1.
RATIONALE OFENDODONTIC
TREATMENT
1
Dr.Basavan Gowda
Reader
Dept.Conservative&Dentistry
Navodaya Dental College
Raichur

2.
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
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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3.
THEORIES 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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4.
Cont 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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5.
Cont 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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6.
CULPRIT 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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7.
PORTALS FOR ENTRY
OF
MICROORGANISMS
 Microorganisms may gain entry into pulp through
o 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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8.
Cont of portal of entry 9
Fig. : Radiograph
showing poorly
obturated canals
Fig. : Deep carious lesion
resulting in pulp necrosis and
periapical lesion

9.
INFLAMMATIO
N
 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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10.
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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11.
Cont of inflammation
Inflammation is of Two Types
1. Acute inflammation
o dominated by PMNLs (Polymorphonuclear lymphocytes)
and few macrophages
2. Chronic inflammation
o 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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12.
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 polymorphonuclearcells.
 It causes release of proteolytic enzymes with resulting liquefaction ofdead
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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13.
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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14.
INFLAMMATORY
CELLS
1. Neutrophils
2. Eosinophils
3. Lymphocytes
4. Osteoclasts
5. Ephithelial
cells
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15.
Inflammatory Response to
Periapical Lesion
1. Cell derived mediators:
– Neuropeptides
– Eicosanoids/arachidonic
acid derivatives
– Cytokines
– Lysosomal enzymes
– Platelet activating factor
– Vasoactive amines
– Prostaglandins
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2. Plasma derived mediators
– The fibrinolytic system
– The complement system
– The kinin system
3.Extracellular matrix derived
mediators
– Effector molecules
Nonspecific Mediators of Periradicular
Lesions
can be classified into following types:

16.
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
Antibodies (Specific Mediators of 17

17.
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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18.
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 nonspecificreactions.
 Cells providing innate immunity are neutrophils, monocytes, eosinophils,
basophils, NK cells, dendritic cells, and odontoblasts.
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19.
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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20.
ENDODONTIC IMPLICATIONS
(PATHOGENESIS OF APICAL
PERIODONTITIS AS EXPLAINED BY FISH)
 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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21.
 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).
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Fig: FISH
zones

22.
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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23.
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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24.
 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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25.
Kronfeld’s
Mountain Pass
Theory
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 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.

26.
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
impervious
healing of
the three-dimensional fluid
obturation will result in complete
periapical area
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27.
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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28.
Endodontic therapy includes:
 Non-surgical endodontic treatment
 Surgical endodontic treatment
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29.
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.
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