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Oral Pathology Physical Chemical Injuries of Oral Cavity

1. Bruxism (night grinding of teeth) can cause physical injuries to teeth like attrition, loosening of teeth, fatigue of muscles, and psychological effects. It is caused by factors like malocclusion, stress, and certain occupations. Treatment involves using a removable splint and addressing underlying causes. 2. Tooth fractures are classified based on the extent of involvement of crown and pulp. Treatment may involve restoration, sedative dressing, pulp capping or pulpectomy depending on the class of fracture. 3. Physical injuries to supporting structures of teeth include concussion, subluxation, avulsion and ankylosis. Complications of jaw fractures include nonunion, malunion and infection.

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0% found this document useful (0 votes)
151 views65 pages

Oral Pathology Physical Chemical Injuries of Oral Cavity

1. Bruxism (night grinding of teeth) can cause physical injuries to teeth like attrition, loosening of teeth, fatigue of muscles, and psychological effects. It is caused by factors like malocclusion, stress, and certain occupations. Treatment involves using a removable splint and addressing underlying causes. 2. Tooth fractures are classified based on the extent of involvement of crown and pulp. Treatment may involve restoration, sedative dressing, pulp capping or pulpectomy depending on the class of fracture. 3. Physical injuries to supporting structures of teeth include concussion, subluxation, avulsion and ankylosis. Complications of jaw fractures include nonunion, malunion and infection.

Uploaded by

thanush.u.20
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© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PPTX, PDF, TXT or read online on Scribd
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PHYSICAL &

CHEMICAL INJURIES
OF ORAL CAVITY

PREPARED BY
Sk..Muskan
Swarna Mukhi Naick. B
T.Mahalakshmi
U..Thanusha
PHYSICAL INJURIES OF ORAL CAVITY
(A) PHYSICAL INJURIES OF TEETH

1.BRUXISM

• Also known as NIGHT-GRINDING or BRUXOMANIA


• “Habitual grinding or clenching of the teeth either during sleep or as an unconscious habit
during walking hours”
• Incidence - 5% & 20%

 ETIOLOGY
(i) Local factors – Malocclusion
(ii) Systemic factors - Nutritional deficiency
- GIT disturbances
- Endocrinal disturbances
- Allergy
- Hereditary
(iii) Psychological factors - Anxiety
- Stress
- Emotional Tension
- Fear
- Rage
- Rejection
(iv) Occupations - Athletes
- Watch Makers
- Other persons associated with precise work
- Voluntary Bruxism seen in persons having habit of chew gum, tobacco,

toothpicks, pencils etc

 CLINICAL FEATURES

• History of clenching during sleep or walking hours is given by patient


• The symptomatic effects of this habit have been reviewed by GLAROS & RAO,
who divide them into 6 major categories:
(a) Effects on the dentition - severe attrition at occlusal & proximal surfaces
- loosening & drifting of teeth
(b) Effects on the periodontium- gingival recession
(c) Effects on the masticatory muscles - fatigue of muscles
(d) Effects on TMJ
(e) Head pain
(f) Psychological & behavioral effects

 TREATMENT

• Removable splint should be worn at night


• Correction of underlying causes should be done
2. FRACTURES OF TEETH
 CAUSES
• Traumatic episodes
• It occurs frequently after endodontic treatment due to brittle nature of non vital tooth

 CLINICAL FEATURES

• Mostly seen in children & maxillary teeth are affected mostly


• Class-1 - Simple fracture of the crown, involving little or no dentin

• Class-2 - Extensive fracture of the crown, involving considerable dentin but not the dental pulp

• Class-3 - Extensive fracture of the crown, involving considerable dentin & exposing the dental
pulp
• Class-4 - The traumatized tooth becomes non vital, with or without loss of crown structure

• Class-5 - Teeth lost as a result of trauma

• Class-6 - Fracture of the root, with or without loss of crown structure

• Class-7 - Displacement of a tooth, without fracture of crown or root

• Class-8 - Fracture of the ‘crown en masse’ & its replacement

• Class-9 - Traumatic injuries to deciduous teeth


TOOTH FRACTURE
 HISTOLOGICAL FEATURES

• Histological features during healing are similar to that of bony fractures


• Clot is organized with deposit of cementum & bone, later restoration & remodeling at
ends of fragments occurs

 TREATMENT

• If enamel is fractured - Restoration of missing tooth structure is done


• If dentin is involved - Placement of sedative base (zinc oxide eugenol) is done at
fractured dentin & tooth is restored
• If pulp is involved - Pulp capping
- Pulpotomy (coronal pulp removal)
- Pulpectomy

3. INJURIES TO THE SUPPORTING STRUCTURES OF THE TOOTH

 CONCUSSION - produce by injury which is not strong enough to cause serious,


visible damage
to the tooth & the periodontal structures
• Characteristic feature- increased sensitivity of tooth to percussion
• Treatment - selective grinding of tooth to eliminate occlusal forces
 SUBLUXATION - abnormal loosening of tooth without displacement due to sudden trauma
- Tooth is mobile on palpation & sensitive to percussion & occlusal forces
- tooth becomes nonvital due to severance of apical blood supply

 AVULSION - dislocation of the tooth from its socket due to traumatic injury
- partial or total
- Partial includes-intrusion, extrusion or facial, lingual or palatal or lateral displacement
- mainly accompanied by fracture of alveolar bone

4. TOOTH ANKYLOSIS

• Fusion of tooth with bone


• Occur mainly after any traumatic episode (occlusal trauma) or periapical inflammatory processes
or after RCT

 CLINICAL FEATURES

• Tooth shows lack of mobility


• There may be evidence of pulpal ds.
• Percussion over tooth gives characteristic solid sound
• Deciduous tooth if affected becomes submerged b/c of eruption of
adjacent permanent teeth & growth of dental arch
 RADIOGRAPHIC FEATURES

• Blending of bone with tooth root is in radiograph

 HISTOLOGICAL FEATURES

• Area of root resorption is found, which have been repaired by bony tissues or cementum

 TREATMENT AND PROGNOSIS

• There is no treatment for ankylosis


• Good prognosis
• Unless removed for some other reason, should serve well indefinitely

(B) PHYSICAL INJURIES OF BONE

1. FRACTURES OF JAW

• Commonly due to automobile, industrial & sports accidents & fight


• Easily occur in bones which are already weakened by developmental
& systemic disorders
• May be - Simple - bone is broken completely
- overlying structure are intact & not exposed to exterior
-Greenstick - common in children
- characterized by break of bone in on side & bend on the

other side
- Compound - external wound in associated with the break
- e.g :road traffic accidents
- comminuted - bone is crushed
- may or may not be exposed to exterior

 Mandible is more prone for fractures

a) FRACTURES OF MAXILLA
- More serious
- In Road traffic accidents, blow, fall & industrial accidents
- Extent of fracture is determined by - Direction , force & location

*CLASSIFICATION
1. Le Fort-I / Horizontal Fracture / Floating Fracture
- separation of body of maxilla from base of skull below the level of zygomatic
process

2. Le Fort-II / Pyramidal Fracture


- vertical fractures through the facial aspects of maxilla & extend
upward to nasal & ethmoid bones & usually extend from maxillary sinus
3. Le Fort III / Transverse Fracture
- high level fracture that extends across the orbits through the base of the nose &
ethmoid
region to the zygomatic arch
- bony orbit is fractured & the lateral rim is separated at the zygomaticofrontal suture
- zygomatic arch is fractured

 Common Features

- Displacement, anterior open bite, swollen face, reddish eye due to subcojuntival hemorrhage
& nasal hemorrhage
- If skull is involved - unconsciousness, cerebrospinal fluid rhinorrhea

b) FRACTURES OF MANDIBLE

- mostly involve angle of mandible followed by condyle, molar region,mental region &
symphosis
- displacement of mandible depends on direction of the line of fracture, muscle pull & direction
of force
 Clinical Features of mandibular fracture
• Pain during movement
• Occlusal derangement
• Abnormal mobility
• Gingival lacerations
• Crepitus on movement
• Trismus
• Loss of sensation of involved side
• Ecchymosis
 Treatment
• Immobilization of fractured bone

 Complications
• Nonunion
• Malunion
• Fibrous union

2. TRAUMATIC CYST
(SOLITARY CONE CYST, HEMORRHAGIC CYST, EXTRAVASATION CYST,
UNICAMERAL BONE CYST, SIMPLE BONE CYST, IDIOPATHIC BONE CAVITY)

• Is a pseudo cyst (lack epithelial lining) & an uncommon lesion comprises about 1% of all jaw cyst
• Occur in other bones of skeleton as well

 ETIOLOGY

• unknown
• THE TRAUMA HEMORRHAGE THEORY in widely accepted theory
• Trauma heals by organization of clot eventual formation of connective tissue & new bone
• Acc. to the theory, clot breaks down & leaves empty cavity within the bone
• - steady expansion of lesion occurs secondary to altered or obstructed lymphatic or venous
drainage
• - this expansion tends to cease when the cyst-like lesion reaches the cortical layer of bone
• - expansion of involved bone is not a common finding in this
• TIME LAG B/W INJURY & DISCOVERY OF THE LESION - 1 MONTH to 20 YEARS

 CLINICAL FEATURES

• Occurs most frequently in young persons


• Maxilla mainly develops it
• Swelling or rarely pain

 HISTOLOGICAL FEATURES

• Thin connective tissue membrane lining the cavity


• There may be presence of few RBCs, blood pigments or giant cells adhering to the
bone surface

 TREATMENT & PROGNOSIS

• 6 to 8 months for filling of space after surgery


• In large spaces, bony chips are used
TRAUMATIC CYST
3. FOCAL OSTEOPOROTIC BONE-MARROW DEFECT OF THE JAW

• Defect of bone closely associated with chronic anemia


• Jaw marrow starts hemopoiesis in response of anemia leading to this defect

 CLINICAL FEATURES

• Asymptomatic condition
• Females are more affected (75%)
• Mandible is affected more than maxilla (85%)

 RADIOGRAPHIC FEATURES

• Poorly defined radiolucency that is found at molar area, a few mm to cm or more


• Poorly defined periphery

 HISTOLOGICAL FEATURES

• Normal red marrow, fatty marrow or both


• Trabeculae of bone present in sections are long, thin, irregular & devoid of
osteoblastic layer
• Megakaryocytes & small lymphoid aggregates may present

 TREATMENT
• No treatment is necessary
FOCAL OSTEOPOROTIC BONE MARROW DEFECT OF JAW
4. SURGICAL CILIATED CYST OF MAXILLA
( SINUS MUCOCELE )

• Sometimes epithelial cells get implanted in maxillary sinus during surgical access maxillary sinus
• When these cells proliferate they form a cyst there

 CLINICAL FEATURES

• Middle aged or older patients are mostly affected


• Nonspecific, poorly localized pain, tenderness or discomfort in the maxilla
• Extraoral or intraoral swelling
• 10-20 years after surgery of maxilla or maxillary sinus when mucocele is infected, the lesion is
called MUCOPYOCELE
• Common in Japan

 RADIOLOGICAL FEATURES

• Well defined radiolucency close to maxillary sinus is seen


• This radiolucency is anatomically separated from sinus
• A filling defect of cyst can be seen after injecting radiopaque material in sinus

 HISTOLOGICAL FEATURES

• Cyst lining is formed by pseudostratified ciliated columnar ep.


• Squamous metaplasia may be found if infection or inflammation is present
• Cyst wall is composed of fibrous connective tissue with or without inflammatory cell infiltration
SURGICAL CILIATED CYST OF MAXILLA
 TREATMENT

• Enucleation of cyst. It doesn’t tend to reoccur

(C) PHYSICAL INJURIES TO SOFT TISSUES

1. LINEA ALBA
• White line seen on the buccal mucosa extending from the commissures posteriorly at the
level of occlusal plane
• Caused by physical irritation & pressure exerted by the posterior teeth
• Usually bilateral
• More pronounced in persons having clenching habit or bruxism

• Histologically - Hyperkeratosis & intracellular edema of epithelium is seen

2. TOOTHBRUSH TRAUMA
• Occurs to gingiva & produced by toothbrush
• Appears as white, reddish or ulcerative lesions or linear superficial erosions,
involving marginal or attached gingiva of maxillary canine & premolar region

 HISTOLOGICAL FEATURE
• Focal ulceration with formation of granulation tissue with diffuse
chronic inflammatory cell infiltration
• Epithelium shows hyperkeratosis & acanthosis adjacent to the ulcers
LINEA ALBA
 TREATMENT
• Symptomatic treatment
• Teaching proper brushing technique

3. TRAUMATIC ULCERS
( DECUBITUS ULCERS)

• Ulcers of mucous membrane formed due to traumatic injury

 MOST COMMON SITES ARE :


• Lateral borders of tongue
• At occlusal level of teeth in buccal mucosa
• Lips

 TRAUMA MAY BE DUE TO:


• Sharp teeth
• Cheek or lip biting

 TREATMENT
• No treatment is required as these ulcers heal within 7 to 10 days
• Symptomatic relief can be provided by lignocaine or any other topical
anesthetic gel
TRAUMATIC ULCER
4. FACTITIAL OR SELF-INDUCED INJURIES

 MAY INCLUDE:
• Lip biting (morsicatio labiorum)
• Cheek biting (morsicatio buccarum)
• May be habitual, accidental or psychological

 LIP & CHEEK BITING

• Holding, biting & tearing of epithelium of lip, buccal mucosa, or tongue, chewing of cheek or
stripping of epithelium using fingers & creating negative pressure by sucking the lips & cheeks
• Gingiva may also be involved

 CLINICAL FEATURES

• Usually bilateral along the occlusal line & vestibular surface of lips
• Mucosa appears white & shredded with areas of redness
• Ulceration is common
• More prominent in females

 HISTOLOGICAL FEATURES

• Extensive areas of hyperkeratosis with keratin projections


• Chronic inflammatory cell infiltration seen in areas of ulceration
 TREATMENT

• Counseling & psychotherapy are treatment of choice


• An acrylic shield will help to prevent the access of teeth to lips & cheeks

5. DENTURE INJURIES

• Caused by denture wearing


• CAN APPEAR AS:

a) Traumatic ulcer (Sore spots)


b) Generalized inflammation (Denture sore mouth, Denture stomatitis)
c) Inflammatory (fibrous) hyperplasia (Denture injury tumor, epulis fissuratum, redundant
tissue)
d) Inflammatory papillary hyperplasia (Palatal papillomatosis)
e) Denture base intolerance or Allergy

a) TRAUMATIC ULCER (SORE SPOTS)


• Caused due to:
- either sharp spicules of bone or high spot on inner aspect of denture
- over extended flanges may also cause sore spots at vestibular area
• CLINICAL FEATURES
- Ulcers are small, painful & irregular
- covered by grey necroting membrane
SORE MOUTH
• TREATMENT
- Correction of underlying cause
- relief of the flange
- removal of high spots

b) GENERALIZED INFLAMMATION
(DENTURE SORE MOUTH, DENTURE STOMATITIS)

- Characterized by burning erythematous granular mucosa, restricted to area beneath the denture

• CAUSES
- Candida albicans
- Saliva retention in glands

• TREATMENT
- Not successful
- denture surface is covered with topical nystatin coating
- For oral condition nystatin tablets(500,000 IU) should de dissolved in mouth
* TDS* 14 days

C) INFLAMMATORY (FIBROUS) HYPERPLASIA


(DENTURE INJURY TUMOR, EPULIS FISSURATUM, REDUNDANT TISSUE)

• One of the most common tissue reaction to a chronically ill-fitting denture


• Occur on buccal mucosa gingiva & angle of mouth
FIBROUS HYPERPLASIA
• CLINICAL FEATURES
- muco- labial or muco- buccal folds may develop excessive enlarged folds of tissues

• HISTOLOGICAL FEATURES
-excessive fibrous connective tissues
- hyperkeratosis is present
- pseudo epitheliamatous hyperplasia is often found
- connective tissue is composed of coarse bundles of collagen fibres with new fibroblasts or blood
vessels

• TREATMENT
- Surgical excision of excessive tissues
- New denture should be made

d) INFLAMMATORY PAPILLARY HYPERPLASIA


(PALATAL PAPILLOMATOSIS)

• It is the condition in palatal mucosa associated with many erythematous &


edematous papillary projections. It is predominantly see in edentulous patients

• CAUSES
- Ill fitting dentures
PALATAL PAPILLOMATOSIS
• HISTOLOGICAL FEATURES
- papillary projections of keratinized stratified squamous epithelium with vascular connective tissue
present

• TREATMENT
- construction of new denture

E) DENTURE BASE INTOLERANCE / ALLERGY

• Allergy may be due to denture base material as in cobalt chromium alloy, it may be due to nickel
or in vulcanite dentures, it may be due to sulphur

• CLINICAL FEATURES
- generalized inflammation of area in contact with denture

• TREATMENT
- First determine the cause of allergy then reconstruct the denture with minimal
or no use of that material

6. MUCOUS RETENTION PHENOMENON


(MUCOCELE, MUCOUS RETENTION CYST)

• It is the most common type of salivary & soft tissue cyst


• It is either due to retention of mucous or extravasation of mucous
into surrounding tissues
 ETIOLOGY
• Obstruction (such as salivary calculi) in duct of salivary gland
• Trauma due to cheek biting or lip biting
• Scar after trauma may also cause retention of mucous in gland

 CLINICAL FEATURES
• Occur most frequently on the lower lip
• May also occur on the palate, cheek, tongue(involving glands of Blandin -Nuhn) & floor of mouth
• Superficial lesion appears as a raised, circumscribed vesicle, several millimeters to a centimeter
or more in diameter with bluish, translucent cast
• Deeper lesion appears as swelling with normal color

 PATHOGENESIS
• Pathogenesis of Retention Cyst
Obstruction of duct -> Pooling of mucous glands -> Retention cyst is formed

• Pathogenesis of Extravasation Cyst


Trauma to Duct -> Mucous escapes in surrounding tissues -> Chronic Inflammation ->
Granulation Tissue formation around mucous without epithelial lining -> Extravasation Cyst

 HISTOLOGICAL FEATURES
• Retention cyst is surrounded by epithelial lining
• No epithelial lining is seen in case of extravasation cyst
 TREATMENT
• Excision of cyst is done completely with underlying salivary gland acini
LIP MUCOCELE
TONGUE MUCOCELE
7. RANULA

• It is a form of mucocele but larger, specifically occur in the floor of mouth in association of ducts
of submaxillary or sublingual glands

 CLINICAL FEATURES
• Unilateral
• Develops as a slowly enlarging painless mass on floor of mouth
• In superficial lesions, mucosa may have a translucent bluish color
• Deep lesion appear normal
• May interfere with speech & mastication

 HISTOLOGICAL FEATURES
• Similar to mucocele except that a definite lining is sometimes present
 TREATMENT & PROGNOSIS
• Treatment either marsupialization or more often excision of the entire sublingual gland

8. RETENTION CYST OF MAXILLARY SINUS


(Secretory cyst of maxillary antrum, mucocele of maxillary sinus,
mucosalcyst of maxillary sinus)

• These are mucous retention cysts of mucous glands, lining the maxillary sinus
 CLINICAL FEATURES
• asymptomatic
RANULA
• Discomfort in cheek or maxilla may be present
• Pain & soreness of face & teeth & numbness of upper lip

 RADIOLOGICAL FEATURES
• Lesion appears as a well-defined, homogenous, dome-shaped or hemispheric radiopacity,
varying in size from a tiny lesion to one completely filling the antrum, arising from antrum &
superimposed on it

 TREATMENT

• Cysts either persists unchanged or disappears spontaneously within a relatively short period
• No treatment is necessary

9. SIALOLITHIASIS
(Salivary duct stone, Salivary duct calculus)

• A stone in salivary ducts or glands is called Sialolithiasis


• Formed by deposition of calcium salts around a central nidus(formed by bacteria,
debris, foreign bodies or epithelial cells)

 CLINICAL FEATURES
• Severe pain occurs during meal time especially when eating citrus fruits
• Salivary gland is painful & swollen
• On palpitation stone may be detected in ducts
• Sialolithiasis is found mostly in submandibular gland because of:
- Tortuous path of Wharton's duct
- Mucinous secretion of the gland
- Gravitational effect of saliva inside duct

 CHEMICAL & PHYSICAL FEATURES

• Round, ovoid or elongated


• Measure just a few millimeters or 2 cm or more in diameter
• Involved duct contain single or multiple stones
• Surface of calculi is rough, which may cause squamous metaplasia of duct lining
• Usually yellow & occasionally white or yellowish-brown in color
• Calculi consist of calcium phosphates & smaller amount of calcium carbonates, organic materials
& water

 TREATMENT & DIAGNOSIS

• Small calculi may sometimes be manipulated or increasing the salivation by sucking a lemon,
leading to expulsion of stone
• I.V. injection of antibiotic like nafcillin is given for bacterial infection due to persistent obstruction
of duct
• Larger stones require surgical removal
• Piezoelectric shock wave lithotropsy is alternative to surgical removal
10. MAXILLARY ANTROLITHIASIS
(Antral rhinolith)

• Rare condition
• Defined as complete or partial calcific encrustation of an antral foreign body, either endogenous
or exogenous, which serves as a nidus
• Endogenous nidus consist of a dental structure such as a root tip or may simply be a fragment of
soft tissue, bone, blood or mucous
• Exogenous nidus is uncommon but may consist of snuff paper

 CLINICAL FEATURES
• Occur at any age in either sex
• May be a complete absence of symptoms
• Some cases are marked by pain, sinusitis, nasal obstruction, foul discharge & epistaxis

 TREATMENT
• Antrolith should be surgically removed

11. RHINOLITHIASIS

• Are calcareous concretions occurring the nasal cavity


• This uncommon lesion is formed by calcification of intranasal endogenous or exogenous foreign
material
• Reported in all ages
• May present for years & frequently give rise to odorous discharge, symptoms of nasal
obstruction, sinusitis, epiphora as well as pain & epistaxis

12. RADIATION INJURY

(A) X-RAYS

• Can ionized the water molecules present inside the cells & form highly reactive radicals. These
radicals can damage the cell by various manners as:
- They can cause mutation
- They can damage enzymes
- They may interrupt cell division

 EFFECTS OF X-RAYS ON ORAL MUCOSA

• Erythema of mucosa occurs initially


• Then Mucositis occurs
• Now mucosa becomes ulcerative with fibrinous exudation. Taste sense is also lost
• Taste sensation is returned 2 to 4 months after treatment of x-ray therapy

 EEFECTS OF X-RAYS ON SALIVARY GLANDS

• Xerostomia occurs due to loss of acinar cells, decrease in secretory granules & inflammation in
connective tissue of salivary glands
• May cause permanent dryness of mouth
• Artificial saliva (Methyl cellulose) should be prescribed

 EFFECT OF X-RAYS ON TEETH

• During formative stage of teeth can cause anodontia or defective root formation
• After development of teeth, may cause cervical caries that may lead to fracture of crown at
cervical third
• TREATMENT : Fluoride treatment & proper oral hygiene

 EFFECT ON BONE

• Have damaging effect on bone forming cells


• Blood vessels necrosed
• When these changes are associated with trauma & infection, OSTEORADIONECROSIS occurs
• This mostly occurs when infected tooth is present in the LINE OF FIRE

(B) LASER RADIATIONS

 EFFECTS ON TEETH
• Enamel – Chalky spots & craters with small holes are seen
• Dentin exhibit a burnt appearance
• Pulp – Hemorrhagic necrosis present
- Inflammatory cell infiltration is seen
- Necrosis of odontoblastic layer
 EFFECTS ON SOFT TISSUES
• Ulcers are formed in epithelium

13. CERVICOFACIAL EMPHYSEMA

• Emphysema is swelling due to presence of gas or air in interstices of connective tissue

 CAUSES
• Blow of air in periodontal pockets or root canals with use of air syringe

 CLINICAL FEATURES
• Painful unilateral swelling with feeling of crepitus on palpation

 TREATMENT
• Antibiotics are given to avoid connective tissue infection, hydration, massages, sialogagues, &
compression
• Puncture of subcutaneous tissues can be done with sharp needle
• Venous air embolism may occur as complication leading to death
CHEMICAL INJURIES OF ORAL
CAVITY:
A)NON ALLERGIC REACTION TO DRUGS AND CHEMICALS USED
LOCALLY :
1)ASPIRIN(ACETYLSALICYLIC ACID):
• Aspirin tablets are used mistakenly by many people as a local obtundent ,especially for the relief of
toothache

• Also available in powder form

• Although effective if used systematically, they are particularly harmful to the oral mucosa if applied locally

• The usual mode of local use is to place the tablet against the offending tooth, allowing the cheek or lip to
hold it in position, and to let it dissolve slowly

• Within a few minutes, a burning sensation of the mucosa will be noted , and the surface becomes
blanched or whitened in appearance

• The drug causes separation and sloughing of the epithelium and frequently bleeding, especially if the area
is traumatized

• The healing of the painful “aspirin burn” usually takes a week or more
ASPIRIN REACTION
2)ENDODONTIC MATERIALS:
• Soft-tissue damage resulting in deep spread of inflammation and necrosis may occur due to the usage of
some endodontic materials or their injection into the hard tissue.

• For instance paraformaldehyde is used to devitalize the inflamed pulp.

• This caustic agent may leak from the pulp chamber into the surrounding tissues and causes necrosis of the
gingiva and bone

• Sodium hypochlorite (NaOCI):and hydrogen per oxide produce similar damage when injected beyond the
reaction

• Sodium hypochlorite is commonly used as root canal irrigant.

• Due to its efficacy against pathogenic organisms and pulp digestion, it is considered to be the medicament
of choice

• It is found to be sporicidal and virucidal and shows far greater tissue- dissolving effects on necrotic than on
vital tissues as well as the organic components of the smear layer

• Although considered safe, it may cause severe tissue damage if it comes in contact with the tissues or
extrudes beyond the apex

• On contact with vital tissue, NAOCL causes hemolysis, ulceration, facial nerve weakness, and necrosis,
inhibits neutrophil migration, and damages endothelial cells and fibroblasts

• Inadvertent injection of NAOCL solution into periapical tissues leads to emphysema, caused by oxygen
liberation into the tissues, permanent facial and trigeminal nerve weakness, and allergic reactions
HYDROGEN PEROXIDE:
• Hydrogen peroxide is a caustic agent and it is used commonly in varying concentrations in
many branches of dentistry.

• On contact, it burns tissues and releases toxic free radicals, perhydroxyl anion, or both.

• It should be handled with care in high concentrations, since it is thermo- dynamically unstable
and may explode if not refrigerated or stored in a dark container.

• About 30-35% hydrogen peroxide (Superoxol) is used along with heat (thermocatalytic) for
bleaching.

• This thermocatalytic process damages the tooth by causing irritation to the cementum and
periodontal ligament
leading to cervical root resorption
SODIUM PERBORATE:
• It has been widely used as a mouth wash and a bleaching agent, and in dentrifices because of
its supposed therapeutic effect on gingival disease

• Clinical studies reveal, however, that the compound may produce an erythema of the oral
mucosa, which may even progress to sloughing of the tissues

• In some instances, the inflammation was aggravated, and edema and ulceration of mucosa
frequently occurred

• The lesions heal spontaneously with cessation of treatment


GUTTA- PURCHA:
• It is a biologically inert latex material used to obturate or fill the empty space inside the root of a tooth
during endodontic treatment.

• It is used along with zinc oxide eugenol to attain apical seal.

• Gutta-percha points extruded past the apices result in infective periapical periodontitis caused by the
transport of bacteria beyond the apex and an incomplete cleansing and foreign body reactions.

• Clove oil is used as a home remedy for tooth ache since decades. It is mixed with zinc oxide to be used
as temporary filling material.

• It has antibacterial properties as well as sedative and anodyne effects. Sometimes clove is directly used
to relieve tooth ache and gum problems.

• Apart from this, clove is also included as a flavoring agent in foods, toothpaste, soaps, cosmetics,
perfumes, and cigarettes.

• Clove oil contains a chemical called eugenol.

• Eugenol is used as an ingredient in dental materials such as impression and filling materials, endodontic
sealers, periodontal dressing materials and dry socket dressings.

• When eugenol comes in direct contact with the oral mucosa, it produces painful ulcerations, necrosis,
swelling and vesicle formation on occasions
• These ulcerations may be secondarily infected.

• The setting reaction of zinc oxide and eugenol produces zinc eugenolate, which is not stable in the
presence of water.

• The surface of this set cement readily undergoes hydrolysis, which releases the free eugenol.

• This release is initially rapid and gradually decreases as all the surface eugenol is hydrolysed.

• Free eugenol can cause harm to human soft tissues.

• Adverse effects of eugenol in the oral cavity have been reported with regards to eugenol containing
surgical and periodontal packs, root canal sealers, mouth washes and in impression materials.

• Adverse reactions to eugenol amongst dental personnel have also been reported, ranging from
localized skin irritation to allergic contact dermatitis.

• The oral soft tissue reactions to eugenol are as follows; Eugenol can act as a contact allergen and
produces a localized delayed hypersensitivity reaction in lower concentrations.

• At times it can cause a more significant generalised allergic response.

• It has an adverse effect on fibroblasts and osteoblast-like cells causing denaturation of cytoplasmic
proteins and is generally cytotoxic at high concentrations.
B)NON ALLERGIC REACTIONS TO DRUGS AND CHEMICALS USING
SYSTEMATICALLY :
• The systemic administration of various drugs and chemicals frequently evokes an oral reaction, which is
not on the basis of an allergy or sensitivity.

• This reaction is often a part of a generalized epidermal reaction, but other times it occurs as a specific
phenomenon apparently due to the anatomic peculiarities of the oral cavity.
A) DILANTIN SODIUM(SODIUM DIPHENYLHYDANTOINATE):
• It is an anticonvulsant drug, extensively used in the control of epileptic seizures

• SIDE EFFECT: Is fibrous hyperplasia of the gingiva

• Most clinicians expert this hyperplasia to occur in less than half of the cases, but if good oral hygiene is
maintained, the incidence may be less than 10%

• Why profileration of fibrous tissue occurs in one case and not in another is not known, nor is it
understood why Dilantin stimulates overgrowth of gingival fibrous tissue

• It has been shown experimentally in cats that in the presence of local irritants in the form of orthodontic
bands on the teeth and in the absence of brushing to remove plaque and debris, inflammation was
produced and gingival enlargement occurred after diphenylhydantoin administration

• However, when no bands were present and the teeth were brushed so that there was no irritation, the
administration of the drug produced no gingival enlargement
• In addition, studies of Shafer and his associates have shown stimulation of wound healing in experimental
animals treated with Dilantin, presumably as a result of stimulation of fibroblastic proliferation and
increased collagen synthesis.

• In other studies, Shafer has also shown remarkable stimulation of growth of human gingival fibroblasts in a
tissue culture system after exposure to Dilantin.

• Interestingly, this drug appeared to be cell- specific in his studies, since there was no similar stimulation of
other types of cells.

• Oral manifestations. Gingival hyperplasia may begin as early as 2 weeks after Dilantin therapy has been
instituted, although usually it takes 2-3 months

• The first change noted is a painless increase in the size of the gingiva, starting with the enlargement of
one or two interdental papillae

• The surface of the gingiva shows an increased stippling and finally a cauliflower, warty, or pebbled surface.
As enlargement increases, the gingival tissue becomes lobulated, and clefts remain between each
enlarged gingiva in many cases

• Palpation reveals that the tissue is dense, resilient, and insensitive

• It shows little tendency to bleed

• The hyperplasia of oral mucosa is almost entirely confined to the gingival tissues surrounding the teeth
• In cases in which a patient is dentulous, but has a few edentulous areas, the gingival tissues around the
teeth may show extreme hyperplasia, while the edentulous regions are generally normal in appearance

• . On rare occasions, hyperplasia may occur in localities apart from the gingiva, such as the palate in
patients wearing a prosthetic appliance, a probable source of chronic irritation (Figure 22.29).

• Histologic features: Microscopic study of the gingival tissue reveals a suggestive but not pathognomonic
appearance.

• The stratified squamous epithelium covering the tissue is thick and has a thin keratinized layer. The rete
ridges are extremely long and thin, sometimes called “test-test-tube “ pegs, with considerable confluence,
but mitotic figures are seldom seen

• The bulk of the tissue is made up of large bundles of collagen fibers interspersed with fibroblasts and
fibrocytes

• Vascularity is not a prominent feature of the lesion

• If chronic inflammation is superimposed on this hyperplasia, plasma cells and leukocytes will be found

• TREATMENT AND PPROGNOSIS:


• No treatment is necessary until the enlargement becomes esthetically objection able

• If the hyperplasia interferes with function, surgical excision is recommended, but the hyperplasia will often
recur

• Discontinuing use of the drug will result in a gradual diminution of the bulk of the gingiva
CYCLOSPORINE:

• Cyclosporine is a selective immunosuppressant(suppresses helper T cells), used primarily in organ


transplant patients to overcome transplant rejection

• It causes generalized gingival hyperplasia and perioral hyperesthesia

• The mechanism for this phenomenon is not known

• CLINICAL FEATURES:

• Not seen in all patients receiving cyclosporine

• Appearance of gingival overgrowth is similar to that induced by Dilantin

• Presence of local factors aggravates the extent of the lesion


NIFEDIPINE:
• Nifedipine is a calcium channel blocker used in cardiovascular disorders.

• Calcium channel blockers interfere with the production of collagenase, through altered calcium influx into
fibroblasts, and collagen keeps accumulating without any degradation.

• Gingival enlargement begins after 1-3 months of taking these drugs.

• Gingiva is firm and nodular, and the clinical appearance is similar to that seen in Dilantin-and
cyclosporine-induced gingival hyperplasia

• LEAD:

• Lead poisoning (plumbism) :occurs chiefly as an occupational hazard today, but occasionally occurs
because of some other accidental exposure of either an acute or a chronic nature.

• In adults, the chief means of poisoning is through inhalation of lead vapor or dust.

• In infants, most cases result from ingestion by the child while chewing on wood painted with lead-
containing paint.

• Many other unusual sources of lead may also result in poisoning


• Clinical features: Lead intoxication is manifested by serious gastrointestinal disturbances which
include nausea, vomiting, colic, and constipation.

• A peripheral neuritis also develops, which may produce the characteristic wrist-drop or foot-drop.

• Encephalitis may also occur.

• Blood changes are those of hypochromic anemia with basophilic stippling of the red blood cells. Skeletal
changes due to deposition of lead in growing bone occur in children and are demonstrable on the
radiograph

Oral manifestations:

• The formation of a "lead line" similar to the "bismuth line" occurs in lead poisoning

• . This gray or bluish black line of sulfide pigmentation occurs in the gingiva, but is somewhat more diffuse
than that of bismuth.

• It is also found occasionally in other areas of the oral cavity.

• Ulcerative stomatitis is an additional reported finding.

• Excessive salivation and a metallic taste are also common complaints in this condition, as is swelling of
the salivary glands

• Lead us deposited In the deciduous teeth of children suffering from lead poisoning, and those teeth may
serve as an index of the body burden of lead
• TREATMENT AND PROGNOSIS:
• Treatment of the oral lesions is secondary to systemic treatment, and the prognosis depends on the
systemic condition of the patient.

• MERCURY :
• Mercury poisoning may be acute or chronic, but the systemic reactions in the acute form are so
serious that the oral features need not be considered.

• Chronic mercurialiism occurs after prolonged contact with mercurial compounds in a variety of
situations, including therapeutic use of these compounds and as an occupational hazard

• Intoxication from repeated exposure to mercury is still reported secondary to liquid mercury spills.

• CLINICAL FEATURES:
• Chronic mercurialism is characterized by gastric disturbances, diarrhea, excitability, insomnia,
headache, and mental depression.

• The patients frequently have fine tremors of the fingers and limbs as well as of the lips and tongue. In
addition, a desquamative dermatitis occurs in some persons.

• Nephritis is common in acute mercurial poisoning, but does not occur in severe form in the chronic
Nephritis

• ORAL MANIFESTATIONS:
• The oral cavity suffers seriously in mercurialism and evidences numerous characteristic but not
necessarily pathognomonic signs and symptoms.
• There is a remarkably increased flow of saliva (ptyalism), and a metallic taste in the mouth due to
excretion of mercury in the saliva

• . The salivary glands may be swollen, and the tongue is also sometimes enlarged and painful.
Hyperemia and swelling of the gingiva are occasionally seen

• Ulcerations of the gingiva, palate, and tongue are common

• In severe cases, pigmentation of the gingiva similar to the bismuth and lead lines may occur as a result
of deposition of the dark sulfide compound.

• Loosening of the teeth, even leading to exfoliation, has been reported.

• toxic reaction from absorption of mercury in dental amalgam has been reported on a number of
occasions.

• The amount of estimated exposure to mercury from dental amalgam is not sufficient to cause mercury
poisoning in the conventional sense

• The treatment of the oral lesions in chronic mercurialism is supportive only and is secondary to the
treatment of the poisoning itself.

• The prognosis is usually good, although severe periodontal destruction and loss of teeth may occur.
• Acrodynia (pink disease, Swift disease):

• is an uncommon disease of unknown etiology, with striking cutaneous manifestations.

• The cause of the disease is a mercurial toxicity reaction, either an actual mercury poisoning or, more
likely, an idiosyncrasy to the metal.

• The source of the mercury is usually a teething powder, ammoniated mercury oinment, calomel lotion,
or dichloride of mercury disinfectant

• CLINICAL FETURES:

• Acrodynia occurs most frequently in young infants before the age of 2 years, although children are
occasionally affected upto the age of 5 or 6 years

• The skin, particularly of the hands, feet, nose, ears, and cheeks, becomes red or pink and has a cold,
clammy feeling

• The appearance has been described as resembling raw beef

• The skin over the affected areas peels frequently during the course of the disease

• The patients also have a maculopapular rash which is extremely pruritic

• Severe sweating is an almost constant feature of acrodynia


• The children will frequently tear their hair out in patches (Figure 22.31).

• The excretion of mercury from the body appears to be a variable phenomenon.

• For this reason, the recovery of unusual amounts of mercury from the urine is not always possible

• Oral manifestations.

• Patients with acrodynia exhibit profuse salivation and often much "dribbling."

• The gingiva becomes extremely sensitive or painful and may exhibit ulcerations.

• Bruxism is a common finding and loosening and premature shedding of teeth often occurs: many times,
the child will extract loose teeth with his/her fingers.

• Mastication is difficult because of the pain

• TREATMENT AND PROGNOSIS:

• It is crucial to identify and remove the source of mercury.

• Immediate chelation therapy is the standard of care for a patient showing symptoms of severe mercury
poisoning
• The administration of dimercapirol, D-pencillamine, or 2,3-dimercapto-1-propanesulfonic acid( DMSA) has proved
successful in most cases unless the disease is of long duration

• Some of the toxic effects of mercury are in some cases partially or wholly reversible

• However, heavy or prolonged exposure can do irreversible damage, particularly in fetuses, infants, and young
children
TETRACYCLINE:
• Discoloration of either deciduous or permanent teeth may occur as a result of tetracycline deposition
during prophylactic or therapeutic regimens instituted either in the pregnant female or postpartum in the
infant.

• Tetracycline and its homologues have a selective affinity for deposition in bone and tooth substance,
possibly through the formation of a complex with calcium ions in the sur face of the microcrystals of
hydroxyapatite

• The severity of the staining by tetracycline is determined by the stage of tooth development at the time of
drug administration.

• Since tetracycline does cross the placental barrier, it may involve the deciduous teeth developing
antepartum, although the discoloration itself depends on the dosage, the length of time over which
administration occurred, and the form of the tetracycline

• . The critical period for tetracycline-induced discoloration in the deciduous dentition (the period of
mineralization of the first millimeter of dentin nearest the dentinoenamel junction) is 4 months in utero to 3
months postpartum for maxillary and mandibular incisors and 5 months in utero to 9 months postpartum
for maxillary and mandibular canines.
• The period for permanent maxillary and mandibular incisors and canines is 3-5 months postpartum to
about 7 years of age.

• The age at which tetracycline administration occurred can easily be pinpointed by reference to a chart
on the chronology of odontogenesis.

• The use of oxytetracycline, or possibly doxycycline, may diminish tooth discoloration if tetracycline
therapy is indicated in the pregnant female or during the first 6-7 years of life

• . After this age, the probability of discoloration need not be considered since the cosmetically important
anterior teeth have completed their formation

• Significant discoloration of the teeth is also produced by minocycline hydrochloride , a semisynthetic


derivative of tetracycline

• Binding of minocycline to certain types of collagenous tissues like dentin, dental pulp, bone , and
dermis results in oxidation and produces the discoloration

• The stained pulp is seen through the overlying translucent dentin and enamel
• Clinical features:

• The teeth affected by tetracycline appear to have a yellowish or brownish-gray discoloration, which is
most pronounced at the time of eruption of the teeth.

• This discoloration gradually becomes more brownish after exposure to light.

• Oxytetracycline and tetracycline give a yellowish color, whereas chlortetracycline tends to cause a
brownish-gray color.

• Tetracycline itself fluoresces under ultraviolet light and, accordingly, the teeth involved by its
discoloration also fluoresce a bright yellow under ultraviolet light.

• However, in time, this fluorescence gradually diminishes

• Minocycline hydrochloride causes discoloration of the skin, nails, conjunctiva, bone, and teeth.

• Palate or anterior alveolar mucosa has a distinctive blue-gray appearance due to the black bone
showing through the thin, translucent mucosa.

• The incisal edge of the fully erupted teeth reveals a blue-gray discoloration, with the middle one-third
being maximally involved and the exposed roots of the erupted teeth reveal dark green discoloration

• The roots of developing teeth show a dark, black color.


• Cancer chemotherapeutic agents :

• A chemically very diverse group of drugs and agents has come into recent use for the treatment of
certain malignant neoplasms.

• Their chief function is the destruction of malignant cells

• . Most of these cytotoxic agents exert their effect preferentially against cells in mitosis.

• Unfortunately, in addition to neoplastic cells, which undergo rapid division, certain normal cells
including the cells of the oral and gastrointestinal mucosa, bone marrow, and skin also exhibit a similar
degree of mitotic activity and are especially prone to manifest the toxic and damaging effect of
anticancer agents .

• Newer and experimental approaches like hematopoietic stem cell transplant (especially in treating
myeloma, lymphoma, and leukemia) and isolated infusion of chemotherapy (to treat neoplasms in the
liver and lung) are in use.

• Clinical features:

• Cancer chemotherapeutic agents are grouped into: (1) alkylating agents, (2) antimetabolites, (3)
antitumor antibiotics, (4) plant alkaloids, (5) nitro- sources , (6) enzymes, (7) hormonally active agents,
and (8) miscellaneous compounds.

• Because the major effect of these materials on cells and tissues is similar, regardless of each agent's
specific mechanism of action, there are a few general manifestations of the group as a whole that can
be emphasized.
• These are1) alopecia , due to arrest of mitosis of the rapidly germinating hair roots, 2) Stomatitis, which
may take a variety of forms, and (3) radiation recall or radiation sensitization , a reactivation of
radiation reaction within the field of radiation following administration of certain of the antineoplastic
agents.

• ORAL MANIFESTATIONS:

• The most common oral manifestation is mucosal erosion is mucosal erosion and ulceration, frequently
diffuse and multiple, often related to the neutropenia produced by the drug but occasionally occurring in
its absence. This may occur anywhere in the mouth but is most likely to be seen on the lips, tongue,
and buccal mucosa.

• Hemorrhage is also a common manifestation resulting from the thrombocytopenia secondary to the
drug therapy.

• These reactions do not occur following use of all cancer chemotherapeutic agents but are especially
common with the alkylating, antimetabolite, and antitumor antibiotic groups

• Another oral finding in patients undergoing this type of therapy is the presence of any one of a variety of
specific or non specific infections(commonly herpes simplex infection, Candida infection, or infection by
staphylococcal or streptococcal organisms) , especially since many of these patients are also
immunosuppressed

• Finally, hyper-pigmentation of oral mucosa has been reported occasionally , especially in patients
receiving alkylating agents and antitumor antibiotics
• Treatment:

• There is no specific treatment for the oral lesions which, although severe, must be considered of only
secondary importance to the patient's major problem.

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