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RATIONALE OF ENDODONTIC
TREATMENT
by: vyomika jadav
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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.
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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.
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Objectives of inflammation
Remove or destroy the irritant
Repair the damage to the tissue.
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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.
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Symptoms :
Pain (due to action of cytotoxic agents released fromhumoral, cellular and microbial elements on nerveendings).
Swelling (due to infiltration of macromolecules and
fluids into the affected tissues). Redness
Heat (produced by vasodilatation of vessels and rushingof blood to affected tissues.
Disturbance of function, resulting from changes inaffected tissues.
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Types of inflammation :
Acute
Chronic Predominant cell in acute inflammation is
polymorphonuclear neutrophil.
Predominant cells in chronic inflammation arelymphocytes, plasma cells, monocytes and
macrophages.
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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.
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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.
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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.
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FUNCTIONS:
They are phagocytic cells that ingest cellulardebris, microorganisms and particulate matter.
They enhance the immunologic reaction by
ingesting, processing and degrading antigenbefore it is presented to the lymphocytes.
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There ability to remove debris from the area
facilitates repair.
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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.
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T-cells
T-cells are responsible for cell mediatedimmunity & 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.
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2. Helper or suppressor T-cells : which stimulate
or supress the development of effector t or b
cells3 . 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
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B-cells
Shorter life span than T-cells & lesser in no.
When activated by an antigen , B-cellsbecome PLASMABLAST which devide to form
1.plasma cells 2. memory cells..
1. memory cells
speed the immunologicreactions in subsequent encounters with the
same antigens.
2. plasma cells - large , oval or round cells witheccentric nuclei containing chromatin in
cartwheel form
- produce Ig..
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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..
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eosinophill
Found during allergic & parasitic reactions..
Involved in phagocytosis of antigen- antibodycomplexes, 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.
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VASCULAR CHANGES
1. VASODILATION
2. INCREASED CAPILLARY
PERMEABILITY, FOLLOWING
INFLAMMATORY CHANGES
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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 theblood supply to the tissues
These changes increase intravascular pressure ,
blood flow
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HISTAMINE : increase contracting the
endothelial cells & produce intracellular gap..
--- filtration of plasma & macromolecules fromvenules
--- plasma less viscous & less protein
contain than blood plasma
proteins like albumin ,
fibrinogen, Igs..
chemical mediators & cells of
inflammation
is called as inflammatory
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it dilutes bacterial toxins , so reduce potentialfor 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
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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
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Inflammatory exudate edema increase
pressure on venules to collapse
reducevenous 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
leucocytesmigration to site called chemotaxis.
first PMNs , followed by monocytes &lymphocytes..
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Vascular responses continues with aggregation of
RBC in vessels. increase resistance of bloodto flowdecrease 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 necrosisof pulp..
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At inflammatory sites .
PMNs
Monocytes & lymphocytes Macrophages
Plasmacells from b-cells
Igs Lymphocyte mediators
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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 therecovery of pulp by allowing return of
macromolecules & fuids to venules.. return the
vascular pressure & tissu pressure to normal &stimulate the repair process..
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Periradicular manifestations
Root canal pathway noxious products of
tissue necrosis & antigenic agent
periradicular area inflammatory &
immunologic responsesif more quantitybone resorption ( by OAF factor ) & granulation
tissue formatoin abscss formation
Tissue changes following
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Tissue changes following
inflammation
Either degenerative changes or proliferative
changes
Degenrative changes :-
Fibrous
Resorptive
Calcific
Necrosis
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Suppuration
Reqiurements for suppuration :-
Necrosis of tissue cells Sufficient number of ploymorphonuclear
leucocytes
Digestion of dean material by proteolyticenzymes
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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.
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Endodontic implications:
Fish established experimental foci of infection inthe jaws of guinea pigs by drilling openings inthe 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
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Zone of Infection
Characterized by polymorphonuclear leucocytes.
Infection present in the center of lesion and
microorganisms were found only in that area.
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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 radiolucencyaround the periapical region of infected tooth.
Prevalence of lymphocytes is seen.
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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.
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Zone of Stimulation
Characterized by fibroblasts and osteoblasts.
Fibroblastlaid down collagen fibers
- which act as - wall of defence aroundzone of irritation
- as a scaffolding aroud
which new boneformation occures.
Osteoblastlaid down new bone which is in
irrregular fashion
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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 mechanismAnd they causes periradicular lesions. (abscess)
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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
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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 bonewill undergo repair
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thanks a lot.