Lect.6- 4th Stage
Endodontic
Dr. Ameer H. AL-Ameedee
The dental pulp is a unique tissue, dental pulp is enclosed in a rigid mineralized structure, low compliant system, no
collateral circulation. Understanding pulp and perapical disease (pathogens) will help in the diagnosis and prescription of the
appropriate treatment for both pulpal and periapical diseases. Apical periodontitis is a sequel to endodontic infection and
manifests itself as the host defense response to microbial challenge emanating from the root canal system.
The lesions most commonly found at the apices of non-vital teeth are the periapical granuloma and radicular cyst. The
treatment and prognosis may differ according to the lesion present. Many studies to determine the diagnostic features and
incidence of these lesions have failed to reach a consensus view, to decide treatment option of periapical lesion, whether surgery
or not, necessitate precise diagnosis of the lesion as being granuloma, true cyst, or pocket cyst within granuloma mass.
The aim of non-surgical root canal therapy is the elimination of infection from the root canal and the prevention of reinfection by root filling.
Etiology of pulpal diseases can be broadly classified into three groups:
1. Bacterial:
a. caries;
b. microleakage around a restoration;
c. periodontal pocket and abscess;
d. anachoresis.
2. Physical:
a. Mechanical:
1. trauma:
e. acute trauma like fracture or avulsion of tooth;
f. iatrogenic dental procedures:
1. pathologic wear like attrition, abrasion, etc.;
2. barodontalgia due to barometric changes.
b. Thermal:
g. heat generated by cutting procedures;
h. heat from restorative procedures;
i. heat generated from electrosurgical procedures;
j. frictional heat from polishing restorations.
3. Chemical:
k. acids from erosion;
l. use of chemicals like monomers, liners, bases, phosphoric acid, or use of cavity desiccants like alcohol.
Pathophysiology of periapical lesion:
inflammatory lesions of dental origin which are the most common of all other periapical lesions, are differentiated by
certain terminologies as “periapical lesions of endodontic origin” or “pulpoperiapical” lesions to indicate that the cause is
infected or necrotic pulp.
Inflammation of periapical membrane around the apex of the tooth is usually due to spread of infection following death
of the pulp. In most cases inflammation remains localized to the periapical region.
Local (periapical) periodontitis must be distinguished from chronic (marginal) periodontitis, in which infection and
destruction of the supporting tissues spread from chronic infection of the gingival margins, and the pulp is vital. Bone destruction
around apex of tooth, mostly secondary to pulp exposure due to caries or trauma.
If the source of the irritants is removed, either by extraction of the tooth or by means of a root canal filling, the abscess
cavity will drain itself and be replaced by granulation tissue, which then will form new bone. A “granuloma” is, literally, a mass
made up of granulation tissue. The periapical granuloma by far represents the most common type of pathologic radiolucencies.
Basically the periapical granuloma is the result of a successful attempt by the periapical tissues to neutralize and confine the
irritating toxic products that are escaping from the root canal.
Classically, more inflammation is seen in the center of the lesion, where the apex of the tooth is usually located, because
at this point the irritating substances from the pulp canal are most concentrated. At the periphery of the lesion, fibrosis (healing)
may already have begun, since the irritants are diluted and neutralized some distance from the apex.
radiographic examination the lesion is a well-circumscribed radiolucency somewhat rounded and surrounding the apex
of the tooth. A periapical granuloma cannot be differentiated from a radicular cyst by radiographic appearance alone , each
one of them may have large, well defined radiolucency with radiopaque (sclerotic) border.
Radiographs are an important part of root canal treatment, especially for the detection, treatment and follow up of
periapical bone lesions. However, routine radiographic procedures do not demonstrate reliably the presence of every lesion and
they do not show the real size of a lesion and its spatial relationship with anatomical structures. Clinical examination and
radiographs alone cannot differentiate between cystic and non-cystic lesions .
Caries: Polybacterial Infection are Gram +ve organisms dominate and change in mix from facultative to obligate
anaerobes as depth of invasion increases, the Gram -ve anaerobes less frequent.
Pulpal reaction to microbial irritation:
1.
2.
3.
4.
5.
Carious enamel and dentin contain numerous bacteria.
Bacteria penetrate in deeper layers of carious dentin.
Pulp is affected before actual invasion of bacteria via their toxic byproducts.
Byproducts cause local chronic cell infiltration.
When actual pulp exposure occurs, pulp tissue gets locally infiltrated by PMNs ( Polymorphonuclear leukocytes, or
granulocyte) to form an area of liquefaction necrosis at the site of exposure.
6. Eventually necrosis spreads all across the pulp and periapical tissue resulting in severe inflammatory lesion.
Degree and nature of inflammatory response caused by microbial irritants depends upon:
1.
2.
3.
4.
5.
6.
Host resistance.
Virulence of microorganism.
Duration of the agent.
Lymph drainage.
Amount of circulation in the affected area.
Opportunity of release of inflammatory fluids.
Pulpal Response to Enamel Caries:
1- Pulp is affected once integrity of its protective chamber is breached, the enamel is permeable.
2-Multirooted teeth could have different pulpal conditions in each root.
3- Pulp is affected once integrity of its protective chamber is breached.
4-Nerve fibers of the pulp are relatively resistant to necrosis. The C fibers are able to function when hypoxic, and the nerves
can be sensitized.
Histopathology: Poor correlation between histopathological condition with clinical signs and symptoms and Variation in
human response/threshold to pain, the variation in pathogens and their virulence.
Vascular System:
1-Pulp has limited ability to withstand increase in pressure because of low compliant system and normal pulp does not
function at 100% capacity.
2- Numerous A-V shunts may open up in inflammation to reduce intrapulpal pressure.
3- Excess interstitial fluid from area of inflammation will be absorbed into the circulation and lymphatic system in
the unaffected areas of the pulp.
Many studies have shown that increase of pressure in one area does not affect the other areas of pulp. Therefore 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 injured
area. Net absorption of fluid into capillaries in adjacent uninflamed area results in increased lymphatic drainage thus keeping
the pulpal volume almost constant.
Limited increase in pressure within affected pulpal area is explained by the following mechanism:
a. Increased pressure in inflamed area favors net absorption of interstitial fluids from adjacent capillaries in
uninflamed tissues.
b. Increased interstitial tissue pressure lowers the transcapillary hydrostatic tissue pressure difference, thus
opposes further filtration.
c. Increased interstitial fluid pressure increases lymphatic drainage.
d. Break in endothelium of pulpal capillaries facilitates exchange mechanism.
Infectious sequelae of pulpitis include apical periodontitis , periapical abscess and osteomyelitis of the jaw. Spread from
maxillary teeth may cause purulent sinusitis, meningitis, brain abscess, orbital cellulitis, and cavernous sinus thrombosis.
Spread from mandibular teeth may cause angina, parapharyngeal abscess, mediastinitis, pericarditis and empyema.
Pulpitis classification (E. M. Gofung, 1928)
1. Acute pulpitis:
a) Partial.
b) General.
c) Purulent.
2. Chronic pulpitis:
a) Fibrous (simple).
b) Hypertrophic.
c) Gangrenous.
American Association of Endodontists Classification
1.
2.
3.
4.
5.
6.
7.
Normal pulp
Reversible pulpitis
Symptomatic irreversible pulpitis
Asymptomatic irreversible pulpitis
Pulp necrosis
Previously treated
Previously initiated therapy
Grossman’s Clinical Classification
1. Pulpitis: inflammatory disease of dental pulp.
a. Reversible papulosis:
1. Symptomatic (Acute).
2. Asymptomatic (Chronic).
b. Irreversible pulpitis:
3. Acute
b. Abnormally responsive to cold.
c. Abnormally responsive to heat.
1. Chronic
d. Asymptomatic with pulp exposure.
e. Hyperplastic pulpitis.
f. Internal resorption.
2. Pulp degeneration:
a. Calcific (Radiographic diagnosis).
b. Other ( Histopathological diagnosis).
3. Pulp necrosis:
a. Coagulation necrosis.
b. Lique faction necrosis.
Ingle’s Classification
1. Inflammatory changes:
a. Hyperreactive pulpalgia.
a. Hypersensitivity.
b. Hyperemia.
b. Acute pulpalgia.
c. Incipient.
d. Moderate.
e. Advanced.
c. Chronic pulpalgia.
d. Hyperplastic pulpitis.
e. Pulp necrosis.
2. Retrogressive changes:
a. Atrophic papulosis.
b. Calcific papulosis.
Baume’s Classification (Based on clinical symptoms):
1– Asymptomatic, vital pulp which has been injured or involved by deep caries for which pulp capping may be done.
2– Pulp with history of pain which is amenable to pharmacotherapy.
3– Pulp indicated for extirpation and immediate root filling.
4– Necrosed pulp involving infection of radicular dentin accessible to antiseptic root canal therapy.
Seltzer and Bender’s Classification (Based on clinical tests and histological diagnosis):
1. Treatable without pulp extirpation and endodontic treatment:
3. Intact uninflamed pulp.
4. Transition stage.
5. Atrophic pulp.
6. Acute pulpitis.
7. Chronic partial pulpitis without necrosis.
2. Untreatable without pulp extirpation and endodontic treatment:
8. Chronic partial pulpitis without necrosis.
9. Chronic total pulpitis.
10. Total pulp necrosis.
Apical Periodontitis:
Apical periodontitis (AP) is an inflammation and destruction of periradicular tissues. It occurs as a sequence of various
insults to the dental pulp, including infection, physical and iatrogenic trauma, following endodontic treatment, the damaging
effects of root canal filling materials. In response, the host mounts an array of defenses, consisting of several classes of cells,
intercellular messengers, antibodies and effector molecules. The microbial factors and host defense forces encounter, clash
with, and destroy much of the periapical tissue, resulting in a formation of various kinds of AP lesions, which most commonly
take the form of reactive granulomas and cysts, with the concomitant resorption of bone surrounding the roots of affected
teeth.
Bacteria has no dentine tubules to provide a “safe haven” when they go beyond the apex, and inflammatory response
at the apex is effective, and Bacteria seldom encountered.
Abscess
Granuloma
Cyst
Chronic Hyperplastic Pulpitis: (Pulp polyp), Exuberant proliferation of chronically inflamed pulp, and open carious lesions in
children/young adults usually first permanent molars.