
■ Regular recalls for routine monitoring for dental health K
■ Reinforcing and motivating parents to continue supervised home care

II. RESTORATIVE

Incipient or white spot carious lesions

■ Professional topical fluoride application and observation of the lesion for reversal
■ Fissure sealant application

Carious lesions in enamel / dentin

■ Preventive resin restoration
■ Glass ionomer fillings
■ Composite crowns in anteriors
■ Posterior composite restoration
■ Amalgam preferably gallium alloy of restoration in posterior teeth
• Nickel chrome stainless steel crowns
• Fuk crowns
■ Polycarbonate crowns

Carious lesions with pulp involvement

■ Pulp therapy with full coverage coronal restoration
■ Extraction with space management
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TEXTBOOK OF PEDODONTICS

13a. VACCINATION SCHEDULE-INDIAN ACADEMY OF PEDIATRICS (1999)

Age Vaccine

Birth BCG
Oral Polio vaccine - 1
* dose
Hepatitis B vaccine -1st dose

6 weeks * dose
DPT - 1
Oral. Polio vaccine - 2nd dose
Hepatitis B vaccine - 2nd dose

10 weeks DPT - 2nd dose

*
Oral Polio vaccine - 3rd dose

14 weeks DPT - 3rd dose

Oral Polio vaccine - 4d dose

6-9 weeks Oral Polio vaccine - 5th dose

Hepatitis B vaccine - 3rd dose

9 months Measles vaccine

15-18 months MMR(Measles, Mumps, Rubella)

DPT - 1st booster \
Oral Polio vaccine - 6th dose

5 years DPT - 2nd booster dose

Oral Polio vaccine - 7th dose

10 year * booster dose

TT(Tetanus) - 3"
Hepatitis B vaccine - booster dose

15-16 years TT(Tetanus) - 4th booster dose

OPTIONAL VACCINE Typhoid fever vaccine

Haemophillus influenzae type - b vaccine
Hepatitis A vaccine
Varicella (chicken pox) vaccine
 APPENDIX I «Cib

13b. VACCINATION SCHEDULE AT K.M.C. MANIPAL

Age Vaccine

Birth Oral Polio vaccine - zero dose

2 months DPT
Haemophilus influenzae
Oral Polio vaccine - 1st dose

4 months DPT
Haemophillus influenzae
Oral Polio vaccine - 2nd do. 3

6 months DPT
Haemophillus influenzae
Oral Polio vaccine - 3rd dose
Hepatitis vaccine (three doses at interval of 0, 1, 6 months)

15th month MMR

1.5 years DPT -1st booster

H.influenzae - 1st booster
Oral Polio vaccine - 1st booster

4-5 years DPT - 2nd booster

Oral Polio vaccine - 2nd booster

10 year * booster
DPT - 3"
Oral Polio vaccine -3rd booster

VACCINE AT RURAL CENTRE KM.C./PAHENT WHO CAN

AFFORD

BCG Birth With 2nd dose of DPT or with

3rd dose of DPT

DPT ■ 1.5 month 1st dose Tetramune (DPT with H

■ 2.5 months 2nd dose influenzae type B)
■ 3.5 months 3rd dose ■ 1.5 month
■ 2.5 month
■ 3.5 month

OPV ■ Birth “0” dose Same as in Rural center

■ 1.5 month (with 1“ DPT)
■ 2.5 month (with 2nd DPT)
■ 3.5 month (with 3rt DPT)

Measles/ MMR Measles at 9 months MMR at 15

* month

Booster dose 1s* booster at 1.5 years

■ DPT 2nd booster at 5 years (DT/DPT)
■ OPV
 I TEXTBOOK OF PEDODONTICS

14a. EFFECTS OF DIFFERENT FLUORIDE CONCENTRATION (PLASMA PEAK) ON ENAMEL FORMATION

Developmental Fluoride level Effect

stages

Cell proliferation 1 p mol/L and above - Cell inhibition

- Cell death
3 p mol/L and above - Delayed differentiation
- Epithelial - mesenchymal interaction
affected
0.2 p mol/L - Cell vacuolation and matrix accumulation
- Slight increase in polar amino acids
- Slight decrease in protein break down

26.5 p mol/L - Slight elevation of existing mineral

53 p mol/L - New matrix fails to mineralize

Transition Upto 159 p mol/L - Accumulation of F * with increasing dose

in tissue
- Persistence of prolin rich matrix
(amelogenin)

Maturation 10.6 p mol/L - Dramatic slowing of ameloblast

modulation
- Increased protein content
- Incomplete maturation and çrystal
growth inhibited z
- Increase in magnesium content

14b. REPORTS ON SLOW RELEASE FLUORIDE DENTAL MATERIALS

Study System Effect

Fazzi et al (1977) Amalgam Release fluoride, decreased with time

Henry and Friedman (1984) Acrylic plates Release fluoride, but frequent
application required

Cooley et al ( 1988) Composite resins Variable rate of fluoride release,

short term

Cooley et al (1990) Fissure sealants Release for 7 days

Habiovisc-Kofman and Glass ionomer Release up to 1 year

Koch (1991) sealants
 APPENDIX I

14c. REPORTS ON SLOW RELEASE FLUORIDE IN HUMANS

Study System Duration Finding

Crowsar et al (1976) Copolymer 30-180 days Salivary F increases

Mirth (1980) Tablets/capsules 16 hr Salivary F increases

Kuala et al (1987) Copolymer 6 months Salivary F increases

Shyama and Tandon Sodium fluoride 19 months Salivary F increases

(1991) tablet even with low
concentration of F

Toumba and Curzon Glass Ionomer 6 months Salivary F increases

(1992)

Tandon and Paul Dentifrice 24 months Both high and low F

(1993) concentration have
shown equal cumulative
effect

15. FLUOROSIS ASSESSMENT (DEAN’S INDEX 1945)

Grade of fluorosis Description DFI (dental

fluorosis index)

Normal None 0

Questionable A few white flecks or white spots. 0.5

Very mild White opacities are more extensive but do not

involve more than 25% of the surface. 1.0

Mild White opacities are more extensive but do not

involve more than 50% of the surface. 2.0

Moderate Distinct brown stains, all enamel surfaces 3.0

affected.

Severe Besides brown staining, the tooth is worn and

hypoplastic. All enamel surfaces affected. 4.0
 | TEXTBOOK OF PEDODONTICS

16. MATERIALS GUIDANCE IN PEDIATRIC DENTISTRY

Primary dentition Materials to be used

Class I • Glass ionomer

■ Amalgam
■ Composite resin

Class II ■ Glass ionomer

■ Amalgam
■ Composite resin
« Stainless steel crown

Grossly carious tooth or endodontically ■ Stainless steel crown

treated

Permanent dentition Material to be used

Occlusal pit and fissure ■ Fissure sealant

Occlusal enamel caries, occlusal enamel

caries with minimal involvement of dentin. • Preventive resin restoration
• Composite resin

Class I, Class II, Class III Caries. ■ Amalgam

■ Composite resin

Class V ■ Glass ionomer

• Composite resin

17. RELATIVE CHARACTERISTICS OF MATERIALS FOR POSTERIOR RESTORATIONS

PROPERTY AMALGAM COMPOSITE COMPOMER RESIN-MODIFIED

GLASS IONOMER

Biocom patability Good Good Good Good

Technique Very low Moderate Moderate Very high

Sensitivity to high to high

Average Survival 10-15 years 5-7 years 3-5 years 2-3 years
time (estimate) (estimate)

Wear Resistance Excellent Occlusal: Fair Fair to poor

Very good
Approximal:
Fair in Poor

Fracture resistance Good Good Fair to good Fair to good

Marginal Integrity Poor Good Good Very good

Esthetics Very poor Excellent Good to excellent Fair to very good

Relative Cost Rs. 300.00 Rs. 600.00 Rs. 600.00 Rs. 400.00
(Two - Surface)
18. P R E V E N T IV E P R O T O C O L F O R P E R IO D O N T A L D IS E A S E

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 I TEXTBOOK OF PEDODONTICS

19. MAJOR EXANTHEMAS IN CHILDREN

DISEASE AGENT EXANTHEMAS ASSOCIATED

FINDINGS

Measles Measles virus (RNA Purple red papules Koplik spots, high fever,
(Rubeolla) paramyxo virus) starting on face, moving toxicity, conjunctivitis,
downward, reaching feet; photophobia, coryza,
coalescent on trunk cough, lymphadenopathy

Rubella Rubella virus (RNA) Discrete pink-red papule Forchheimer spots, mild
starting on face, spreading fever, malaise, occipital
downwards rapidly. and posteroauricular
adenopathy.

Roseola Unknown Discrete pink non-coalescent High fever 3-5 days,

macules in central distribut­ children seem well
ion (trunk, face, and proximal despite fever.
extremities) appear as fever
decreases.

Enterovirus Coxsackie virus A Highly variable, macular, Non-specific fever,

and B, echovirus papular rubelli form, petechiae. myalgias, headache.
- V .............. . ..... ..

Coxsackie A16, A5, Ulcers of buccal mucosa, -do-

A10 scattered vesicles on hands
and feet

Erythema Human parvovirus “slapped cheeks”, pink red Children appear well,
infectiosum lacy reticular eruptions' on trunk occasional mild flu like
and extremities, recrudescent symptoms.
up to several week.

Varicella Varicella zoster Pruritic papulo-vesicles in Fever, malaise,

virus (DNA herpes different stages of develop­ myalgias.
virus) ment in central distribution,
mucous membrane
involvement common.

Scarlet fever Group A-B-hemolytic Tiny red papules with rough, Pharyngitis, strawberry­
streptococci. sand- pappery texture, more resembling tongue,
intense in skin folds and areas generalized
of warmth, Pastia’s lines. lymphadenopathy,
late desquamation.
 Index

A Anxiety 134
Anxiety Rating Scale 134
A.R.T. Restorations 307
Apexification 357. 520
Abdominal reflexes 59
~Apexogenesis 357,520
Abnormalities of deciduous dentition 724
Aphthous ulcers 679
Access opening for puipectomy 350
Apicoectomy 487
Acute necrotising ulceratice gingivitis 659
Aplastic anemia 554
Acute toxicity 261
Appraisal 134
Acyanotic congenital heart disease 547
Arch height 111
Adenoids 56
Arch length 111
Adsorption and ion exchange method 263
Arch mark 706
Adult caries 181
Arch width 111
Advanced diagnostic aids 11
Arrested caries 180
Age changes in mandible 73
Arterial haemangioma 676
Age changes in maxilla 71
Askali - extract 265
Aggressive bite marks 707
Associated syndrome 576
AIDS 566
Asthma 553
AIDS vaccine 572
Asymmetric tonic neck reflex 58
Alteration in the size of teeth 99
Attached gingiva 654
Alteration of shape 99
Attitude of the dentist 536
Alternative to amalgam 305
Attitude of the parents 536
Alveolar process 73
Attitude of the patient 536
Amalgam 303
Attitude of the society 536
Ambulatory, outpatient or day care
Attitudes of children 34
anesthesia 154
Attribution 134
Amniocentesis 638
Audio analgesia 150
Amorous bite marks 707
Autism 554
Analytical epidemiology 691
Autosomal disorders 632
Aneuploidy 623
Autosomal dominant 632
Anger 131
Autosomal recessive 634
Anhydrous 294
Aversive conditioning 151
Anorexia nervosa 175
Anterior space regainer 408 B
Anthropometry 77
Babinski’s reflex 58
Antibiotic prophylaxis 529
Balanced diet 224
Antibiotic resistance 529
Band 390
Antibiotic therapy 528
Band and loop 394
Anticipatory guidance 214
Band construction 390
 I TEXTBOOK OF PEDODONTICS

Band material 390 Capillary haemangioma 676

Band pinching 390 Capillary lymphangioma 678
Battered baby 700 Carbohydrates 201, 225
Behaviour 121,139 Caries 178
Behaviour management 121, 146 Caries activity tests 194
Behaviour shaping 147 Caries detection 196
Behavioural Pedodontics 139 Caries index 9
Behavioural science 139 Caries management 727
Benign micro-organisms 267 Caries risk assessment 192
Bichat’s fat pad 56 Caries tetralogy 187
Biocompatibility 297 Caries vaccine 268
Biofeed back 150 Carlo gram 195
Biometrics 75 Case-control study 691
Bionator 424 Cause of anxiety 134
Biostatistics 692 Cavernous lymphangioma 678
Biotransformation 463 Cavitation 179
Birth history 8 Cellulitis 684
BIS-GMA 234 Cementation 322
Bite 706 Cephalometric radiography 24
Bite mark 706 Cerebral palsy 541
Bite mark analysis 709 Cervical lymphodenopathy 571
Bite registration 422 Chairside general anesthesia 160
Bitewing 20 Characteristic of human dentition 86
Bitewing radiograph 22 Characteristics of phobia 136 K
Bizarre marks 703 Cheek biting 456
Black’s classification 278 Chemico parasitic theory 185
Bleeding 720 Chemistry of fluoride 245
Blindness 546 Cherubism 685
Blink reflex 58 Chewing gums 268
Blood analysis 639 Chickenpox 681
Body proportions 47 Child abuse 698, 700
Body type 366 Child psychology 121
Bonded space maintainers 398 Chin 73
Bone grafting 589 Chin cap 425
Bone morphogenetic protein 347 Choking off phenomenon 255
Bottle feeding 212 Chondrocranium 48
Bovine milk and whey 270 Chorionic villus sampling 639
Bowen 234 Chromosomal abnormalities 622
Breast feeding 212 Chronic marginal gingivitis 658
Broadbent phenomenon 116 Chronic Myeloid leukemia 637
Bruxism 450 Chronic renal failure (CRF) 564
Bunocore 233 Chronic sialadenitis 684
Burkitt’s Lymphoma 637 Circumference 111
Burns 510 Clamps 285
Clark twin block 424
C
Classes of nutrients 224
Calcium hydroxide 306, 340, 354, 360 Classical conditioning 125
 INDEX | ^EE>
Classification of analgesics 526 Cyclic neutropenia 669, 672
Classification of child’s behaviour 139 Cystic fibrosis 552
Classification of early childhood caries 201
D
Classification of pit and fissure 234
Classifications for cavity 278 Deafness 545
Clay minerals 265 Deciduous dentition 107
Cleaning of gum pads 215 Deep sedation 154
Cleft lip and palate team 581 Defiant person 171
Cleft palate 574 Defluoridation 263
Cluster sampling 693 Deletion 622
Cohort study 691 Demineralization 244
Cold beverages 246 Dental aae 95
Colour of gingiva 656 Dental materials containing fluoride 259
Combined nalgonda and calcined magnesite Dentifrice 245
technique 264 Descriptive epidemiology 691
Common developmental disturbances of teeth 97 Desensitization 148
Communication 29 Determination of age 713
Communicative management 146 Development of fear 132
Community water fluoridation 250 Devitalization 342
Compensatory cry 131 Diabetes mellitus 550
Complete dentures 603 Diabetic emergencies 551
Compomer 294 Diagnosis 6
Composite inclines 416 Diagnostic values 722
Composite resins 298 Diet 224
Composition of films 20 Diet counseling program 225
Computerized tomography 25 Diet diary 228
Concious sedation 154, 157 Different types of cry 130
Condensation 304 Differential diagnosis 6
Conditioning the cavity 296 Differential growth 66
Considerations for stainless steel crown 323 Direct pulp capping 338
Consistency of gingiva 657 Discolouration 719
Contingency management 150 Diseases of the pulp 330
Contour of gingiva 656 Disking 409
Convenience form 281 Displacement injuries 518
Coping 151 Distal shoe 396
Corpus adiposum 56 Distal step 377
Correlational studies 691 Distal step type 110
Cotton rolls 283 Distress or cry 130
Cotton test 367 DNA chip 649
Craniometry 75 DNA vaccination 648
Crimping 322 Doll’s eye reflex 58
Cross bite 412 Dose calculation 528
Cross sectional surveys 691 Down’s syndrome 539
Crowding 408 Drumstick plant (Moringa Cleifera) 265
Crown contouring 321 Duplication 622
Curve of spee 388 Dyes 200
Cyanotic congenital heart disease 547
 €Eß> I TEXTBOOK OF PEDODONTICS

Features of teething 93
E
Feeding plate 586
Early childhood caries 180 Ferric sulfate 347
Early interventions 402 Festooning 392
Early mesial shift 114 Fetoscopy 638
Early orthodontic intervention 12 Fiber optic transillumination (FOTI) 199
Ego 122 Fields of Forensic Odontology 698
Electra complex 122 Final diagnosis 6
Electronic dental anesthesia 468 Finger springs 419
Electronic resistance measurements 199 Finishing and polishing 322
Electrosurgical pulpotomy 345 First transitional period 112
EMLA 468 Fish bone charcoal 264
Emotion 121 Fissure 234
Enamel fractures 517 Fissure eradication 233
Endocrine growth axis 721 Fissured tongue 676
Enlow’s 'V Principle 68 Fixed lingual arch 396
Ephebodontics/adolescent 168 Fixed partial denture 607
Epidemiology 691 Fixed splint 521
Epidemiology of dental caries 181 Floss 260
Epilepsy 543 Fluid absorbents 283
Epulis 684 Fluorescence 199
Eruption cyst 478 Fluoridated milk 252
Eruption rhythm 93 Fluoridated salt 252
Eruption status 90 Fluoride 240 ‘
Erythroblastosis fetalis 8 Fluoride content 247 v
Estimation of dental age 95 Fluoride impregnated prophylaxis paste 259
Ethics 646 Fluoride in amalgams 259 t.
Etiologic agents in nursing caries 201 Fluoride in blood 249
Examining child abuse 701 Fluoride in body tissue 249
Exanthemas in children 735 Fluoride in bone 249
Exarticulation 518 Fluoride in enamel and dentin 249
Excretion of fluoride 249 Fluoride in placenta and foetus 249
Exogenous theories 185 Fluoride in plaque 249
Expression 645 Fluoride in saliva 250
Extinction 125 Fluoride in sugar 253
Extraction 471 Fluoride metabolosm 245
Extraoral and specialized radiographs 24 Fluoride rinses 260
Extraoral films 20 Fluoride toxicity 261
Extrusion 518 Fluorosis assessment 731
Flush terminal 110
F
Folate deficiency anemia 554
Factors affecting development of dentition 95 Folded flap method 392
Factors affecting the physical growth 80 Fontanelles 50
Factors which affect child’s behavior 141 Food 224
Fear 132 Food guide 231
Fear assessments 137 Fordyces granules 681
Features of fear 133 Forensic dentistry 697
 INDEX | OEB

Forensic odontology 697

H
Forensic science 697
Formocresol pulpotomy 342 Haemangioma 675, 676
Foundation foods 225 Hamartoma cheek 679
Four handed dentistry 33 Hand marks 703
Frankel's classification 139 Hawley 416 j
Fraud 699 Head circumference 49 j
Free end loop space regainer 408 Head gear 424 |
Frenectomy 483 Health history 6 j
Hemolytic anemia 554 f
Frenum thrusting 458
Frictional keratosis 679 Hemophilia 559 I
Frightened Cry 131 Heredity 192 \
Herpangina 681
G
Herpes simplex 569
Gag reflex 58 Herpes zoster 681
Gender 712 Herpetic gingivostomatitis 661 [
Gene 620 Herpetic stomatitis 681 !
General anaesthesia 154, 160 Herpetiform ulcers 679 |
Generalisation 125 Hierarchy of needs 128 j
Genetic counselling 640 High copper alloy 303 !
Genetic factors 576 High fluoride 245
Genotype 614 Histiocytosis X 669,672
Geographic tongue 678 Histologic approach 713 ;
Gerber space maintainer 406 History of Pedodontics 2 |
Gingiva 654 HIV associated gingivitis 570 i
Gingival abscess 659 HIV associated periodontitis 570 j
Gingival cyst 667 Hixon and Oldfather 388 j
Gingival diseases in childhood 658 HOME (Hand over mouth ^exercise) 151
Gingival fluid 656 Horse shoe appliance 424 i
Gingival sulcus 656 Hot beverages 246
Glass ionomer 259, 292, 306 Hotz lingual arch 407
Global AIDSTstrategy 571
Human cloning 650
Glucosyltranferase 267 Humor 150
Glutaraldehyde 346 Hump 8
Grand Rapids-Muskegon 242 Hurt Cry 131
Grasp reflex 57 Hybridization 341
Gravimeric method 713 Hypnosis 151
Greater palatine 465 Hypophosphatasia 671
Growth 36
I
Growth assessment parameters 77
Growth factors 82 Id 122
Growth of gum pads 55 Idiopathic thrombocytopenic purpura 563
Growth of the ramus 73 Implosion therapy 151
Growth spurts 66 Incipient caries 179, 244
Growth Theories 68, 70 Incipient malocclusion 364
Growth trends 67 Incisal liability 115
Gumpads 54 Incisor extraction 412
 GSi I TEXTBOOK OF PEDODONTICS

Indications for general anaesthesia 160 Learning disability 541

Indigenous products 268 Leeway space 115,388
Indirect pulp capping 335 LeFort I, II and III fractures 512
Infantile swallow 58 Legend of the worm 185
Infantile swallowing 374 Leukemia 548, 664
Infected vs affected dentin 338 Lignocaine Patch 467
Infective bacterial endocarditis 547 Limb placement reflex 57
Inferior alveolar 465 Linear enamel caries 180
Innate fear 132 Lingual arch 394
Inter transitional period 116 Lingual arch construction 396
Intercanine arch width 409 Lingual thyroid 676
Intercanine width 114 Lining 305
Interceptive orthodontics 381 Lip bumper/plumper 407
interdental clefts 656 Lip habit 454
Interdental gingiva 656 Up print 699, 709
Interincisal angle 114 Lipids 225
*
Intervention trials 692 Literature review 687
tntra-oral films 19 Litigation 698
Intca-oral periapical (IOPA) radiographs 20 Loop 390
Intraoral radiographs 19,20 Ludwigs angina 683
Intravenous induction 165 Luxation 518
intrusion 518 Lymphangioma 678
Inversion 622
M
Iodoform paste 354
Ion exchange adhesion 297 Macroglossia 676
Iontophoresis 259 Magnetic resonance Imaging 25
iron deficiency anemia 554 Major aphthous ulcers 679
Isobutyl cyanoacrylate 341 Marginal gingiva 654
Isolation 283 Materials in pediatric dentistry 733
Maternal attitude 144
J
Maxillary height 69
Jack screw 408 Maxillary length 71
Jet injection 467 Maxillary width 71
Juvenile periodontitis 667 Maxillo-mandibular relation 73
Mean 694
K
Median 694
Kinetic cavity preparation 290 Membrane separation 263
Knutson and Feldman technique 255 Mental retardation 538
Koplik’s spots 682 Mesial step 377
Mesial step type 110
L
Microdentistry 268
Lamination techniques 308 Microglossia 676
Landau reflex 58 Midline diastemas 419
Laser 245, 341 Mineral trioxide aggregate 361
Laser Pulpotomy 346 Minerals 225
Late mesial shift 114 Minor ulcers 679
Lateral oblique view 25 Mirror test 367
Mitchell and Gordon 234 Observational and intervention studies 691
Mixed dentition period 111 Obstinate cry 130
Mode 694 Obturation techniques 354
Modeling 148 Obturators 609
Modifications of cavity preparation in primary Occlusal radiographs 22
teeth 288 Occult caries 179
Modified bonded space maintainer 399 Odontogenic cysts 478
Monoclonal antibodies 270 Oedipus complex 122
Moro reflex 57 Ointments and Jelly 468
Morphologic differences 274 Opacities of enamel 717
Mouth breathing 445 Open coil space regainer 406
Moyer’s analysis 388 Operant conditioning 125
Mucocele 478, 675 Oral features of the neonate 54
Muhler (1957) technique. 255 Oral habits 427
Multifactorial diseases 636 Oral manifestation 550,559
Multistage sampling 693 Osteomyelitis 486
Mumps 684 Outline form 280
Overdentures 609
N
P
Naevus 681
Nalgonda technique 264 Panoramic radiograph 24
Nasal fractures 513 Papilloma 679
Nasal reflex 58 Papillon Lefevre syndrome 669, 670
Nasomaxillary complex 52 Parachute reflex 58
Nasopalatine nerve 465 Paranasal sinus view 27
Nature and prevalence of space loss 383 •Parent history 8
Negative reinforcer 150 Parotid fistula 684
Neglected child 700 Passivation 396
Neonatal and natal teeth 107 Periodontic Triangle 4
Neonatal skeleton 47 Pedodontics in India 2
Neonatorum jaundice 8 Periodontists’ attitude 34
Neoplasms of the lip 675 Period of embryo 38
Neurocranium 48 Period of fetus 43
Neutropenia 669 Period of ovum 38
Nitrous oxide 158 Pernicious anemia 554
Hazards 159 Persecuted chid 700
Noma 683 Personalty types 171
Non-nutritive sucking habits 429 Pharmacogenomics 649
Non-probability sampling 693 Phases of mixed dentition 112
Non-vital pulpotomy 342 Phases of treatment planning 12
Normal distribution 695 Phenotype 614
Nursing caries 207 Phobia 136
Nutrition 224 Physical restraints 152
Nutritive sucking habits 429 Physiologic/developmental spaces 109
Physiology of emotion 130
O
Physiology of growth 69
Objective fear 133 Pioneer bacteria 210
 tZO I TEXTBOOK OF PEDODONTICS

Pit 234 Protocol preparation 688

Plaque 9, 190 Provisional diagnosis 6
Plaque index 9 Proximal approach 313
Platelet disorders 562 Psychological therory 122, 128, 724
Poisoning 699 Psychology 121
Polyploidy 623 Psychology of adolescence 170
Position of gingiva 657 Puberty and adolescence 64
Positive reinforcer 150 Pulp physiology 329
Post natal 54 Pulp testing 332
Post natal period 60 Pulp therapy 329
Post operative instructions 475 Pulpectomy 347, 520
Postero-anterior view 25 Pulpotomy 341
Postnatal 47
Postnatal history 8 R
Posture 48
Prasanti technology 264 Radiation caries 180
Pre-orthodontic trainer 425 Radiation hygiene 27
Precipitation method 263 Radio-visiography 27
Precociously erupted teeth 107 Radiographs 20
Predisposing factors 496 Radiography 638
Preformed bands 390 Radioisotopes 77
Preimplantation diagnosis 640 Rampant Caries 207
Prenatal counseling 219 Range 694
Prenatal development 87 Ranula 478,676
Prenatal diagnosis 640 Recommended dietary allowancesJRDA) 225
Prenatal fluoride 254 Recommended radiographic 23
Prenatal history 8 Recording of child abuse 701
Prenatal period 38 Recurrent/secondary caries 180 *
Preschool period 64 Reflexes 57 .
Prevalence 491 Reframing 147
Prevalence of fear 132 Rega fede disease 678
Prevalence of nursing caries 201 Regaining the space 405
Prevention of child abuse 711 Relative analgesia 157
Prevention of dental injuries 525 Relative pulpectomy 352
Preventive orthodontics 381 Relaxation 151
Preventive resin restoration 306 Remineralization 243
Primary dentition 107 Removable lingual arch 394
Primary palate 574 Removable partial denture 605
Primate spaces 107 Rrmovable space regainers 408
Principles of bone growth 68 Removable splint 521
Principles of cavity preparation 280 Renal diseases 564
Probability sampling 692 Repetitive DNA sequence 621
Progression of the lesion 205 Research problem 687
Properties of composite resins 300 Resin modified 294
Prophylactic odontotomy 233 Resistance form 280
Protein 225 Respiratory diseases 552
Protocol for nursing caries 728 Response to fear 133
Retained infantile swallowing 374 Slot cavity 313
Retention form 281 Smart materials 313
Retrocuspid papilla 656 Social learning theroy 129
Reverse - town projection 27 Social phobia 137
Rhabdomyosarcoma 679 Soldering 394
Rheumatic Fever 547 Space control 386
Risk assessment 162 Space loss 383
Role of pediatricians 216 Space maintenance 389
Root filling materials 353 Space management 387
Root fracture 517 Special child 535
Rooting reflex and sucking 58 Split labial bow 419
Rubber dam 284 • Split saddle 408
Rubber dam frame 285 Sprays 468
Rubber dam punch 285 Stages of human tooth eruption 91
Rubber dam sheet 285 Stages of nursing-bottle caries 727
Stages of tooth bud development 88
S
Stainless steel crown 314
Saliva 190 Stainless steel crown 413
Salivary factors related to dental caries 190 Stainless steel crown modification 324
Sampling 692 Standard deviation 694
Scarlet fever 682 Startle reflex 57
School period 64 Storage of fluoride 249
School water fluoridation 251 Strap marks 703
Scope of pedodontics 4 Stratified random sampling 693
Seating the crown 321 Streptococci mutans 194
Second transitional period 117 Streptococcus mutans 201
Secondary palate 574 Sub-stages of adolescence 173
Sectional arch technique 407 Subjective fear 132
Selective filling 353 Sublingual dermoid 676
Self adaptive person 171 Su bmentovertex view 27
Self assembling polypeptides 268 Submissive person 171
Self-correcting anomalies 118 Submucous Cyst 675
Self-directed 171 Substitutes for food items 231
Sequelae of dental injuries 522 Substrate 201
Serial extraction 409 Superego 122
Setting reaction for glass ionomers 294. Surface active polymeric agents 267
Setting reaction of compomer 296 Surface texture of gingiva 657
Setting reaction of resin modified 296 Suture materials 477
Shape of gingiva 656 Sutures of cranium 50
Shoe leather survey 242 Symptom 6
Sialadenitis’ 684 Synchondroses 50
Sialography 25 Syphilitic lesion 683
Sickle - cell anemia 554 Systematic sampling 693
Simple phobia 137 Systemic fluoride 250
Simple random sampling 692
T
Single visit calcium hydroxide 360
Situational phobia 137 Tactile examination 196
Size of intraoral filrr^ 19 Tailored bands 390
Sling shot 408 Tanaka and Johnston 388
 >¿4г» I TEXTBOOK OF PEDODONTICS

Techniques of Local Anesthesia 464 Types of Genes 620

Teenage caries (adolescent caries) 180 Types of Phobia 136
Teething 93 Types of stainless steel crowns 316
Teledentistry 268
U
Telomere 624
Tendon reflexes 59 Ugly duckling stage 116
Terminologies and definitions 201 Ultrasonics 200
Tests of significance 695 Ultrasonography 638
Thalassaemia 558 Ultrasound 25
Theories of child psychology 122 Unadjusted person 172
Theories of eruption 92 Universal space maintainer 399
Throat shields 284
V
Thrush 682
Thumb sucking 428 Vaccination schedule 730
Timely extraction 411 Variations in composite resins 299
Tin-fluoro phosphate complex 255 Venous hae’mangioma 676
TMJ 54 Vertical plane type 110
Tongue blade therapy 413 Visual and radiographic method 713
Tongue thrusting 439 Visual examination 196
Tongue tie 678 Vital pulpotomy. 341
Tonsils 56 Vital staining 76
Tooth defects in cleft lip and palate 581 Vital statistics 7
Tooth development 87 Vitamin B-12 deficiency anemia 554
Tooth evolution 85 Vitamins 225
Tooth friendly sweets 268 Voice control 151
Tooth mark 706
w
Topical anesthesia 468
Topical applicaitons 254 W-arch 416
Toxicogenomics 649 Walking/stepping reflex 57
Trace elements 187 Wand 467
Transgenic plants 271 Water 225
Translocation 622 Water test 367
Transpalatal arch (TPA) 398 Welding 392
Transverse centromeric division 622 Wilkinson’s extractions 412
Traumatic injuries 490 Working length 353
Tri cure 296 Working mother 432
Tricalcium phosphate (TCP) 265 Wrist radiography 25
Trimming 392
X
Trituration 304
Tubercular lesion 683 X-linked dominant 634
Tunnel cavity 311 X-linked recessive 634
Turner’s syndrome 95 X-linked disorders 634
Tweed 411
Z
Type of child abuse 700
Types of anxiety 134 Z springs 416
Types of child neglect 700 Zinc oxide - Eugenol paste 306, 353
Types of dental amalgam alloy 303 Zinc phosphate cement 305
Types of eruption 91 Zygomatic complex 512
Types of fissures 234