The document discusses the rationale and process of endodontic treatment. The aim is to remove infected tissue and restore the tooth with a bacteria-tight restoration to preserve pulp health. Inflammation is the body's response to irritants, involving vascular changes, increased permeability and blood flow, and recruitment of immune cells like neutrophils, macrophages and lymphocytes to remove irritants and repair tissue damage. The inflammatory response must be resolved for healing to occur. Endodontic treatment aims to reduce inflammation and allow for pulp recovery and resolution of periradicular manifestations.

1. RATIONALE OF ENDODONTICRATIONALE OF ENDODONTIC
TREATMENTTREATMENT

2.  The aim of the treatment is to remove allThe aim of the treatment is to remove all
infected hard or soft tissue and to restore theinfected hard or soft tissue and to restore the
tooth with a bacteria-tight restoration in order totooth with a bacteria-tight restoration in order to
preserve the health of the residual pulp tissue.preserve the health of the residual pulp tissue.

3. INFLAMMATIONINFLAMMATION
 Inflammation is the local physiologic reaction ofInflammation is the local physiologic reaction of
the body to noxious stimuli or irritants.the body to noxious stimuli or irritants.
 Any irritant, whether of traumatic, chemical orAny irritant, whether of traumatic, chemical or
bacterial origin, produces a sequence of basicbacterial origin, produces a sequence of basic
physiologic and morphologic reactions inphysiologic and morphologic reactions in
vascular, lymphatic and connective tissues.vascular, lymphatic and connective tissues.

4. Objectives of inflammationObjectives of inflammation
 Remove or destroy the irritantRemove or destroy the irritant
 Repair the damage to the tissue.Repair the damage to the tissue.

6.  Injurious agent may cause reversible orInjurious agent may cause reversible or
irreversible changes to the tissues.irreversible changes to the tissues.
 Irreversible damage leads to tissue necrosisIrreversible damage leads to tissue necrosis
whereas reversible damage leads to repair.whereas reversible damage leads to repair.
 Inflammatory process resolves when the repairInflammatory process resolves when the repair
has been completed.has been completed.

7. Symptoms :Symptoms :
 Pain (due to action of cytotoxic agents released fromPain (due to action of cytotoxic agents released from
humoral, cellular and microbial elements on nervehumoral, cellular and microbial elements on nerve
endings).endings).
 Swelling (due to infiltration of macromolecules andSwelling (due to infiltration of macromolecules and
fluids into the affected tissues).fluids into the affected tissues).
 RednessRedness
 Heat (produced by vasodilatation of vessels and rushingHeat (produced by vasodilatation of vessels and rushing
of blood to affected tissues.of blood to affected tissues.
 Disturbance of function, resulting from changes inDisturbance of function, resulting from changes in
affected tissues.affected tissues.

8.  Types of inflammation :Types of inflammation :
 AcuteAcute
 ChronicChronic
 Predominant cell in acute inflammation isPredominant cell in acute inflammation is
polymorphonuclear neutrophil.polymorphonuclear neutrophil.
 Predominant cells in chronic inflammation arePredominant cells in chronic inflammation are
lymphocytes, plasma cells, monocytes andlymphocytes, plasma cells, monocytes and
macrophages.macrophages.

9. Polymorphonuclear neutrophilsPolymorphonuclear neutrophils
 Contain nucleus with 3 or more interconnectedContain nucleus with 3 or more interconnected
lobules and cytoplasm containing lysosomal andlobules and cytoplasm containing lysosomal and
specific granules.specific granules.
Functions :-Functions :-
 Phagocytize bacteriaPhagocytize bacteria
 Phagocytize and lyse fibrin, cellular debris.Phagocytize and lyse fibrin, cellular debris.

10.  They are the first cells to migrate from vessels.They are the first cells to migrate from vessels.
 The PMNs, along with the products of cellularThe PMNs, along with the products of cellular
lysis and nuclear debris, are the principallysis and nuclear debris, are the principal
constituents of pus.constituents of pus.

12. MACROPHAGESMACROPHAGES
 These cells are derived from circulatingThese cells are derived from circulating
monocytes.monocytes.
 Immature monocytes in the extravascular areas,Immature monocytes in the extravascular areas,
such as inflammation, differentiate intosuch as inflammation, differentiate into
macrophages.macrophages.
 They are mononucleated cells that, in periods ofThey are mononucleated cells that, in periods of
great activity, fuse with other macrophages togreat activity, fuse with other macrophages to
produce multinucleated giant cell.produce multinucleated giant cell.

14. FUNCTIONS:FUNCTIONS:
 They are phagocytic cells that ingest cellularThey are phagocytic cells that ingest cellular
debris, microorganisms and particulate matter.debris, microorganisms and particulate matter.
 They enhance the immunologic reaction byThey enhance the immunologic reaction by
ingesting, processing and degrading antigeningesting, processing and degrading antigen
before it is presented to the lymphocytes.before it is presented to the lymphocytes.

15.  There ability to remove debris from the areaThere ability to remove debris from the area
facilitates repair.facilitates repair.

16. LYMPHOCYTESLYMPHOCYTES
 Lymphocytes appear in chronic stage ofLymphocytes appear in chronic stage of
inflammatory reaction.inflammatory reaction.
 They have a large, spherical, or slightly indentedThey have a large, spherical, or slightly indented
nucleus surrounded by a thin band of cytoplasmnucleus surrounded by a thin band of cytoplasm
containing small granules.containing small granules.
 Two types of small lymphocytes: B-cells and T-Two types of small lymphocytes: B-cells and T-
cells.cells.

18. T-cellsT-cells
 T-cells are responsible for cell mediatedT-cells are responsible for cell mediated
immunity & for immunosurveillance of theimmunity & for immunosurveillance of the
human organisms..human organisms..
when T-cells are stimulated by an antigens ,when T-cells are stimulated by an antigens ,
foreign substances , they develop in to tforeign substances , they develop in to t
lymphocytes ; they have followinglymphocytes ; they have following
manifestation……manifestation……
1.1. Memory T-cells : which speeds theMemory T-cells : which speeds the
immunologic reaction in subsequentimmunologic reaction in subsequent
encounters with the same antigen.encounters with the same antigen.

19. 2. Helper or suppressor T-cells : which stimulate2. Helper or suppressor T-cells : which stimulate
or supress the development of effector t or bor supress the development of effector t or b
cellscells
3 . Effector T-cells : which may produce cell –3 . Effector T-cells : which may produce cell –
madiated immune reactions , such as delayedmadiated immune reactions , such as delayed
hypersensitivity.hypersensitivity.
 Lymphokines : released by T lymphokinesLymphokines : released by T lymphokines
- activate macrophages , PMNs , non- activate macrophages , PMNs , non
sensitised T-cellssensitised T-cells
 Interferon : inhibit viral replicationInterferon : inhibit viral replication

20. B-cellsB-cells
 Shorter life span than T-cells & lesser in no.Shorter life span than T-cells & lesser in no.
 When activated by an antigen , B-cellsWhen activated by an antigen , B-cells
becomebecome PLASMABLASTPLASMABLAST which devide to formwhich devide to form
1.plasma cells 2. memory cells..1.plasma cells 2. memory cells..
1. memory cells –1. memory cells – speed the immunologicspeed the immunologic
reactions in subsequent encounters with thereactions in subsequent encounters with the
same antigens.same antigens.
2. plasma cells -2. plasma cells - large , oval or round cells withlarge , oval or round cells with
eccentric nuclei containing chromatin ineccentric nuclei containing chromatin in
cartwheel formcartwheel form
- produce Ig..- produce Ig..

21.  Ig - typesIg - types
Ig M , Ig G , Ig A , Ig D , Ig EIg M , Ig G , Ig A , Ig D , Ig E
includes various reaction includes…includes various reaction includes…
1.1. Neutralisation of bacterial toxins by antitioxinsNeutralisation of bacterial toxins by antitioxins
2.2. Coating of bacteria by antibodies , orCoating of bacteria by antibodies , or
opsonisation , to facilitate phagocytosis..opsonisation , to facilitate phagocytosis..
3.3. Lysis of bacteria by complement activationLysis of bacteria by complement activation
4.4. Agglutination of bacteriaAgglutination of bacteria
5.5. Combining of antibody with viruses to preventCombining of antibody with viruses to prevent
their entry into the cells..their entry into the cells..

22. eosinophilleosinophill
 Found during allergic & parasitic reactions..Found during allergic & parasitic reactions..
 Involved in phagocytosis of antigen- antibodyInvolved in phagocytosis of antigen- antibody
complexes…, in detoxification of histamine…complexes…, in detoxification of histamine…
Basophill & mast cellsBasophill & mast cells
 Found in hemopoitic system & tissueFound in hemopoitic system & tissue
 Contain granulesContain granules
 Stimulated by tissue injury or antigen ;Stimulated by tissue injury or antigen ;
degranulate & release chemical mediators suchdegranulate & release chemical mediators such
as histamine , vasodilator , heparin….as histamine , vasodilator , heparin….

24. VASCULAR CHANGESVASCULAR CHANGES
1.1. VASODILATIONVASODILATION
2.2. INCREASED CAPILLARYINCREASED CAPILLARY
PERMEABILITY, FOLLOWINGPERMEABILITY, FOLLOWING
INFLAMMATORY CHANGESINFLAMMATORY CHANGES

25. initially brief VASOCONSTRICTION followedinitially brief VASOCONSTRICTION followed
by VASODILATATION of arterioles &by VASODILATATION of arterioles &
capillary sphincter…..due tocapillary sphincter…..due to histaminehistamine releasedreleased
from mast cellsfrom mast cells
 so ,increased blood flow through vessels &so ,increased blood flow through vessels &
reduction in vascular reactivity ; opening ofreduction in vascular reactivity ; opening of
dormant capillary bed that increases thedormant capillary bed that increases the
blood supply to the tissues…blood supply to the tissues…
 These changes increase intravascular pressure ,These changes increase intravascular pressure ,
blood flowblood flow

26.  HISTAMINE : increase contracting theHISTAMINE : increase contracting the
endothelial cells & produce intracellular gap..endothelial cells & produce intracellular gap..
--- filtration of plasma & macromolecules from--- filtration of plasma & macromolecules from
venulesvenules
--- plasma--- plasma  less viscous & less proteinless viscous & less protein
contain than blood plasmacontain than blood plasma
 proteins like albumin ,proteins like albumin ,
fibrinogen, Igs..fibrinogen, Igs..
 chemical mediators & cells ofchemical mediators & cells of
inflammationinflammation
 is called as inflammatoryis called as inflammatory

27.  it dilutes bacterial toxins , so reduce potentialit dilutes bacterial toxins , so reduce potential
for tissue damage. , helps to form fibrin to contain thefor tissue damage. , helps to form fibrin to contain the
inflammatory reaction…inflammatory reaction…
 HEGMAN FACTOR ( factor xii ) :HEGMAN FACTOR ( factor xii ) :
-- released in infl.. Exudate-- released in infl.. Exudate
-- activate by collagen ; by damaged-- activate by collagen ; by damaged
basement membrane of blood vessels ; orbasement membrane of blood vessels ; or
by Ag-Ab complexesby Ag-Ab complexes
-- reacts with prekallikrein of plasma or tissus-- reacts with prekallikrein of plasma or tissus
to produceto produce kininskinins ( vasodilator )( vasodilator )
-- also activates the fibrinolytic & blood-- also activates the fibrinolytic & blood
coagulating systemcoagulating system

28.  Also PLASMINOGEN in infl. ExudateAlso PLASMINOGEN in infl. Exudate
activated to plasmin..activated to plasmin..
-- activate complement system-- activate complement system
-- digest fibrin (fibrinogen) & aid in removal-- digest fibrin (fibrinogen) & aid in removal
of blood clotsof blood clots
 IgIg  actvate complement & produceactvate complement & produce
anaphylatoxinanaphylatoxin act on mast cellsact on mast cells  releaserelease
histamine..histamine..
 Also some chemotactic factorAlso some chemotactic factor  aid inaid in
leucocytosis & lysis of bacteria…leucocytosis & lysis of bacteria…

29.  Inflammatory exudateInflammatory exudate  edemaedema  increaseincrease
pressure on venules to collapsepressure on venules to collapse  reducereduce
venous drainage & blood flow..venous drainage & blood flow..  stasis ofstasis of
blood in venules ( due to increase viscosity ofblood in venules ( due to increase viscosity of
blood)blood)  leucocytic migration from center toleucocytic migration from center to
peripheryperiphery  adhere to vessel wall calledadhere to vessel wall called
pavementation of leucocytespavementation of leucocytes  emigration ofemigration of
leucocytesleucocytes migration to site called chemotaxis.migration to site called chemotaxis.
 first PMNs , followed by monocytes &first PMNs , followed by monocytes &
lymphocytes..lymphocytes..

30.  Vascular responses continues with aggregation ofVascular responses continues with aggregation of
RBC in vessels.RBC in vessels.  increase resistance of bloodincrease resistance of blood
to flowto flow decrease in O2 conc. ; increase in CO2decrease in O2 conc. ; increase in CO2
conc. & iower the pH at infl. Siteconc. & iower the pH at infl. Site  decreasedecrease
removal of metabolites..removal of metabolites..
 The aforementioned changes may spreadThe aforementioned changes may spread
inflammation to adjacent tissue ; this visciousinflammation to adjacent tissue ; this viscious
cycle of inflammation may lead to total necrosiscycle of inflammation may lead to total necrosis
of pulp..of pulp..

31.  At inflammatory sites ….At inflammatory sites ….
 PMNsPMNs
 Monocytes & lymphocytesMonocytes & lymphocytes
 MacrophagesMacrophages
 Plasmacells from b-cellsPlasmacells from b-cells
 IgsIgs
 Lymphocyte mediatorsLymphocyte mediators

32.  Recovery of pulpRecovery of pulp
--- arteriovenous anastomoses & U-turn loops--- arteriovenous anastomoses & U-turn loops
open in pulpal vasculature to reduce the flow theopen in pulpal vasculature to reduce the flow the
area of inflammation ; so decrease vasculararea of inflammation ; so decrease vascular
pressure..pressure..
--- increased tissue pressure plays a role in the--- increased tissue pressure plays a role in the
recovery of pulp by allowing return ofrecovery of pulp by allowing return of
macromolecules & fuids to venules..macromolecules & fuids to venules.. returnreturn
the vascular pressure & tissu pressure to normalthe vascular pressure & tissu pressure to normal
& stimulate the repair process..& stimulate the repair process..

33. Periradicular manifestationsPeriradicular manifestations
 Root canal pathwayRoot canal pathway  noxious products ofnoxious products of
tissue necrosis & antigenic agenttissue necrosis & antigenic agent 
periradicular areaperiradicular area  inflammatory &inflammatory &
immunologic responsesimmunologic responses if more quantityif more quantity 
bone resorption ( by OAF factor ) & granulationbone resorption ( by OAF factor ) & granulation
tissue formatointissue formatoin  abscss formationabscss formation

34. Tissue changes followingTissue changes following
inflammationinflammation
 Either degenerative changes or proliferativeEither degenerative changes or proliferative
changeschanges
 Degenrative changes :-Degenrative changes :-
 FibrousFibrous
 ResorptiveResorptive
 CalcificCalcific
 NecrosisNecrosis

35.  SuppurationSuppuration
 Reqiurements for suppuration :-Reqiurements for suppuration :-
 Necrosis of tissue cellsNecrosis of tissue cells
 Sufficient number of ploymorphonuclearSufficient number of ploymorphonuclear
leucocytesleucocytes
 Digestion of dean material by proteolyticDigestion of dean material by proteolytic
enzymesenzymes

36. Proliferative changes :-Proliferative changes :-
 Produced by irritants mild enough to act asProduced by irritants mild enough to act as
stimulants.stimulants.
 In the center of inflammatory area, irritant mayIn the center of inflammatory area, irritant may
be strong enough to produce destrcutionbe strong enough to produce destrcution
whereas at the peiphery irritant may be mildwhereas at the peiphery irritant may be mild
enough to stimulate proliferation.enough to stimulate proliferation.


37. Endodontic implications:Endodontic implications:
 Fish established experimental foci of infection inFish established experimental foci of infection in
the jaws of guinea pigs by drilling openings inthe jaws of guinea pigs by drilling openings in
the bone and packing in wool fibers saturatedthe bone and packing in wool fibers saturated
with broth culture of microorganisms.with broth culture of microorganisms.
 4 well defined zones of reaction found are :-4 well defined zones of reaction found are :-
 Zone of infectionZone of infection
 Zone of contaminationZone of contamination
 Zone of irritationZone of irritation
 Zone of stimulationZone of stimulation

38. Zone of InfectionZone of Infection
 Characterized by polymorphonuclear leucocytes.Characterized by polymorphonuclear leucocytes.
 Infection present in the center of lesion andInfection present in the center of lesion and
microorganisms were found only in that area.microorganisms were found only in that area.

40. Zone of contaminationZone of contamination
 Surrounding the zone of infection.Surrounding the zone of infection.
 Characterized by round cell infiltration.Characterized by round cell infiltration.
 Cellular destruction observed in this zone.Cellular destruction observed in this zone.
 Bone cells die due to toxins released from zoneBone cells die due to toxins released from zone
of infection. Thus, lacunae appear empty.of infection. Thus, lacunae appear empty.
 Radigraphically seen as initial radiolucencyRadigraphically seen as initial radiolucency
around the periapical region of infected tooth.around the periapical region of infected tooth.
 Prevalence of lymphocytes is seen.Prevalence of lymphocytes is seen.

41. Zone of IrritationZone of Irritation
 Characterized by macrophages and osteoclasts.Characterized by macrophages and osteoclasts.
 Irritation due to dilution of toxins.Irritation due to dilution of toxins.
 Distinguished by small, round cells, normal boneDistinguished by small, round cells, normal bone
cells and osteoclasts could just above survive.cells and osteoclasts could just above survive.
 Collagen framework digested by phagocytes,Collagen framework digested by phagocytes,
macrophages while osteoclasts attack bonemacrophages while osteoclasts attack bone
tissue.tissue.
 Overall histologic picture is one of much activityOverall histologic picture is one of much activity
preparatory to repair.preparatory to repair.

42. Zone of StimulationZone of Stimulation
 Characterized by fibroblasts and osteoblasts.Characterized by fibroblasts and osteoblasts.
 FibroblastFibroblast – laid down collagen fibers– laid down collagen fibers
- which act as - wall of defence around- which act as - wall of defence around
zone of irritationzone of irritation
- as a scaffolding aroud- as a scaffolding aroud
which new bonewhich new bone
formation occures.formation occures.
 OsteoblastOsteoblast – laid down new bone which is in– laid down new bone which is in
irrregular fashionirrregular fashion

43.  Root canal is site of infection through whichRoot canal is site of infection through which
- micro organisms (in sufficient quantity)- micro organisms (in sufficient quantity)
- metabolic product of microorganisms- metabolic product of microorganisms
- toxic product of tissue necrosis…….- toxic product of tissue necrosis…….
may be diffused to the periradicular tissue.may be diffused to the periradicular tissue.
 They are destroyed by PMNs. But whenThey are destroyed by PMNs. But when
microorganisms are sufficiently virulant or inmicroorganisms are sufficiently virulant or in
enough quantity……. They overwhelm theenough quantity……. They overwhelm the
defensive mechanismdefensive mechanism
 And they causes periradicular lesions. (abscess)And they causes periradicular lesions. (abscess)

44.  Thus toxins ( pus ) may diluted enough to actThus toxins ( pus ) may diluted enough to act
as stimulant & form granulomaas stimulant & form granuloma
fibroblast form fibrous tissue &fibroblast form fibrous tissue &
osteoblast delimit the area with wall of scleroticosteoblast delimit the area with wall of sclerotic
bone…bone…
 If in addition, the epithelial rest of malassesIf in addition, the epithelial rest of malasses
are stimulated , a cyst will form…are stimulated , a cyst will form…

45.  When root canal has been treated , theWhen root canal has been treated , the
reservoir of bacteria or noxious products getsreservoir of bacteria or noxious products gets
eliminated ; when the root canal is cleanedeliminated ; when the root canal is cleaned
and obturated , the destroyed periapical boneand obturated , the destroyed periapical bone
will undergo repair…will undergo repair…

46.  thanks a lot….thanks a lot….