﷽

Endodontics Sheet

4th Year Dentistry

By: Dayasiq (47)

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‫‪Typed and revised by Dayasiq (batch 47), from Rawan Hafiz notes,‬‬
‫‪of Dr. Riham Nabil lectures.‬‬

‫الحمد هلل الذي أعاننا‪ ،‬إن أصبنا فمن هللا‪ ،‬وإن أخطأنا فمن أنفسنا ومن الشيطان‪.‬‬
‫ال تنسونا من صالح الدعوات ‪):‬‬

‫أدعية قبل المذاكرة‪:‬‬

‫‪ ‬اللهم ارزقني قوة الحفظ وسرعة الفهم وصفاء الذهن اللهم ألهمني الصواب في‬
‫الجواب‪ ،‬وبلغني أعلى المراتب في الدين والدنيا واآلخرة‪ ،‬واحفظني وأصلحني‬
‫وأصلح بي األمة‪.‬‬

‫المقربين‪ ،‬اللهم اجعل‬

‫ّ‬ ‫‪ ‬اللهم إنّي أسالك فهم النّبيين‪ ،‬وحفظ المرسلين والمالئكة‬
‫ألسنتنا عامرة ً بذكرك‪ ،‬وقلوبنا بخشيتك‪ ،‬وأسرارنا بطاعتك‪ ،‬إنّك على ك ّل شي‬
‫قدير‪ ،‬وحسبنا هللا ونعم الوكيل‪.‬‬

‫ونيال لكل مقصد‪ ،‬وارزقنا القمة في درجات‬ ‫ً‬ ‫‪ ‬اللهم ارزقنا نجا ًحا في كل أمر‪،‬‬
‫ي بالحفظ‬
‫ي رحمتك‪ ،‬وامنن عل ّ‬ ‫العلم‪ .‬اللهم افتح لي أبواب حكمتك‪ ،‬وانشر عل ّ‬
‫والفهم‪ ،‬سبحانك ال علم لنا إال ما علمتنا‪ ،‬إنّك أنت العليم الحكيم‪.‬‬

‫‪2‬‬
Contents:

1. Introduction 4
2. Pulpitis + 3. Periradicular diseases 6
4. Microbiology of root canal infections 13
5. Endodontic diagnosis and treatment planning 17
6. Case history 21
7. Examination of chief complain 24
8. Endodontic radiology 30
9. Pulp diseases 34
10. Periradicular diseases 1 40
11. Periradicular diseases 2 52
12. Root canal anatomy 58
13. Access cavity 1 66
14. Access cavity 2 73
15. Access cavity 3 82
16. Working length and apical considerations 93
17. Irrigants and irrigation techniques 107

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 LECTURE #1 – Introduction

What is Endodontics?

• Dealing with the internal structure of the tooth, to study the diseases of the dental pulp.

* Vital pulp therapy: pulpotomy and pulpectomy (treatment).

• To know the normal physiology of the pulp.

SO, ENDODONTIC IS:

The science that deals with anatomy, physiology, pathology and prevention of the pulp and
periradicular tissue. " Endodontic periodontal disease ".
* The main aim of endodontic treatment is to prevent spread of the infection.
(spread to tissue space > abscess > Ludwig angina > airway obstruction > Death).

* To prevent periapical tissue infection - unless it reaches the periapical tissue, the aim here is
treatment *

Causes of endodontic diseases:

1. Caries (most common cause).
2. Trauma
3. Filling procedure.
4. Tooth wear (Non-caries tooth surface loss).
5. Cracks.
6. Developmental anomalies (developmental grooves, dens invagenatus, dense evagenatus - as
a source of entry).
• Usually toxins of bacteria precede bacterial invasion (simple caries > pain > pulpal inflammation
" even without invasion by bacteria itself ").
• If the bacteria reach the pulp, severe inflamed pulp with periapical inflammation will occur.
• Periodontal inflammation may start without complete inflammation of the whole pulp.
• Periodontal infection: actual presence of the bacteria in the periapical tissue, which has poor
prognosis.
• Periodontal inflammation: inflammation of the periapical tissue without reaching of bacteria.
• Indirect pulp capping: if there is 0.5 mm before reaching the pulp.

Pulp Therapy:
• According to the health of the pulp, treatment may be partial pulpotomy or complete pulpectomy
(RCT).

• Bacteria may not reach the whole pulp but the whole pulp is inflamed: here the treatment will be
RCT.

• If the inflammation restricted to a certain area, the treatment will be partial pulpotomy.

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• A Healthy pulp has the ability to regenerate itself = vital pulp therapy.
• Blood supply is necessary for pulp healing

Conditions of the pulp:

1. Vital healthy pulp.

2. Vital inflamed pulp. *
3. Partially inflamed pulp (Here the coronal pulp is vital but inflamed and the radicular pulp is
healthy).
4. Necrotic pulp. *

**Two conditions are indicated for RCT = (vital inflamed pulp and the necrotic pulp).

• Periapical inflammation = conventional RCT.

• Excessive periapical infection = 1- primary treatment: RCT "super".

2- Secondary treatment: Surgical treatment.

A patient can be:

1- Primary treatment.
2- Retreatment.
3- Surgical endodontics.

SCOPE of ENDODONTICS:
1. Diagnosis and differentiation/differential diagnosis of orofacial pain, pulpal and periradicular
diseases (typical facial pain, sinusitis).
2. Vital pulp therapy (pulp capping, pulpotomy, apexogenesis, apexification)
3. RCT: Non-surgical treatment for root canal system or pulpectomy + widening + disinfect
canals + obturation + adequate sealing.
4. Retreatment.
5. Surgical endodontics.
6. Advances in endodontics.

• Biomechanical preparation: mechanical by instrument, and chemically by intracanal irrigation.

• Access Cavity: cavity preparation with removal of the coronal pulp and radicular pulp
(Biomechanical preparation).
• Working length determination: Where should I stop?
• Obturation material: for filling the canal.

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 LECTURE #2 + #3 – Pulpitis and periradicular diseases

• Pulpitis and neurological response.

Pulp consists of:

1- Pulp chamber: the part of the pulp located in the crown.

2- Radicular pulp: the part of the pulp located in the root.

• Pulp is soft tissue enclosed by hard tissue (the dentine) like "the brain".

Except that the brain is a nervous tissue and has no ability to regenerate, while the (only the vital)
pulp is a connective tissue and has the ability to regenerate.
• Pulp is loose connective tissue: it has blood supply, innervation so it can regenerate itself (high
ability to regenerate if an injury occurs).

* The problem is that it is enclosed by hard tissue which cause:

1. Restrict the tissue expansion in response to edema "inflammation".
Edema => stasis in blood flow which lead rapidly to necrosis.
2. There is no collateral blood supply, which limits its ability to cope w/ inflammation.

* Rapid necrosis occurs due to low rate rush of immunity and low rate of absorption of edema from
interstitial fluid.
Rapid degeneration = Necrosis

• So although it is vascular connective tissue and if it is vital, it has the ability to regenerate itself, it
has rapid rate of degeneration.
* If the irritant is chronic and the rate of injury is very slow, tertiary (reparative) dentine will be
formed.
 Etiology of pulpal diseases
Classification of etiology of pulpal diseases (Wein’s Classification):

1. Bacterial: mainly caused by bacterial damage, it is the most common and most important
cause of pulpal disease.
2. Mechanical:
a) Trauma: may be just fractured enamel, lead to bacterial entry.
b) Tooth wear: Non carious tooth surface loss
It may be physiological, occur with eating or Pathological occur due to (attrition, erosion,
abrasion and abfraction).

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 c) Cracked tooth syndrome (crown originating fracture)
Development of crack in the tooth which not related to trauma or developmental anomaly
like "palatogingival groove > extended to the pulp" in the palatal surface of the upper lateral
incisor.
d) Barometric changes (barodontalgia): injury to the pulp due to change in pressure, in
case of low atmospheric pressure Pulpitis will occur (pulpitis in the plane).

3. Iatrogenic:
a) Hand peace exposure.
b) Lack of cooling with cavity preparation.
c) Thermal injury and mercury component (chemical injury with amalgam).
d) Non setting monomers associated with composite = injury.
e) Zinc phosphate cement (phosphoric acid injury).
f) Phosphoric acid of composite = injury.
g) Excessive polishing of composite with excessive generation of heat.
h) Very deep scaling.
i) Excessive orthodontic movement.
j) Periapical and bone surgery "impaired vascular supply to the pulp".
4. Idiopathic:
a) Aging.
b) Resorption.

Bacterial Cause "Most common":

 May be by bacteria or by its byproducts (pulp infection by bacterial toxins reach through
dentinal tubules).
 Odontoblastic process starts to initiate innate immunity by stimulating chemokines and
cytokines through "TLR" => (Nonspecific receptors recognize foreign antigens > chemokines >
pulp > vasodilation > activate the local leukocytes).
 Once the injury gets close to the pulp > stimulation of adaptive immunity occurs > produce
specific antibodies.
 Routes of entry of bacteria:
1- Carious lesions (through cavitation)
2- Accidental exposure by the dentist
3- Fracture
4- Percolation around restorations (due to polymerization shrinkage for instance)
5- Extension of periodontal infection through lateral canals, accessory canals as well as
apical foramen, aka endoperio lesion.
6- Anachoresis, which refers to the transportation of bacteria through blood, from a
systemic infection for example. Rare.

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 Note:
* Carious exposure: soft dentine.
* Iatrogenic exposure: hard and even glossy.

PULPITIS
- Immune and neurological response to an irritant (‫)ردة فعل‬
- It can be acute or chronic depending on many factors.
- Immune interaction can be just innate (resolve), and/or adaptive when the infection is close
to the pulp.

Pathogenesis:

Irritation occur => the cells (odontoblast, fibroblasts and NK cells) have TLR => activate the innate
immunity => chemokines activating => vasodilation => edema => PMNs recruitment => stasis in
blood flow => degeneration => hypoxia. Neutrophils start to engulf toxic metabolites => rupture =>
further chemokines => cycle of immunity.

Theories of pulpitis:

 Strangulation theory:

Once bacteria (or their toxins) reach to the pulp >> complete pulpal inflammation.

*On irritation, there is local inflammation in pulp, which results in vasodilation, increased capillary
pressure and permeability. These result in increased filtration from capillaries into tissues, thus
increased tissue pressure. By this, thin vessel walls get compressed resulting in decreased blood
flow and increased venous pressure. This results in vicious cycle, because increase in venous
pressure further increases capillary pressure. Consequently, choking/strangulation of pulpal blood
vessels occur because of increased tissue pressure. This results in ischemia and further necrosis.
(Textbook of Endodontics)

 Current theory:
Local inflammation in the pulp result in tissue pressure only in inflamed area, and not in the entire
pulp cavity >> pressure in the inflamed area favor net absorption into interstitial fluid of the
adjacent capillaries in the uninflamed area (net of pulp volume can keep constant for certain
amount of time), but if the lesion ignored >> total inflammation + total necrosis

*Local inflammation in pulp results in increased tissue pressure in inflamed area and not the entire
pulp cavity.
It is seen that injury to coronal pulp results in local disturbance, but if injury is severe, it results in
complete stasis of blood vessels in and near the injured area. Net absorption of fluid into capillaries
in adjacent uninflamed area results in increased lymphatic drainage thus keeping the pulpal volume
almost constant. (Textbook of Endodontics)

Initial >> Localized >> Local venous collapse >> inflammation + edema >> Complete collapse +
complete edema >> Necrosis

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*If we intervene when it is localized, the remaining intact pulp will absorb the edema.

 Factors that affect the degree and nature of inflammation:

1. Severity of irritant (or virulence of the microorganism)
2. Type of bacteria
3. Host resistance/immunity
(Auto immune disease can cause pulpitis, also immunodeficiency)
4. Depth of penetration of bacteria
5. Lymphatic drainage and blood circulation
Less in old age, more in young age (immature teeth have adequate blood supply, incomplete
root, open apex)
6. Opportunity of inflammatory drainage
(The cavity may be large but painless... due to continuous release of edema)
7. Intervention: early >> reduce inflammation
*Note:
 We don’t say “pulpitis” unless the pulp is vital
 Pulpitis is either: Total, or Local
 When the pulp is non vital “pulp necrosis” >> no immune response

*Summary of immune response:

Innate Adaptive
 Non specific  Specific
1. Dentinal fluid (pushing out toxins  B cells
and bacteria)  T cells
2. Immunoglobulins  Macrophages (effective killers)
3. Odontoclasts  Cytokines and chemokines
4. Neuropeptides  Specific antibodies
5. Immature dendritic cells  Adaptive immunity reacts when
6. Monocytes & macrophages microorganisms are about 2mm from
(nonspecific) the pulp
If it didn’t >> irreversible pulpitis

 Neurological response:

Mainly mediated by neurological mediators from nerve endings within dentinal tubules (have TLRs
as in TLRs of cells) -innate immunity-

Neuropeptides that act as chemoattractants for other immune cells and has an indirect action
(Vasodilation).
*Sensory nerve fibers can mediate pathology as well as healing, because it has TLRs.

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Any external stimulation of dentin can cause release of pro-inflammatory neuropeptides from pulp
afferent nerve, and has 2 actions:
1. Direct action: can stimulate immunocompetent recruitment (adaptive immunity cells)
2. Indirect action: vasodilation, etc.
* Examples of neuropeptides:
1. Substance P
2. Calcitonin gene related peptides (CGRP)
3. Neurokinin A & γ
4. Vasoactive intestinal peptide (VIP)

All these can play a role in pulpal inflammation, periradicular inflammation and in healing process.
*New studies proved that even if the pulp is irreversibly inflamed and not necrotic there may be
periradicular disease (inflammation)

*How can the pulp be necrotic and there is periradicular inflammation?

Because necrotic pulp has no immune response >> bacteria and their toxins reach the apex.

Initially small lesion but become larger with time.

*So periradicular diseases happen when the inflammatory response involve the whole pulp with
partial or complete necrosis (by high virulent bacteria)*

*When does periradicular inflammation happen?

1. When the bacteria proliferate in large numbers, and the bacterial toxins and necrotic
materials reach the periradicular area.
2. When the virulence of the bacteria overcome the immunity.
3. Some cases are sterile, like in trauma >> death of pulpal cells >> inflammatory mediators
reach the periradicular area.

*Is the host response the same for pulpitis and periradicular disease?

The only difference is that in periradicular inflammation there is bone resorption. Otherwise,
inflammatory and neurologic reaction is similar to pulpitis eventually there is:
formation of granulation tissue and bone resorption >> chemoattractants >> stimulation of
osteoblasts >> bone lay down >> at the same time: fibroblasts >> granulation tissue >> collagen >>
restrict the spread of the infection.
* The whole mark of apical periodontitis is bone resorption.

Sometimes it does not appear in acute cases but appear when it became chronic.

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*Bone resorption occur when the lesion reaches the cortical bone, when it is still in spongy bone it
does not appear in regular X-ray images; because there is superimposition with cortical bone. We
need to do CBCT image.

*Bone resorption may not be manifested as radiolucent lesion, may be manifested just as change in
trabeculae.

*Bone resorption occur to accommodate formation of soft tissue lesion (advantage: give chance to
immune cells to be recruited).

 Periradicular diseases:
1. Apical periodontitis
Acute and chronic, symptomatic and asymptomatic
2. Apical abscess
Highly virulent bacteria, severe necrosis >> neutrophils >> pus (dead bacteria, dead
neutrophils, pulp tissue, fibroblasts, purulent exudate) usually acute >> cellulitis >> intense
inflammatory response surround the pus.
3. Granuloma and cyst
Low virulent bacteria or good immunity.
On X-ray: radiolucent lesion surrounded by radiopacity (granulation tissue and bone) >>
Granuloma.
* Periapical bone destruction on X-ray image:

- Could be “granuloma” or “cyst”

- Abscess on X-ray usually there is no bone destruction (especially acute abscess it doesn’t cause
bone destruction), but it could be “acute exacerbation of chronic abscess.”

- It is mostly either granuloma or cyst.

It can’t be diagnosed from the signs and symptoms, diagnosis needs biopsy and histopathology.
- If the radiolucent lesion > 3mm it is a cyst.
But small lesion could be either of them granuloma or a cyst (on exam just write periradicular
disease).
*Cyst: Cells are “epithelial rests of Malassez”
Stimulation of these cells >> proliferation >> prevent blood supply >> death of the cells >> cyst.

Fish study:
4 zones of periradicular disease:

1. Zone of infection: in the center and part of it in the tooth structure, full of bacteria and their
toxins + PMNs.
2. Zone of contamination: Toxins (no microorganisms)
these toxins cause death of bone cells >> bone resorption >> empty lacunae.
In this zone there is lymphocytes; so no bacteria.
3. Zone of irritation: full of macrophages >> macrophages ingest collagen and dead cells.
Osteoclasts are also present in this zone and the initiate bone resorption.

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 Toxins are also present here are diluted so they only cause irritation they fail to kill normal bone
cells (still vital in this zone), immunity can control toxins >> first attempt of body to repair.
At the same time granulation tissue and osteoblasts act in the last zone to prevent further
spread of infection.
4. Zone of stimulation.
- Full of fibroblasts and osteoblasts (form fibrous tissue and bone).
- Toxins here are very mild enough to act as a stimulus to these cells to elicit their function
- They need stimulation to lay down fibrous tissue that act as a wall of defense around the
zone of irritation, and as a base for the new bone (scaffold).
*Microorganisms are only found in the zone of infection.

*Healing: the level of healing of pulpitis depends on 3 factors:

1. Degree and extent of tissue injury.

2. Host immunity and systemic condition (DM, immune disease…).

3. Intervention (CaOH stimulates stem cells >> odontoblasts)

Net result:

1. Regeneration (back as it was before).

2. Repair (formation of a scar).

These two may not occur or they may occur both together, according to the 3 factors that affect
healing.

e.g., (1) Mild injury to the pulp stimulate cells of the pulp, (2) Pulp capping materials stimulate and
make the stem cells differentiate.

The level of healing in apical periodontium also depends on factors:

1. Extent of the lesion specially bone destruction (usually if severe >> repair more than
regeneration).
2. Severity of irritant.
3. Quality of intervention.
4. Host systemic condition.

Mesenchymal stem cells =>stimulation=>osteoblast+cementobalst+fibroblast to form bone,

cementum and periodontal ligament (PDL).
(the last tissue to heal is PDL although it’s the first tissue affected because it is the zone of
infection).

but in bone healing start before cementum and PDL because it is the zone of irritation and zone of
stimulation.

*Usually healing reach final limit after 4 years from treatment.

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 LECTURE #4 – Microbiology of root canal infections

Source.. Entry:

 Exposure of the dentine-pulp complex to the oral microorganisms.

 Exposure may occur as a result of minimal crack, dental caries, trauma, to name a few.
 The risk of the microorganisms entering the pulp increases as the lesion gets deeper, why?
1- Close association (location)
2- Dentinal tubules are wider close to the pulp (compared to the dentinal tubules at the
DEJ), thus, it is easier to allow for bacterial entry.
toxins ‫ بال‬inflammation ‫ لكن ممكن يكون فيه‬infection ‫ هنا اتوقع العصب ما فيه‬DEJ‫يعن مثال السوسة واصلة ال‬
‫ي‬ 
‫ السبب شنو؟‬pulp‫ هنا بتوقع انها وصلت ال‬dentine‫ بتاع ال‬inner quadrant ‫ لكن السوسة لو وصلت ال‬
 Because close to the pulp, the dentinal tubules are very wide, even cells can pass.
 The microorganisms inhabit the whole pulp space only when the whole pulp tissue becomes
necrotic (because necrotic pulp doesn’t stop bacterial invasion, due to lack of immunity, unlike
vital pulp).

Classification of endodontic infection according to anatomical location:

1- Intraradicular (we may have intra radicular infection with periapical inflammation due to
toxins that reach P.A area)
2- Extraradicular (P.A area infection the bacteria itself in P.A area)

Intraradicular infection is further classified into primary and secondary.

(Remember: this is not a diagnostic classification, the purpose behind it is to study the lesion
histologically to determine the treatment).

Intraradicular Infection:
1- Primary infection: New bacteria (oral commensal), pulp is sterile.
2- Secondary infection: There is already previous infection and get treated but there is
secondary infection.
 Any class (primary/secondary) is caused by bacteria totally different from the other, differ in
features and genetic consequences.
 Primary infection is caused by bacteria that initially invades and colonized the necrotic pulp.

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 Secondary infection is caused by microorganisms that are not present in the primary infection
but are introduced to the root canal system during or after treatment.
 So isolation is important (so we don’t introduce new bacteria to the area)
(Pain and swelling)  Flare up ‫ ما متعودة عليها عشان كدا حتعمل‬immunity‫البكتييا الجديدة ال‬
‫ر‬ 
 To avoid:
1- Use sterile instruments
2- If one canal has pus use file for it only
3- Restoration TF is stable
4- Good obturation

Persistent infection (with primary):

 Bacteria get trapped in the dentinal tubules and lateral canals and remains dormant, when it
has source of nutrients, it will cause infection (not secondary)
‫ كويس‬disinfection ‫البكتييا األوىل زاتها لكن انا ما عملت ليها‬
‫ر‬ ‫دي‬

*The most common cause of failure of RCT is persistent infection and secondary infection.
Causes of secondary infection:

1- Leakage through TF between visits.

2- Not strict antiseptic techniques.

interdental adaptation ‫ ما مزبوط ما عملت‬rubber dam‫ال‬-

leakage‫ بختو يف حتة ال‬resin ‫ هو‬gingival dam ‫مرات بعمل‬-
That’s why in case of RCT for class II , we build up the missing wall with permanent restoration or
strong temporary restoration (GIC for eg) but not ZOE. This provides 2 advantages:
A- Adequate isolation of the access and good rubber dam grip.
B- Preserve the irrigant in the access cavity for as long as possible
pre-access build up ‫*الخطوة دي اسمها‬

3- Non sterile/contaminated instruments or delivery systems (irrigation syringe for eg)

The most common microorganisms in secondary infection is enterococcus fecalis (not commensal in
oral cavity).
4- Delay of permeant restoration.

rotary system‫ وانت شغال ب ـ‬posterior ‫ او‬anterior ‫ ممكن لو كانت السن‬single visit ‫*عشان كدا احسن تكون‬

*persistent and secondary infection are responsible of several clinical problems including:
persistent exudation, continuous symptoms (persistent pain), inter-appointment flare ups and
failure of endodontic treatment.

Exrtaradicular infection:

 Microbial invasion and proliferation into inflamed periapical area.

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 ‫ اال يف حاالت معينة بيحصل‬endodontic problem ‫ دايما بيكون نتيجة ل‬،‫ براهو‬periapical infection ‫ ما بيحصل‬
perio-endo lesions ‫بتمش العصب اسمها‬
‫ي‬ ‫ بعداك‬periapical area‫العكس ببدا من ال‬
 Also in cases of trauma.
 usually if the intra radicular infection is properly controlled, extra radicular infection can heal
by itself (by immunity) except if patient has osteoradionecrosis so it is preferred to perform
RCT before radiotherapy.
 So no intervention (because irrigant is toxic) and should not reach the periradicular area, just
treat the intraradicular infection.
 In some cases, antibiotics can be prescribed, NSAIDS if there are systemic symptoms (fever,
headache).

Biofilm:

 May be single species or multiple species. Resistant to the action of the immunity because:
o It has polysaccharide polymer (covers bacteria from action of immunity and
antibiotics)
o Bacteria communicate with each other (although it is normal commensal)
 It has certain genetic changes and become violent.
 Biofilm microorganisms in the root canal => multi species biofilm community.
 Any hard tissue is susceptible to biofilm formation.
‫يعن ما بتكون يف اي حتة يف الجسم‬
‫ي‬
 Biofilm micro-colonies irreversibly attach to substratum (dentin) and to each other.
 Each environment has different biofilms. (biofilms in coronal parts differ from in middle
part, differ from in apical part).
 Why?! According to interaction to oxygen and immunity.

Biofilm formation:

 Start by cells attachment to the surface, cell proliferation, matrix production, adherence of
other microorganisms, microbial colony maturation (Quorum sensing),
biofilm ‫تمش حتات تانية عشان تعمل‬
‫ي‬ ‫ يف ر‬
‫بكتييات بتطلع‬
Does the biofilm environment affect the pathogenicity of the infection? Yes, by: 
1- Matrix will act as protective shield, highly nitrogen matrix composed of extra cellular
polymeric substance (EPS) act as protective barrier.
2- Increase the size of biofilm make the treatment difficult.
3- Microbial organization and maturation (coagulation of expression points or genes
between bacterial species).
‫ى‬
‫ ما بتقدر تشتغل‬immunity‫ وال‬drug‫ فبيحصل شنو؟ ال‬dormant ‫وبتبق‬ metabolism ‫مرات بتقلل ال‬

*Also this communication controls density of biofilm (Quorum sensing)

Quorum sensing = (synergism, digestion, regeneration, exchange, competition, antagonism,
sorption, resistance, adherence, renewal, import, protection, aggregation)

15
 4- Presence of certain types of bacteria in biofilm increase the pathogenicity
(under research)
Bacteria:

non culture DNA study ‫وهش‬‫ي‬ culture ‫ كانت بتعتمد عىل‬study‫ زمان ال‬
 Porvetella, fisibacteria, strept, lactobacelluous, candida also. In culture base.
 In cultural independent =>DNA => systematic revision of 12 studies of next generation DNA
sequences.
 The most abundant phyla, Firmicutes, Actinobacteria, Bacteriods, Proteobacteria and
Fusobacteria.
 The most detected genera were Prevotella ,fusobacteriam.
 Temperature map classified bacteria into general and apical.
 Bacteroids are present in apical more than general.
 Prdo bacteria, Fusobacteria are present in general more.

Virulence:

 An innate ability to switch on genes that enable survival and propagation in different
environment and encode a range of variant factors.
 Ex: lipopolysaccharide (gram –ve)
 It has been suggested that symptoms appear with certain microorganisms.
 A study was made between symptomatic and asymptomatic patients to study types of
bacteria, they found that they have the same types of bacteria, why?! Variation in
expressions of the virulence factors in different strains of the same species.

*The reference for this lecture is

Endodontics principles and practice 6th edition. EVERYTHING HAS
BUEATY BUT NOT
EVERYONE SEES IT.

16
 LECTURE #5 – Endodontic diagnosis and treatment planning

Clinical classification of pulp and periradicular disease:

1. Depends on the patient’s symptoms (subjective), thus, not reliable (because they differ from
person to another).
1- We can’t determine the extent of inflammation, if pulp is infected or sterile.
2- It only differentiates between symptomatic and asymptomatic cases.
3- No correlation between clinical presentation and histopathology.
4- Used to determine the type of treatment and prognosis.

There are 2 classifications:

1- Grossman (just for pulpal disease, without classification of periradicular disease):

A-pulpits [inflammatory disease of the dental pulp]

B- pulp degeneration [not inflammatory]

C- pulp necrosis
Pulpits is either reversible or irreversible.
Types of irreversible:
1. Symptomatic
2. asymptomatic
3. Hyperplastic
4. Internal resorption.
 Types of pulp degeneration:
1- Calcific => radiographic diagnosis. Here reaction of pulp to inflammation is laying
down reparative dentin, also known as (calcific metamorphosis).
2- Atrophic (histological diagnosis)
3- Fibrous (histological diagnosis)
 Pulp necrosis:
When the pulp is irritated, it has 3 options:
1- Inflammation (initially is reversible) if no intervention=> irreversible
2- Pulp is vital but severely inflamed => symptomatic.
 If no symptoms:
1- chronic hyperplastic pulpitis
2- A symptomatic irreversible pulpitis
3- internal resorption
irreversible‫ دي أنواع ال‬

17
B. Ischemia occurs in severe trauma.

C. Degenerative type of calcification (in the X-ray).

American Association of Endodontics (AAE) Classification: (Used in university clinic)

 It has two parts, pulpal diagnosis and periapical diagnosis.

 You have to right the two parts for diagnosis (pulpal diagnosis + P.A diagnosis)

A. Pulp:
1. Normal pulp:

 Simple caries with no symptoms.

 Diagnosis (Dx): dental caries with normal pulp.
 In necrotic pulp there is no pain also, how to differentiate?
 X-ray is not reliable; because it's a 2D image for a 3D structure => caries may extend buccal
or lingual but may appear as if it's extending inside the pulp;
‫ش بس عشان أشوف السوسة واصلة وين‬‫بعملها آخر ي‬
2. Reversible pulpitis.

3. Irreversible pulpitis:
I. Symptomatic. II. Asymptomatic.

4. Pulp necrosis.
5. Previously treated pulp.

6. Previously initiated therapy.

18
B. Apical tissue:
1. Normal apical tissues.

2. Symptomatic apical periodontitis (A.P).

3. Asymptomatic apical periodontitis.

4. Chronic apical abscess.

5. Acute apical abscess.

6. Condensing osteitis.

Diagnostic procedure:
‫(الزم يكون ى‬
MUST BE IN ORDERED SEQUENCE )‫باليتيب‬

1. History taking of dental and presenting complaint.

‫لو وصلت لتشخيص هنا ما ضوري أواصل وال ى‬
vitality test ‫حن اعمل‬ 

2. Clinical examination => ‫ممكن أصل للتشخيص هنا‬

3. Clinical tests " Vitality test ".

4. Preoperative radiographs => if indicated for RCT or a previously filled tooth.

5. Interpretation of the radiograph.
6. Formulation of the diagnosis.

7. Treatment plan.

 ‫يفي للبيشنت ألي قسم‬

‫كل حاجة محتاجة معالجة اعمل ر ر‬
 The sequence of the treatment plan is also important:
1. Emergency: severe pain or swelling.
2. Refer to: (order is important)
o Surgery.
o Periodontics.
o Restorative.
o Prosthesis.
o Orthodontics, implant.

8. Finalization by discussing treatment options.

19
Case History:

 Name, disease, current systemic or local condition...etc

 e.g. If the pt. Is a chronic alcoholic don't do composite; life span of the filling will be reduced
=> do a porcelain crown.

1. Chief complaint (C/C): the complaint which made the pt. visit the clinic. If there are other findings
write it in others.

 It should be it pt.'s own words:

 e.g. First molar => ❎
 In the lower right tooth => ✅
 Commonly pain.

2. History of C/C: the severity and the emergency of the c/c

 If pain is the chief complaint, you should ask about the following:
1- First onset: tell if the condition is chronic or acute.
2- The quality:
Sharp, electrical, piercing => A delta fibers.
Dull, throbbing => C fiber.
3- Intensity of pain (‫)الشدة‬:
numerical pain scale (NPS) from 1-10 (1-3 mild, 4-6 moderate, 7 -10 severe)
4- Location:
If localized => periapical because the pulp has no proprioceptive fibers.
If pure pulpitis => referred or radiating pain.
It may be non-odontogenic pain (sinusitis, trigeminal neuralgia)
5- Duration:
If it is continuous or intermittent.
If it is initiated or spontaneous.
If more than 5 sec => irreversible pulpitis.
If spontaneous => irreversible pulpitis
6- Aggravating factors.
7- Relieving factors.
 In late stage of irreversible pulpitis, pain is initiated by heat and relieved by cold (very
characteristic)
 Relieved by medication (meaning that there is still as healthy part in the pulp) not severely
inflamed.

20
 LECTURE #6 – Case history (continued)

 Medical history: there is no medical history that absolutely contraindicate endo tx.
 Patients susceptible to bacterial endocarditis, congenital heart defects, prosthetic heart
valve, patients on anticoagulants, patients on corticosteroids -especially those who stopped
it-).
 There is a checklist of medical history described by Scully and Cawson:

 In addition, L, which stands for

Likelihood of pregnancy, in which
case care should be taken regarding
radiographs and chair positions.
 Contraceptives are known to cause
gingival changes, periodontitis, this
imposes a challenge for composite
restorations, difficult isolation due
to gingival bleeding.

Dental history:

1. Previous restorative and endodontic treatment, this will affect the current condition.

2. Other dental treatment or conditions:

 scaling and root planning => root sensitivity.

 Ortho => crack or root resorption.

3. Possible complications.
4. Previous response, unfavorable response.
5. History of trauma (if a pt. came with non-vital tooth without caries).

6. Any previous radiograph?

‫ ؟ ال‬retreatment ‫ هل دا طوالي‬،‫ ممتاز‬obturation‫ وماف أعراض وال‬RCT ‫ وهو كان عامل‬P.A Lesion‫لو زول جاك ب‬
‫ وال أل‬healing ‫ عشا اقارن هل بدا يحصل ليه‬preoperative x-ray ‫هل عنده‬

7. Habits:

 Tooth wearing <= ‫لو زول قال ليك أنا نجار أو أستاذ‬
 Smoking, tooth brushing, lemon and acids, ‫ العرديب‬, you expect to see tooth wearing.

21
Examination:

 Examination, objective findings, any deviations, abnormalities should be checked.

 How do we differentiate between deep fissures and caries?
Any deviation from the normal in 3Cs: color, consistency & contour.

1. Visual examination: bluish hue => caries

2. Tactile examination by probe, explorer => Catching (both deep fissures and caries cause
catching) => softening => caries
A. Tactile exploration of dental caries.

B. Palpation of soft and hard tissues. (with your finger)

If it was fluctuant => cyst or abscess.

If hard => bone lesion.

C. Periodontal probe.
Extra-oral examination:

 Deviation from normal in 3Cs must be checked.

 General look > if good => NAD. Eyes, skin (sinus tract) => may be dental or dermal, lips,
facial symmetry, muscles of mastication, mouth opening (normal: male: 45-50mm, female
40 - 45mm)
 Must know the cause of limitation: TMJ or muscles?
.‫ لناس السيرجري بسبب‬refer ‫عشان بعدين اعمل ليهو‬
 TMJ examination anterior to the ala of the ear, and ask pt to open his mouth and check if
there’s Clicking, deviation, limitation, tenderness.
 If there is no problem then you should mention all of them, no clicking, no deviation, no
limitation, no tenderness.
 Mouth opening should be written in millimeters.

Lymph nodes:

 Palpation of submental, submandibular & cervical lymph nodes.

 If there is swelling, write whether it's hard (malignancy) or soft (infection), and if it's mobile
or fixed, if there is tenderness (infection) may be due to dental, periodontium, sinusitis, eye
infection, tonsillitis (you must know the source of infection).
 So briefly you write: L.N:
1. Palpable or not. 2. Soft or hard.
3. Mobile or fixed. 4. Tender or not.

22
Intra-oral examination:

 Same steps: inspection and tactile

- palpate the mucosa, vestibule...etc.
- oral hygiene (should be written)
 Examination of the gingiva:
1- Calculus or plaque:
write if it's localized => overhanging restoration
generalized => systemic disease, pregnancy, poor oral hygiene.
2- Gingival recession => localized or generalized. (if more than 6 => generalized)

Examination of occlusion:

 Angle classification.
Increased, decreased or zero overjet (important in the treatment plan of class iv).
 Over bite
 Deep bite
 Cross bite: area of interference
crack in the cross bite area ‫ بجي العيان يشكي من ألم تعاين تلقى مافي تسوس فتلقى‬crack ‫لو السن فيها‬
 Scissor bite.
 Anterior guidance:
‫ لو‬،occlusion‫ األسنان القدام بيكونو هابشين بعض واألسنان الورا بيكونوا برا ال‬،‫لمن تقول للبيشنت يعضي على أسنانه‬
interference posteriorly ‫بقى في أسنان ورا هابشة بعض معناها في‬
‫ (مفروض يكونوا الوحيدين‬edge to edge ‫ خلي األسنان القدام‬،‫ بتقول للبيشنت اقفل فمك وجيب أسنانك التحت لقدام‬
) out of occlusion ‫الهابشين والورا‬
 Lateral interference:
(non-working side)‫ ال‬opposite side‫ بشوف بعداك مفروض ال‬laterally ‫بتقول للبيشنت يحرك‬
out of occlusion ‫يكون‬
 If there were teeth touching in the non-working side => non-working side interference.
 Occlusal vertical dimension (OVD):
treatment plan ‫ بيحدد لي حاجات كتيرة في ال‬،‫بعمل تعليق جنرال‬
 If the tooth is over erupted => not indicated.
 Chart.

*‫صور نهاية اللكشر‬

23
 LECTURE #7 – Examination of chief complain

1. Percussion (vertical & horizontal):

 Start with normal tooth, better to do it on the same tooth in the contralateral side.
 By the tip of the mirror handle on the incisal edge and each cusp => look at the eye
response.
 Horizontal => on lingual and buccal => inflammation beyond the pulp.
 In case of vertical => there is apical involvement but we don’t know to which extent, in
horizontal => periodontal involvement.
 If pt felt pain on percussion, X ray is mandatory.
 Also in case complaint in tooth with previous restoration, x ray is mandatory to see if there
is secondary caries or material and there extension.

2. Biting test:

 Must be on hard object, in mirror handle for example.

pain on biting ‫الحاجة دي مهمة في حالة العيان شكى من‬ 
objective  subjective ‫الزم أحول أي حاجة‬ 
‫ لوحده‬each cusp ‫الزم يعضي على‬ 

3. Sensibility test: to know if the pulp is vital or not and to differentiate between reversible and
irreversible.

4. Mobility test: grades.

 Abscess can cause mobility =< treatable.

 The cause can be periodontal => extraction.
 These two tests determine whether there’s periodontitis or not => 1- PPD (periodontal
pocket depth) and 2- PAL (periodontal attachment loss) (by probe), they are important
because their symptoms mimic pulpits.
 Also important in endo-perio lesion, and treatment plan.

5. Palpating test: Soft tissue around the tooth, palpable? swelling? hard? Soft? Tender or not?

 Mobility test: by 2 blunt instruments.

Grades:

 grade one - tooth move horizontally less than 1mm

 Grade 2 - tooth move horizontally 1-2 mm
 Grade 3 - tooth move in all directions V/ H

Biting test: by tooth slooth device.

Have rounded tip that goes into each cusp individually.

24
 If vertical percussion +ve: inflammation on apical periradicular area.
 If horizontal percussion +ve: inflammation on lateral periradicular area.
 Percussion pain on specific direction on specific cusp => cracked tooth syndrome.
1- Confirm by biting test (pain is relieved with biting)
2- pain of specific direction.
 Palpating test: to detect soft tissue swelling or bony expansion, the patient should be asked
about tenderness during palpation.
 If the swelling is facing apex of the tooth => P.R.D
 Above this may be periradicular or endodontic (from lateral canal), periodontal.
 PAL = measured from cementoenamel junction
bone loss ‫لو نزل تحت معناها في‬
 Cal = distance from pocket depth to bone loss
 Mobility test: DDx:
1- Trauma (sub luxation and luxation injuries)
2- Para functional habits: bruxism
3- Periodontal diseases
4- Root fracture: no trauma in crown (crown is intact).
5- Rapid orthodontic movement
6- Endoperio lesion (or periapical abscess)
 Vitality test: blood supply: all tests that we use they test nerve supply.
 some cases when the pulp is partly necrotic, when I do sensibility test: necrotic products
conduct sensation to nerve ending => false positive +
(nerve supply) ‫ لكن في‬blood ‫هنا في الحالة دي ماف‬
 That’s why it’s called sensibility test not vitality test (check blood supply).
 Methods: 1- Neural sensibility test 2- Pulp vascularity test

*Homework: pulp vascularity tests ‫مسؤولي منه م يف االمتحان‬

‫ر‬

25
  Neural sensibility test:
1. Thermal test.
2. Electrical pulp test.
3. Anesthetic test.
4. Test cavity.
3 and 4 are not very reliable.

1. Thermal test: (heat and cold)

Indirectly tell about the vitality of the pulp by stimulating the neural fibers in the pulp tissue.
 Cold => give its sensation through outward hydrodynamic fluid flow to stimulate A delta
fibers (shrinkage of the fluids, stimulate odontoblastic processes, on its end there is A delta
fibers (very fast fibers) found peripherally.
 Heat test => inward (expansion) direction of fluids.
 C fibers are found deep inside.
 If the patient complains from sharp electrical pain => A delta fibers = they are not destructed
yet => early stage of reversible pulpits.
 If patient complain from dull and throbbing pain => C fibres => A delta fibres are destructed
=> late stage of irreversible pulpits.
.‫ دي بشرى كويسة‬pain on cold and sweets ‫ لمن العيان يشتكي من‬
.‫ دي ما كويسة‬pain on hot ‫ أما العيان يشتكي من‬
=> Late stage of irreversible pulpitis and necrosis of most part of the pulp.
 Heat >> fluid or necrotic tissue expansion; in case of necrotic pulp; there is no dentinal fluids
(because dentinal fluid is serum), here the necrotic tissue itself expands, and stimulates the
remaining vital part.

a) Cold test:
 Is most reliable and most commonly used.
 When I say pulp is vital then it’s vital.
 But when I say pulp is not vital doesn’t necessarily mean non vital => false –ve.
 Methods:
1- Ice stick (small).
2- Carbon dioxide (dry ice): have very low temperature (-80) very painful, so we don’t use it
in normal conditions, used in pts with crowns.
3- Endo ice.

b) Heat test:
Not used unless the pt came complaining of pain o heat, sometimes in late stages of irreversible
pulpitis the pain is relieved with cold; why?
Because contraction of atrophic tissue -that causes the pain- occurs.

26
  Heat test is done by heated gutta percha or electrical heat carrier or probably cup (polishing,
used without water cooling) or by hot water.

 Advantages and disadvantages of cold test:

- Cold water:
temperature of cold water is not less than 5 ֯ = not very cold = not very reliable.
 Advantages:
Entire tooth can be cold down + Can be used to replicate patient symptoms.
 Disadvantages:
Require single tooth isolation, time consuming, not as sensitive as other methods? Less rapid
cooling.
- Refrigerated Spray (-50 ֯ ):
The best one; can produce a response even through restorations and crown, cheap.
- Carbon dioxide (-78 ֯ ):
Can produce a response even through restorations and crowns, quick response (very low temp.);
but less available and can be painful to the patient.

2- Electrical Pulp Test:

Neural pulp test gives electrical current, start with low current and increase gradually and see
reaction of pulp and interpret the numerical scale of pulp response => tingling sensation => vital (0-
40 => vital, 40-80 => degeneration, more than 80 non vital)
 Not reliable on its own, (unlike cold test).
 You must isolate the tooth.
 Start at control tooth (sound tooth), you should repeat the test at least twice.
 Lubricate with electrolyte medium. (heat test: lubricate with Vaseline or glycerin, cold test
no need, just isolate and dry).
 Apply in the crown in the middle 1/3 in posterior, (because cervical third will give false +ve)
 While in anterior in the Incisal third, if the patient has delayed in response, go toward the
middle 1/3.
 Avoid contact with any restoration and gingiva.
 Remove test immediately after response, if no immediate response; stay applying until 15
seconds
sensation‫ وزيادة >> بدا يحس بـ‬normal tooth‫تخليه زي ما خليته على ال‬
Normal teeth: usually no pain, or just cold sensation. (compare normal response with the
offending tooth).
pulp is non vital = ‫( وما حس بحاجة‬beyond 15 sec without response) normal tooth‫ قعد أكتر من ال‬-
 Repeat test buccally and lingually because in multi rooted teeth there may be a vital canal
and other is non vital.
 Technique for the test:
Explain the procedure to the patient, isolate the tooth, dry the tooth, tell the patient to raise

27
 their hand if they felt pain and never put it down until pain totally disappear (once there is
pain = vital, duration tells the type of pulpitis).

 Combination of cold pulp test and electrical pulp test is ideal.

Mechanism of cold test:

1- Cold application for 15 sec.
- If +ve response similar to that of the contralateral sound tooth = normal.
- If sharp pain and disappear when the stimulus is removed = reversible pulpitis.
- In comparison with normal tooth, if in normal tooth patient pt had the same severe
reaction= hypersensitivity.
 Tell the patient to close his mouth immediately after you remove the test, to heat the tooth.
- If the pain duration is less than 5 sec = reversible pulpitis.
- If pain is persistent after removal of the stimulus more than 5 sec is irreversible pulpitis.
- No response in necrotic pulp / or late response in late stage irreversible pulpitis.

Electrical pulp tester:

- Normal response of pulp tester: patient starts to feel a +ve response at similar numerical
value as control.
- Early response = reversible pulpitis = responds to less excitation of electrical level.
*Gives a clue that the pulp is diseased, but to determine which type of pulpitis it needs to be
combined with cold test.
- if response at high level of electrical excitation = also diseased pulp but vital.
- (-ve) response, no response even in highest electrical value = necrotic pulp.

*Homework:
1 - Pulp vascularity test.
2- False -ve and false + ve of pulp testing.

Other tests (adjunctive tests):

 Gutta percha tracing sinus test: if there is abscess and sinus tract, insert gutta percha and
do X-ray.

28
 Transillumination and light cure (for cracks).
After performing bite test, the pt felt pain on release, or on percussion the pt felt pain in certain
direction => look for crack either clinically , if not seen clinically => apply light cure on certain
surface, if all surface is light => no crack, if part of the surface was dark => this is the crack
location. Why does it appear dark? The crack scatters the light.

 Test cavity:
Stimulation of dentin without anaesthesia, destructive, historical procedure, applied only when
sensibility test results are inconclusive and tooth already have previous restoration.

 Selective anesthesia:
- selectively anesthetize specific area.
- For patients who complains of diffuse pain.
- In multiple caries or multiple crown, to detect the source of the pain.
.‫ تبدا تخدر األسنان واحد واحد وتشوف األلم بيروح وال ال‬،‫لما يكون البيشنت ما قادر يحدد؛ يقول األلم في الجهة كلها‬ -
- Start with maxillary teeth moving from mesially to distally .
.mesially ‫ لكل األسنان القاعدة‬anesthesia ‫ أول حيحصل‬distally ‫ألنو لو أديت‬ -

Diagnosis is not the

end, but the
beginning of practice.

29
 LECTURE #8 – Endodontic radiology

During the treatment, recall and follow up.

Importance of radiology:

1- To confirm diagnosis of defect extension caused by caries, old restoration, crack and trauma (2
types: pulpal extension, gingival extension). It also tells if there is periapical lesion or not, chronic
apical abscess appear in X-Ray while acute does not except in case of acute exacerbation of chronic
abscess. So it aids in periapical diagnosis not pulpal.
2- To know the tooth anatomy. In deep caries to know the extension for RCT.
3- Reflect the state of surrounding tissue (periapical tissue). If in clinical examination periodontitis is
suspected = to know the bone level if there was bone loss more than middle third of tooth =
indicated for RCT.
4- Assess in setting of treatment plan.
5- Assessment of treatment state outcomes during treatment. (At working length, master con,
obturation, composite) if healing occurs if there is success or failure
6- Follow up

Types of important radiographs in endodontics:

Radiographs are broadly classified into extraoral and intraoral radiographs.

Intraoral radiographs are performed either using plain film or digital sensor.
1- Periapical (2D) 2- bitewing (2D)
Limited information (2D) and distortion from surrounding anatomical guides (super imposition) like
zygomatic bone in x-ray of upper 6, upper 7 but it is still the gold standard in endodontics.

Extraoral: CBCT (3D).

Advantage of digital sensor over plain film:

1- 80% to 90% reduction in exposure to ionizing radiation.

2- No need for dark room processing.
3- Eliminate the use of some environment and chemicals (fixer).
4- Facilitate storage of the image to the computer.
5- Modify and monitor by clinician to enhances ability to discrete
variation by contrast, sharpening.
6- Better interpenetration and correction of under or over exposure,
optimize the image for diagnosis.
7- Can be shared with others.

Disadvantage:

1- The sensor is bulk compared to conventional film.

2- Expensive.

30
What will we see?

 Hard tissue = radiopaque

 Soft tissue = radiolucent

How to interpret radiograph?

1- Type of X-Ray.
2- The area showed in the radiograph, which teeth by number.
3- The offending tooth from coronal to apical.
 In coronal part there is caries, we should mention its extension, to which part, upper third,
middle third, inner third, pulp is involved or not, pulp horn extension.
 Then radicular pulp, then periodontal tissue, then crestal bone and then lamina dura.
 So you should interpret the: enamel, dentin, cementum. Presence of restoration, tooth
morphology, numbers & level of roots, canals, pulp chamber dimension, pulp space (stones),
PDL & its relation to the root structure, adjacent anatomical structure such as maxillary
sinus, IANC.
 Variation of these structure from normal.

Periapical radiograph clinical consideration:

 It shows individual tooth & neighboring & surrounding bone.

 The primary type & the gold standard in endodontics.
 It should include the whole length of the tooth & 3mm of periapical tissue.

Technique:

1-Parallel: film with film holder, film and tooth are parallel to each other. Features include:
1- Same size no distortion, no elongation, no shortening.
2- Reproducible: it can be taken after 10 years for example with the same angle for the same
pt, so it is important in follow up not like bisecting angle.
3- The central ray directed perpendicular to both film and tooth => give better diagnostic
quality (no angulation errors).

2- Bisecting angle:

 The dentist/technician holds the film by his finger, not parallel to the tooth.
‫ واألشعة بتكون عليه‬tube‫ الخط حيكون عودي لل‬،‫التكنشن بيسلط األشعة عىل خط بيقسم الزاوية ربي السن والفيلم‬ 
 The image will be distorted so we can’t calculate the W.L
 Less accurate dimension and extra radiation to eye, maxillary sinus, parotid gland.
 Not used in follow up.
 Used when pt has shallow palatal vault or when the floor of the mouth is very high, in
pediatric patient.

31
Advantage of parallel technique:
1- Accurate image reflect the true length of the tooth with minimal distortion no elongation or
shortening. In bisecting angle technique if:
 Under angulation = elongation ‫نزلت التيوب تحت‬
 Over angulation = shortening ‫ = طلعت التيوب فوق‬occlusal will be shown.
 Con cut=partial image

2- Highly reproducible best in follow up.

3- Less superimposition of bony structure and no overlap (mesial &distal overlap; the tube was
shifted mesially or distally -if there is class II caries it will not be seen-).

Disadvantage of parallel technique:

1- Technical consideration needs film holder.
2- Clinical consideration: in single rooted tooth 1 radiograph sufficient, but in multi rooted teeth
(superimposition) more than one X-rays are required, by tube shift technique (move the tube
mesial or distal), but the problem is how do I differentiate between M.L & M.B

 Tube shift: the aim is to recognize buccolingual relationships of adjacent so the objects
within the tooth and the alveolus appear. If the lesion moves with the tooth => related to it.
If anyone moves to a different direction then the lesion is not related to the tooth.
 The best method is CBCT.
 How to distinguish superimposed structures?
SLOB= Same Lingual Opposite Buccal, if I do tube shift mesially=> canal, root, object
(lingual= ‫االتحرك مع الشيفت‬, buccal = ‫)عكس الشيفت‬
‫عشان كدا مهم أعرف الشيفت كان عىل وين‬
 Upper 5 has 2 canals in Sudanese, tube shift moves distal or mesial 20 degree.
‫مفروض التكنشن يوريك حول لـ وين‬
 Bitewing is an adjunct in some cases but it is necessary in operative to determine caries
extension, in initial pre endodontic assessment of the tooth and overall restorability of the
tooth provide additional information detecting mainly the crown & interproximal area till
the middle surface
 crown is very clear pulp chamber, caries extension, pulp chamber extension, alveolar crest
position, presence of pulp stones, fracture area.

Radiograph in different stages of endo:

1- Preoperative stage is for diagnostic purposes => periapical using parallel tech. Sometimes the
lesion more than 3mm in this case do OPG or upper & lower occlusion OR CBCT buccolingual
 Lower 6 has 2 distal roots each root may have 2 canals
it is not calcification ‫كبية فجأة اختفت معناها اتقسمت لكمية‬
‫أول ما تشوف الكنال ر‬
 See radiographic anatomy => PDL space black line, lamina dura white line.
 Alveolar crest must be in CEJ if below => bone resorption.
 Widening in lamina dura => infection, irregularities.

32
  Mostly in chronic periapical, not acute.
 Widening in lamina dura may be from trauma from occlusion.
 Also estimation the root apex.
 Other anatomical structures superimposition (super imposition of maxillary sinus,
nasopalatine foramen, canine fossa). Detection of canine fossa is by looking at lamina dura
in the opposite side; if we find same radiolucency that means its canine fossa NOT a lesion.
 Mental foramen: also can appear radiolucent lesion adjacent to five.
 Radiopaque shadow, like mylohyoid ridge, body of zygoma.

2- Working length stage:

 Use a file of at least 15mm to show the tip then take an x-Ray
 Has special end holder => Rinn Endoray

3- Master cone:

 After removal of plup tissue we use gutta percha to full working length.
 The cone should not be more than 1 mm from apical constriction.

4- Obturation stage:

 Periapical with or without shift to assess the quality of obturation and condensation process
and should be checked before the pt goes.
 Also check coronal seal and coronal restoration.

5- Recall stage:

 No radiographic changes before a year or 6 months.

 If after 4 years there is no lesion and complete healing this is success.

33
 LECTURE #9 – Pulp diseases

Grossman’s classification:

1. Pulp inflammation [Reversible, irreversible (symptomatic... asymptomatic... chronic hyperplastic

“pulpal hyperplasia, pulp polyp”). Internal root resorption]

2. Pulp degeneration [x-Ray (calcific), Histo (fibrous)

3. Pulp necrosis {pulp necropiasis}: (part is vital and part is necrotic)

AAE classification: (Pulpal and periapical classification):

Pulp Diagnosis:

1/ Normal pulp
2/ Reversible pulpitis
3/ Irreversible pulpitis (symptomatic and asymptomatic)
4/ pulp necrosis
5/ previously treated
6/ previously initiated

Reversible pulpitis:
Is mild to moderate inflammatory condition in which the pulp is capable to retain to un inflamed
state following removal of the stimulus

Histopathologically:

1/ Starts with just local hyperemia => vasodilation => late stage recruitment to inflammatory cells,
limited to the area of stimulus.
2/ Destruction of odontoblastic layer.
3/ Formation of reparative dentin.
4/ Blood vessels are dilated and extravasation of edema predominant of chronic inflammatory cell.

Signs and symptoms: " due to stimulation of a delta fibers "

 Pain => nature of it => provoked pain with sweet and cold
 Character of pain => sharp electrical pain
 Relieved immediately after removal of the stimulus
 May be Asymptomatic
 Patient has no symptoms but when I do sensibility test, he will have
Sensibility test exaggerated response. Usually in these cases the cavity is so large (because
symptoms are caused by edema, in this case there is continuous relief for exudate so pt has
no symptoms). Caries may even reach deep areas and require direct pulp capping and pts is
asymptomatic.

34
‫ ; ممكن‬necrotic pulp ‫ والبيشنت ما بيشتكي من أعراض ما شرط يكون دا‬deep caries ‫ اذا شفت‬x-ray‫ يعني في ال‬
. sensibility test ‫ فالزم أعمل‬reversible pulpitis ‫يكون‬
 So :
 Feature of pain => short (important), sharp, lasting for seconds (not more than 5 sec)
 More than that is considered lingering pain
 *Although in the new classification: (up to 12 sec is Reversible pulpitis)!
 Symptoms:
 Pain is specific (not dull), (and usually in the early stage of Reversible and irreversible pulpitis
pts can detect the tooth) while in late stage pts cannot, pain must be provoked, relieved by
removal of the stimulus (cold or sweet)
 Sign: clinical and then radiographic if needed. Visual inspection to detect the source of
irritation (caries, trauma, crack, sensitivity, tooth wear)
 Then,

Palpation, percussion=> usually no pain except with associated periodontal condition (pain on
horizontal percussion).
If there is pocket => associated periodontal problem and if no caries symptoms may be due to
periodontal problem.
Symptoms may also be due to orthodontic movement.
Then:
Sensibility test: pain 2-5 seconds compared with normal tooth.

Then X ray if:

1- I can’t detect the extension (pulpally and gingivally).
2- If caries is deep (did it reached the level of bone or not? To determine whether we need to
do crown lengthening or not).
3- To see if it’s near the pulp to prepare for pulp capping.
4- If there is restoration.
5- If trauma pt to see if there is root fracture.

Usually there is no periapical change, I just interpret the extension of caries (as a radiolucent lesion)
and the extension => upper, middle, or inner third. also gingival extension=> did it reach apical bone
crest or above it. and if above do we need crown lengthening or just gingivectomy (to know if it’s
restorable or not).
*E.g in lower6caries subgingivally , If it reach furcation area  No need for crown lengthening
tooth for extraction even with reversible pulpitis.
Treatment: -

 Removal of irritant, if deep I must reach hard dentin in the walls, in the floor against the
pulp I must reach affected dentin (firm dentin), but wall it must be with sound dentin (why)?
To prevent microleakage, to make base before the adhesive restoration ((deep caries
composite)).

35
  In other cases, you should remove the irritant and restore the cavity (if present), and
consider pulp protection (if needed).
 In tooth hypersensitivity=desensitizing agent varnish in the area /and follow up by sensibility
test every 6 months, or each year.
Prognosis: - is favorable but in case of early treatment may be turned to irreversible.

- X-Ray pic = P.A X-Ray, showing 36,37,35 and periapical areas.

- In 37: - when interpreting the X-Ray =don’t say caries but radiolucent lesion. Extending to the
inner 1/3 at dentin even it could expose the distal pulp horn.
- Radicularly: pulp canals are intact /periradicular area and periodontal lamina is normal = no
widening and no irregularities, crestal bone at the level cementoenamel junction so no bone
loss.
- Why s/s are for reversible pulpitis while in X-Ray pulp horn is exposed? because x-ray is 2D
view for 3D structure, caries clinically extended buccally and lingually, so it is extending
around the pulp but not actually exposing it as it appears in X-Ray.

-Irreversible pulpitis: -
It is persistent inflammatory condition of the pulp, so it become incapable of healing.
-Histopathology: -
Chronic and acute inflammatory stages ((while reversible are chronic)),The same stage of
reversible but more diffused.
-most capillary venules congestion affect the circulation Necrosis (start partial and then
complete)attraction PMMNPSAcute inflammatory.

Chronic acute exacerbation  fibrosis around micro abscess

*So in partial pulpotomy we separate the chronically inflamed tissue and leave the to be
healed.
S/S=severe pain, sharp, shooting, piercing in nature; in early stages is not spontaneous, it is
stimulated -by cold and sweet-, to differentiate it from reversible  it is lingering pain
(stimulated lingering pain) (for several sec to mins, and change in position, e.g ‫)الصالة‬.
At late stages  spontaneous, and then if interfere with sleeping, may be represented as pain
on biting (combination of irreversible pulpitis with periapical diseaseat late stage may be
as stimulated by hot (dilatation of necrotic products).
-May be symptomatic.
-If spontaneous =I must ask if it Is intermittent or spontaneous.
-Nature in late stage is throbbing, bowing or dull.
.‫البيشنت بيجي يقول ليك حاسي السن فيها ضغطة أو "نتاحة" أو حاجة مزعجة‬

.And it could be associated with slight discomfort when biting

‫ بعرف كيف؟‬،‫ ؟ ال‬A.P ‫في الحالة دي هل بقدر أقول‬

36
Due to stimulation of proprioceptive fibers in the apical 1/3 of canal, caused the pain through the
apical tissue is not inflamed.

Signs:
1. Visual examination: inspection: source of irritation (usually extensive) deep caries
2. Percussion: may be no pain or there is a slight discomfort (discomfort differs from pain).
Patient in tenderness: closes his eyes or flinch. )‫ ينزعج‬،‫ ينط‬،‫(يغم ض عينه‬
Patient in discomfort (in late stages): the tooth feels different.

3. Sensibility test:
In early stages: immediate heightened pain lingers for several secs to mins after the removal of the
test.
(sometimes you need to give potent anesthesia to stop the pain.
In late stages: late week linger pain
In the late stage the coronal pulp start becoming necrotic
‫ ألنو البيشنت بعداك بيبدا يحس‬necrotic pulp ‫بنتظر شوية ما بقول‬
*In necrotic pulp no response at all.

Radiographic examination:
Usually no periapical changes till the late stages:
1. Widening of the PDL space may occur,
irregularities ‫ بيحصل‬widening ‫ ما بيحصل فيها‬lamina dura‫ال‬
2. Deep radiolucent lesion.

Treatment:
1. Complete removal of the pulp (pulpectomy or RCR)
2. Extraction if the tooth is not restorable

Prognosis:
It is favorable if:
1. The pulp is removed.
2. Proper endodontics treatment.
3. Appropriate restoration.

Once the infection reaches the periradicular area the prognosis is very poor.

Types:
1. Chronic hyperplastic “a flesh extruded from the cavity”, it is type of irreversible.
2. Internal resorption.

 Pulp polyp:
DDX of pulp polyp?
May be from gingiva (gingival hyperplasia).

37
How to differentiate between pulp polyp and gingival hyperplasia?
Catch it with a tweezer to see the source from where it is coming (in class II).
*It is always associated with large cavity.
*It is a productive inflammation due to extensive exposure of young pulp
*Caused by chronic, low grade, slow progressive irritation. (gave a chance to the pulp avoiding pulp
death, instead it proliferates).

Histopathology: granulation tissue.

Signs and symptoms: Usually asymptotic because there is no edema, may be painful in mastication
due to ulceration.
Sign: Pink, reddish, swelling originating from a large cavity.

Treatment: extraction or RCT.

 Internal resorption:
- X-ray: widening in the canal.
- Clinically there is reddish or pink hue (pulp tissue).
Due to enamel and dentine resorption >> thinner layer of enamel >> showing the color of the pulp.
- It is irreversible but idiopathic resorptive process.
Stem cells >> clast cells (odonto-, cemento-, osteo-) eat the hard tissue.
This occur in dentine in the pulp chamber or in the root canal system.
- Cause is Unknown but usually the patient gives history of trauma (it is asymptotic) or history of
chronic infection.
- May be a slow progression or very fast.

Signs and symptoms: Asymptotic

Radiograph:
Very important in diagnosis; sometimes discovered accidentally on x-ray.
- In periapical x-ray: rounded or ovoid radiolucent area show change in the appearance on the wall
of root canal or pulp chamber (very important to differentiate it from external root resorption).
**External root resorption doesn’t cause change in the shape of the canal.
On x-ray you see the shadow of the canal in the middle of the resorption, in contrast to internal
where change in the canal occurs.
- CBCT: to check 3D buccolingual extension because if there is perforation diagnosis will differ and
the treatment plan will differ.
Or to know the amount of the remaining dentin wall; is it able to withstand the force of mastication
or not.

Treatment:
A) in early stages minor resorption with no perforation in the walls >> pulpectomy (RCT) but
obturation will be difficult (need to be by “thermal plasticized technique” the gutta percha is
heated/melted to enter the irregularities) “lateral condensation” doesn’t work here.

38
B) In late stage: when perforation occurs…
Integration dentistry must contact surgeon (to open a flab then MTA to the perforation; then we
proceed to do the obturation).
If not repairable: extraction.

Prognosis: Depend on the stage, treatment and repairability of the tooth.

*Homework: Pulp degeneration, calcific degeneration what is it and the appearance on x-ray; its
types, pulp stone and calcific metamorphosis. (Grossman’s textbook, radiographs in Google “dental
pulp stones”, “calcific metamorphosis”). ‫مسؤولين منهم في االمتحان‬

Pulp necrosis:
S/S: if without periapical periodontitis > no symptoms, but if with PAP there will be pain on biting.
Sensibility test: no response
Radiograph: may or may not show cavity (could be due to trauma), or periodontal change.
Treatment: RCT or extraction if not restorable.
Prognosis: usually it is favorable for proper endo therapy.

* If the pulp is necrotic or there is periapical lesion — multiple RCT visits.

* If pulp vital and irreversibly inflamed — single visit RCT.

Reference of the lecture: Grossman’s.

39
 LECTURE #10 – Periradicular diseases 1

 Causes of periradicular disease:

(Seen as radiographic changes).

1. Dental caries; when pulp and P.A area are infected (invasion of pulpal infection by bacteria
or its products by inflammatory mediators into periradicular area).
2. Trauma (pure trauma; without affecting the pulp, the pulp could be sound).
3. Iatrogenic.
4. Periodontal condition (the radiographic change may be due to pure periodontitis; the tooth
may be sound).
5. Developmental disorders.
6. Neoplastic disorder.
These are the DDs for radiographic changes (radiolucency or radiopacity).

 AAE’s clinical classification – Apical diseases:

1. Normal apical tissue.

2. Symptomatic apical periodontitis.
3. Asymptomatic apical periodontitis.
4. Chronic apical abscess.
5. Acute apical abscess.
6. Condensing osteitis.

 Grossman’s clinical classification of periradicular diseases:

1. Symptomatic periradicular diseases.
2. Asymptomatic periradicular disease.
3. Persistent apical periodontitis.
4. External root resorption.
5. Diseases of periradicular tissues of non-endodontic origin (read about them for the
exam).
*We use AAE’s in our clinical practice because it is easier and clearer.

In Grossman’s:
Within symptomatic periradicular disease:
a. Symptomatic apical periodontitis.
b. Symptomatic apical abscess (acute abscess).
And within Asymptomatic peri radicular disease:
a. Asymptomatic apical periodontitis.
b. Chronic apical abscess.

40
 Sequelae by Grossman:

- Periradicular disease could start from irreversible pulpitis stage

pulp necrosis ‫يعن ما شط يبدا بعد ال‬
‫ي‬
- Periradicular disease could be: primary symptomatic periodontitis or asymptotic apical
periodontitis.
- Phoenix abscess = Secondary symptomatic apical periodontitis
Why is it called secondary? The dentist intervened when the pt has no symptoms >> the pt
then came having symptoms and abscess.
- In diagnosis when there is a periradicular lesion, we don’t say cyst or granuloma (because
these terms are pathological diagnosis not clinical diagnosis, and they couldn’t be diagnosed
from the radiograph and clinical symptoms); that’s why they are not included in the clinical
classification.
- Abscess is a diagnosis because there are certain clear signs and symptoms for it.
- Cyst and granuloma have the same treatment (primary endodontic treatment then wait; if
not relieved then surgical treatment need to be done).

41
In Symptomatic pt probably have:
1) Symptomatic apical periodontitis (pure), or
2) Cellulitis (if neglected by the pt), or
3) Symptomatic abscess.
In Asymptomatic pt probably have:
4) Condensing osteitis (discovered accidentally on X-ray), or
5) Asymptomatic apical abscess, or
Secondary acute apical abscess (after intervention), or
6) Cyst (preceded by granuloma), discovered by histopathology.
* Sometimes symptomatic apical abscess becomes an asymptomatic apical abscess, when?

If it opens a sinus tract >> relieve of pus.

And the symptoms relieve (from acute to chronic asymptomatic).

•Grossman made a histopathological classification:

1. Apical granuloma.
2. Apical abscess.
3. Apical cyst.

The AAE included the apical abscess in their classification because it can be identified
clinically and distinguished; acute or chronic.

A/ Symptomatic peri-radicular diseases:

1) Symptomatic apical periodontitis.
2) Symptomatic or acute apical abscess.
3) Acute exacerbation of chronic abscess (phoenix abscess).
They are all symptomatic, whether they were acute or chronic.

1) Symptomatic apical periodontitis (SAP):

An inflammation of the periodontium regardless of whether the pulp is vital or non-vital, producing
clinical symptoms including painful response to biting and percussion.

i.e. the pulp could be irreversibly inflamed “vital” + there is apical periodontitis (1ry symptomatic
apical periodontitis).

* Could there be Asymptomatic apical periodontitis with irreversible pulpitis?

Asymptomatic is a chronic apical periodontitis, low grade irritation caused this form of disease; so
the pulp can’t still be vital; except in one case: in multirooted teeth; when one of the canals is vital
and the other became necrotic and surrounded by asymptomatic apical periodontitis, on vitality
test = there is response, on percussion: no pain, these 2 are features of asymptomatic apical
periodontitis.

42
*This definition is important; this is the difference between 1ry Symptomatic apical periodontitis
and Asymptomatic apical periodontitis:

1ry symptomatic apical periodontitis: the pulp could be vital but irreversibly inflamed, usually in a
late stage of irreversible inflammation (on sensibility test: delayed response).
+ Painful response to biting and percussion.

Causes:

1- Occlusal trauma (usually the tooth is vital).

(Example from previous lecture: a radiographic picture of a lower 8 with simple caries and the pulp
is vital and healthy, but there was widening in PDL space, why? Widening occurred due to a trauma
from occlusion).
- Or due to over-hanging restoration.
- Or the pt already has occlusal interference in the tooth.
- Or due to high force on the tooth because many teeth are missed.
All these can lead to trauma from occlusion.
2- Sequelae of pulpal diseases.
3- Iatrogenic causes.
e.g. over-hanging restoration, over-instrumentation (instrument or irrigant goes beyond the
apical constriction), over-obturation, or sealer leakage outside the root canal; the periradicular
region was sterile >> bacteria reach it by these iatrogenic causes.
* That’s why we use crown-down technique in preparation of root canal (removing the
infection and bacteria from the coronal part first, the apical part could be pure and may even
have sound vital pulp).

Diagnosis of SAP:
 Symptoms:
Pain and tenderness on biting/ pressure, recent onset, very severe.
(Unable to tolerate even gentle percussion, very severe pain).
Characteristic and distinguished from the asymptomatic apical periodontitis.

Recent onset= because it’s acute caries, if the pt. delayed >> chronic.

 Signs
Signs= clinical and radiographic examination.

Clinical examination:
1- Visual inspection: usually we can detect the source irritation?
Caries, trauma, crack, …
No swelling, and no sinus tract.

43
 Also check the occlusion to exclude occlusal trauma.
2- Palpation: to mucosa over root apex may or may not tender, (palpate over the opposing side
first).
May not tender if the lesion is not such huge to reach the alveolar crest, SAP usually very fine
lesion.
Is there swelling or not = to exclude acute apical abscess, if there was abscess the swelling will
be detected by inspection.
3- Percussion: perform both vertical and horizontal= to exclude acute periodontitis. Response:
tender and severely painful (perform the percussion gently).
4- Sensibility test: usually no response, but in early conditions may give response as IRP
(irreversible pulpitis).
Could be vital or non-vital, in multirooted teeth this response (vital or non-vital) may be also
seen in apical abscess, but usually only in SAP.

Radiographic examination:

No change (didn’t take time to make changes) or slight widening of the apical PDL space and loss of
the apical lamina dura (no peiapical radiolucency)

Treatment:
Remove cause of irritation (eg RCT, relieving occlusion) as early as
possible.

Radiographic pic of 6 and 7 with symptomatic apical periodontitis

- Almost no change, although there is a slight widening in some

areas of PDL space + loss of lamina dura (it is normally a clear
white line >> becomes irregular or not visible).
- Onlay on one tooth and deep restoration on the other, the cause may be occlusal trauma or
infection.

2) Secondary Symptomatic Apical Periodontitis (phoenix abscess):

An acute inflammatory reaction superimposed on an existing asymptomatic apical periodontitis.

At the beginning, the pt may be having a necrotic pulp or chronic asymptomatic irreversible pulpitis
(on vitality test= lingering response).

‫تان يوم ىبق عنده‬

‫ ي‬،RCT ‫ وانت عملت ليه‬esthetic problem ‫ وال‬food impaction ‫ جا بمشكلة تانية؛‬pain ‫ما عنده‬
cellulitis + severe pain on biting

The cause is not always the intervention, sometimes it occurs due to sudden decrease in body
immunity (may be due to severe illness); how is this can be detected?

44
Pt comes with symptomatic apical periodontitis and when X-ray is done = there clear periapical
radiolucency This means it is not SAP, the pt was already having asymptomatic AP >> acute
exacerbation

Causes:

Irritation of dormant asymptomatic apical periodontitis by:

- Lowering of body's defenses

- Excessive Influx of bacterial toxins from the root canal or external source
The bacteria suddenly arrive to the root canal without intervention >> evolution in genes >> release
if new types of byproducts

- latrogenic (improper isolation, wrong technique, etc. lead to introduction of new bacteria
into the interior)

2ry SAP- Diagnosis

 Symptoms:
- Pain and tenderness on biting/ pressure, recent onset, very severe

 Signs:
Clinical examination:
1. Visual inspection usually we can detect the source of irritation.
- No swelling; because it is not actually an abscess.
- The pt sometimes come with cellulitis = it is inflammation of soft tissue, not abscess
- There may be redness and swelling of the face but it is inflammation
- There might be a sinus, because it was asymptomatic apical periodontitis (chronic) >> secondary
symptomatic
2. Percussion: tender and painful
3. Palpation to mucosa over root apex: may or may not tender
4. Sensibility test: no response, no possibility to find the pulp vital

Radiographic examination:
Penapical radiolucency (clear)

45
Because it was already there and was asymptomatic.

... irritation ‫ وصل هنا وعمل‬intracanal medicaments ‫ النقط البيضاء دي‬iatrogenic ‫واضح انه‬

Pt was asymptomatic >> RCT was done >> came complaining of severe pain

 Treatment:
Remove cause of irritation (e.g RCT, relieving occlusion) as early as possible.

3) Symptomatic (acute) apical abscess:

An inflammatory reaction to pulpal infection and necrosis characterized by rapid onset,
spontaneous pain, tenderness of the tooth to pressure pus formation, and eventual swelling of
associated tissues.

 Causes:
Bacterial infection extending from root canal to periodontal and alveolar bone through apical
foramen / lateral canals

)‫البكتييا نفسها وصلت‬

‫ر‬ ‫(هنا‬

SAA – Diagnosis:

 Symptoms:
- Severe recent pain and tenderness on biting/ pressure (pain to biting not pulpal pain).
- Swelling (recent < 1 day), occasionally fever, malaise, and headache.
*The main chief complain is severe pain.
‫ ساعة؛ إذا ى‬24 ‫ والزم يكون أقل من‬،‫ لكن انت ممكن تشوفه‬extensive ‫غالبا ما بيكون وصل مرحلة‬
‫اكي دي حاجة‬ ً swelling ‫ال‬
chronic abscess ‫ ممكن يكون‬،‫تانية‬
(In chronic abscess the swelling may be the main chief complain).

46
  Signs:
Clinical examination:

1. Visual inspection: usually we can detect the source irritation, mucosal swelling at level of root
apex (early), later-on extending to surrounding tissues maybe to the the keratinized gingiva, cheek,
or even causing facial swelling, and may be disfiguring (if in anterior teeth areas >> may cause eye
closure, premolar area >> swollen cheek, lower teeth >> in the neck and this is dangerous, could
develop Ludwig’s angina)
inflammation (cellulitis) ‫ دا‬، abscess ‫ دا ما كله‬facial swelling‫ مرات ال‬-

- Tooth may be or may not be slightly extruded and mobile

2. Percussion: tender and painful ‫الزم‬

3. Palpation to mucosa over root apex tender,

ً lymph nodes ‫ لل‬palpation ‫الزم أعمل‬
lymphadenopathy ‫دايما بيكون يف‬

4. Sensibility test: no response

* Acute abscess is an emergency and must be drained as soon as possible “before sunset”:
- Either through the canal + RCT
- Or through the canal + open intraorally
* When the lesion is very small, it is not very fluctuant upon palpation, because there is no
perforation to the cortical bone yet (but there is pus inside)
‫ف الحالة دي ى‬
pus ‫حن لو فتحته ما حيطلع‬ ‫ي‬
* But when it is clearly fluctuant upon palpation
lesion‫ وتفتح ال‬RCT ‫ هنا الزم تعمل‬perforation to the cortical bone ‫(كأنه كيس مليان موية) دا عمل‬

47
Radiographic examination:

Not expected to see any radiographic changes (like SAP) if it was pure acute apical abscess not
secondary.
Or there may be slight widening of the apical PDL space and loss of the apical lamina dura (no
periapical radiolucency).

 Treatment:
- Drainage in the same day, either through canal alone by RCT, or through canal and open the intra
oral lesion.
*If there is a systemic condition (fever, malaise) give antibiotic, otherwise don’t give.
- Relieve the occlusion (this must be done whenever there is pain on biting = for all symptomatic
lesions).
The pt sometimes can’t close their mouth because of severe tenderness, reduce the cusp by about
0.5 mm.

B/ Asymptomatic periradicular diseases:

1. Asymptomatic Apical Periodontitis

2. Asymptomatic (chronic) Apical Abscess
3. Condensing Osteitis

1) Asymptomatic Apical Periodontitis:

It is the symptomless sequelae of symptomatic apical periodontitis.
How to know if it is a sequela of SAP? From the history of pain.

 Causes:
1. Low grade chronic irritation.
i.e. It could start asymptomatic.
‫شنو بيحدد الحاجة دي؟‬
- Type of bacterial biofilm
- Size of carious cavity
- Immunity of the pt (strong immunity >> chronic disease)
2. Sequelae of SAP
3. Pulp death products, bacterial/ products, inflammatory mediators invade PR area (started as a
primary disease).

48
aSAP- Diagnosis:

 Symptoms:
No symptoms or slight discomfort upon biting, tooth feeling different.
(the pt could give a previous history of pulpalgia)
- What makes symptomatic become asymptomatic? The immunity… symptomatic after 2-3 days >>
asymptomatic
Pt maybe neglected the symptoms, took NSAIDs, or drainage of inflammatory products through the
canal has occurred.
 Signs:
Cinical examination:

1. Visual inspection: source of irritation.

2. Percussion: not tender, or slight discomfort, or feeling different.
3. Palpation to mucosa over root apex: may or may not tender.
4. Sensibility test: no response.

Radiographic examination:

Clear radiolucency; well defined radiolucent lesion + loss of lamina dura

- DDx: granuloma, cyst
Asymptomatic apical periodontitis cannot be differentiated from
other periradicular diseases unless the tissue is examined
histologically (to be in the safe side you say it is asymptomatic apical
periodontitis).

 Treatment:
Pulpectomy (RCT)
Prognosis: good with proper treatment.

Pic: aSAP occurred just due to the tooth preparation for crown (no caries) >> low grade irritation to
the pulp >> aSAP

2) Asymptomatic (chronic) Apical Abscess:

A longstanding, low grade infection (real infection not inflammation) of the periradicular alveolar
bone, generally symptomless and characterized by the presence of an abscess draining through a
sinus tract.

49
  Causes:
- Low grade chronic irritation (started chronic).
- Sequalae of acute abscess: started as acute abscess >> continued until it penetrated the bone >>
sinus tract >> spontaneous drainage.
‫وش اتورم وجنب الضس اتورم وألم شديد بعدين يف مادة بدت تطلع (خراج) وبعده‬
‫يومي ي‬
‫البيشنت بيقول ليك انا اخدت ر‬
.‫ارتحت من األلم‬
This was acute abscess, now >> chronic abscess.

aSAA - Diagnosis:

 Symptoms:
No symptoms or slight discomfort upon biting, tooth feeling different
‫ ) بس أغلبهم ما بيالحظوها‬sinus tract‫ممكن البيشنت يقول يف فتحة (دي ال‬
The pt could give a previous history of pulpalgia and pus drainage (something bitter or salty)

 Signs:
Clinical examination:
1. Visual inspection usually we can detect
the source of irritation + sinus tract ‫الاازم‬
‫تشوفه‬
2. Percussion: not tender or slight
discomfort or feeling different.
3. Palpation to mucosa over root apex
may or may not tender.
4. Sensibility test: no response.

Sinus could be small and with no

swelling, or there could be white fibrous
tissue, and could be through the skin.

Radiographic examination:

Well defined radiolucent lesion + loss of continuity of lamina dura.

Gutta-percha tracing test: to detect the source of sinus tract.

- Needed specially when there are two neighboring carious teeth, or

in cases of trauma, to know from which tooth it is.

50
- Sinus goes towards the weakest point of the bone and opens there, that’s why the source might
be confusing.

 Treatment: Pulpectomy.

3) Condensing osteitis:
A diffuse radiopaque lesion believed to represent a localized body reaction to a low-grade
inflammatory stimulus.
(Here stimulus to the osteoblasts instead of osteoclasts)

 Causes:
- Low grade, long-standing pulpal pathosis.
Pulp could be still vital, or necrotic.
- Mild irritation stimulates osteoblastic activity.

Condensing osteitis - Diagnosis

 Symptoms:
No symptoms

 Signs:
Clinical examination:

1. Visual inspection: usually we can detect the source irritation, sinus tract.
2. Percussion: not tender or feeling different.
3. Palpation to mucosa over root apex: may or may not tender.
4. Sensibility test: no response or response of IRP (irreversible pulpitis).

Radiographic examination:

Localized area of radiopacity surrounding the affected root (very

dense bone with loss of trabecular pattern of normal bone)

Tube shift is done to confirm that it is from this root, if the lesion
didn’t move with the root = this is another type of lesion, could be a
bone lesion.

 Treatment: pulpectomy (RCT)

51
 LECTURE #11 – Periradicular diseases 2

 Post treatment sequelae after apical periodontitis:

1- scar tissue formation.

2- healing (complete deposition of new bone).

3- persistent apical periodontitis.

C/ Persistent apical periodontitis:

Causes of persistent lesion

1- Case no 1 to the left: not proper endodontic treatment or there is shortage in obturation
(shadow of canal, no cleaning and shaping).
2- Case no 2: widening at palatal root, although the treatment is good to some extent, there is a
gap, palatal root has opened apex, should not be obturated with gutta percha, instead; MTA
plug was supposed to be placed in this area).
3- Case no 3: widening in apical part, although obturation seems proper (good obturation in x ray
doesn’t mean good preparation) but if you are sure that all of your work is good persistent
lesion may be from other causes like <<
Maybe this lesion was already big before the treatment, and now it is starting to heal (so previous
X-ray is needed).

X-ray of endodontic treatment + apical periodontitis = Persistent apical periodontitis;

But if the apical periodontitis appeared after the treatment = this is not persistent apical
periodontitis this is conventional apical periodontitis).

 So the cause could be:

1- Improper endodontic treatment or there is shortage in obturation or a gap.

2- Complex canal anatomy (there is lateral canals).

52
 ‫ه السبب‬
‫ممكن تكون مشيت بكل الخطوات الصاح لكن الكنال فيها حتات ما بقدر اصلها ممكن تكون ي‬
3- Apical biofilm or periapical plaque.
‫ى‬
‫االميونن لكن ممكن من األول اتفاداها‬ ‫البكتييا نفسها وصلت وهنا صعب اسيطر عليها واتدخل وبتعتمد عىل‬
‫ر‬ ‫هنا‬
‫ي‬
step down or crown down technique‫كيف؟ بأنه نشتغل ب‬
‫ى‬
.‫ستيب باك بتدخل الحاجات لالبيكال‬.‫البكييا والتيشوز بدري‬ ‫نشيل كل‬

4- Actinomycosis infection.
5- Cholesterol crystals.

6- Foreign body reaction to the over-extended gutta percha or sealer.

7- This radiolucency may be a periapical scar tissue.

Most of micro.organisms in persistent apical periodontitis are: yeast and candida albicans,
gram +ve cocci, filament, and enterococcus vecalis "the most associated bacteria".

Enterococcus vecalis is very resistant to treatment, and can cause “mono-infection” = can elicit the
infection alone without being in a biofilm.
And it also can survive for long starvation period.

 Treatment of persistent apical periodontitis:

Retreatment; if…:
A- patient develops symptoms, and

B-if RCT is non proper also do retreatment,

C- if tooth is abutment for (crown and bridge).

D/ External root resorption:

(Internal root resorption is in pulpitis; type of irreversible pulpitis).
* To differentiate between external and internal root resorption; in tests:

1- Usually internal root resorption at early stage pulp is vital (in vitality test give response of
irreversible pulpitis) but in external root resorption there is no response.

2- External root resorption is lytic process occurring in the cementum only or cementum and dentin
and it continues inward to reach the canal. (while internal occurs inside and extend outwards
making perforation).

53
May be laterally or apically, when it is buccal or palatal it will appear inside the canal on X-ray and
you will be confused whether it is external or internal.
.‫ ما مشكلة‬lateral ‫لكن لو‬

 Types of external root resorption:

1- External surface resorption.
2- Inflammatory root resorption.
3- External replacement resorption " ankylosis ".
4- Cervical root resorption (sometimes classified as a separate entity, but it is external root
resorption occurs cervically).

 Causes of external root resorption generally are:

a. Periradicular inflammation.
b. Trauma.
c. Periapical lesions: odontogenic or non-odontogenic (cyst, granuloma, keratocyst, neoplasm).
d. Excessive force e.g. orthodontic force.
e. Bleaching " internal bleaching". ‫التبييض‬
f. Reimplantation (when tooth falls and reimplanted, in some cases resorption occurs with
time).
g. Impacted tooth.
h. Systemic diseases (Paget's disease).
i. Idiopathic.

 Signs and symptoms:

External root resorption is asymptomatic, just in x-ray, or pts complain of signs of apical
periodontitis then you discover it.

*But at late stages "when most of root resorbed >> mobility or Infra occlusion.

*In some types of cervical root resorption, when resorption reach pulp chamber >> appear as pink
spot in the crown.

Also pink spot is in internal root resorption when it is coronally, resorption in dentin and enamel is
remain = Shadow of the pulp, but in external= pulp is non vital, this pink spot is not shadow of the
pulp, it's shadow of the gingiva (resorption area is empty >> gingiva enters in it).

Signs:

Clinical examination:

1- In visual examination: usually you can detect the cause trauma, caries, old restoration, bleaching,
etc.

2- Percussion: like apical periodontitis may or may not be tender.

54
In replacement resorption "ankylosis" metallic sound is heard upon percussion ‫كأنه بضب يف حديدة‬
because the tooth is ankylosed on the bone directly no periodontal ligament.
3- Palpation to mucosa: may be tender or not, according to stage.

4- Sensibility test: may be vital (depending on the cause).

When the cause is apical periodontitis = tooth is non vital.
Radiograph:
X-ray is diagnostic; most lesions appear on routine radiograph.
- lesion appear concave/ scooped radiolucent lesion and irregular ‫كأنه غرفته بملعقة‬
- While in internal root resorption: “ballooning” of the canal and usually is regular.
- If resorption occur in the apex >> blunting apex ‫كأنه مقطوع‬
- Replacement resorption on x-ray: no PDL space.

* Pic in lecture:
1- External can be buccal or palatal, but it's irregular, the canal is clear.
2- External resorption in many areas.
3-Replacement resorption in late stage, the root is completely resorbed, the crown will fall soon.

* Pic of blunted apex.

CBCT is mandatory in cases of severe resorption associated with lesions (e.g. cyst, granuloma, etc.)
>> for treatment plan, to know whether the tooth is going to be extracted or restored. In some
cases, resorption in buccal or lingual side may not appear on normal x-ray, but appear on CBCT.

 Pathogenesis and management:

1. External inflammatory resorption:

- Infection or inflammation of the pulp >> pulp inflammatory mediators extend to periapical
area, passing through dentinal tubules or through the apical foramen >> cause damage to
the periodontal tissue cells >> this stimulates osteoclasts to start resorption of exposed root
surface.
- External inflammatory resorption may also be due to trauma >> PDL damage cells >>
apoptosis >> inflammatory mediators >> stimulate osteoclasts.

(action of osteoclast).
2. Replacement resorption: the main cause of is damage to PDL not infection.
That’s why most of resorption due to trauma is replacement resorption, but could be inflammatory.

The stimulation is initially to osteoclasts, and then osteoclasts start the process of remodeling by
stimulating osteoblast >> lay down bone, PDL already damaged, replacement of PDL by bone
instead of periodontal tissue (action of osteoblasts).

55
  Management:

1- CBCT: to determine the extension and if the tooth is restorable or not.

External inflammatory resorption:

(if the tooth is restorable):

2- Endodontic treatment as soon as possible in multi-visits + CaOH management between visits.

3- Micro surgery in case of perforation (perforation reached the canal).

Replacement resorption: has no management.

if the pt is young don’t extract the tooth immediately, leave it as space maintainer and bone
maintainer until the pt reach proper age for implant.
If the pt is old: exract and implant, or any other replacement.

 Cervical root resorption:

Type of external root resorption with some different features.

 Causes:

1- Bleaching ‫التبييض‬
2- Scaling and root planning (if you damaged the cementum).

 Characterized by:
- It is localized at the cervical margin.
- Usually asymptomatic, until late stage >> pink spot (gingival tissue).
- On probing (subgingivally): Profuse bleeding + you feel sharp edge on tooth structure due to
resorption.

- Sometimes on early stage pulp can remain vital.

56
 Pathogenesis:

Damaged cementum at the cervical area >> exposure of the dentin >> stimulation of osteoclasts

Or in cases of internal bleaching when bleaching agent is applied inside the pulp chamber if you
didn’t perform good sealing to the pulp, bleaching agent (hydrogen peroxide) will leak through the
dentinal tubule to the periodontal tissue >> stimulation of osteoclasts.

 Management:

1- CBCT to determine the extension of the lesion.

Treatment depends on accessibility and restorability (deal with it like any other type of trauma).

2- Repair: external repair if the lesion is accessible (restoration) or internal repair (from inside the
canal)
+/- endodontic treatment
3- Endodontic treatment depends on whether the pulp vital or not, reversibly or irreversibly
inflamed, this is when the cause isn’t apical periodontitis (trauma, ortho, external bleaching,
periodontal treatment).

4- Usually need crown lengthening or orthodontic extrusion to access the lesion or extract the root
and do restoration then reimplantation.

5- If tooth is not restorable >> extraction.

The problem of resorption is that it is a silent lesion, patients always come at late stages.

57
 LECTURE #12 – Root canal anatomy

 The components of pulp cavity are: Pulp chamber, root Canals and other anatomic features.

 The pulp chamber found in anatomic crown (that start from the CEJ).

# What is the difference between anatomic and clinical crown?

 The root canals found in anatomic root.

# What is the difference between anatomic and clinical root?

 The other features of pulp cavity are: Pulp horns, accessory canals, furcation canals, canal
orifices, isthmus, Pins, apical deltas, apical foramina.

 In pulp chamber I should reach the pulp chamber floor that as the CEJ.

 The lateral canals emerging from accessory foramina.

 Between the lateral and main canal there is the apical deltas.

 The furcation canals are lateral canals at furcation area.

 Isthmus, Pins, deltas: are communication between canals.

◾Pulp Chamber:

 The goals in access cavity is pulp chamber.

 The outline of pulp chamber is corresponding to the external contour of the crown except
the upper molar teeth (6,7,8).

 In access cavity you must reach the pulp chamber floor which is at cement-enamel junction.

 Pulp chamber is found at the center of the tooth except for upper molars.

 Pulp chamber roof has pulp horns point where the pulp chamber extends towards the tooth
cusp.

 Sometimes these horns are not complete because the formation of the tertiary dentin. (Sees
on x-ray).

 Floor is at or below the level of cemento-enamel junction.

How to know that you reach the floor?

Using periodontal probe, measure the distance to the CEJ, then measure it from inside the
cavity. Or just by eyes…

 . Floor also has maps, I have to see orifices and developmental grooves between them

58
Sometimes when you see openings and they may be the pulp horns; how to distinguish?
they are above the level of CEJ.
The color of the roof of the pulp chamber is the same color of the dentin on the walls, while the
floor is darker than the dentin on the walls and contain orifices and developmental grooves .

*Developmental grooves are made by the fusion of root shelfs.

 RULES:

Applied on all teeth except upper molars.

95% successful, the 5% is anatomical variations.

1. Orifice location :at the junction of wall and floor, search at the corners ,if it open in the center it
is not the orifice and you did furcation perforation .

Orifices also locate at terminals of developmental fusion lines.

At the end of developmental groove, I should find the orifice, if I not find it that's mean it closed by
dentin bridge, I should open it.

The orifices are equidistant and perpendicular from to line drawn in mesiodistal direction through
the pulp chamber floor. (If you draw an imaginary line from mesial to distal at the center of the
floor; the orifices will be located at equal distances from this line and at 90 ֯ with it).

*Ex: Lower6 = has 2 roots and 3 canals , may be 4 or 6 canals . how to differentiate ?
Usually mesial root has 2 canals )MB , ML( distal root has one canal usually ) most commonly 2 in
Sudanese).

On x-ray may appear but may not )superimposed even by tube shift it may start as one canal ).
When I draw imaginary line at the center of pulp chamber if the distal canal is located at this line
that's mean it is one orifice, but if it dislocated from this line lingually or buccally that's mean there
is another orifice I should search for it, I should know this from the tooth contour.

Lower 6 triangular = 1 orifice, wide lower 6 = 2 orifices.

The other orifices will be at same distance from this line and at perpendicular line.
PC = Pulp chamber.

◾Upper Molars:

 Pulp chamber are located mainly mesiobuccally, not at the center of the tooth. (the distal
side is empty).

 Usually if oblique ridge is sound dont remove it in the access cavity (oblique ridge important
for strengthen of the tooth) unless it is carious.

59
  The orifices position: the upper 6 contain 3 roots and more than 80% contain 4 canals.
‫ بس بفتش يف األركان‬،imaginary line‫ما بتنطبق عليها قاعدة ال‬

 MB1 = just under MB cusp tip but usually MB cusp tip is destructed by caries.

 DB orifice = just distal to palatal plain.

 Palatal orifice = so far from the center.

◾Root canal:

 Root canal is funnel shape start from canal orifice at cement-enamel junction or just below
it or just apical to the cervical line and end in the apical foramen which open on the root
surface at or within 3mm from the center of the root apex (That's mean the apical foramen
may open at root apex or 3 mm above it ).

 The apical foramen may locate buccal or lingual (don't appear on x-ray).

 Nearly all root canals curve in faciolingual direction, straight canals are exception.

 Generally, the no. of root canals corresponds to the no. of roots but not a rule, and oval root
may have more than one canal even when there is one orifice.

◾Vertucci Classification:

 Vertucci classified 8 basic formations of canal structure:

- Type I: (1 - 1) starts as one orifice and ends as one foramen (only in central and lateral incisors).

- Type II: (2 - 1) 2 orifices and it will fuse to form one canal.

60
61
 ‫بتختق معناها اتقس مت‬
‫ي‬ ‫كبية بعد داك‬
‫مرات الكنال بتظهر ر‬
 In x- ray canal start big and then disappear that's mean it divided to small canals.

 In access cavity if there is a lingual canal I will extend until I reach it.

As you are inserting the file straight, you suddenly feel resistance and the file goes buccally or
lingually = there is other canal.

 Lower 6 is type II.

 Upper central and lateral = 1 orifice, 1 canal and 1 apical foramen in 100 % of cases.

 But in lower anteriors 58% of cases one orifice, in 40% of cases start as 2 and end as one,
and in 1% of cases start as 2 and end as 2.

 Almost one half of the lower anteriors have 2 canals.

62
◾Root canal Special features:

1. Accessory canals: minute canals extend in horizontal vertical or lateral direction from the pulp
space to the periodontium and mostly in the apical third.

*In case of vital tooth have irreversible pulpitis do the RCT by “step down/ crown down” technique,
because if bacteria inter the lateral canals it will not go out of it and these lateral canals have
connective tissue and vessels and that is the problem.

2. Furcation canals: accessory canals at the furcation area and branch out from pulp chamber.

3.Apical deltas: Multiple accessory canals that branch out from the main canals at or near the apex
(we should remove the connective tissue from it and seal it with a sealer).
Obturation to deltas = proper RCT.

63
 Apical delta:

Pic: There is radiolucent lesion in the furcation area, the source of infection is the sealer leakage out
of the lateral canal, after follow-up (D): healing; that mean the dentist did adequate cleaning and
disinfection.

The sealer will be absorbed by the body.

*Clinical significance: of lateral canal it can acts as a way for passage of irritant from the pulp to the
periodontium and vice versa (most common cause of peri-endo lesions lateral canal).
*Gutta percha can't enter inside it.

4.Anastomosis: have roman name (culs-de-sac) /fine /webs /isthmuses >> are connection between
canals:
• Narrow, ribbon-shaped communication between two root canals (contain pulp tissue) (it is a
problem also).
• Common in mid-root area, junction of mid and apical ⅓.
• Sometime connection is so severe >> shape canal.
• C shape canal are common in molars (especially lower 7).

64
  C shape canal classification:
Isthmus classification described by Kim and colleagues:
- Type 1: incomplete isthmus (faint communication).

*.‫شعرة بس‬
- Type 2: definite connection.

- Type 3: very short complete isthmus.

(‫)لدرجة بتحس نفسك داخل يف كنال واحدة‬.

- Type 4: complete or incomplete isthmus between 3 or more canal.

- Type 5: 2 or 3 canals opening without visible connection.
(may or may not be seen from the pulp chamber).

“Believe you can

and you are half way
there”.

65
 LECTURE #13 – Access cavity 1

Is convenient direct preparation, used to remove pulp chamber roof, coronal pulp tissue, locate and
enter all root canals.

*Should be convenient, aimed to:

1. Remove all roof to clearly see the floor.

2. Remove all coronal pulp tissue.
3. Locate and enter the root canal /s (all orifices should be located and through them enter to
the canals).

Tooth morphology is the guide (very huge tooth= more accessory canals).
Position of the tooth also can modify access cavity preparation.
Previous attempt or actual restoration.

So it is dictated by:

1- Clinical morphology of the crown (differences in size of the pulp chamber, numbers of canals
according to the size of the tooth).
2- Size and extension of the pulp chamber "x-ray".

pulp ‫صغي اتوقع انو ال‬

‫ر‬ ‫ البيشنت‬, ‫صغية‬
‫ر‬ ‫ وبقت‬formation of tertiary dentin ‫ هل فيها‬calcification ‫(هل فيها‬
)‫كبية‬
‫ دي ر‬chamber
3- Previous restorative attempt or procedure, inclination of the crown and tooth.

‫ بعدين لمن اي‬lower4 ‫ زي ال‬inclined ‫ ممكن الروت يكون عديل لكن الكراون شوية‬tooth ‫ و ال‬crown ‫(ف فرق ربي ال‬
‫ي‬
)‫ حقو بميل يدي مع الكراون‬access ‫اعمل ال‬

4- Extension of the lesion

‫ ى‬mesial and buccal ‫ بتاع السن لكن مايلة‬center ‫ ف ال‬mainly ‫ حقتهم‬access ‫ ال‬lower molars ‫يعن مثال ال‬
‫اكي فلو‬ ‫ي‬ ‫ي‬
: distal ‫ يف ال‬2 ‫عندك سوسة كالس‬

‫ لكن حأرجع لل‬distally ‫ عشان حادخل‬,‫روح يف البلب‬ ‫اولردي واصلة البلب لمن اخلص ى‬, caries ‫ من ال‬A.C ‫حأبدا ال‬
‫حالق‬
‫ي‬
pulp chamber ‫ حقت ال‬dimension ‫ حاواصل لغاية ما أصل لكل ال‬A.C ‫ عشان اعمل‬canals ‫ بتاع ال‬main position
5- Root curvature.

Goal of access cavity:

1- Removal of all carious tissue, to avoid further infection.

66
Specially in irreversible pulpitis “sterile tooth” the pulp is inflamed but the bacteria didn’t enter yet
or entered in few numbers, if A.C was opened without removing all the caries >> infection enters
the pulp >> pt will come complaining of flare up.

)Presence of carious tissue after you finished A.C is a fatal mistake).

2- Conservation of sound tooth structure (convenient cavity but it is conservative at the same time)
because success rate mainly depends on the strength of the tooth.

3- Complete deroofing of the pulp chamber, if there's weak shoulder, and I can access the canal
orifice, it should be removed also, because some infection might be remained under pulp horn, and
shoulder interfere with proper instrumentation.

4- Complete removal of the coronal pulp tissue (vital or necrotic) no remnant of the tissue by the
end of A.C.
When coronal pulp is vital= bleeding

Necrotic= no bleeding (there is remaining tissue and should be removed)

This is not removed mechanically; it is removed mechanically + biologically (by irrigation).

5- Location of all root canals: (there should be no shoulder, no calcified tissue).

6- To achieve straight line access to the apical ⅓ or first curvature, and file must be free in the
access.

‫ لو يف ميالن يكون مايل يىل‬، ‫يعن لمن ادخل الفايل مفروض الفايل دا يخش يىل عديل ماف حاجة مدقرة ليهو ومخلياهو مايل‬
‫ي‬
.‫ه المايلة‬
‫ ي‬root canal ‫سبب انو ال‬
(File should be free not attached to any wall)

If there's shoulder that make the file tilted this may cause 2 problems:
A- File will not inter in proper position "straight" >> will cause error.

B- File may fractured due to excessive load during preparation.

(File does not only bind to canal but also binds to the wall of access cavity = torsion and cyclic
fatigue on file).

*The less the walls that binds the file = the less cyclic fatigue on it.
*At the end of access cavity walls must be funnel-shaped to avoid any contact between file and
walls, clear outlines, adequate access for files and irrigants, no any pulp tissue and roof, all orifices
are clear and reach the floor.

: cavity prep ‫عكس ال‬

● In cavity prep = walls converge occlusally
● In access cavity = walls diverge occlusally

67
  How to do access cavity?

A. Preoperative assessment: (clinically and radiographically).

1. Assessment of the occlusal tooth anatomy.

2. Radiographic assessment of the pulp chamber extension through radiograph.

3. Assessing possible complicating factors.

1. Assessment of the occlusal tooth anatomy:

It determines the shape of access cavity

Two steps:

1- Outline form (working from outside to inside).

2- Refinement step (working from inside to outside).

External and internal anatomy dictates the external outline form, while extending preparation form
the inside of the tooth to the outside dictates Refinement step.
Pulp ‫ (بشوفه من برة ) وال‬morphology ‫ هنا أساسنا ال‬، ‫ بس‬caries ‫ بحكمنا كان شكل ال‬cavity prep ‫ يف ال‬:‫بمعن‬
‫الىل هو ال‬
‫ ي‬3rd dimension ‫ حيظهر ال‬3D ‫ و بعد ادخل حيظهر يىل الشكل‬,2D ‫) لكن‬x-ray ‫(ف ال‬ ‫ ي‬chamber extension
: ‫ دي الفكرة بتاعتو‬، ‫حق اذا احتجت‬‫ ى‬outline ‫ لل‬further extension‫ بعد ما ادخل ممكن اعمل‬، buccolingual
‫ي‬
From outside to inside [outline form] and then from inside to outside [Refinement step].

 Outline form:

Any additional cusps, any change in morphology= expect other canal than normal i.e. additional
canal.

e.g.:
A- Lower central: have 2 canals, may have 1, or 1 orifice with 2 canals.

How to know?

68
From the external tooth anatomy (if the tooth was sound not so destructed).
- When the cingulum is so pronounced and so prominent = 2 canals for sure (the may join at
some point or continue as 2 separate canals) so extension of access cavity lingually is done till
the cingulum, until it is found.

If you don’t reach the cingulum you will not find the other canal; why?

buccolingual ‫ وقاعدين‬superimposed ‫ النهم‬x-ray ‫ما بتكون ظاهرة يف ال‬

In x ray you will not know.

Even if there aren’t 2 canals for sure there are 2 orifices.

- If the cingulum is not prominent= may be one orifice and then two canals.

B- In premolars: lower 5 has 2 shapes (2 cusps and 3 cusps forms "molarized premolar").

Lower 5 usually has one canal (or 2 orifice), 3 cusps type l should expect 3 canals, so outline will not
be like normal premolar (oval) but some sort of triangular outline form.

C- lower 6 has 3 canals (triangular outline) so access cavity usually is triangular, but in some cases
just from morphology you know the access cavity is rectangular, also if you did triangular and enter
then you can make extension after, some things will guide you. ‫حنعرفها لقدام‬

2. Radiographic assessment of the pulp chamber:

What to see?

a) The mesiodistal tilting of the tooth, sometimes doesn’t appear clinically.

‫ وبحدد يىل مسكة اليد‬extension of the access cavity ‫ بحدد يىل ال‬tilting ‫ ال‬-1

(The bur should be parallel to the crown to avoid perforation).

‫ بميل‬straight‫ عشان ادخل الفايل‬mesial extension of the access cavity ‫ بنعمل‬mesially ‫ لمن السن تكون مايلة‬-2
wall mesially ‫ال‬

b) Size and shape of the pulp chamber

‫ وبعداك‬، pulp chamber‫ حق ال‬roof ‫ لحدي ال‬external groove ‫حقن وبقيس المسافة من ال‬ ‫ ى‬x-ray ‫بشيل ال‬
‫ي‬
‫ عشان تحدد‬floor‫ لحدي ال‬roof ‫البي االنا شغال بيهو هو شنو وطولو كم ولغاية وين مفروض ادخل وبرضو من ال‬
‫بحدد ر‬
‫ وال ال‬perforation ‫عىل‬
‫ماش ي‬ ‫ي‬ ‫انت‬
c) Thickness of the roof of the pulp chamber
‫ شديد ى‬calcification ‫ دا حاصل فيهو‬roof ‫مرات بكون ال‬
‫وبق بعيد جدا‬

This determines the types of the instrument and case selection.

d) Presence of pulp stone, is the pulp chamber open or there is calcification and if there is
calcification, can I remove it?

69
e) Variation in the number of the canals and/or roots.
Preoperative x-ray for multi rooted teeth: tube shift 20 degree + parallel.

f) Extension of the root curvature.

If curvature of the root start early in the root (obtuse root), should extend the outline form (from
inside to outside).
g) Periradicular area lesions, and furcation area lesions.

.‫ يف الفلور‬perforation ‫ عامل‬furcation ‫ يف ال‬lesion ‫مرات بيكون يف‬

3. Assessing possible complicating factors:

1- Rotated and malposition teeth.

e.g.: Crowding is not indicated for RCT "case selection" or at least not for GP (difficult access cavity,
difficult isolation).

2- Tipping and mesial tilting of the tooth.

‫كتي عشان الفايل يدخل مستقيم‬
‫ ر‬tooth structure ‫حاضطر أشيل من ال‬mesially tilted lower molar ‫صورة‬
3- Grossly decayed teeth.

soft ‫حيج يف ال‬

‫ي‬ irrigant‫ ال‬irrigation ‫اح اعمل‬
‫ لمن ي‬+ crown build up ‫ اال بعد اعمل‬، isolation ‫ما بقدر اعمل‬
: ‫ وبعمل يىل حاجة اسمها‬tissue
sodium hypochlorite accident (fatal condition)

‫ بعداك بشتغل‬build up for the walls ‫ش بعمل‬

‫اح اشتغل اول ي‬
‫فلمن ي‬
‫ "بعييد جدا" النه مزمن‬receded ‫ يكون‬pulp ‫ اتوقع ال‬x-ray ‫يف ال‬

70
4- Previous attempts of restoration:
) ‫االناتوم‬ ‫(ف زول اشتغل قبىل ر‬
‫غي‬
‫ي‬ ‫ي ر‬ ‫ي‬
(Pic of a bridge) pt complaining of symptoms of irreversible pulpitis on one of the abutments.
The complication is: there is no occlusal anatomy I can operate on…

Teeth with full coverage restorations and abutment teeth for fixed prosthesis are of the
complicating factors in access cavity preparation. I can’t see real extension of the anatomy.

#pic: x-ray A tooth treated with RCT >> poor treatment quality >> caused a periapical lesion, there's
a crown/large amalgam restoration with pin, it is difficult to remove the restoration and the pin to
retreat the tooth (complicated anatomy) + has 2 roots.

5- Teeth with extensive calcification >> require special equipments.

#X-ray pic: A preiapical radiograph showing lower 6, part of lower 5 and part of 7, distal
radiolucency extending to the pulp exposing the distal pulp horns, calcification (pulp stones), 2 root,
2 canals, widening in lamina dura in distal root and apical 1/3 (periapical diagnosis: asymptomatic
apical periodontitis in distal root, pulp diagnosis: can’t be diagnosed from the x-ray, could be
irreversible pulpitis or necrosis).

 Steps of access cavity

1. Outline:
Remove caries (or restorations) then do your outline, but in case of class II caries you build up the
missing wall first then make the outline form (pre-endodontic build-up).

*If there is a crown (fixed) it's preferable to be removed, but if it's well cemented and the patient
has no complaints about it and its removal may cause fracture; open through the crown.
So, it is better to remove the whole restoration; unless the extension of the secondary caries was
obvious on the radiograph.
‫ بس تكون معوضة‬، ‫ماف سوسة تحتها ح اخليها ربي الجلسات‬ ‫ى‬
‫كلينيكاىل ي‬
‫ي‬ ‫باف حشوة و انت متأكد منها‬
‫قمت شلتها و فضل ي‬
.‫ جديدة‬restoration ‫االخي بشيلها و بعمل‬
‫ر‬ ‫؛ يف‬wall‫ال‬

*The outline form is just through the enamel (could be up to the DEJ).

2. Penetration of pulp chamber roof + deroofing:

‫تج نازل من الروف‬
‫ لمن ي‬، ‫البي مفروض يخش كم لغاية الروف‬
‫يعن انا عارف ر‬
‫حادخل بالمقاسات االنا قايسها من صورة االشعة ي‬
‫( كدا انت قديت الروف‬tactile sensation( ‫ كانك وقعت يف حفرة‬drop‫ح تحس ب‬
“APICAL MOTION” ‫من فوق لتحت‬

- Then complete deroofing.

Once you penetrate the roof; the motion should be “SPOONY MOTION” from inside to outside no
more apical motion. Until complete deroofing is done.

71
*Sometimes the tooth is irreversible pulpitis, acutely inflamed; once you penetrate the pulp
chamber >> extensive bleeding ⚠️
!!! bleeding ‫إياك تواصل تشتغل بالهاندبيس و يف‬

At this stage you are not required to have completed the deroofing… the idea is to remove a little
portion of the roof to excite the coronal pulp tissue to stop the bleeding; just a small opening so
you can: (1) Insert a hand instrument (e.g. endodontic excavator) and remove this pulp tissue that
caused the bleeding. And (2) irrigate to remove this organic tissue + stop the bleeding.

After the bleeding stops and you have a clear visibility; you continue the deroofing. Complete
deroofing is not accomplished without the handpiece.

3. Identification of root canal orifices:

Any shoulders, calcification, etc., should be removed at this step.

4. Refinement:
Extension from inside to outside.

*Steps of access cavity preparation:

A: outline form, until the enamel (or up to the DEJ).

B: change in bur direction > exposure of pulp chamber roof.
C: refinement step > if not done:

1. File fracture. 2. Ledge. 3. Perforation. 4. Remnants pulp tissue >> discoloration. 5. infection
D: complete debridement of pulp chamber space.

Refinement step: to make the cavity funnel shaped, straight and divergent occlusally.
Sometimes we need to make further extension when we have obtuse roots or tilted crown.

72
 LECTURE #14 – Access cavity 2

Steps:

1. Removal of caries and restorations + pre-endodontic build-up:

A. All caries should be removed before entering the pulp space; to prevent secondary infection
(pulp may be sterile), or if there is already infection in the canal, immunity is already adapted to it,
but if we entered new type of stratae will cause >> flare up or phoenix abscess.
Caries is usually removed by round bur usually size 2, 4, 6 according to the size of access cavity,
round bur may be diamond or carbide. >>> High speed.

B. All restorations should be removed whenever possible:

If direct restorations (composite, amalgam) >> removed by round bur like caries.

If Crown/ inlay/ onlay (according to type of material will be removed) >> If porcelain fused to metal
>> cutting the layer of porcelain using high speed diamond bur (new diamond bur) most coarse type
(with green or black line color). (Blue, yellow or red round burs can’t remove porcelain)

Layer of metal should be removed by metal cutting bur (trans-metal bur)

C. Pre-endodontic build-up: After removing of caries, cover access cavity (to prevent entry of
material into the access cavity and being set inside it will cause problems) by Teflon or cotton, apply
matrix, build up by composite, better by GIC; because in composite the use of etching and bonding
without isolation may cause a problem.

1. For rubber-dam stabilization.

2. For irrigant retention.

73
3. Prevention of tissue irritation by the irrigant.
4. For provisional restoration retention and prevention of micro-leakage which can cause secondary
asymptomatic apical periodontitis (phoenix abscess) caused by Micro-leakage between visits which
will complicate your treatment (every visit you try to obturate you can’t because there is exudate
from the abscess, and pt will still have symptoms and facial swelling).

# Better to use RMGIC (Resin Modified GIC) for build up; because it's retentive without etching and
bonding, we inject the RMGIC in the whole cavity, then with cotton by tweezer we remove it from
access cavity, then curing of remaining in wall.

N.B: sometimes I have to deroof before buildup due to presence of caries in area of buildup (I can’t
buildup on caries), But otherwise the outline form is done after the build-up.

2. Preparation of the outline form:-

Determined by:

I. Dimensions of the coronal pulp (pulp chamber).

II. Morphology of the tooth.

III. Position of the tooth.

IV. Curvature of the canal.
Start outline from outside to inside and consider it's perfect, then we move from inside to outside
if needed.
So:

After removal of caries and restorations, remove the remaining enamel and dentine according to an
imaginary outline that dictated by the pulp chamber anatomy and canal location.
I have to imagine all dimensions specially the buccolingual dimension which is absent in x-ray.

E.g. lower anterior mesiodistal outline at the center of the tooth extended to the cingulum

approximately.

In buccolingual outline extends to the cingulum and to the incisal edge.

# All anterior teeth buccolingual pulp chamber is wider than mesiodistal.

# Extension to the cingulum because 53% of lower anteriors has other lingual canal; so if I didn’t
extend it to the cingulum I will miss the other canal.

As beginners we should start the outline form from outside to inside then we should refine from
inside to outside if we suspected a second canal. (If from X ray we found to canals we open it
directly)

# Outline forms of all maxillary and mandibular teeth:

74
The extension of mesiodistal dimension detected by pulp horns.

Maxillary:
- Central: triangle (has 3 pulp horns) base of the triangle is toward incisal edge.
- Laterals: triangle but with rounded angles.

- Canine: almost ovoid.

- Premolars: ovoid.

Upper 6, 7, 8: Tringle, but sometimes in upper 6 we do extension (because of mesiobuccal 2 canals)

and become rhomboid in shape.

75
Mandibular:
Lower anterior: all of them are ovoid in shape.

Premolars: ovoid to circular (1 canal usually).

Molars: between triangular (3 orifices) and rectangular (4 canals).

* This is an overview, but every tooth has its own rule.

-after outline from pulp chamber is not exposed.

3-penteration of pulp chamber and de-roofing of pulp chamber roof:

A-Should be penetrated at it largest point: (There are large and narrow areas of pulp chamber we
know it from anatomy and X ray); because if we started from narrow area we may perforate
furcation area without feeling it.

Usually the largest point in the anterior +lower premolar =at the center
Usually the largest point in posterior upper=towards the palatal root.

Usually largest point in lower molars =towards distal root. But sometimes this is ruled by carries
extension, if caries was distal in lower molars, there will be accumulation of tertiary dentin in distal
area, in this case distal area will be the narrowest area and vice versa. That’s why from X ray I
determine the largest point; to direct the bur towards it.
On penetration of pulp chamber roof bur should be directed with the long access of the crown not
the tooth; so we don’t do perforation.

B-Feeling of drop into pulp chamber cavity: when we penetrate the roof. If tooth is vital >>>
bleeding.

*there is a certain consideration to the direction of the bur in anterior teeth (during outline form
and initial perforation it is not with the long axis of the crown).
C- Complete de-roofing:

Once enter the pulp chamber =irrigation.

Sometimes when the tooth is vital and bleeding compromises visibility, I should irrigate through the
penetration and try to excavate the coronal pulp tissue by Endodontic excavator (like conventional
excavator but with long shank).

*if bleeding doesn’t subside, stop further instrumentation +apply eugenol +close the cavity + give
the patient NSAIDs + dismiss the patient and continue in the next visit.

* Complete de-roofing is not in an apical direction. It’s done with spooning action from inside to
outside towards lateral walls to remove remaining roof and avoid perforation.

76
It’s done with high speed large round bur (size 4, 6) especially in large pulp chambers, long shank
(for better visibility), diamond or carbide. Then funneling to the access >>now this is complete de-
roofing.

Once there is still dentin normal color (not dark) and there is bleeding, this is pulp horn not canal
orifices. You should know from preoperative assessment from X ray the length of space to pulp
chamber roof; so you should already know how much you should enter bur until you reach the roof.

4- Explore pulp chamber and root canal identification:

Anatomical land mark of the floor of pulp chamber is CEJ, (if you don’t have X ray or measurements
use CEJ as anatomic land mark).
*usually pulp chamber depth 2-4 mm (space between pulp chamber roof and floor is very small).
How do I know that I reached the floor? By using endodontic explorer or periodontal probe and see
if you reached the level of CEJ.

 Kranser and Rankow’s laws of access opening:

1- Law of centrality:

The floor of the pulp chamber is always located in the center of the tooth at the level of CEJ.
Applied at 95% of human teeth except upper molars (6, 7, and 8).
This means even if pulp chamber was located mesiobuccally, the floor is still in the center; so I have
to do refinement from inside to outside.
*CEJ: cementoenamel junction
*AC: access cavity.

2-Law of concentricity:

The walls of the pulp chamber are always concentric to the external surface of the tooth at the
level of CEJ (floor).

(Photos on lecture’s pdf)

Photo1: from left: 6 with rounded pulp chamber and have 1 orifice.

Photo2: lower 6 rectangular =pulp chamber is rectangular and 2 orifices in distal canal.
Photo3: canine =shape of access cavity like shape of outer anatomy of the tooth.

Photo4: molarized premolar = has 2 canals mesially.

*e.g: you may not find out the shape of access cavity of lower 6 is rectangular unless you reach the
floor and figure out possibility of another canal and do refinement to adjust the shape of outline
form which will eventually give rectangular shape.

77
3-Law of CEJ:
The distance from the external surface of clinical crown to the wall of the pulp chamber is the same
throughout the circumference of the tooth at the level of CEJ. the CEJ is the most consistent
repeatable landmark for locating the position of the pulp chamber.

Photo slide21: lower 6 one with3 canal and the other with 4 canals.

How do I know if there is lost canal? By law of symmetry 1and 2

4-Law of symmetry 1:
Except for maxillary molars the orifices of the canals are equidistant from a line drown in
mesiodistal direction throughout the pulp chamber floor.

Draw an imaginary line at the middle of the floor, canals distance from it are equal (equidistant), if
canal was located in the line this means it’s single canal, but if canal distanced from line even if half
mm, I should look for another one at same distance on other side, it would be covered by dentin
shoulder.
5-Law of symmetry 2:
Except for maxillary molars the orifices of the canals lie on a line perpendicular to a line drawn in a
mesiodistal direction across the center of the floor of the pulp chamber.
This law shows you the direction of the other canal, it is perpendicular to the canal.

*Dentin shoulder is in the floor not the roof, it is on the floor.

Photo: Floor is darker +no complete de roofing.

6-Law of color change:

The color of the pulp chamber floor is always darker than the walls.

(canal orifices darker than the floor ).

Floor=gray. VS orifices=black
7-Law of orifice location:

The orifices of the root canal are always located at junction of the walls and the floor.
Orifices are not at the middle of pulp chamber, if you found something looks like an orifice in the
middle this means perforation! Do not enter any file (that’s why we don’t use burs, we only
excavate the remaining pulp tissue and irrigate to avoid perforation).
8- Law of orifices location 2:

The orifices of the root canals are located at the angles in the floor -wall junction. (Found between 3
angles).

78
9-Law of orifices location 3:
The orifices of the root canal are located at the terminus of the root developmental fusion lines.

Follow developmental groove, if you didn’t find the orifice means it’s covered with dentin shoulder,
you should remove this dentin shoulder. (you will not see developmental groove unless you’ve
done adequate removal of coronal pulp tissue and adequate irrigation with sodium hypo chloride
and EDETA >> to remove smear layer).

Slide 27 =upper 6 right

Lower 6 left

5- Refinement:

The aim: achieving straight line access to the apical part or to the first canal curvature (if canal is
curved).
Means when I enter instrument through the access cavity to canal, instrument should go straight
without impairment from the access cavity until reaching the apical third of the tooth or the first
curvature.
*The path of the file is determined by the shape of the canal not the shape of the access cavity.

Straight line access cavity>> file is free in AC (not the literal meaning of straight).so AC can be
diverged with straight line AC.

Dentin shoulder is not special anatomical entity, but results from AC.it impairs file entry (prevent
straight line AC), the more the obtused canal (early curvature in canal)>> the bigger the dentin
shoulder, so in refinement of this case not only remove dentin shoulder, but also remove the wall
to allow file entry (difficult case).if I didn’t I will have 3 problems:

1. Excessive load on the file =easy fracture.

2. Error (ledge or perforation)

3. Wrong working length. Firstly it will increase working length due to longer pathway, and with
preparation automatically part of dentin shoulder will be removed but you will continue with the
same increased working length leading to apical perforation!, or over extension in obturation.

79
 At the end of refinement: access cavity and wall of the canal should be at the same level; so the file
can enter free (Proper refinement = decrease cyclic fatigue on file).
-Techniques of refinement:

1. Extension of lateral walls as necessary: in some cases e.g: obtuse canal, pulp chamber is not at
the center, when expecting or searching for other canal.

2. Identify and explore undetected canal/possible canal orifices.

3. Removal of dentin shoulder: by using lateral cutting (toward the wall) motion instead of
proceeding in an apical cutting direction using low speed hand peace with non-cutting tips. Use
Gates Glidden bur (has non cutting tip to avoid perforation).

The shape of dentin shoulder looks like mouse hole defect.

Instruments:

a. Gate Glidden: have sizes according to the drawn line (1 line > size 1, 2 lines > size 2……size 10),
in refinement we usually size 2 or 3.

b. Rotary file special for coronal preparation and removal of dentin shoulder.

c. Endo Z bur: have non cutting edge with tapered tip carbide or diamond. It can remove dentin
shoulder and extend the lateral wall (Gate Glidden or rotary file Don’t extend lateral wall)

d. Endodontic ultrasonic tips: it differs from periodontal tips at speed (periodontal tips are very
speed while endodontic ones are slow, they should be fixed to ultrasonic device has endo mode
for slow osculate movement or slow ultrasonic movement) used in refinement, calcification and
pulp stones.

80
ENDODONTIC ULTRASONIC TIPS ENDO Z BUR

ROTARY FILES GATE GLIDDEN BURS

The dentinal shoulders should be taken into consideration to achieve straight line access and avoid
preparation errors.
Mand ant = lingual shoulder.

Max ant = palatal shoulder. When there is remaining pulp tissue with dentin shoulder, in addition to
problems of dentin shoulder, there will be infection or discoloration or pain.

Premolars = mesial and distal shoulders.

Mand molars = mesial and distal shoulders. Some lower molars have mid mesial canal (normally
there are 2 mesial canals but in this case they are 3) it can be hidden under dentin shoulder, if it’s
not removed, we’ll miss the canal.

Max molars = mesial and buccal shoulders.

4. Removal of pulp chamber calcifications (if any).

81
 LECTURE #15 – Access cavity 3

5.Refinement:

Extension of lateral walls:

In sagittal section cavity may need further extension from inside to outside = end result is increase
in the outline form…
And this is for many reasons:
1. Identification of the canals

- There is a missed canal you want to see. or

- There is a calcified canal and you want to open it and achieve straight line access.

e.g., Upper 6 and 7 when there is MB2 we sometimes convert the access cavity from triangular
form >> rhomboid shape, to detect this canal, and to achieve a straight-line access to it.
Also in lower 6 when we have other distal canal we need to convert from triangular shape >>
rectangular form = extension in the lateral walls.

*At the end lateral wall must be diverge occlusally forming a funnel shape and connect with the
coronal 1/3 of the canal. (i.e., the lateral wall of the access cavity at the same level of the lateral
wall of the canal in the coronal 1/3)

Another reason for extension of lateral walls is to have:

2. Obtuse curvature: curvature starts from the coronal 1/3

In this case it is difficult to achieve straight line access without extending the lateral walls.

82
The file will enter curved, it is not a problem with small-sized files, but larger files are more rigid and
less flexible, and perforation can occur.
Here it is not a dentin shoulder, it is an entire wall need to be extended.

*How do I measure the curvature?

From an angle located between the straight line of the tooth and the line along the curvature.

This angle determines the amount of curvature, if it was…

- Minimal curvature: straight or reached 5° (≤5°)
- Moderate curvature: 10°-20°

- Severe curvature: 25°-70°

Moderate and severe need to be referred to a specialist.

*We need to do extension of lateral walls to allow the file to enter straight as long as possible in the
canal, and curve only in the area of curvature (in severe curvature), so the cyclic fatigue will be just
in the curved part of the file, if the cyclic fatigue was in the whole file this would lead to: fracture of
the file, ledge formation, or perforation.

*Eventually: the lateral wall of the canal in the coronal 1/3 must be confluent with the lateral wall
of the access cavity.
How do we test this? By “endodontic explorer”.

- If the endodontic explorer entered the access cavity straight = you did the straight line
access.
- If the endodontic explorer diverged due to tissue in the access cavity = you need further
extension.
*Any divergence of the endodontic explorer must be due to angulation in the canal, not due to any
tissue present in access cavity.

83
One of the problems that happen if you didn’t do adequate refinement (e.g., you left a dentin
shoulder) or you didn’t do further extension of the lateral wall:
Errors in the working length; if you leave a dentin shoulder then you measured the working length,
the dentin shoulder will be removed automatically with the preparation, but then the working
length will be wrong, the file would be longer, and cause over obturation.

*Pictures in lecture slides*:

1- Access cavity, removal of pulp chamber without complete de-roofing

2- complete de-roofing + identification of canal orifices

3- Refinement

Part of the preparation of the coronal 1/3 is part of the refinement; as one of the instruments that
removes the dentin shoulder is rotary file which is also called “coronal shaper file” it does the
preparation of the coronal 2/3 of the canal, and at the same time it removes the dentin shoulder.

So, the idea of refinement is going from inside to outside.

84
  Outline form of the teeth:

1. Anteriors:

(The standard of anteriors is the central incisor)

 Central incisors:
triangular shape, due to the extension of pulp chamber (has 3 horns) mesial-middle-distal

pulp chamber is triangular in mesiodistal direction, but in labiolingual direction it is inverted triangle
(apex of the triangle towards insical edge and base towards the cervical 1/3)

- canals in upper anterior teeth = wider L.L than M.D; that’s why preparation is done more in
the L.L direction than in M.D direction, to avoid an error called “strip perforation”.
- According to Kransner and Rankow laws; access cavity is in the center of the crown
equidistant from the dentinal walls, pulp chamber floor is at the level of CEJ (upper and
lower anterior teeth are included in this law).
- Broad L.L with its broadest part insicaly aligned.

- Generally, slightly triangular outline in young centrals, get more ovoid in old centrals and
laterals, and when the tooth is chronically inflamed >> recession of the pulp chamber >>
more ovoid, triangular to ovoid (the angles of the tringle become confluent), while it is
circular ovoid in canines and lower incisors.
- Laterals and canines: are always ovoid not triangular.

- Extension of the outline of the pulp chamber is determined from the preoperative X-ray.

85
How to enter to the pulp?

Through the enamel size 2 or 4 round bur at high speed (the first bur used, to make the outline
form).

1- Incisally: bur is perpendicular to lingual wall, in a right angle to the lingual wall.
2- Once I reach DEJ = direction of bur with the long axis of the crown; this is the position of the
axis cavity.

Only anteriors are started perpendicular then shift to the long axis of the tooth.

3- Apical direction towards the roof of the pulp chamber, once the bur drops down = reached
the roof.

4- The movement now is from inside to outside removing the whole roof, moving according to
the outline form “spooning movement”, until complete deroofing is done. And canal is
identified (upper anteriors: 1 canal, lower anteriors: could be 2), as there is one canal = no
need for extension of lateral walls.

5- Refinement: removal of dentin shoulders, by using “gate glidden bur” or any other
instrument of refinement (endo Z or rotary file) moving to outside or laterally.
Then checking by using endodontic explorer, making sure that it enters through the access cavity
straight, if there is angulation it is because of the tissues inside the canal (not in the access cavity).

86
  Upper central = triangular

 Lateral = more rounded

 Upper canine = almost ovoid

 Lower central = ovoid but so extended up to the cingulum (susceptibility for additional
canal), -but as beginners we first open until the upper part of the cingulum and see then
extend the lateral walls-.

The extension almost through the whole cingulum (to locate the other canal)
Sometimes one orifice but 2 canals, how is it going to be discovered? After refinement and removal
of dentin shoulders, you find the bur going more buccally, in this case you suspect that this single
orifice opened into 2 canals, so you have to go back to the access cavity and extend the lingual wall
-in this case-, to get a straight access to the other division of the canal.
* central (lower): 75% one canal, but 35% more than one.
* Lateral (lower): more than central (more likely to have additional canal).

Errors in the access cavity:

87
All of them are due to inadequate access cavity.
1- Access cavity gouging:

Continuously moving with the bur, without changing the angulation (keeping perpendicular rather
than changing into the long axis) leading to perforation.

Commonest error in the upper anteriors = gouging; because they’re already angulated.
destruction in tooth structure << ‫ إذا اتلحق كويس لكن حيكون حصل‬-

2- Perforation.
3- Remaining pulp tissue due to incomplete de-roofing, leading to:

- Infection (because this tissue contains bacteria) + discoloration.

- Line access will not be straight.

4- Missed other canal in lower anteriors, very common.

5- Incomplete de-roofing >> dentine shoulder >> file curves >> ledge formation (the file exits from
the pathway of the canal and enters in the walls >> making a step in the wall).

This causes 2 problems:

1) Some tissue will remain not cleaned.

2) This area will not be reached in the obturation.

Also...
3) If continued in this ledge with the file >> perforation.

4) Instrument fracture, due to the high cyclic fatigue on the file.

5) Errors in the working length.

2. Premolars:

- Upper 4: usually 2 roots, but sometimes one root; in both cases there are 2 canals.

- Upper 5: usually one root (very common 2 canals in Sudanese pts).

88
- Lower 4 and 5 usually one root and one canal.
Hence; Access cavity of…

upper premolars: ovoid extended (to see the 2 canals).

lower premolars: circular.

After pre-operative assessment, enter with the bur to the central groove with the long axis of the
tooth, until perforating the roof (drop) >> then de-roofing >> then lateral extension (buccolingual)
>> check >> refinement = the access cavity is ready.

Usually the extension of the access cavity in upper premolar is to the middle of the buccal and
lingual cusps, because the orifices are located at these areas not under the cusp tips; unless there is
caries or the cusp tips are so destructed, because they should be removed if they were weak so
they don’t make wrong reference for the WL. =(in normal cases you don’t reach the cusp tips,
orifices are found under the middle of the cusps).

*Crown of lower 4 is tilted; so the bur should be “tilted” with the long axis of the crown not the
long axis of the tooth.

Errors:

Same errors in anterior teeth may occur in premolars…

- Gouging and perforation
- Dentin shoulder >> fracture instrument
- Ledge
- Missed canal
A canal could be missed due to unremoved dentin shoulder.
(slide 26) Why missed? In access cavity when drawing the MD imaginary line to locate the orifices,
they aren’t at the same level, so there is a missed canal need to be searched for.

3. Maxillary molars:

Rhomboid outline form, and as moving toward the floor it becomes triangular; because the orifices
become near to each other.
- Usually has 3 roots, MB root has 2 canals (MB1,MB2)

MB orifice = under MB cusp tip

DB orifice = palatal and distal to MB

Palatal = just palatal to MB

- Usually outline doesn’t reach the oblique ridge nor the marginal ridge -if it was sound-, and
also doesn’t reach the cusp tip of the MB, DB or P canals.

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*HOW TO FIND MB2?

After finding 3 canals >> refinement >> preparation of the coronal third… now we look for MB2,
where to search for it?

Draw a line from MB1 to the Palatal + a line from the DB until it meets the first line at some point;
at this point search for the MB2 (where the line from DB meets the line between MB1 and Palatal
canal orifices)

- Sometimes the MB2 is too close to MB1 forming “Vertucci type II” which is: 2 orifices and 1
canal.

Always when the orifices are too close to each other they become Vertucci type II; they are
connected (looks like glasses) and they are removed in one file.

 Steps: the same steps of premolars; entered with the long axis but when you near perforating
the roof, you orient palatally (toward the largest area) and the largest area of pulp chamber
here is toward the palatal, while in lower molars is toward the distal, unless the caries extension
obligated you and the pulp was calcified in this area. This is always seen in the pre-operative
radiograph.

4. Mandibular molars:

Usually 3 orifices, the distal might be 1 orifice but opens into 2 canals…
How to know that? By the law of symmetry, if it was in the middle = 1 orifice, but could open into 2
canals.

But if the orifice wasn’t in the middle = 2 orifices, you need to make extension and search for the
other one.

 Perforation of the pulp chamber roof will be toward the distal.

 Errors in molars:

90
1- In tilted molar: gouging; if the bur wasn’t following the long axis of the crown.
2- Perforation to the furcation area.

3- Gouging then >>

‫ فتفتكر انك خالص وصلت وانت لسه بعيد‬blood ‫ ويطلع‬horns ‫تظهر ليك ال‬

 Tips and tricks for identification of canal anatomical variations:

1- Orifice shape and location:

- The closer the orifices = the greater the chance the canals join and vice versa.
- The more separation between orifices = the less the degree of canal curvature.
= (orifices close to each other = more chance they join “Vertucci type II” + more chance of greater
curvature)
And (orifices more separated = less chance to join “single/ Vertucci type IV” + less curvature)
- When the orifice shape is oval = possibility of 2 canals but have single orifice origin.

2- Direction of the file upon introduction into the orifice:

- Point either in a buccal or lingual direction = a second canal is often present, need to make
extension to find it.
- If a canal appears radiographically patent coronally, but disappears apically, it may bifurcate
(Vertucci type V)
<< ‫وكبية وفجأة اختفت = معناها اتقسمت‬
‫ واسعة ر‬canal‫بتشوف ال‬
Then you should consider it in the access cavity in the refinement step.
from inside to outside ‫ حتضطر تعمل‬clue ‫ ما اداك‬X-ray‫ لكن لو ال‬،‫ كويس‬X-ray‫يعن لو الموضوع واضح من ال‬
‫ ي‬-

91
*Homework: (Need to be studied for clinical work and for the exam).
Morphology of roots and canals of different teeth types:

- Average length, no. of canals, roots, Vertucci classification

- Cross section at levels.

- Common root curvatures (e.g., common curvature of upper anteriors -specially centrals-: either
buccal or palatal, laterals: distal/ disto-palatal; that’s why in lesion of lateral the abscess appears in
the palate not in the buccal vestibule).

- Possibility of anatomical deviations and impact upon procedural errors (C-shaped canals, S-shaped
canals, dens invagenatus, dens evaginatis).

92
 LECTURE #16 – Apical morphology and working length

We mean by “apical morphology”: the last 3-4mm of the canal.

 Apical considerations:
important terms we need to know:

 Apical foramen: connection between root canal and periodontal tissue, usually not at
the tip of the root but 0.5-3.0mm above the tip of the root (root apex).
 Lateral canal: very common in this area (apical third).
 Apical constriction: the narrowest part of the root canal (minor diameter).
 Apex: tip of the root.
 Anatomic apex: the tip or the end of the root that is determined morphologically.
 Radiographic apex: the tip or the end of the root that is detected radiographically.

*Note: the radiographic apex and anatomical apex maybe the same but most of the time
they are not , for example when there is root curvature buccally or palatally this can't be
detected by plain radiograph (in this case we see radiographic apex and we measure the
length of the canal but this is not the actual apex “anatomic apex”).

 CDJ (cemento-dentinal junction) “histological landmark” can’t be detected clinically.

*It's not constant for the rest of life; it changes, it becomes narrow and far away from the
apex due to accumulation of cementum.

Histologically it must be with the apical constriction, while with aging the cementum may go
coronally and leave the apical constriction apically, for this reason we can't say that the CDJ
is at the level of the apical constriction.

 Major diameter: the widest area in the root canal (the apical foramen).

93
The main apical foramen of RC it’s frequently eccentrically located away from anatomical or
radiographic apex

 Minor diameter (apical constriction): the narrowest area of the root canal, sometimes at
the level of CDJ.

The distances:

*Distance between radiographic apex and apical foramen = 0 - 3mm.

i.e. could be at the same level of the radiographic apex or it could be far away from it up to
3 mm).

*Distance between apical constriction and apical foramen = 0.5 - 1mm.

Working length is usually measured from the radiographic apex, according to textbooks it
should be 0 – 2 mm from the R.A (this is in case the radiographic apex concise with the
anatomic apex).
But if the R.A wasn’t at the same level A.A; for example, 3 mm >> you will be over-extended.

 The apical foramen (A.F):

Circumference rounded edge, like a funnel or crater that differentiate the termination of the
canal from the exterior surface of the root.
*Usually is offset from the anatomic apex by 0.5 - 3mm.
NOTE:
A.A stand for anatomic apex
R.A stand for radiographic apex
C.S: clinical significance
*In the canal preparation we stop at the apical constriction not the apical foramen.
When measuring the R.A or the A.A is our landmark; it is noted that the apical foramen is
actually far away from the apical constriction by at least 0.5mm up to 3mm.

*Apical foreman coincides with apical root vertex (R.A or A.A) in 17-46% of cases.
‫ او ما بنعتمدو شديد؟‬R.A‫ عىل ال‬working length ‫عشان كده لو سالك ليه ما بتحسب ال‬
94
 apical ‫ ؛ وال‬apical constriction‫ نحن مفروض نقيف يف ال‬R.A ‫النو نحن اصال ما مفروض نقيف يف ال‬
at R.A ‫ عادة ما بتكون‬apical foreman ‫ وال‬، 0.5-1mm‫ ب‬apical foramen ‫ اصال ابعد من ال‬constriction
0.5-3mm‫بتكون فوقه ب‬
‫ى‬
A.F ‫ معناها حأفوت ال‬R.A ‫ عىل ال‬W.L ‫ وانا حسبت ال‬0.5mm = A.F‫ وال‬apical constriction ‫نفيض انه ربي ال‬
1mm ‫ ب‬over extension ‫وحأعمل‬

 Apical constriction:
The most important part of the canal; because it is where the canal preparation and the
obturation ends.
0.5 — 0.75 mm, but in some literatures (it may be 1—1.5 or even 2 mm coronal to the A.F).
*The part of root canal with the smallest diameter.
C.S: the reference point for the apical termination for shaping, cleaning, disinfecting, and
filling.
*Pic in slides: over extension (W.L was measured from R.A) >> apical perforation + severe
irritation to periodontal tissue by file and irrigant.
In addition, there will be a problem in the obturation because it should be done up to the
apical constriction (the narrowest area), not up to the apical foramen because it is the
widest area, gutta percha cannot reach that area to form sealing there.
Furthermore, there is part of the cementum and the periodontal tissue within the A.F = this
area is highly vascularized >> and it is the exit for any bacteria and irritant to the periodontal
tissue.

That’s why preparation must stop at the narrowest area; to perform a proper obturation, if
the preparation extended to the A.F; there is no more narrowest area >> there will be
flaring; and when inserting any gutta percha there will be no “tug-back” (tug-back: diameter
of the gutta percha is the same as the diameter of the apical constriction), which guarantees
adequate apical seal.

But once there is no adequate apical seal; there will be failure, because this means you did
just disinfection not sterilization, there will be remnants of bacteria inside the dentinal

95
tubules; due to the lack of apical seal; this will provide a source of nutrients and oxygen to
the bacteria through the blood supply in this area >> new biofilm + new infection.
If this error occurred; how to manage it?
Refer to a specialist; to do either:
1- MTA plug.
2-Endodontic surgery.

 Working length:

Extracted teeth >> file exit through the A.F.

Rarely to find the A.F at the radiographic apex.

 Objective: To determine the position of canal terminus (the apical extent of root
canal obturation and preparation).
*The terminus is at the apical constriction, why?
1- Because it is the point at which the safe manipulation ends.
(Where the pulpal tissue ends and the periodontal tissue starts). Any preparation beyond
the apical constriction, i.e. outside the root canal = in the periodontal tissue >> consistent
inflammation and periapical periodontitis.

96
2- It is the narrowest area = allowing adequate obturation against a very narrow area; and
hence adequate apical seal.

Very sensitive procedure requires adequate skills, instruments and patience.

*Clinical significance: over-extension can reduce success rate by 62%, while under-extension
can reduce success rate for each mm under-extension by 12% (i.e. 2mm above the A.C =
reduced success rate by 24%).
-A.C = apical constriction.
*What is the problem with under-extension?
Remnants of pulp tissue and bacteria, no apical seal and area of microleakage.

 Working length methods:

Apex locater + X-ray (both at the same time)
*Always go with the apex locater (even if the x ray said it's wrong)

Old methods:
1-Apical gouging by tactile sensation.
i.e. after being experienced you can sense when the file stick in a narrow area (the apical
constriction), nevertheless; a study found that 72% of endodontic specialists couldn’t detect
the A.C.
2- instrumentation without local anesthetic.
Not ethical + the pt may feel pain because there is remaining pulp tissue not always
because you reached the A.C.

3- Using preoperative radiograph alone.

Used for “estimated W.L” according to which preparation is initiated after the A.C. The
“actual W.L” is measured using the Apex locater; by entering the patency file (size 10)
until the estimated W.L (which was measured from the x-ray), start measuring from a
reference point in the occlusal surface of the tooth; and it must not have neither
unsupported enamel nor caries, to be a fixed point. It is preferable to be the same point
when there are multiple canals.
It is better that the reference point is written down, because if you forgot it you have to
remeasure the W.L. You write for example that your reference point is the incisal edge -
if the tooth is anterior-, or if premolar e.g. the palatal cusp tip, or the margin of the
cavity… etc.

97
W.L on x-ray is measured from reference point to 0.5 to 1 mm from the radiographic apex
(R.A) = EWL (estimated working length).
First file inserted is the “exploration file” or “patency file” (size 10).

* Using preoperative x-ray alone to measure the WL is wrong, why?

- Because the R.A is not an accurate landmark, since stop point is the A.C which is far away
from the R.A.
- X-ray is 2D view to 3D structure, maybe apical curvature is present and is not visible on x-
ray >> result in under-extension.

4- The paper point technique:

Paper point: a stick made of absorbing material. It is used to dry the canal and remove any
excess liquid in it.
The paper point is inserted until beyond the A.C then pulled out and checked if there is
bleeding or not, and the point where the bleeding stopped, then substitute 0.5mm and
insert a new one, if no bleeding = this is the A.C it hasn’t been exceeded.
Also a wrong method because the bleeding may be from remnant of pulpal tissue, or the
cause of bleeding is there could be root resorption.

5- Proper technique:
A- working length radiograph (WLR) with file in situ.
x-‫ بعداك انقصو او ازيدو حسب االنا شايفاو يف ال‬x-ray ‫ ووديت البيشنت ال‬EWL‫معناها انا دخلت الفايل لحدي ال‬
ray.
B- The use of electronic apex locater (EAL).
Should be followed with a confirmatory x-ray.
C- Combination technique (EAL + WLR)

A- Working length radiograph with file in situ (WLR):

- The most widely accepted method.
- Placing a file to the estimated working length.
‫ بكون مكتوب الطول‬anatomical knowledge ‫ او من ال‬radiograph‫ يا اما من ال‬EWL‫يعن تخت الفايل يف ال‬ ‫ي‬
X-‫ بتاعك وبتيل الفايل عليه بعداك بتودي العيان ال‬EWL‫ كم فانت بناء عىل الموضوع ده بتقيس ال‬root ‫بتاع كل‬
‫وه‬‫ ي‬R.A ‫ لكن يف النهاية المرجعية حقتنا‬X-ray ‫تان‬
‫ وتعمل ي‬،‫ ننقص والعكس‬overextended ‫ بنشوف اذا الفايل‬ray
.‫مرجعية ما دقيقة ممكن تزبط وممكن ال‬
98
Then taking confirmatory radiograph using parallel technique.-
*Problems:
1- Radiographic apex rarely corresponds with root canal foramen.
2- Only give an estimation (based on assumption AC is 0.5-1 mm short of the RA up to 3.8
mm in some cases).
3- Represent 2D view of a 3D structure.
That’s why it is not reliable alone.

File measured on ruler >> the EWL determined >> 0.5-1 mm measured from the R.A >> x-ray
on x-ray it is 0.5 – 1 m from R.A, but actually there is overextension, the file is outside the
A.F >> then after obturation; the gutta percha is overextended outside the A.F.
* Radiography method alone or as the first step = wrong; EAL then confirmatory x-ray.

 The use of electronic apex locators (EALs):

–Reliable and accurate in >90% of the times.
–Read the connection between periodontal tissue and pulp space (detect the point at
which the file leaves the tooth and enters the periodontium = the A.C).

99
 CDJ is the A.C; cementum is a periodontal tissue, and as long as there is cementum there
is PDL; so the point where the file leaves the canal, it enters an entirely different
environment (the periodontal tissue); this is the A.C, this is what the electronic apex
locater reads.

Mode of action:

‫ واقيس الفايل‬، file ‫والتان بوصله بال‬

‫ي‬ lip ‫ واحد بييل يف ال‬2 calipers ‫ فيه‬، ‫ عشان توصل دائرة كهربائية‬clips ‫فيه‬
‫ يف‬readings ‫طواىل الجهاز حيبدا يعمل يىل‬
‫ي‬ ‫ شديد وابدا انزل الفايل‬stopper ‫ ازح ال‬،‫ او ما شط أقيسه‬، EWL ‫عىل‬
‫( ويعمل صوت‬zero zero) 00 ‫يبق‬ ‫ى‬
‫ لغاية ما ي‬، 0.5mm ، 1mm ، 2mm ، 3mm ‫ يف االول‬، digital screen ‫ال‬
‫ ليه ؟‬، out of the canal ‫ معناها الفايل‬zero zero ، ‫كده أو فالش‬
great resistant ‫ عندها‬root canal ‫ كلو ال‬pulp tissue ‫ لو انت شلت ال‬root canal ‫ ال‬within ‫النه‬
ً
electrolyte ‫ حتة فاضية ما فيها‬root canal ‫ لكن ال‬، ‫ الكهربا بتطلع اصال من الجهاز‬، electrolyte current‫لل‬
‫ دي حيحصل فيها فجاة‬resistance ‫طواىل ال‬ ‫ي‬ periodontium ‫ أول ما الفايل ييل حتة ال‬، ‫فالدائرة ما بتكتمل‬
، patient mouth ‫ يف ال‬clip ‫تمش عشان ماف مقاومة والزم يكون يف‬ ‫ي‬ ‫طواىل الكهربا تبدا‬
‫ي‬ ، zero ‫ وتصل‬drop
‫ ومنها ترجع‬، patient mouth‫الق ال‬ ‫ ي‬clip ‫ ومنها لل‬periodontium ‫تمش خالل الفايل وتنتقل من ال‬ ‫ي‬ ‫الكهربا تبدا‬
.(zero zero) ‫للجهاز وهو يقرا ودي البوينت بتاعت‬

SO, THE MODE OF ACTION:

*Use the human body to complete an electrical circuit, sudden flow of current due to
sudden reduction of resistance (the point of zero zero) reading.
*measure of electric current using pair of electrodes.
1- Oral mucosa through a lip clip
2- Endodontic file

100
Both of them conduct electricity but need media between them to deliver the electrons
from the file to the lip; this medium is the periodontium and patient’s mucosa
So as long as the file is inside the canal, it is not supposed to give reading; unless there is
remnant of pulp tissue >> this gives false reading; that’s why preparation is done (crown
down technique) before taking the WL. Apex locater doesn’t work properly with “step-back
technique”.

0.5 ‫ وبعداك اطلع الفايل واقيس الطول وانقص‬reference point ‫ يف ال‬stopper ‫ بوقف ال‬zero zero ‫*لمن ي قرا‬
. ‫ للتأكد‬X-ray ‫واخىل البيشنت يعمل‬
‫ي‬ ‫ دا‬WL ‫تان عىل حسب ال‬
‫ وادخل الفايل ي‬، WL ‫دا ال‬

* Interpretation of reading:

- Zero reading = the file reach PDL = still over extension…

So:

- Subtract 0.5 mm from length at 0 reading = WL.

- ESE (European Association of Endodontists) recommendation = the reading should be

confirmed by WLRs (combination).

 Classification according to generation of EALs (Evolution of EALs):

- The first two generations of electronic AL were very sensitive to the contents of the canal
and irrigants used during treatment
101
 WL ‫كان الزم تنشف الكنال كويس قبل ما تقيس ال‬
- While new generations are not affected by presence of any liquid in the canal (may get
affected by liquid in pulp chamber).

3rd - 6th generations: Electrolytes did not have a significant effect on the accuracy of the unit
(clinically the canal contents need not to be dried).
‫ى‬
irrigation ‫ نعمل فيها شوية‬excessively dry ‫حت مرات بيقولو لو كانت‬

*Homework: ‫ اقروا عنها ممكن ت تسألوا عنها يف سنة خامسة‬،‫دا باختصار‬

102
103
104
 Problems associated with the use of apex locators:
1- Remnant pulp tissue >> need cleaning.

2- Saliva >> use rubber dam (saliva contain electrolytes, saliva or water in access cavity
will lead to wrong reading). Access cavity should be dry, but the canals not necessarily.

Also there should be no GCF, if there is a missed wall in the access isolate properly, or
build up the missed wall.
3- EAL is contraindicated in pts who have pacemakers (will die in the chair).

4- Amalgam restoration in some wall, or A.C through porcelain fused to metal crown or
metal crown (all these are good electrical conductors) >> isolation of the file with Teflon
tip.

105
So, causes of inaccurate reading:

1- Intact vital tissue or inflammatory exudate (in preapical abscess and I drained it through
canal) can conduct electric current.

What to do in this case? work according to the EWL and take an X-ray, then finish the
preparation, and before the obturation when the canal is clean and dry; repeat with EAL.

2- Fluids in contact with crowns or coronal metallic restoration materials could conduct
current and lead to false reading.
3- Canal shape (narrow or calcified), lack of patency (severe curvature and the file used is
SS not NT and it can’t reach to the end of the canal), accumulation of dentin debris and
calcification.
4- Open apex (death of the pulp before apexification) fracture, perforation (area of
perforation will give zero reading before reaching the apex), broad lateral canal (has
pulp tissue).
5- The potential to interfere with cardiac pacemakers.

 To avoid errors with EAL:

1- Crown down technique (coronal 2/3).
2- Rubber dam isolation.
3- Drying coronal part of the tooth would increase the accuracy of reading.
4- Avoid contact between file or lip electrodes and any metallic restoration or dental
appliances.
5- Moisten of excessively dry canal for stable reading.
6- The size of the file most correspond the size of the canal.

SUCCESS IS NOT FINAL;

FAILURE IS NOT FATAL:
It is the courage to
continue that counts.

106
 LECTURE #17 – Irrigants and irrigation techniques

Mechanical preparation is not enough?

•The bacterial present in anatomical complication “anatomical complex areas" of the canal
(dentinal tubules, Lateral canals, anastomosis and fins …)

•Mechanical prep did not remove microbial biofilm stuck in dentin (some canals are not
circle in cross section “most of them ovoid” while files work in circle dimensions)
SO = bio mechanical prep is done (this is the concept of preparation in endodontic
treatment)

Importance of irrigation:
The only way to clean and disinfect areas of the root canal wall that can’t be touched by
mechanical instrumentation (35% or more)
The apical 1/3 is full of anatomical complication, curvature, ledge may occur, so your best
not to do over instrumentation

The most of errors happened in apical third (ledge, transportation...)

How to disinfect the apical third?

If reach 2 mm from the WL the disinfectant is enough

(Even we use master apical file in very severely curved canal size 25 and then use very small
irrigation needle to reach 2 mm from the WL)

Generally the irrigant extend 1 mm beyond the tip of the needle

So if I do adequate penetration till minus 2 mm from WL and activation of irrigant that is

enough for the apical third

(35%) areas:
1.The apical part of the canal

Depends on biological prep more than mechanical prep

If you work by crown down technique, must take the whole infection and this area to some
extent be sterile

So in this situation you don't need excessive mechanical prep

2.Lateral canals, anastomoses, accessory canals, fins and isthmus

3.compormise anatomy (oval and flat canals)

Files not work in all walls of the oval and flat canals

4.dentinal tubules
107
Goals of irrigation:

1. Killing and removal of microorganism biofilm.

Endodontic infection mainly is biofilm infection, so must penetrate the biofilm and kill the
bacteria inside it; not kill the planktonic bacteria only.
2. Dissolution of organic dental structure.
(organic structure pulp tissue and organic part of infected dentine)
If didn't remove all of pulp tissue that's source of infection “persistent infection"
* infected dentin has : organic and inorganic components, part of the infected dentin
removed by mechanical prep.

3. Dissolution of inorganic part in the smear layer.

4. Disinfection of non-accessible areas.

5. Mechanical flushing out of debris.

6. Lubrication and cooling of endodontics files (prevent fracture, friction, and improve
cutting action).
*Don't insert the file in dry canal; even if it was a new file, the friction action of file in dry
canal can generate thermal irritation of the periodontal ligament; especially in rotary system
(because it works without water).
So, irrigate before and after inserting the file. Irrigation after: to avoid the debris
accumulation that's lead to canal blockade.
characteristics of optimal irrigation solution:
1- the ability to dissolve organic and inorganic matter.
2-killing of planktonic and biofilm microbes.
3- washing action (have very low viscosity and adequate flowability).
4- lubricants (special feature in its surface action).
5-good penetration within the root canal system.
6- low cost.
7- non-toxic and non-allergic.
8- do not interact negatively with other dental materials.
9- does not weaken dentin.

The ideal single endodontic irrigant does not exist.

108
 Irrigation protocol:
Multiple irrigants at least two irrigants because there is no single irrigant can perform all
these actions.

 Delivery mechanisms:

1. Manual passive irrigation

In pic: endodontic irrigation needles

- Sizes: 25 - 27 - 30 gauge
- Increase in gauge = decrease in diameter
(The needle with 30 gauge in master apical file 25 can reach minus 2mm from WL, while the
conventional needle "5 ml" does not reach beyond the coronal 1/3, and the irrigant reach
only 1mm beyond the needle).
Advantages of endodontic irrigation needle:
1- Very thin easily reaches minus 2 mm from WL with same master file.
2- These needles are “side-vented”, opening of the needle is on the side, the tip is blunted.
There is single / double / multi side vented needles.
 Importance of side-venting:
Solution is extruded through the sides of the needle not the tip; hence, it guarantees
washing of the walls + it prevents the solution from reaching the periapical area.

109
A.B.C = conventional needles.
D(single). E(double). F(multi) = endodontic irrigation needle
In manual passive irrigation = by your hand / passive means = no positive action from you,
you just irrigate without doing further activation to irrigant.
*Using conventional syringe + endodontic needle: 5 or 1 ml syringe “Luer lock design”
(prevent needle disengagement), single use.

during irrigation ‫ ألنو لو ديزاين بيتكبس ممكن يتفتح‬، ‫ ال بتلفو ما بتكبسو‬Luer lock design

-The needle should be flexible (Nickel-titanium or polymer) for curved canals, don’t use SS
(stainless steel) it may fracture.

-Needle penetration: at the end of apical prep.: 1-2 mm from WL

-Manual passive irrigation is not enough to reach canal complexities, or in severely curved
canals (even the smallest needle didn't reach 1-2 mm from wall).
What should I do? Use “Optimizing irrigant action” (activation of irrigant), (Agitation):
-Must be done in any irrigation protocol.
-Irrigant doesn’t reach the lateral canals unless you activate it. (manual passive technique
irrigates the main canal only).

Objectives of agitation: -
1.To circulate (refresh) and activate the irrigant.
2.To push into canals irregularities and complex anatomical area.
3.To break vapour lock concept (air entrap in apical 1/3).
In irrigate; the oxygen accumulates in the apical third >> locks the area and prevents the
irrigant from entering >> this is called “dead zone”

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 Agitation mechanisms: -

1/ Manual:
a) Syringe and needle:
Up and down movement.
The needle must be loose not close within the canal.
b) Gutta percha:
Large gutta percha (but not locked within the canal).
Measure minus 2mm from WL.
By tweezer move the gutta percha up and down.
Effective in curved canal.

2/ Machine – assisted:
a) Sonic device:
(< 20 KH)

b) Ultrasonic device:
(>20 KH)
Entering the tip >> vibration occur.

c) Pressure alteration:
-ve activation.
Tube connects to needle.
This tube pulls the irrigant (activation and pull the debris to avoid the blockade of the canal).
Called “endo bac”.
*Manual and (sonic + ultrasonic) >> called positive activation: you give an action (pressure).
While pressure alternation device >> negative pressure.

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 Irrigation solutions:

A/ antimicrobial irrigation solutions

B/ smear layer irrigants
A- Antimicrobial irrigants:

1. Sodium hypochlorite (NaOCl):

The most important irrigant and principle part in each protocol (gold stander) WHY??
1- It is the only used solution that can dissolve organic (vital, necrotic tissues, organic part of
smear layer and bacteria)
2-broad spectrum antiseptic and antibacterial (planktonic and biofilm) only irrigant has
action on biofilm.
3-low viscosity.
4-cheap.
5-safe when use with care
Its complications are disaster, can lead even to cavernous sinus thrombosis.
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Disadvantage of NaOCl: it can’t dissolve inorganic tissue (can’t completely remove smear
layer).

Photo for experiment: -

tweezer hold pulp tissue within a tube contain NaOCl (1%conc) it takes 30 mins to reach
complete dissolution.

So, if you use low conc you should elevate time, activation and temperature.

Conventional NaOCl conc is 5.25 %

NAOCL Mechanism of action: -

NaOCl+H2O<—>NaOH+HOCl<—>Na+OH+H+OCl-

(HOCL): hypochlorous (very active oxidizing agent)

1-Free radicals:
positively charged that binds to organic tissue"-ve charge" and causes apoptosis to the
organic tissue.

2-High PH -> bacteria can’t live in high PH (dissolution activity, degradation of cell protein +
inhibition of cell metabolism … cell death and dissolution).

Refreshment and temperature (increase effectiveness)

+if NaOCl with low conc, after dilution use it immediately (not after 24 from dilution) and
save it in opaque bottle because exposure to sun makes it inactive.

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NAOCL - Clinical consideration: -
- Concentration :(0.5-6%)
- If used in low conc; refreshment and temp. must be done.
- 1% antimicrobial activity as 5.25% if will refreshment and activated.
- 1% NAOCL at 95 c can dissolve human dental pulp = 5.25% solution at 20 c.
- (In our protocol we use 3% with activation)
- You should irrigate throughout the perp with rubber dam isolation (before and after
every file)/ 1-2 mins after cleaning >> then drying >> obturation.
* Not less than 30-60 minutes.
Activation:
- The root canal system and pulp chamber should be contentiously flooded and
replenished with fresh irrigant.
- Kept in motion.

Shelf life:
Degradation caused by light (store NAOCL in refrigerator and in a dark bottles).

jNAOCL - accidents:
•Damage to clothes.
•Damage to the eyes.
•Soft tissue damage (tongue, mucosa, your hand).
•Extrusion beyond the apex.
(So must measure it 1_2 ml from wl with stopper in needle to avoid the extrusion)

How to avoid?
- Plastic bib to protect clothes.
- Protective eye wear.
- Immediate washing and referral to ophthalmologist if warranted.
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 - Rubber dam isolation (if there is a missed wall you build up it to do gingival dam the
isolate by rubber dam).
- Use of side vented luer-lock needles.
- Irrigation needle a minimum of 2 mm if the working length.
- Avoidance of wedging the needles into the root canal.
That’s why the needle must be loose.
- Avoidance of excessive pressure (use index finger; thumb exerts high pressure).

Management:

1. Stop sodium hypochlorite irrigation and reassure pt as to likely event.

2. Irrigate canal with normal saline or sterile water.
3. Dress tooth with calcium hydroxide and place temporary double seal.
4. Administer long acting local anesthetic such as Bupivacaine.

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Why? To decrease the absorption of the irrigant into systemic circulation" cause
vasoconstriction"
5. Recommend analgesics NSAIDs if no allergy or asthma, and antibiotics if there is a
risk of infection.

6. Recommend extra-oral cold compress for swelling (consider urgent hospital referral
if airway compromised or swelling or pain not likely to be controlled by local
measures).

7. After 1 day recommend warm compress with frequent warm mouth rinses to
stimulate local circulation.

8. Daily recall to ensure recovery (consider oral maxillofacial referral if

ulceration/necrosis, evident of persistent neurological deficit occurs.
9. Calcium hydroxide will reduce the acidity.
10. Administration of long acting anesthesia to act as vasoconstrictor and to reduce
systemic effects.

Make TF and ice packs and prefer the pt stay in the clinic for 1 hour. Follow up after leave
and if happened any complications like swelling that affects the air way must referral to
hospital " write NaOCl injury after RCT"

2/ chlorohexidine digluceriate (CHX):

- Wide spectrum antimicrobial (specially against E. fecalis and C. albican associated with
retreatment).
- Permeate the cell wall and disturb the bacterial cytoplasm.

Studies: comparable to NaOCL against planktonic bacteria, but NaOCL superior against
biofilm.
retreatment ‫ خاصة يف حالة ال‬CHX ‫ كمادة أساسية وبعداك‬NaOCl ‫عشان كدا بستخدمو‬

- Inherent substantivity (ability to bind to tissue and exert long lasting action).
dentin‫بكون قاعد يف ال‬
‫ بكون‬intracanal medicament ‫ وكـ‬irrigant ‫ ممكن نستخدمه كـ‬CHX‫ حق ال‬application ‫ عشان كدا يف ال‬-
‫ ربي الجلسات‬canal‫قاعد جوا ال‬
- Low toxicity.
But have no tissue dissolving capability (only adjunctive final irrigant (not organic none
inorganic)).

‫ ؛ لكن يف حاالت‬intracanal medicament ‫ ممكن نستخدمه كـ‬،CHX‫ ما بحتاج لل‬primary ttt ‫يف ال‬
NaOCl ‫ بستخدمه مع‬retreatment ‫ال‬

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CHX clinical consideration:
Concentration: 0.1 to 2% liquid(irrigant) or gel (intracanal medication).

Application phase: as irrigant and intracanal medication especially in re ttt because of low
cytotoxicity and substantivity) but only adjunctive to NaOCL.

Shouldn’t be mixed with NaOCL (carcinogenic precipitate and obliterate dentinal tubules)
after NaOCL use an intermediate flush of saline or distilled water and dry the canal prior to
CHX.

3/ Iodine potassium iodide:

Wide spectrum antimicrobial properties (bacterial and yeasts).

Concentration: 2%

Penetrate cell membrane and destroy organelles.

Low toxicity

No tissue dissolving capability (only adjunctive as final irrigation).

Studies found to be effective in some failed cases (effective against E. faecalis) (used in re
ttt).

B/ irrigation solutions that used to remove the smear layer:

1.EDTA: Used as adjunctive irrigant.

EDTA- mechanism of action and properties:

EDTA: Ethylenediaminetetraacetic acid.

Chelator and dissolute only inorganic tissue.
React with the calcium ions of hydroxyapatite to form soluble chelates that can then be
rinsed out.
Very poor antibacterial action.
Doesn’t dissolve organic component.
EDTA- clinical consideration:

Concentration: 15-17% liquid.

Application phase: is used after NaOCL as final irrigant for smear layer removal. Just an
adjunctive irrigant to NaOCL (can’t be used as sole irrigant).
The contact time: for smear layer removal is 2 minutes, or more for thick layers.
*Precautions:
- EDTA greatly weakens the effect of NaOCL and should not be mixed or alternating
with it.

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 - Used only as final irrigation after NaOCL.
- When mixed with CHX, EDTA forms a white cloudy cytotoxic precipitate.
Note:
To complete removal of the smear layer (the organic part) and to penetrate opened dentinal
tubule 2 ml NaOCL should be used following EDTA.

EDTA:
- Not used in combination with NaCl, because it will affect the action of it, by reducing the
antibacterial and tissue dissolution of it.
- Before the final flowing of NaCl, all EDTA should wash out with normal saline.

 Other Irrigants:

1- Hydrogen peroxide:
History (cause tissue injury so not more used as an endo irrigant)
It produces oxygen free radicles, and spread to the periodontium.
2- MTAD
M: mixture
T: Tetracycline (or doxycycline), which have antibacterial action.
" tetra cause staining"
A: Acid (Citric acid): for removal of inorganic part of the smear layer.
D: Detergent: polysorbate
But the removal of organic part is not involved, so use of NaCl is highly important and we
can’t work without it even with the use of MTAD

3- Tetraclean:
The same structure of MTAD, with different in the type of the acid and detergent
(polypropylene glycol).

So, MTAD and Tetraclean are alternative to EDTA not to NaOCl.

But the advantage of them over EDTA, that the EDTA can't be used during instrumentation
with NaCl, just used at the end of the visit, but other irritant like the MTAD and Tetraclean,
they can be used alternatively during instrumentation in combination with NaCl without
altering its proteolytic or antimicrobial action.
4- QMix:
Mixture of EDTA, CHX & Detergent
Used for smear layer removal and as disinfectant.

COMBINED IRRIGATION PROTOCOL

 Chemical disinfectant is administered in a proper manner to fulfil irrigation goals

without compromising their action.

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  The protocol can be modified according to the condition (vital pulp, infected
necrotic pulp, periapical lesion, retreatment...).

Modifications:

- In vital pulp: no need for excessive antibacterial irrigant (just NaCl and EDETA).
- In (infected necrotic pulp, periapical lesion, retreatment): consider other
antibacterial solution like (CHX, Iodine K, Q mix).

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  Intracanal medicaments:
What is intracanal medicament?
A temporary antimicrobial agent that is placed inside the root canal system between
treatment appointments in an attempt to destroy remaining microorganisms and prevent
reinfection.
*Prevent reinfection: because the TF is not final restoration that can be source of
microleakage so antimicrobial agent prevent the reinfection.

Role:
Used to dress the canals in multi-visit approach to achieve the following roles:
1. To further enhance reduction of remaining intra canal micro-organisms following chemo-
mechanical preparation.
2. Prevent recolonization during the intermediate period prior to obturation.
3. Reducing inflammation of the periapical tissues.
*Sometimes not all the bacteria are removed in biomechanical prep like in periapical lesion -
chronic infections- necrotic pulp due to large number of bacteria so need intracanal
medicament.
*Recolonization: by bacteria from outside or remaining bacteria inside the canal.

Requirements:
1. The ability to eradicate all intra-canal bacteria.
Have wide spectrum role and bactericidal or bacteriostatic.
2. Long-lasting antibacterial affect.
Because it remains in canal for days between the visits.
3. Not inactivated in the presence of organic material.
If there is remaining of organic material like necrotic pulp tissue should be active.
4. Ability to degrade residual organic material (necrotic pulp tissue remnants and microbial
biofilm).
Not active only but should be degrade this material.
5. Well tolerated and no toxicity or irritation if extruded beyond the confines of the canal.
6. Ability to induce regeneration of the periapical tissues.
In cases where there is destruction in periapical tissue like in periapical inflammation.
7. No effect on the physical properties of the temporary access restoration or subsequent
root canal sealer.
Not interacting negatively with them.
8. Ease of placement and removal.
Certain consistency.
9. Radiopaque so easily discernible on radiographs.
10. Inability to stain and weaken the tooth.
11. Ability to suppress pain if present.

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Examples:
• Calcium hydroxide.
• Halogens (iodine solution).
• Corticosteroids.
• Antibiotics.
• Eugenol.
• Chlorhexidine/ a mixture of calcium hydroxide and chlorhexidine (Pure or mix).
• Bioactive glass.
•Phenolic and formaldehyde compounds (fixation-history-carcinogenic).
Fix the organic structure (used in past not nowadays.)

1) Calcium hydroxide:

• Pure calcium hydroxide paste is a strong base (high pH 12.5-12.8)

• Wide spectrum Anti-microbial action; how?
1. High alkalinity prevent bacterial growth.
2. Ionic dissociation into Ca2+ and OH-ions resulting in bacterial cell protein denaturation
and damage to DNA and cytoplasmic membranes.
• But Less effective against Enterococcus faecalis and Candida albicans; because those
microorganisms have certain proton pumps that lower the level of cytoplasmic pH so they
are not effective by high alkalinity.

Ca(OH)-advantages:
• Not expensive.
• Low solubility (allow release ions gradually and provide long duration action).
• Simple application and removal (paste format).
(Have paste and powder form "paste is easier in application and removal").
• Doesn't stain teeth.
(And not weakening the tooth structure).
• Can degrade remining organic tissue.
• Help in drying out of any exudate from the periapical tissues.

Ca(OH)-clinical considerations:
 Dry powder form (powder mixed with liquid such as water, saline, local anesthetic
before use).
 Suspension or paste form.

Indications:
 Routine intra-canal medicament especially in primary cases with necrotic pulp and
infection.
*In retreatment cases use combination between CaOH and other intracanal medicament
agent.
*Primary cases= no E.fecalis and candida albicans in large amounts.
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  One week application gives the most significant action.
 Applied as in thin slurry using spiral instrument.
*Thin slurry accelerates the ionization.
*Using spiral instruments like k file or the syringe found with the paste.

 The root canal should be filled homogeneously to the WL.

BUT Avoid extrusion into periapical tissue (pain, necrosis).
*If small extrusion no problem "reabsorption occurs".
If it is large it can cause pain or necrosis.

2) Chlorhexidine digluconate (CHX):

• Either CHX gel (2 %) or Mixture of CHX and calcium hydroxide.

• Wide range of antibacterial activity, antifungal activity (E. faecalis, candida species).
• Substantive properties.
Remain attached to the tissue.
• Ability to absorb onto dentine, preventing microbial colonization for some time beyond
the actual medication period.
•Retreatment of failed endodontic cases

Used pure or mix.

3) Halogens (iodine):
• Iodine potassium iodide (2 % iodine, potassium iodide 4 % and distilled water 94 % (2 % IPI
4 %)).
• Used in re-treatment cases for its effectiveness in killing E. faecalis and C. albicans.

Intracanal Medicaments Containing Antibiotics:

• Questionable role!!
Most of the antibiotics are bacteriostatic which subside the action if the bacteria to allow
the immune system to eradicate them but we haven't blood supply inside the canal so the
effect on immune not good.
• e.g. Ledermix paste: antibiotic-corticosteroid compound.
Tetracycline antibiotics, demeclocycline, HCL (3.2 %) and a corticosteroid triamcinolone
acetonide (1 %).
• Pain and inflammation control.
• Endodontic periodontal lesions before Ca(OH).
• Can be mixed with Ca(OH) (50:50).

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Corticosteroids:
• Provide pain relief and anti-inflammatory actions.
• Inhibit external root resorption.
Because the external is due osteoclast "inflammation" so if the inflammation is reduced the
external resorption reduced.
• No antibacterial effects.
• e.g. Ledermix (not used anymore, it causes staining).
Substituted by Odontopaste (zinc oxide-based + 5 % clindamycin hydrochloride and 1
% triamcinolone acetonide).

 Indication: to relief pain and inflammation:

- Symptomatic irreversible pulpitis.
No necrotic pulp no high amount of bacteria
- Symptomatic apical periodontitis.
Relief the pain and symptoms but need combination with calcium hydroxide due to bacteria
- Dental traumatology.

“IF YOUR DREAMS

DON’T SCARE YOU,
THEY ARE TOO SMALL”.

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