Endodontic treatment aims to remove infected pulp from the tooth canal and fill the space to prevent further infection. Inflammation is the body's response to injury or infection and involves vascular changes, immune cell infiltration, and tissue changes. The goal of inflammation is to destroy the irritant and repair the tissue. Successful endodontic treatment relies on controlling or resolving inflammation in the tooth and surrounding tissues.

1. RATIONALE OF ENDODONTIC TREATMENT
INTRODUCTION
INFLAMMATION
- Definition
- Causes
- Signs and Symptoms
- Cells of inflammation
- Inflammatory process
- Tissue change
- Periradicular manifestation
- Repair
ENDODONTIC IMPLICATION
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2. INTRODUCTION:
The term “Rationale” can be defined as the fundamental
reason or the rational basis for a procedure.
The rationale for endodontic therapy is based on the
belief that a natural tooth function more efficiently and
comfortably than a bridge, partial denture or an implant
tooth.
Endodontic therapy allows the removal of vital or
necrotic pulp from the canal system of an infected tooth and
replaced by an inert filling material. This is mainly done to
prevent extension of the disease from the pulp into the
periapical tissues.
INFLAMMATION:
Definition: Can be defined as a local physiologic response of
a living tissue to injury. The main objective of inflammation
is to destroy the irritant causing tissue changes and bring
back the tissue to a normal form and function.
Mediators of inflammation:
The agents that cause the changes in inflammation, the
alterations in the blood vessels, the escape of proteins and
cells into the tissues, and the change in the tissue – are
called the mediators of inflammation.
The initiated, transient vasoconstriction in due to the
direct stimulation of the blood vessels and the flare is
caused by an/ or on reflex.
“Nerves are not necessary for the inflammatory
process.” Inflammation develops normally in derivated
tissue, except that the flow is absent. Nerves may play some
part in modifying the severity of the vascular change, but in
most circumstances their effect is slight.
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3. Agents causing inflammation:
a. Physical agents: Heat, cold, mechanical trauma as in
sports injuries, bruxism, accidental exposure during
cavity preparation, rapid tooth movement during
orthodontic treatment.
b. Chemical agents: ZnPO4, Silicate, acid etching agents
etc.
c. Infection agents: Bacterial, Virus, Parasites.
d. Immunological agents: Cell mediated reaction antigen –
antibody, reaction.
Factors modifying the inflammatory respond
1) Host resistance
2) Intensity
3) Duration
4) Virulence of irritant / microorganism
(pathogenicity of stimulus).
Based on these premises we can generalize that mild or
moderate noxious stimuli to the pulp may produce sclerosis
of dentinal tubules, formation of reparative dentine, or
reversible inflammation.
Irreversible inflammatory changes caused by severe
injury can lead to necrosis of pulp and subsequent
pathologic changes in periradicular tissues.
The inflammatory process allows:
1. The arrival of phagocytic cells to digest bacteria or
cellular debris.
2. Antibodies to recognize attack and destroy foreign
material.
3. Edema or fluid to distribute and neutralize the irritant.
4. Fibrin formation to limit the spread of inflammation.
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4. Symptoms of inflammation:
According to Roman hunter Celcus in 1st
century A.D.
typical signs of inflammation can be witnessed.
1. Dolar (Pain): Caused by the action of cytotoxic agents
released from humoral, cellular and microbial elements of
the nerve endings.
2. Tumor (Swelling): Produced by infiltration of
macromoleculars and fluids into the affected tissues.
3. Rubor + Color (Redness + Heat): Produced by
vasodilatation of the vessels and the rushing of blood to
the affected tissues.
4. Loss of function: was later added by Verchow resulting of
from changes in the affected tissues.
As in any other inflamed organ of the body these
symptoms also occur in inflamed pulp but only pain and loss
of function can be clinically appreciated because of the
encasement of pulp with in dentin does not permit swelling.
But in case of inflammation including the periapical tissues
all the symptoms of inflammation may be clinically
recognized.
Cells of inflammation:
Glanulocytes Agranulocytes
- Neutrophils - Lymphocytes
- Eosinophils - monocytes
- Basophils
The main cells of acute inflammation are poly
morphonuclear neutrophil (PMN’s).
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5. Chronic inflammation: lymphocytes, plasma cells,
monocytes and macrophages.
Poly morphonuclear neutrophils (PMN’s) (Neutrophils
or Polymorphs).
1. Their cells constitute 40-75% of Leucocytes.
2. Seen in acute inflammation.
3. They contain
a. Nucleus having 2-4 lobes, which is connected.
b. Cytoplasm containing characteristic violet pink
granules.
These granules are said to contain enzymes
i. Lysosomes
ii. Alkaline phosphatase
iii. Collagenase
iv. Lactoferrin
1. These cells get attached to the area of inflammation by
chemotactic factors produced by bacteria or the
complement system.
2. They then allow the binding of opsonised bacteria onto
this surface.
3. In the binding sites the bacteria are encapsulated into
the neutrophils where lysosomal enzymes are released
that kill the bacteria.
4. These PMNs have a narrow range of life. They are
destroyed in the inflammatory site when the pH of the
tissues falls to 6.5.
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6. 5. This change in pH is brought about due to the release
and production of lactic acid by the neutrophil during
phagocytosis.
6. Destruction of the PMN’s also cause the release of 2
proteolytic enzymes.
a. Pepsin
b. Cathepsin
These enzymes result in tissue lysis.
1. The PMN’s with the products of cellular lysis and debris
are principal constituents of pairs.
Eosinophils:
1. They are fewer in number, constitute, 1-6% of leukocytes.
2. They consist of;
a. Nucleus usually has 2 lobes.
b. Cytoplasm made up of cause deep red staining
granules.
3. They are most predominant in allergic reactions and
parasitic infection.
4. During the immune response, they are involved in
phagocytosis of Ag-Ab complexes and in detoxicate on of
histamine.
Basophils:
1. These cells are least in number contain 1% of all
incubating leukocytes.
2. They resembles all other leukocytes but can be
distinguished by their coarse intensity basophilic
granules which usually fill the cytoplasm.
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7. 3. These granules contain Heparin, Histamine and Hydroxy
tryptamine and when these granules are stimulated by
tissue injury or antigen they degranulate and release
these substances, which can initiate an inflammatory or
a allergic response.
4. Basophils and masts cells are considered similar cells
except that Basophils are found in hemopoetic system
and mast cells in tissues. Functions of both these cells
are same.
Macrophages:
1. These cells are derived from circulating monocytes.
Immature monocytes in extravascular areas of
inflammation differentiate into macrophages.
a. Macrophages are phagocyte cells that ingest
- Cellular debris
- Microorganisms
- Particulate matter
b. They release mediation of inflammation such as
lysosomal enzymes, complement proteins and
prostaglandins.
c. They enhance the immunological reaction by ingesting
processing and degrading the antigen before presenting it
to the lymphocytes.
d. Then capacity to remove debris from area facilitates
repair.
e. Macrophages are mononucleated cells that, in periods of
great activity, may fuse into other macrophages to
produce a multinucleated giant cell.
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8. They release enzymes like
1. Acid hydrolases.
2. Neutral proteases, these enzymes result in digestion of
dead cells.
3. Collagenase.
4. Elastase.
Lymphocyte:
1. These cells appear in the chronic stage of inflammation.
They are intimately related to the immunological system
of the organism.
2. It is seen that immune system also fights infection along
with the inflammatory process.
3. If the normal inflammatory process fails to sum up with
the infection then the body mounts up a more massive
highly efficient response that is capable of memory as
well as specificity – viz., the immune system.
The immune system is comprised of two basic.
1) B cells
2) T cells
Both derived from the haemopoitic system. These cells
have a large spherical or slightly indented nucleus
surrounded by a thin band of cytoplasm containing small
granules.
The stem cells are carried by the blood to the thymus
where they differentiate as
T - Cells B - Cells
1. In thymus they become 1. Become immuno
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9. immuno comp. T cells. competent in bone manner
2. Most common cells of
lymphocytes
2. Lesser in number than T
cells.
3. Responsible for cell
mediated immunity +
immuno surveillance of the
human organisms
3. Responsible for humoral
immunity.
4. Circulate through the
lymphoid tissues and other
organs of body except
thymus.
4.
5. Found in para cortical
area of lymph nodes.
5. Found in cortical areas
of lymph nodes.
6. When stimulated by
foreign body they form
sensitized T. lymphocytes
6. When stimulated by
foreign body they become
large cells called plasma
blasts.
Plasma blasts divide into
c. Plasma cells
d. Memory B Cells
7. Types
a) Memory T-cells – Speed
up immunological reaction
when in contact with same
antigen.
b) Helper or suppressor
cells– which stimulate or
suppress the development
of effects T or B cells.
7. Types
a) Plasma cells – Large oral
round cells with chromatic
nucleus, which contains
chromatic network in
cartwheel form. These cells
produce immunologlobulin
or antibodies.
c) Effector T cells –
Produce cell mediated
immune reaction such as
delayed hypersensitivity
b) Memory B cells – speed
up the immunologic
reaction in subsequent
encounters with same
antigen.
8) Cells release chemical
mediations known as
lymphokines
8)
9) Lymphokines- may
activate
9) Immunoglobulin or
antibodies of which have
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10. a) Macrophages
b) PMNS
c) Non-sensitized T cells or
d) Produce interferron
which inhibits viral
replication
five classes IgM, IgG, IgA,
IqD & IgE.
Antibodies in humoral immunity
IgM: In the first antibody to be produced when host is
stimulated by an antigen. Plasma cells then produce IgG.
IgG + Igm: are the circulatory antibodies and one the most
important of the serum antibodies. IgG + IgM base the
capacity to bind to the antigen on specific receptor sites.
This process is termed as Opsonization and the antibodies
are called opsonins.
IgA: Is found in saliva, tears etc.
IgE: In conjunction with eosinophil serves a function of
protection against parasitic infection.
IgD: Function is not yet known but is considered to be a
surface on B-lymphocytes hence triggering antigen related
lymphocytes differentiation.
These antibodies combine with specific antigen to form
a complex that activates the compliment system. The
complement system then release chromatic factors that
attract phagocytic cells to the area that eugenol the antigen
and destroy it.
Inflammatory Process
Acute inflammation: This process can be studied as
a. Vascular changes
b. Escape of cells from blood vessels into tissues
c. Tissue changes
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11. Vascular Changes:
In any kind of injury 2 types of vascular changes can
be appreciated
a. Vasodilatation.
b. Increase in vascular permeability
Immediate response to injury results in transient vaso
constriction of blood vessels, which lasts for few seconds.
This is followed by vasodilatation of blood vessels that
persists for day to weeks that is as long as the inflammation
persists. This vasodilatation of arterioles is caused by the
relaxation of anterior and capillary sphincters. As a result of
vasodilatation there is increased rate of blood flow, which
also results in opening of dormant capillary beds that
increases the blood supply to the affected area.
This causes rise in intra vascular pressure leading to
redness and heat.
Simultaneously because of release of proteolytic
enzymes from injured cells, bacterial toxins and traumatic
mechanical forces, histamine is triggered off from the mast
cells. This histamine contracts the endothelial cells and
increases the intracellular gaps between them. These gaps
along with the intra vascular pressure results in some
plasma fluid to leave the vessels. This fluid is less in protein
and is termed as inflammatory transudate.
This transudate is soon over shadowed by the blood
plasma which contains rich plasma proteins such as
albumin, fibrinogen, immunoglobulin, which is called as
inflammatory exudates.
1. This blood plasma helps in bringing the chemical
mediation and cells of inflammation to start the
inflammatory reaction.
2. It also dilutes bacterial toxins.
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12. 3. It helps to form fibrin to contain the inflammatory
reaction. This exudate accumulates in the tissue
producing edema.
As the increased blood flow through the vessels fills up
the capillary beds, the volume of capillary bed increases so
there is slowing down of blood flow. This alteration in the
caliber of blood flow results in structural changes in the
micro vasculature i.e.,
1. The RBCs come in the center
2. Leukocytes move towards the vessel wall.
This process is called margination of leukocytes.
After margination the leukocytes adhere to the vessel
wall, which is termed as pavementation.
After the procedure the next step is Emigration of
Leukocytes.
At the site of inflammation these leukocytes are
attracted by
- Compliment system
- Prostaglandins
- Kallikrein
Which acts a chemotactic agent. This is called as
‘chemotoxis’ where the leukocytes migrate through the vessel
wall by amoeboid movements.
The PMN’s migrate 1st
followed by monocytes and
lymphocytes.
Simultaneously ‘Heggman factor’ or factor XII is also
released into the tissue in the inflammatory exudates.
This factor is activated by collagen; damaged blood
vessels; Ag-Ab complexes.
Reacts with PreKallikrien – Kinin.
Kinin produced 1) Helps in dilatation of blood vessels,
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13. 2) permeability of blood vessels.
The Heggman factor also activates the fibrinolytic and
blood co-aggulating systems.
Fibrinogen XII---- Fibrin ---– confines the inflammatory
reaction to a limited area.
Plasminogen XII----- plasmin
--- activates the complement system
- --- digests fibrin to remove blood clots.
- ---Activates kinin system.
This complement system in turn releases the
chemotactic factors, which aid in chemotoxis.
The vascular response continues with the aggregating
of RBC in the vessel causing resistance of blood flow.
This resistance along with the increase in blood
viscosity produced by the loss of plasma causes metabolic
changes such as
1. Decrease in oxygen concentration.
2. Increase in carbon dioxide.
3. Low pH.
Relating these changes to pulpal tissues as elsewhere
in the body are detrimental as they prevent the removal of
waste products. The spread of inflammation is faster in pulp
tissue as it is in a closed chamber, which may lead to total
necrosis of the pulp. Also the migration of monocytes and
lymphocytes at the inflammatory sites start a immunologic
reaction. The macrophages, plasma cells derived by B-
lymphocytes and lymphocytes mediators of the immune
response are also found at the site.
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14. Extra vascular immunoglobulins found are
predominantly IgG apart from IgE, IgA, IgM.
The recovery of pulp can be explained by some unique
vascular responses.
Anterior venous anastamoses and U turn loops open in
the pulpal vasculature to reduce the flow to the area of
inflammation there by decrease in the vascular pressure.
The increased tissue pressure plays an important role
in the recovery of pulp by allowing return of macromolecules
and fluids to the venules.
Therefore these 2 changes return the vascular pressure
and tissue pressure to normal and stimulate the repair.
Phagocytosis:
This is defined as process of engulfment of solid
particulate material by the cells. This is carried out by cells
called as Phagocytes mainly
1. PMN’s;
2. Circulating monocytes or Macrophages.
Phagocytosis takes place in 3 stages
1. Attachment stage: The serum at the injury site
contains naturally occurring opsonins. These opsonins get
coated on the microorganisms.
Main opsonins are:
1) IgG opsonin
2) C3B opsonin
2. Engulfment stage: The phagocyte gets attracted to this
opsonised microorganism and sends out cytoplasmic
pseudopods that envelop and encloses the organism
forming a vacuole. The plasma membrane enclosing the
phagocytic vacuole breaks. The lysosomes fuse to the
phagocytic vacuole to form a phagolysosome.
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15. 3. Degranulation stage: Degranulation takes place releasing
antibacterial substances, which kills the microorganisms.
The enzyme released help in digestion and liquefying of
the dead cells and damaged tissues.
Tissue changes following inflammation:
Can be either
1. Degenerative
2. Proliferative
1. Degenerative changes: Degenerative changes in the pulp
may be
i. Fibrous
ii. Resorptive
iii. Calcific
iv. Necrosis
v. Supportive
Suppuration occurs due to release of proteolytic
enzymes from the PMN resulting in liquifaction of dead
tissue resulting in to pus formation.
Accumulation of this pus forms an abscess.
Requirements for pus formation
a. Necrosis of tissue cells
b. Sufficient number of PMN’s and Leukocytes
c. Digestion of the dead material by protolytic enzymes.
2. Proliferative changes: These are produced by irritants
mild enough to act as a stimulatant. Within an area, a
substance may be both irritant and a stimulant.
For e.g. Ca(OH)2 in the center of inflammatory area may
act as an irritant strong enough the produce regeneration or
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16. distruction where as at the periphery it may be mild enough
to stimulate proliferation.
When a gap is present between tissue parts, repair is
made by granulation tissue.
Periradicular manifestations:
If the inflammatory response over whelms the pulp
there is partial or total necrosis of the pulp in the root
canal, this serves as a pathway to the periradicular area for
the noxious products of tissues necrosis and antigenic
agents.
The inflammatory and immunologic reaction continue in
the periradicular area as in pulp
In the periradicular area the noxious products cause.
Bone resorption and resorbed bone is replaced by
granulation tissue.
The affected tissue contains neutrophils, lymphocyte,
plasma cells, macrophages, mast cells along with
immunoglobulins IgG, IgA, IgM, IgE and complement.
Some recent reports indicate that some endodontic flare
-ups are mediated by IgE reactions and that have bone
resorption is mediated by lymphokine called ostoelastic
activating factor. These findings tells us the important role
that immunology plays in the physiology, and pathology of
the periradicular tissue.
Repair:
Repair is the return of tissue to normal structure and
function and it begins as the tissue becomes involved in the
inflammatory process.
Repair of the tissue depends on
1. Severity of injury
2. Host resistance
Reversible damage  Repair
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17. Irreversible damage  Necrosis
Stages of Repair:
1. After organization of the blood clot there is formation of
granulation tissue.
During this stage the endothelial loops become canalized
by the pressure of the blood allowing new channels for
circulation of blood.
Anastomasis of these loops occur forming a rich network
of small blood vessels.
2. In the soft tissues, development of scar tissue begins
fibroblasts grow along fibrin strands and help to form the
protein matrix by laying down collagen fibres. After this
both the fibroblast and the capillaries become fewer in
number and an avascular fibrous tissue i.e. scar tissue
is formed.
3. In bone the process is more complex as soft tissue, has
to get converted into hard matrix.
Bone is composed of protein matrix infiltrated by
calcium salts like calcium phosphate Ca(PO4)2 and calcium
carbonate Ca(CO3)3. This protein matrix is formed by
osteoblasts.
Surrounding the matrix is a fluid subsaturated with
calcium salts. The osteoblasts produce alkaline phosphatase
which help in forming Ca(PO4)2 which gets precipitated as
matrix.
There areas or islands in which the Ca(PO4)2 is
precipitated unite to form spongy trabecular.
Repair always proceeds from periphery towards the
center
Therefore to summarise. Granulation tissue-------
fibrous connective tissue ----- bone.
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18. Endodontic Implications:
Fish described the reaction of periradicular tissues to
noxious products of tissue necrosis, bacterial products, and
antigenic agents from the root canal and established an
experimental focci of injection, which he described as 4
zones.
Four zones of reaction are
1. Zone of infection
2. Zone of contamination
3. Zone of irritation
4. Zone of stimulation
Zone of infection:
1. Infection is present in the center of the lesion.
2. Micro-organisms are also present only in that area.
3. It contains pus fluid, which contains
i. Dead cells.
ii. Destructive components released from phagocyts.
iii. Intermediate and end products of protein
decomposition (Proteolysis).
4. Main cells are polymorphoneuclear leukocytes
5. Micro-organisms are attacked by these leukocytes.
6. The microorganisms not attacked by leukocytes are found
in the Haversian canals or in the fissures of bone matrix
made by bur.
Zone of contamination:
1. The principal difference cells are the round cells mainly
‘lymphocytes’.
2. Macrophages are less in number. These appear later
because they are less motile and survive longer than
neutrophils or lymphocytes.
3. Dilution of toxic elements takes place.
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19. 4. Fish observed cellular distortion around the central zone,
not from bacteria themselves but from toxins discharged
from the central zone.
5. Bone cells die and undergo Autolysis. Therefore the
lacunae appear empty as opposed to that of the central
zone.
Zone of irritation:
Toxicity diminishes as distance increases from central zone.
1. Principal cells
a. Macrophages.
b. Osteoclass.
2. Undifferentiated cells join to form osteoclast which resorb
the contaminated bone.
3. Phagocytosis takes place of collagen network by
macrophages and cells.
4. The activity of osteoclasts on bone open up gap in the
bone all around the center of lesion.
This space gets filled with leukocytes
Because in this;
-Healing starts to take place
-Repair.
5. Capillary proliferation.
6. Cells like plasma cells, lymphocytes, macrophages etc.,
starts developing more from undifferentiated cells.
Zone of stimulation:
Toxicity reduced to mild stimulatant
1) Cells
a. Fibroblasts
b. Osteoblasts
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20. This zone takes care of periphery i.e. peripheral
orientation takes place.
2) Collagen fibres are laid down by fibroblast which act as
a. Wall of difference around zone of irritation.
b. Scaffolding on which osteoblasts lays new bone.
New bone is irregular in pattern.
By this experiment fish concluded that root canal is a
seat of infection. The microorganisms from the root canal are
rarely motile. However they can multiply sufficiently enough
to grow out of the root canal or the metabolic products of
microorganisms or toxic products of tissue necrosis may
diffuse into the periradicular tissue.
As the microorganisms gain entry into the periradicular
area they are destroyed by the leukocytes.
If the number of microorganisms is less a stalemate
occurs. If it is more, chronic abcess occurs.
The toxic products of microorganisms and the necrotic
pulp in the root canal acts as irritants and destroy the
periradicular tissues along with proteolytic enzymes
resulting in pus formation.
At the periphery of the lesion there is stimulation of
fibroblasts to build the fibrous tissues and osteoblasts to
limit the area with a wall of sclerotic bone. This happens
because of dilution of toxic products, which acts as a
stimulant. If in addition the epithelial cell rests of mallesez
are stimulated a cyst develops. Once the root canal has been
treated and the reservoir of bacteria or noxious products has
been eliminated and the root canal thoroughly obturated the
destroyed periapical bone undergoes repair.
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21. REFERENCES:
 Grossman – Endodontic Practice.
 Robbins – Basic Pathology.
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