ionale of Endodontic Treatme

Resource faculties:
Dr. Navin Agarwal
Dr. Mannu Vikram
Dr. Vimmi Singh Presented by:
Dr. Ashok Ayer Ashma ojha
Department of Conservative BDS 2011 (477)
Dentistry and Endodontics
Contents:
Inflammation
Objectives of inflammation
Symptoms
Types of inflammation
Inflammatory cells
Vascular changes
Periradicular manifestations
Endodontic implications
References
 Inflammation

Inflammation is the local physiologic

reaction
of the body to noxious stimuli or
irritants.

Any irritant, whether of traumatic,

chemical or
bacterial origin, produces a sequence
of basic
physiologic and morphologic reactions in
vascular,
lymphatic and connective tissues.
Objectives of
inflammation
Remove or destroy the irritant.

Repair the damage of the tissue.

 Injurious agent may cause reversible or
irreversible changes to the tissues.

Irreversible damage tissue necrosis

Reversible damage repair.

Inflammatory process resolves when the repair

has been completed.
 Symptoms:
Pain (due to action of cytotoxic agents released
on nerve endings).

Swelling (due to infiltration of macromolecules

and fluids into the affected tissues).

Redness

Heat (produced by vasodilatation of vessels and

rushing of blood to affected tissues.

Disturbance of function , resulting from

changes in affected tissues
Types of inflammation :

- Acute

- Chronic
Predominant cell in acute inflammation is
polymorphonuclear neutrophil.

Predominant cells in chronic inflammation are

lymphocytes, plasma cells, monocytes
and macrophages.
Polymorphonuclear neutrophils

Contain nucleus with 3 or more interconnected

lobules and cytoplasm containing lysosomal
and specific granules.

Functions :-
Phagocytize bacteria

Phagocytize and lyse fibrin, cellular debris.

Macrophag
es:
These cells are derived from circulating
monocytes.

Immature monocytes in the extravascular

areas, such as areas of inflammation,
differentiate into macrophages.
FUNCTIONS:
They are phagocytic cells that ingest cellular debris,
microorganisms and particulate matter.

They enhance the immunologic reaction by ingesting,

processing and degrading antigen.

In periods of great activity, may fuse with

other macrophage to produce multi-
nucleated giant cells.
 Lymphocy
tes:
Lymphocytes appear in chronic stage of
inflammatory reaction.

They have a large, spherical, or slightly indented

nucleus surrounded by a thin band of cytoplasm
containing small granules.

Two types of small lymphocytes: B-cells and T-

cells.
 T- cells
T-cells are responsible for cell mediated
immunity .
Different types are:

1. Memory T-cells : speeds the immunologic

reaction in subsequent encounters with the
same antigen.

2. Helper or suppressor T-cells : stimulate or

suppress the development of effector T or B cells

3. Effector T-cells : produce cell mediated

immune reactions such as delayed
hypersensitivity.
 Lymphokines : released by sensitized T
lymphocytes:
activate macrophages , PMNs, or
may produce
interferon.

Interferon : inhibit viral replication.

 B-

cells
Shorter life span & lesser in number than T-cells.

When activated by an antigen, B-cells become

PLASMABLAST which divide to form:
1.plasma cells
2. memory B cells.

1. Memory B cells speed the immunologic reactions

in subsequent encounters with the same antigen.

2. Plasma cells - large , oval or round cells with

eccentric nuclei containing chromatin in cartwheel
form ,
- produce Immunoglobulin
Ig - types :
Ig M , Ig G , Ig A , Ig D , Ig E

1. Neutralization of bacterial toxins.

2. Coating of bacteria by antibodies or

opsonization, to facilitate phagocytosis.

3. Lysis of bacteria by complement activation.

4. Agglutination of bacteria.

5. Combining of antibody with viruses to

prevent their entry into the cells.
 Eosinophils
Found during allergic & parasitic
reactions.

Basophill & Mast cells

- Stimulated by tissue injury or antigen.

- Degranulate & release chemical mediators such
as histamine,
vasodilator and heparin an anticoagulant that
can initiate inflammatory or allergic response.
 Vascular
changes :
Initially brief VASOCONSTRICTION
followed by
VASODILATATION of arterioles & capillary
due to
histamine released from mast cells.

Increased blood flow through vessels

that increases
the blood supply to the tissues.

Decrease in flow resistance.

These changes increase intravascular

 HAGEMAN FACTOR ( factor xii ) :

Released in inflammatory exudate.

Activated by collagen, damaged basement

membrane of blood vessels and Ag-Ab
complexes.

Reacts with prekallikrein of plasma to produce

kinin( dilates and increases permeability of vessel) .

Activates fibrinogen and produce fibrin which confines

inflammation to limited area.

Also PLASMINOGEN in inflammatory exudate is

activated to plasmin, activate complement system
digest fibrin & aid in removal of blood clots.
Periradicular
Manifestation
Root canal pathway noxious products
of tissue necrosis & antigenic agent
periradicular area inflammatory &
immunologic responses in periradicular
area if more quantity bone
resorption & granulation tissue
formation abscess formation.
 Tissue changes following
inflammation:
Either degenerative changes or
proliferative changes.

Degenerative changes :-

Fibrous
Resorptive
Calcific
Necrosis
Suppuration :

Reqiurements for suppuration :-

Necrosis of tissue cells.

Sufficient number of polymorphonuclear

leucocytes.

Digestion of dead material by proteolytic

enzymes.
 Proliferative
changes:

Produced by irritants mild enough to act as

stimulants.

In the center of inflammatory area, irritant

may be strong enough to produce
destruction whereas at the periphery irritant
may be mild enough to stimulate
proliferation.
 Endodontic implications:

4 well defined zones of reaction as found by Fish are :-

Zone of infection
Zone of contamination
Zone of irritation
Zone of stimulation
 Zone of Infection:
Characterized by polymorphonuclear leucocytes.

Infection present in the center of lesion and

microorganisms were found only in that area.
Zone of contamination:
Surrounding the zone of infection.
Characterized by round cell infiltration.
Cellular destruction observed in this zone.
Bone cells die due to toxins released from zone of infection.
Thus, lacunae appear empty.
Radigraphically seen as initial radiolucency around the
periapical region of infected tooth.
Prevalence of lymphocytes is seen.
Zone of Irritation:
Characterized by macrophages and osteoclasts.
Irritation due to dilution of toxins.
Distinguished by small, round cells, normal bone cells and
osteoclasts could just above survive.
Collagen framework digested by phagocytes, macrophages
while osteoclasts attack bone tissue.
Overall histologic picture is one of much activity preparatory to
repair.
Zone of Stimulation:
Characterized by fibroblasts and osteoblasts.
Fibroblast : collagen fibers are laid down, which act as:
- wall of defense around zone of irritation.
- as a scaffolding around which new bone
formation
occurs.
Osteoblast : new bone are laid down which is in
irregular fashion.
References:
Grossmans Endodontic practice.(12th edition)

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