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RATIONALE OF ENDODONTIC TREATMENT

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2Contents of these presentation

INTRODUCTION

THEORIES OF SPREAD OF INFECTION

CULPRIT OF ENDODONTIC PATHOLOGY

PORTALS FOR ENTRY OF MICROORGANISMS

INFLAMMATION

TISSUE CHANGES FOLLOWING INFLAMMATION

INFLAMMATORY CELLS

INFLAMMATORY RESPONSE TO PERIAPICAL LESION

ANTIBODIES (SPECIFIC MEDIATORS OF IMMUNE REACTIONS)

ROLE OF IMMUNITY IN ENDODONTICS

ENDODONTIC IMPLICATIONS (PATHOGENESIS OF APICAL PERIODONTITIS AS EXPLAINED BY FISH)

KRONFELD’S MOUNTAIN PASS THEORY

RATIONALE OF ENDODONTIC THERAPY

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3INTRODUCTION

Endodontic pathology is caused by Physical , chemical or bacterial injury

These injury results in reversible or irreversible changes in the pulp & periradicular tissues. Changes depends on the

o Intensity , duration , pathogenicity of the stimulus and

o host defense mechanism

Changes mediated by a series of inflammatory & immunological reactions

All these reaction take place to eliminate the irritant and repair any damage

However, certain conditions are beyond the reparative ability of the body and need to be treated endodontically to aid the survival of tooth

Rationale of endodontic therapy is complete debridement of root canal system followed by three-dimensional obturation

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4THEORIES OF SPREAD OF INFECTION Focal Infection

Definition: It is localized or general infection caused by the dissemination of microorganisms or toxic products from a focus of infection.

Focus of Infection

Definition: This refers to a circumscribed area of tissue, which is infected with exogenous pathogenic microorganisms and is usually located near a mucous or cutaneous surface.

Theory Related to Focal Infection William Hunter first suggested that oral microorganisms and

their products involved in number of systemic diseases, are not always of infectious origin.

In year 1940, Reimann and Havens criticized the theory of focal infection with their recent findings

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5Cont of theories

Mechanism of Focal Infection

There are generally two most accepted mechanisms considered responsible for initiation of focal infection:

1. Metastasis of microorganisms from infected focus by either hematogenous or lymphogenous spread.

2. Carrying of toxins or toxic byproducts through bloodstream and lymphatic channel to site where they may initiate a hypersensitive reaction in tissues.

For example: In scarlet fever, erythrogenic toxin liberated by infected streptococci is responsible for cutaneous features of this disease.

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6Cont of theories

Oral Foci of Infection

Possible sources of infection in oral cavity which later on may set up distant metastases are:

1. Infected periapical lesions such as:

i. Periapical granuloma

ii. Periapical abscess

iii. Periapical cyst

2. Teeth with infected root canals.

3. Periodontal diseases with special reference to tooth extraction.

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7CULPRIT OF ENDODONTIC PATHOLOGY

Root canal infections are multibacterial in nature.

In 1965, Kakehashi describe the Importance of microorganisms for the development of pulpal and periapical pathologies

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8PORTALS FOR ENTRY OF MICROORGANISMS

Microorganisms may gain entry into pulp througho Most common route for entering of microorganisms to dental pulp

is dental caries Microorganisms can pass into the dentinal tubules and subsequently

to the pulp resulting in its necrosis

Through the periodontal ligament or the gingival sulcus, microorganisms can enter into the pulp via accessory and lateral canals which connect pulp and the periodontium

o Entry into pulp cavity via mechanical or traumatic injury, through gingival sulcus and via bloodstream

o Anachoresis Anachoresis refers to the attraction of blood borne bacteria in the

areas of inflammation

Microorganisms are transported in the blood to an area of inflammation where they establish an infection.

o Through defective restorations, faulty restoration with marginal leakage can result in contamination of the pulp by bacteria.

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9Cont of portal of entry

Fig. : Radiograph showing poorly obturated canals

Fig. : Deep carious lesion resulting in pulp necrosis and periapical lesion

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INFLAMMATION

Inflammation is defined as the local response of living mammalian tissue to injury due to any agent.

Agents that cause inflammation Physical

Cold, heat, echanical trauma or radiation

Chemical

• organic and inorganic poisons

Infective

• bacteria, viruses and their toxins

Immunological

• antigen-antibody cell mediated reactions

inflammation is distinct from infection. Inflammation is the protective response by the body,

while infection is invasion into the body by harmful microbes and their resultant ill effects by toxins

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Cont of inflammation

Signs of Inflammation

The roman writer celsus in 1st century AD gave four cardinal signs of inflammation:

1. Rubor i.e. redness

2. Tumor i.e. swelling

3. Color i.e. heat

4. Dolor i.e. pain

Virchow later added the fifth sign of inflammation function lasea,

i.e. loss of function

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Cont of inflammation

Inflammation is of Two Types

1. Acute inflammation o dominated by PMNLs (Polymorphonuclear lymphocytes)

and few macrophages

2. Chronic inflammationo dominated by lymphocytes, macrophages and plasma

cells.

The balance between the host defense and microbial factor determines the formation of lesion

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TISSUE CHANGES FOLLOWING INFLAMMATION

1. Degenerative changes

The pulp can be:

Fibrous, Resorptive and Calcific

Continuous degeneration of the tissue results in necrosis.

Suppuration

is another form of degeneration which is due to injury to polymorphonuclear cells.

It causes release of proteolytic enzymes with resulting liquefaction of dead tissues thus leading to formation of pus or suppuration.

Three requisites which are necessary for suppuration

Tissue necrosis

Polymorphonuclear leukocytes

Digestion of the necrotic material by proteolytic enzymes released by injured polymorphonuclear cells

Clinical significance: An abscess can result even in absence of microorganisms because of chemical or physical irritation. It results in formation of sterile abscess

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Cont of tissue changes

2. Proliferative changes The irritant may be strong enough to produce

degeneration or destruction, whereas at the periphery, the irritant may be mild enough to stimulate proliferation.

The principal cells are Fibroblasts, which lay down cellular fibrous tissues.

In some cases collagen fibers may be substituted by a dense acellular tissue.

In either case it results in formation of fibrous tissue.

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INFLAMMATORY CELLS

1. Neutrophils

2. Eosinophils

3. Lymphocytes

4. Osteoclasts

5. Ephithelial cells

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Inflammatory Response to Periapical Lesion

1. Cell derived mediators:

– Neuropeptides

– Eicosanoids/arachidonic acid derivatives

– Cytokines

– Lysosomal enzymes

– Platelet activating factor

– Vasoactive amines

– Prostaglandins

2. Plasma derived mediators – The fibrinolytic system – The complement system – The kinin system3. Extracellular matrix derived mediators – Effector molecules

Nonspecific Mediators of Periradicular Lesions

can be classified into following types:

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Antibodies (Specific Mediators of Immune Reactions)

These are produced by plasma cells and are of two types

1. Polyclonal antibodies are nonspecific like IgE mediated reactions which interact with

antigen resulting in release of certain chemical mediators like histamine or serotonin

2. Monoclonal antibodies like IgG and IgM, interact with the bacteria and its by-

products to form antigen-antibody complexes that bind to the platelets resulting in release vasoactive amines thus increasing the vascular permeability and chemotaxis of PMNs.

The monoclonal antibodies exhibit antimicrobial effect.

In acute abscess, the complex enters the systemic circulation. The concentration of these complexes return to normal levels after endodontic treatment.

In chronic lesions, the Ag-Ab complexes are confined within the lesion and do not enter into the systemic circulation

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Cont.…

The response of periapical/host tissue is controlled by:

Cells

Molecular mediators (Nonspecific mediators of inflammation), and

Antibodies (Specific mediators of inflammation)

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Role of Immunity in Endodontics

Immunity is of two types:

1. Innate immunity

2. Acquired/adaptive immunity

1. Innate immunity It is responsible for the initial nonspecific reactions.

Cells providing innate immunity are neutrophils, monocytes, eosinophils, basophils, NK cells, dendritic cells, and odontoblasts.

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2. Acquired/Adaptive immunity

It involves release of specific receptor molecules by lymphocytes which recognize and bind to foreign antigens.

Adaptive immunity is provided by: T-Lymphocytes that release T-cell antigen receptors

B-Lymphocytes that release B-cell antigen receptors or immunoglobulins.

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21ENDODONTIC IMPLICATIONS

(PATHOGENESISOF APICAL PERIODONTITIS AS

EXPLAINED BYFISH) FISH described the reaction of the periradicular tissues to bacterial

products, noxious products of tissue necrosis, and antigenic agents from the root canal

FISH in 1939 theorized that the zones of infection are not an infection by themselves but the reaction of the body to infection.

Thus he concluded that the removal of this nidus of infection will result in resolution of infection.

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Four well defined zones of reaction were found during the experiment

a. Zone of infection or necrosis (PMNLs)

b. Zone of contamination (Round cell infiltrate – lymphocytes)

c. Zone of irritation (Histiocytes and osteoclasts)

d. Zone of stimulation (Fibroblasts, capillary buds and Osteoblasts).

Fig: FISH zones

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Zone of Infection

Infection was confined to the center of the lesion.

This zone is characterized by polymorphonuclear leukocytes and microorganisms along with the necrotic cells and detructive components released from phagocytes.

Zone of Contamination

Area of cellular destruction.

This zone was not invaded by bacteria, but the destruction was from toxins discharged from the microorganisms in the central zone.

This zone is characterized by round cell infiltration, osteocyte necrosis and empty lacunae.

Lymphocytes were prevalent everywhere.

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Zone of Irritation

FISH observed evidence of irritation further away from the central lesion as the toxins became more diluted.

This is characterized by macrophages, histocytes and osteoclasts.

The degradation of collagen framework by phagocytic cells and macrophages was observed while osteoclasts attack the bone tissue.

The histologic picture is much like preparatory to repair.

Zone of Stimulation

FISH noted that, at the periphery, the toxin was mild enough to act as stimulant.

This zone is characterized by fibroblasts and osteoblasts.

In response to this stimulatory irritant, fibroblasts result in secretion of collagen fibers, which acted both as wall of defense around the zone of irritation and as a scaffolding on which the osteoblasts synthesize new bone.

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The knowledge gained in FISH study can be applied for better understanding of reaction of periradicular tissues to a nonvital tooth.

The metabolic byproducts of these microorganisms or the toxic products of tissue necrosis may also get diffused to the periradicular tissues.

As the microorganisms enter in the periradicular area, they are destroyed by the polymorphonuclear leukocytes.

But if microorganisms are highly virulent, they overpower the defensive mechanism and result in development of periradicular lesion.

The toxic byproducts of the microorganisms and the necrotic pulp in the root canal are irritating and destructive to the periradicular tissues. These irritants along with proteolytic enzymes (released by the dead polymorphonuclear leukocytes) result in the formation of

chronic abscess

Granuloma

Sclerotic bone and then

Cyst

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Kronfeld’s Mountain Pass Theory Kronfeld explained that the granuloma does not

provide a favorable environment for the survival of the bacteria

Zone A: He compared the bacteria in the infected root canalwith the invaders entrenched behind high and inaccessible“mountains”, the foramina serving as mountain passes.

Zone B: The exudative and granulomatous (proliferative) tissueof the granuloma represents a mobilized army defending theplains (periapex) from the invaders (bacteria). When a fewinvaders enter the plain through the mountain pass, they aredestroyed by the defenders (leukocytes). A mass attack ofinvaders results in a major battle, analogous to acute inflammation.

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Zone C:

Only complete elimination of the invaders from their mountainous entrenchment will eliminate the need for a defense forces in the “plains”. Once this is accomplished, the defending army of leukocytes withdraws, the local destruction created by the battle is repaired (granulation tissue) and the environment returns to its normal pattern

This explains the rationale for the non-surgical endodontic treatment for teeth with periapical infection. The complete elimination of pathogenic irritants from the canal followed by the three-dimensional fluid impervious obturation will result in complete healing of periapical area

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Rationale of Endodontic Therapy The rationale of RCT relies on the fact that the nonvital

pulp, being avascular, has no defense mechanisms

The damaged tissue within the root canal undergoes autolysis and the resulting breakdown products will diffuse into the surrounding tissues and cause periapical irritation associated with the portals of exit even in the absence of bacterial contamination.

It is essential therefore, that endodontic therapy must seal the root canal system three-dimensionally so as to prevent tissue fluids from percolating in the root canal and toxic byproducts from both necrotic tissue and microorganisms regressing into the periradicular tissues.

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Endodontic therapy includes:

Non-surgical endodontic treatment

Surgical endodontic treatment

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Non-surgical endodontic treatment includes three phase

1. Access preparation

2. Shaping and cleaning

3. Obturation

Surgical Endodontic Treatment

The rationale of surgical endodontics is to remove the diseased tissue present in the canal and around the apex, and retrofil the root canal space with biologically inert material so as to achieve a fluid tight seal.