RATIONALE OF ENDODONTIC[1]

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RATIONALE OF ENDODONTIC TREATMENT by: vyomika jadav:

RATIONALE OF ENDODONTIC TREATMENT by: vyomika jadav

Slide 2:

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 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:

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.

Symptoms ::

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.

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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:

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.

MACROPHAGES:

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 cellular debris, microorganisms and particulate matter. They enhance the immunologic reaction by ingesting, processing and degrading antigen before it is presented to the lymphocytes.

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There ability to remove debris from the area facilitates repair.

LYMPHOCYTES:

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 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…… 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 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

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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 ..

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Ig - types Ig M , Ig G , Ig A , Ig D , Ig E includes various reaction includes… Neutralisation of bacterial toxins by antitioxins Coating of bacteria by antibodies , or opsonisation , to facilitate phagocytosis .. Lysis of bacteria by complement activation Agglutination of bacteria 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- 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:

VASCULAR CHANGES VASODILATION 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 the blood 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 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

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 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

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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  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..

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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..

Slide 31:

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 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:

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 :

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 proteolytic enzymes

Proliferative changes :-:

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: :

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:

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:

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:

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:

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

Slide 43:

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)

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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 bone will undergo repair…

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thanks a lot….