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RATIONALE OF ENDODONTIC
TREATMENT

Contents 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

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ANTIBODIES (SPECIFIC MEDIATORS OF IMMUNE REACTIONS)

ROLE OF IMMUNITY IN ENDODONTICS
ENDODONTIC
IMPLICATIONS
(PATHOGENESIS
PERIODONTITIS AS EXPLAINED BY FISH)
KRONFELDS MOUNTAIN PASS THEORY
RATIONALE OF ENDODONTIC THERAPY

OF

APICAL

INTRODUCTION
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

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Intensity , duration , pathogenicity of the stimulus and

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

Focal Infection

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THEORIES OF SPREAD
OF 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

Cont of theories

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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.

Cont of theories

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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.

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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CULPRIT OF
ENDODONTIC
PATHOLOGY

Microorganisms may gain entry into pulp through

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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

Entry into pulp cavity via mechanical or traumatic injury, through

gingival sulcus and via bloodstream

Anachoresis

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PORTALS FOR ENTRY

OF MICROORGANISMS

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.

Through defective restorations, faulty restoration with marginal

leakage can result in contamination of the pulp by bacteria.

Cont of portal of entry

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Fig. : Radiograph
showing poorly
obturated canals

Fig. : Deep carious lesion

resulting in pulp necrosis and
periapical lesion

INFLAMMATION

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Inflammation is defined as the local response of living mammalian

tissue to injury due to any agent.

Agents that cause inflammation

Physical

Chemical

organic and inorganic poisons

Infective

Cold, heat, echanical trauma or radiation

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

Cont of inflammation

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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

Cont of inflammation

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Inflammation is of Two Types

Acute inflammation

1.

dominated by PMNLs (Polymorphonuclear lymphocytes)

and few macrophages

Chronic inflammation

2.
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dominated by lymphocytes, macrophages and plasma

cells.

The balance between the host defense and microbial

factor determines the formation of lesion

TISSUE CHANGES FOLLOWING

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INFLAMMATION
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Degenerative changes

The pulp can be:

Fibrous,

.Continuous

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1.

Resorptive and Calcific

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

Cont of tissue changes

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2. Proliferative changes

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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.

INFLAMMATORY CELLS

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1.

Neutrophils

2.

Eosinophils

3.

Lymphocytes

4.

Osteoclasts

5.

Ephithelial
cells

Inflammatory Response to
Periapical Lesion

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Nonspecific Mediators of Periradicular Lesions

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can be classified into following types:

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 system
3. Extracellular matrix derived
mediators
Effector molecules

Antibodies (Specific Mediators of Immune Reactions)

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These are produced by plasma cells and are of two types

1.

Polyclonal antibodies

2.

are nonspecific like IgE mediated reactions which interact with

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

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.

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The response of periapical/host tissue is

controlled by:
Cells
Molecular

mediators (Nonspecific
mediators of inflammation), and

Antibodies

(Specific mediators of
inflammation)

Role of Immunity in Endodontics

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Immunity is of two types:

1.
2.

Innate immunity
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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ENDODONTIC IMPLICATIONS
(PATHOGENESIS
OF APICAL PERIODONTITIS AS
EXPLAINED BY
FISH described the reaction
FISH)of the periradicular

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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
Cyst

bone and then

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 canal
with the invaders entrenched behind high and
inaccessible
mountains, the foramina serving as mountain passes.
Zone B:
The exudative and granulomatous (proliferative)
tissue
of the granuloma represents a mobilized army defending
the
plains (periapex) from the invaders (bacteria). When a
few
invaders enter the plain through the mountain pass, they
are
destroyed by the defenders (leukocytes). A mass attack
of
invaders results in a major battle, analogous to acute
inflammation.

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Kronfelds Mountain
Pass Theory

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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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Zone C:

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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.