This document discusses the rationale for endodontic therapy. It begins by explaining that endodontic pathology is mainly caused by injury to the tooth from physical, chemical, or bacterial factors. This injury can result in reversible or irreversible changes to the pulp and surrounding tissues depending on factors like the intensity and duration of the stimulus and the host's defense mechanisms. A series of inflammatory and immunological reactions then occur in the tissues to eliminate the irritant and repair any damage. However, some conditions exceed the body's repair ability and require endodontic treatment to aid tooth survival. The rationale for endodontic therapy is then described as complete debridement and disinfection of the root canal system followed by three-dimensional filling of the

1. Rationale of Endodontic
Treatment
5
 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
 Bibliography
Endodontic pathology is mainly caused by injury to the tooth
which can be physical, chemical or bacterial. Such injury can
results in reversible or irreversible changes in the pulp and
periradicular tissues. These resultant changes depend on the
intensity, duration, pathogenicity of the stimulus and the host
defense mechanism. The changes that occur are mediated by
a series of inflammatory and immunological reactions (in the
vascular, lymphatics and connective tissue). All these reactions
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.
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
About a century ago, 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.
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.
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.
CULPRIT OF ENDODONTIC PATHOLOGY
Many studies have shown that root canal infections are
multibacterial in nature. In 1965, Kakehashi found that when
dental pulps of conventional and germ free rats were exposed
to their own oral microbial flora, the conventional rats showed

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pulpal and periapical lesions whereas the germ free rats did
not show any development of lesion. So he described
importance of microorganisms for the development of pulpal
and periapical pathologies.
PORTALS FOR ENTRY OF MICROORGANISMS
(FIGS 5.1 AND 5.2)
Though microorganisms may gain entry into pulp through
several routes, most common route for entering of micro-
organisms to dental pulp is dental caries. They can also gain
entry into pulp cavity via mechanical or traumatic injury, through
gingival sulcus and via bloodstream.
Entry of Microorganisms into Pulp Through
Dental caries—Caries is the most common way of entry of
microorganisms into the dental pulp.
Through open dentinal tubules-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.
Anachoresis—Anachoresis refers to the attraction of blood
borne bacteria in the areas of inflammation. In other words,
anachoresis is a process by which 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.
INFLAMMATION
Inflammation is defined as the local response of living
mammalian tissue to injury due to any agent.
It is a body defense reaction in order to limit the spread
or eliminate it or to remove consequent necrosed cells and
tissues. Following agents cause inflammation:
a. Physical agents like cold, heat, mechanical trauma or
radiation.
b. Chemical agents like organic and inorganic poisons.
c. Infective agents like bacteria, viruses and their toxins.
d. Immunological agents like antigen-antibody cell mediated
reactions.
Therefore, we can say that 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.
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
Fig. 5.1: Radiograph showing poorly obturated canals
Fig. 5.2: Deep carious lesion resulting
in pulp necrosis and periapical lesion
Virchow later added the fifth sign function lasea, i.e. loss
of function.
Inflammation is of Two Types
• Acute inflammation dominated by PMNLs (Polymorpho-
nuclear lymphocytes) and few macrophages
• Chronic inflammation dominated by lymphocytes,
macrophages and plasma cells.
The balance between the host defense and microbial factor
determines the formation of lesion. In an infected canal, the
microbes are usually confined within the canal. As the blood
supply is compromised, the host defense mechanisms do not
totally eliminate the bacteria. These bacteria release certain
enzymes that stimulate the inflammatory process in the
periapical tissue.
TISSUE CHANGES FOLLOWING INFLAMMATION
As a result of inflammation, tissues exhibit two types of changes
viz degenerative changes and proliferative changes.
1. Degenerative changes in the pulp can be:
• Fibrous
• Resorptive
• Calcific.
Continuous degeneration of the tissue results in necrosis.
Suppuration is another form of degeneration which is due

3. TextbookofEndodontics
to injury to polymorphonuclear cells. This injury 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.
2. Proliferative changes (Fig. 5.3) are produced by irritants
which are mild enough to act as stimulants. These irritants
may act as both irritant and stimulant, such as calcium
hydroxide and its effect on adjacent tissues.
In the approximation of the inflamed area, 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
of proliferation or repair are the 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.
In an infected canal, the microbes are usually confined
within the canal. As the blood supply is compromised, the
host defense mechanisms do not totally eliminate the
bacteria. These bacteria release certain enzymes that
stimulate the inflammatory process in the periapical tissue.
INFLAMMATORY CELLS (FIG. 5.4)
1 . Neutrophils (PMNLs) (Fig. 5.5): Along with basophils
and eosinophils, polymorphonuclear neutrophils are called
granulocytes because of presence of granules in the
cytoplasm. Neutrophils are attracted to the site of injury
within 24 hours and phagocytose the bacteria and cellular
debris releasing lactic acid. Because of its low pH, this lactic
acid results in death of the PMNLs and release of proteolytic
enzymes (pepsin and cathepsin) prostaglandins and
leukotrienes. All these changes result in breaks down of
the tissue resulting in the formation of an abscess (dead
PMNLs + debris).
2. Eosinophils (Fig. 5.6): They have many functional and
structural similarities with neutrophils like their formation
in bone marrow, phagocytosis, presence of granules in the
cytoplasm, bactericidal and toxic action against many
parasites. However, granules of eosinophils lack lysozyme
and they are richer in myeloperoxidase than neutrophils.
Number of eosinophils increase in following conditions:
• Allergic conditions
• Skin diseases
• Parasitic infestations
Macrophages (Fig. 5.7): When the PMNLs fail to remove
the bacteria, the circulating monocytes reach the site of
60
Fig. 5.3: Inflammatory cells present at the healing site
Fig. 5.4: Inflammatory cells
Fig. 5.5: Neutrophil
inflammation and change into macrophages. These
macrophages are slow moving and remain at the site of
inflammation for a longer time (approximately 2 months). This
result in development of chronic inflammation.
Macrophages perform following functions:
• They help in phagocytosis and pinocytosis
• Perform immunological function
• Secrete lysosomal enzymes
• Secrete complement protein and prostaglandins

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Fig. 5.6: Eosinophil
Fig. 5.7: Macrophage
• Provide antigen to the immunocomplement cells
• They act as scavenger of dead cells, tissues and foreign
bodies
• They fuse with other macrophages to produce multi-
nucleated giant cells like osteoclasts, dentinoclasts and
foreign body giant cells.
3. Lymphocytes (Fig. 5.8): They are the most numerous
cells (20-45%) after neutrophils. There are two types of
lymphocytes seen in apical periodontitis:
a. T-lymphocytes
– T-helper cells (Th): They are present in the acute
phase of lesion expansion.
– T-suppressor cells (Ts): They predominate in later
stages preventing rapid expansion of the lesion.
b. B-lymphocytes – On getting signals from antigens and
T-helper cells, they transform into plasma cells and
secrete antibodies. Their number increases in following
conditions:
– hypersensitivity state
– prolonged infection with immunological response.
4. Osteoclasts: In the physiologic state, the preosteoclasts
remain dormant as monocytes in the periradicular bone.
Fig. 5.8: Lymphocyte
Fig. 5.9: Inflammatory response to periapical lesion
In case of apical periodontitis, they proliferate and fuse on
stimulation by cytokines and other mediators to form
osteoclasts. These osteoclasts are responsible for deminerali-
zation of the bone and enzymatic dissolution of organic
matrix at the osteoclast-bone interface. This results in bone
resorption.
5. Epithelial cells: Cytokines and other mediators stimulate
the dormant cell rests of malassez. These cells undergo
division and proliferation which results in inflammatory
hyperplasia.
INFLAMMATORY RESPONSE TO
PERIAPICAL LESION (FIG. 5.9)
Nonspecific Mediators of
Periradicular Lesions
Nonspecific mediators can be classified into following types:
1. Cell derived mediators:
– Neuropeptides
– Eicosanoids/arachidonic acid derivatives
– Cytokines
– Lysosomal enzymes

5. TextbookofEndodontics
Fig. 5.10: Cell derived mediators
– 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
Cell Derived Mediators (Fig. 5.10)
1 . Neuropeptides: These are generated following tissue injury
by the somatosensory and autonomic nerve fibers.
Neuropeptides include:
– Substance P (SP): Causes vasodilation, increased vascular
permeability and increased blood flow.
– Calcitonin-gene related peptide (CGRP): results in
vasodilation.
2. Eicosanoids: The injury to cells results in release membrane
phospholipid, arachidonic acid which is metabolized by
either cyclooxygenase pathway or lipoxygenase pathway to
form prostaglandins (PGs) or leukotrienes (LTs) respectively,
which are involved in inflammatory process.
a. Prostaglandins are of various types:
– PGE2,
– PGD2,
– PGF2a,
– PGI2
In cases of acute apical periodontitis and areas of bone
resorption, PGE2 and PGI2 are commonly observed.
Action of PGs can be inhibited by administration of
indomethacin which inhibits the enzyme cyclooxygenase
thus inhibiting formation of prostaglandins.
b. Leukotrienes: These are produced by activation of
lipoxygenase pathway of arachidonic acid metabolism.
Studies have shown the presence of LTB4, LTC4, LTD4
and LTE4 in periradicular lesions which cause different
effects on the tissues as shown in (Fig. 5.11).
3. Cytokines – These are low molecular weight polypeptides
secreted by activated structural and hematopoietic cells.
62 Different cytokines such as interleukins and tumor necrosis
Fig. 5.11: Leukotrienes
factor (TNF) cause development and perpetuation of
periradicular lesions.
They are of two types:
a. Proinflammatory cytokines – IL1 α and β,
(Interleukins) – IL6 α and β,
– IL8 α and β.
b. Chemotactic cytokines – TNFα (macrophage
derived)
(Tumor necrosis factor) – TNFβ (T-lymphocyte
derived)
– TNFγ.
a. Proinflammatory cytokines
IL1 – The local effects of IL1 are –
– Enhanced leukocyte adhesion to endothelial walls.
– Stimulate PMNLs and lymphocytes.
– Activates production of prostaglandins and proteolytic
enzymes.
– Enhances bone resorption.
– Inhibits bone formation.

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IL1 β is predominant in cases of periapical pathology.
IL6 – It is secreted by lymphoid and non-lymphoid cells
and causes inflammation under the influence of IL1, TNF
α and interferon γ (IFN). It is seen in periapical lesions.
IL8 – It is produced by macrophages and fibroblasts under
the influence of IL1 β and TNF α and is associated with
acute apical periodontitis.
b. Chemotactic cytokines
TNF – They are seen in chronic lesions associated with cytotoxic
and debilitating effect. TNF α is seen in chronic apical lesions
and root canal exudates.
1. Colony stimulating factor (CSF) – They are produced by
osteoblasts and regulate the proliferation of PMNLs and
preosteoclasts.
2. Growth factors (GF) – They are the proteins produced by
normal and neoplastic that regulate the growth and
differentiation of non- hematopoietic cells. They can
transform a normal cells to neoplastic cells and are known
as transforming growth factors (TGF).
They are of two types -
a. TGF α (produced by malignant cells) – not seen in
periapical lesions.
b. TGF β (produced by normal cells and platelets).
They counter the adverse effects of inflammatory host
response by:
– Activating macrophages.
– Proliferation of fibroblasts.
– Synthesis of connective tissue fibers and matrices.
Lysosomal Enzymes
Lysosomal enzymes such as alkaline phosphatase, lysozyme,
peroxidases, collagenase cause increase in vascular permeability,
leukocytic chemotaxis, bradykinin formation and activation of
complement system.
Platelet Activating Factor
It is released from IgE—sensitized basophils or mast cells. Its
action include increase in vascular permeability, chemotaxis,
adhesion of leukocytes to endothelium and broncho-
constriction.
Vasoactive Amines
Vasoactive amines such as histamine, serotonin are present in
mast cells, basophils and platelets. Their release cause increase
in tissue permeability, vasodilation used vascular permeability
(Fig. 5.9).
Prostaglandins
These are produced by activation of cyclooxygenase pathway
of arachidonic acid metabolism. Studies have shown high levels
of PGE2 in periradicular lesions. Torbinejad et al found that
periradicular bone resorption can be inhibited by administration
of indomethacin, an antagonist of PGs. This indicates that
prostaglandins are also involved in the pathogenesis of
periradicular lesions.
Plasma Derived Mediators (Fig. 5.12)
1. The fibrinolytic system: The fibrinolytic system is activated
by Hageman factor which causes activation of plasminogen.
This results in release of fibrinopeptides and fibrin
degradation products which cause increase in vascular
permeability and leukocytic chemotaxis.
2. The complement system: Trauma to periapex can result
in activation of kinin system which in turn activates
complement system. Several studies have shown elevated
levels of kinins and C3 complement component in
periradicular lesions. Products released from activated
complement system cause swelling, pain and tissue
destruction.
3. The kinin system: These are produced by proteolytic
cleavage of kininogen. Release of kinins cause smooth
muscle contraction, vasodilation and increase in vascular
permeability (Fig. 5.13).
Effector Molecules
The inflammatory process causes not only the destruction of
the cells but also the extracellular matrix in the periapical
pathosis. The extracellular matrix is degraded by enzymatic
effector molecules by various pathways like
• Osteoclast regulated pathway,
• Phagocyte regulated pathway,
• Plasminogen regulated pathway and
Fig. 5.12: Plasma derived mediators
Fig. 5.13: Kinin system

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• Metalloenzyme regulated pathway (Matrix Metallo Proteases-
MMPs)
The collagen (proteins) based matrices are degraded by
MMPs.
ANTIBODIES (SPECIFIC MEDIATORS
OF IMMUNE REACTIONS)
These are produced by plasma cells and are of two types:
• Polyclonal antibodies – 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.
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
The immune system of human being is a complex system
consisting of cells, tissues, organs as well as molecular mediators
that act together to maintain the health and well-being of the
individual. The cells and microbial irritants interact with each
other via a number of molecular mediators and cell surface
receptors to result in various defense reactions.
Immunity is of two types:
• Innate immunity
• Acquired/adaptive immunity
Innate immunity: It consists of cells and molecular elements
which act as barriers to prevent dissemination of bacteria and
bacterial products into the underlying connective tissue. The
innate immunity is responsible for the initial nonspecific
reactions.
Cells providing innate immunity are neutrophils, monocytes,
eosinophils, basophils, NK cells, dendritic cells, and odonto-
blasts.
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
Histopathology of Periapical Tissue
Response to Various Irritants
Root canal of teeth contains numerous irritants because of some
pathologic changes in pulp. Penetration of these irritants from
infected root canals into periapical area can lead to formation
and perpetuation of periradicular lesions. In contrast to pulp,
periradicular tissue have unlimited source of undifferentiated
cells which can participate in inflammation and repair in
inflammation and repair. Also these tissues have rich collateral
blood supply and lymph drainage.
Depending upon severity of irritation, duration and host,
response to periradicular pathosis may range from slight
inflammation to extensive tissue destruction. Reactions involved
are highly complex and are usually mediated by nonspecific and
specific mediators of inflammation.
ENDODONTIC IMPLICATIONS (PATHOGENESIS
OF APICAL PERIODONTITIS AS EXPLAINED BY
FISH) (FIG. 5.14)
FISH described the reaction of the periradicular tissues to
bacterial products, noxious products of tissue necrosis, and
antigenic agents from the root canal. He established an
experimental foci of infection in the guinea pigs by drilling
openings in the jaw bone and packing it with wool fibers
saturated with a broth culture of microorganisms. FISH in 1939
theorised 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.
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)
immunoglobulins. Fig. 5.14: FISH zones

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RationaleofEndodonticTreatment
c. Zone of irritation (Histiocytes and osteoclasts)
d. Zone of stimulation (Fibroblasts, capillary buds and
Osteoblasts).
Zone of Infection
In FISH study, 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
Around the central zone, FISH observed the area of cellular
destruction. This zone was not invaded by bacteria, but the
destruction was from toxins discharged from the micro-
organisms in the central zone. This zone is characterized by
round cell infiltration, osteocyte necrosis and empty lacunae.
Lymphocytes were prevalent everywhere.
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.
So the knowledge gained in FISH study can be applied for
better understanding of reaction of periradicular tissues to a
nonvital tooth.
The root canal is the main source of infection. The
microorganisms present in root canal are rarely motile. Though
they do not move from the root canal to the periapical tissues;
but they can proliferate sufficiently to grow out of the root
canal. 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 pus. This results in development of
chronic abscess.
At the periphery of the destroyed area of osseous tissue,
toxic bacterial products get diluted sufficiently to act as stimulant.
This results in formation of a granuloma.
After this fibroblasts come in the play and build fibrous
tissue and osteoblasts restrict the area by formation of sclerotic
bone. Along with these if epithelial rests of Malassez are also
stimulated, it results in formation of a cyst.
KRONFELD’S MOUNTAIN
PASS THEORY (FIG. 5.15)
Kronfeld explained that the granuloma does not provide a
favorable environment for the survival of the bacteria. He
employed the FISH concept so as to explain the tissue reaction
in and around the granulomatous area.
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 inflam-
mation.
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.
Fig. 5.15: Kronfeld’s mountain pass theory

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RATIONALE OF ENDODONTIC THERAPY
The rationale of root canal treatment 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.
Endodontic therapy includes:
• Non-surgical endodontic treatment
• Surgical endodontic treatment
Non-surgical endodontic treatment includes three phases:
• Access preparation: The rationale for this is to create a
straight line path for the canal orifice and the apex.
• Shaping and cleaning: The rationale for this is the complete
elimination of vital or necrotic pulp tissue, microorganisms
and their byproducts.
• Obturation: Main objective of obturation is to have a three
dimensional well fitted root canal with fluid tight seal so
as to prevent percolation and microleakage of periapical
exudate into the root canal space and also to prevent
infection by completely obliterating the apical foramen and
other portals of communication.
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.
QUESTION
Q. What is rationale of endodontics? Explain in detail
about fish zones.
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