rationale of tics

8/2/2019 Rationale of tics

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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.

rationale of tics

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