RATIONALE OF

ENDODONTIC
TREATMENT
CONTENTS
 INTRODUCTION
 The aim of the treatment is to remove all
infected hard or soft tissue and to restore the
tooth with a bacteria-tight restoration in order
to preserve the health of the residual pulp
tissue.
 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 to the tissue.
 Injurious agent may cause reversible or
irreversible changes to the tissues.
 Irreversible damage leads to tissue necrosis
whereas reversible damage leads to repair.
 Inflammatory process resolves when the repair
has been completed.
 Symptoms :
 Pain (due to action of cytotoxic agents released from
humoral, cellular and microbial elements 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
NEYTROPHILS
 Contain nucleus with 3 or more interconnected
lobules and cytoplasm containing lysosomal
and specific granules.

Functions :-
 Phagocytize bacteria

 Phagocytize and lyse fibrin, cellular debris.

 They are the first cells to migrate from vessels.
 The PMNs, along with the products of cellular
lysis and nuclear debris, are the principal
constituents of pus.
 MACROPHAGES
 These cells are derived from circulating monocytes.
 Immature monocytes in the extravascular areas,
such as inflammation, differentiate into
macrophages.
 They are mononucleated cells that, in periods of
great activity, fuse with other macrophages to
produce multinucleated giant cell.
FUNCTIONS:

 They are phagocytic cells that ingest cellular

debris, microorganisms and particulate matter.
 They enhance the immunologic reaction by
ingesting, processing and degrading antigen
before it is presented to the lymphocytes.
 There ability to remove debris from the area
facilitates repair.
 LYMPHOCYTES
 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 &
for immunosurveillance of the human organisms..
when T-cells are stimulated by an antigens , foreign
substances , they develop in to t lymphocytes ; they
have following manifestation……
1. Memory T-cells : which speeds the immunologic
reaction in subsequent encounters with the same
antigen.
2. Helper or suppressor T-cells : which
stimulate or supress the development of
effector t or b cells
3 . Effector T-cells : which may produce cell –
madiated immune reactions , such as delayed
hypersensitivity.
 Lymphokines : released by T lymphokines

- activate macrophages , PMNs , non

sensitised T-cells
 Interferon : inhibit viral replication
 B-cells
 Shorter life span than T-cells & lesser in no.
 When activated by an antigen , B-cells become
PLASMABLAST which devide to form
1.plasma cells 2. memory cells..
1. memory cells – speed the immunologic reactions in
subsequent encounters with the same antigens.
2. plasma cells - large , oval or round cells with
eccentric nuclei containing chromatin in cartwheel
form
- produce Ig..
 Ig - types
Ig M , Ig G , Ig A , Ig D , Ig E
includes various reaction includes…
1. Neutralisation of bacterial toxins by antitioxins

2. Coating of bacteria by antibodies , or

opsonisation , 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..
 Eosinophill
 Found during allergic & parasitic reactions..
 Involved in phagocytosis of antigen- antibody
complexes…, in detoxification of histamine…
Basophill & mast cells
 Found in hemopoitic system & tissue
 Contain granules
 Stimulated by tissue injury or antigen ;
degranulate & release chemical mediators such
as histamine , vasodilator , heparin….
 VASCULAR CHANGES
1. VASODILATION
2. INCREASED CAPILLARY
PERMEABILITY, FOLLOWING
INFLAMMATORY CHANGES
initially brief VASOCONSTRICTION followed by
VASODILATATION of arterioles & capillary
sphincter…..due to histamine released from mast
cells
 so ,increased blood flow through vessels & reduction
in vascular reactivity ; opening of dormant capillary
bed that increases the blood supply to the tissues…
 These changes increase intravascular pressure , blood
flow
 HISTAMINE : increase contracting the endothelial cells
& produce intracellular gap..
--- filtration of plasma & macromolecules from venules

--- plasma  less viscous & less protein

contain than blood plasma
 proteins like albumin ,
fibrinogen, Igs..
 chemical mediators & cells of
inflammation
 is called as inflammatory
exudate
  it dilutes bacterial toxins , so reduce potential
for tissue damage. , helps to form fibrin to contain the
inflammatory reaction…
 HEGMAN FACTOR ( factor xii ) :
-- released in infl.. Exudate
-- activate by collagen ; by damaged
basement membrane of blood vessels ; or
by Ag-Ab complexes
-- reacts with prekallikrein of plasma or tissus
to produce kinins ( vasodilator )
-- also activates the fibrinolytic & blood
coagulating system
 Also PLASMINOGEN in infl. Exudate
activated to plasmin..
-- activate complement system
-- digest fibrin (fibrinogen) & aid in removal
of blood clots
 Ig  actvate complement & produce
anaphylatoxin act on mast cells  release
histamine..
 Also some chemotactic factor  aid in
leucocytosis & lysis of bacteria…
 Inflammatory exudate  edema  increase
pressure on venules to collapse  reduce
venous drainage & blood flow..  stasis of
blood in venules ( due to increase viscosity of
blood)  leucocytic migration from center to
periphery  adhere to vessel wall called
pavementation of leucocytes  emigration of
leucocytes migration to site called
chemotaxis.
 first PMNs , followed by monocytes &
lymphocytes..
 Vascular responses continues with aggregation
of RBC in vessels.  increase resistance of
blood to flow decrease in O2 conc. ; increase
in CO2 conc. & iower the pH at infl. Site 
decrease removal of metabolites..
 The aforementioned changes may spread
inflammation to adjacent tissue ; this viscious
cycle of inflammation may lead to total
necrosis of pulp..
 At inflammatory sites ….
 PMNs
 Monocytes & lymphocytes
 Macrophages
 Plasmacells from b-cells
 Igs
 Lymphocyte mediators
Recovery of pulp
--- arteriovenous anastomoses & U-turn loops
open in pulpal vasculature to reduce the flow
the area of inflammation ; so decrease
vascular pressure..
--- increased tissue pressure plays a role in the
recovery of pulp by allowing return of
macromolecules & fuids to venules..  return
the vascular pressure & tissu pressure to
normal & stimulate the repair process..
 Periradicular manifestations
 Root canal pathway  noxious products of
tissue necrosis & antigenic agent 
periradicular area  inflammatory &
immunologic responses if more quantity 
bone resorption ( by OAF factor ) &
granulation tissue formatoin  abscss
formation
 Tissue changes following
inflammation
Either degenerative changes or proliferative changes
Degenrative changes :-
 Fibrous

 Resorptive

 Calcific

 Necrosis
 Suppuration
Reqiurements for suppuration :-
 Necrosis of tissue cells

 Sufficient number of ploymorphonuclear

leucocytes
 Digestion of dean 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 destrcution
whereas at the peiphery irritant may be mild
enough to stimulate proliferation.
 Endodontic implications:

Fish established experimental foci of infection

in the jaws of guinea pigs by drilling openings
in the bone and packing in wool fibers saturated
with broth culture of microorganisms.
4 well defined zones of reaction found 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 – laid down collagen fibers
- which act as - wall of defence around
zone of irritation
- as a scaffolding aroud
which new bone
formation occures.
 Osteoblast – laid down new bone which is in
irrregular fashion
 Root canal is site of infection through which
- micro organisms (in sufficient quantity)
- metabolic product of microorganisms
- toxic product of tissue necrosis…….
may be diffused to the periradicular tissue.
 They are destroyed by PMNs. But when
microorganisms are sufficiently virulant or in
enough quantity……. They overwhelm the
defensive mechanism
 And they causes periradicular lesions. (abscess)
 Thus toxins ( pus ) may diluted enough to act
as stimulant & form granuloma
fibroblast form fibrous tissue &
osteoblast delimit the area with wall of
sclerotic bone…
 If in addition, the epithelial rest of malasses
are stimulated , a cyst will form…
 When root canal has been treated , the
reservoir of bacteria or noxious products gets
eliminated ; when the root canal is cleaned
and obturated , the destroyed periapical
bone will undergo repair…