RATIONALE OF ENDODONTIC TREATMENT

INTRODUCTION INFLAMMATION Definition Causes Signs and Symptoms Cells of inflammation Inflammatory pro ess Tissue !ange "eriradi ular manifestation Repair

#NDODONTIC IM"LICATION

INTRODUCTION: T!e term $Rationale% an &e defined as t!e fundamental reason or t!e rational &asis for a pro edure' T!e rationale for endodonti partial denture or an implant toot!' #ndodonti from t!e t!erapy allo)s t!e remo*al of *ital or ne roti pulp anal system of an infe ted toot! and repla ed &y an inert t!erapy is &ased on t!e &elief t!at a omforta&ly t!an a &ridge( natural toot! fun tion more effi iently and

filling material' T!is is mainly done to pre*ent e+tension of t!e disease from t!e pulp into t!e periapi al tissues' INFLAMMATION: Definition: Can &e defined as a lo al p!ysiologi irritant ausing tissue response of a li*ing tissue to in,ury' T!e main o&,e ti*e of inflammation is to destroy t!e !anges and &ring &a - t!e tissue to a normal form and fun tion' Mediators of inflammation: T!e agents t!at ause t!e !anges in inflammation( t!e alterations in t!e &lood *essels( t!e es ape of proteins and ells into t!e tissues( and t!e !ange in t!e tissue . are alled t!e mediators of inflammation' T!e initiated( transient *aso onstri tion in due to t!e dire t stimulation of t!e &lood *essels and t!e flare is refle+' $Ner*es are not ne essary for t!e inflammatory pro ess'% Inflammation de*elops normally in deri*ated tissue( e+ ept t!at t!e flo) is a&sent' Ner*es may play some part in modifying t!e se*erity of t!e *as ular !ange( &ut in most ir umstan es t!eir effe t is slig!t' aused &y an/ or on

Agents causing inflammation: a. !"sical agents: 0eat( old( me !ani al trauma as in sports in,uries( &ru+ism( a idental e+posure during a*ity preparation( rapid toot! mo*ement during ort!odonti treatment'

#. C!emical agents: 1n"O 2 ( Sili ate( a id et !ing agents et ' c. Infection agents: 3a terial( 4irus( "arasites' d. Immunological agents: Cell mediated rea tion antigen . anti&ody( rea tion' Fa tors modifying t!e inflammatory respond 56 76 86 26 0ost resistan e Intensity Duration 4irulen e of irritant / mi roorganism 9pat!ogeni ity of stimulus6'

3ased on t!ese premises )e an generali:e t!at mild or moderate no+ious stimuli to t!e pulp may produ e s lerosis of dentinal tu&ules( formation of reparati*e dentine( or re*ersi&le inflammation' Irre*ersi&le inflammatory !anges aused &y se*ere in,ury an lead to ne rosis of pulp and su&se;uent pat!ologi !anges in periradi ular tissues' T!e inflammatory pro ess allo)s< 5' 7' 8' 2' T!e arri*al of p!ago yti ells to digest &a teria or ellular de&ris'

Anti&odies to re ogni:e atta - and destroy foreign material' #dema or fluid to distri&ute and neutrali:e t!e irritant' Fi&rin formation to limit t!e spread of inflammation'

$"m%toms of inflammation: A ording to Roman !unter Cel us in 5 s t entury A'D' typi al

signs of inflammation an &e )itnessed'

&. Dolar ' ain(: Caused &y t!e a tion of ytoto+i agents released from !umoral( ellular and mi ro&ial elements of t!e ner*e endings' ). Tumor '$*elling(: "rodu ed &y infiltration of ma romole ulars and fluids into t!e affe ted tissues' +. Ru#or , Color 'Redness , -eat(: "rodu ed &y *asodilatation of t!e *essels and t!e rus!ing of &lood to t!e affe ted tissues' .. Loss of function: )as later added &y 4er !o) resulting of from !anges in t!e affe ted tissues' As in any ot!er inflamed organ of t!e &ody t!ese symptoms also o ur in inflamed pulp &ut only pain and loss of fun tion an &e lini ally appre iated &e ause of t!e en asement of pulp )it! in dentin does not permit s)elling' 3ut in re ogni:ed' Cells of inflammation: =lanulo ytes - Neutrop!ils - #osinop!ils - 3asop!ils T!e main ells of a ute inflammation are poly morp!onu lear Agranulo ytes - Lymp!o ytes - mono ytes ase of inflammation in luding t!e lini ally periapi al tissues all t!e symptoms of inflammation may &e

neutrop!il 9"MN>s6' C!ronic inflammation: lymp!o ytes( plasma ma rop!ages' ol" mor%!onuclear neutro%!ils ' MN/s( 'Neutro%!ils or ells( mono ytes and

ol"mor%!s(. 5' T!eir ells onstitute 2?-@AB of Leu o ytes' 7' Seen in a ute inflammation'

8' T!ey ontain a' Nu leus !a*ing 7-2 lo&es( )!i ! is onne ted' &' Cytoplasm ontaining !ara teristi *iolet pin- granules' T!ese granules are said to ontain en:ymes i' ii' iii' i*' 5' Lysosomes Al-aline p!osp!atase Collagenase La toferrin ells get atta !ed to t!e area of inflammation &y !emota ti

T!ese

fa tors produ ed &y &a teria or t!e omplement system' 7' 8' T!ey t!en allo) t!e &inding of opsonised &a teria onto t!is surfa e' In t!e &inding sites t!e &a teria are en apsulated into t!e

neutrop!ils )!ere lysosomal en:ymes are released t!at -ill t!e &a teria' 2' T!ese "MNs !a*e a narro) range of life' T!ey are destroyed in t!e inflammatory site )!en t!e p0 of t!e tissues falls to C'A' A' T!is !ange in p0 is &roug!t a&out due to t!e release and

produ tion of la ti a id &y t!e neutrop!il during p!ago ytosis' C' Destru tion of t!e "MN>s also en:ymes' a' "epsin &' Cat!epsin T!ese en:ymes result in tissue lysis' 5' T!e "MN>s )it! t!e produ ts of prin ipal onstituents of pairs' Eosino%!ils: ellular lysis and de&ris are ause t!e release of 7 proteolyti

5' 7'

T!ey are fe)er in num&er( onstitute( 5-CB of leu-o ytes' T!ey onsist ofD a' Nu leus usually !as 7 lo&es' &' Cytoplasm made up of ause deep red staining granules'

8' T!ey are most predominant in allergi infe tion'

rea tions and parasiti

2' During t!e immune response( t!ey are in*ol*ed in p!ago ytosis of Ag-A& omple+es and in deto+i ate on of !istamine' 0aso%!ils: 5' T!ese ells are least in num&er ontain 5B of all in u&ating

leu-o ytes' 7' T!ey resem&les all ot!er leu-o ytes &ut t!eir oarse intensity &asop!ili ytoplasm' 8' T!ese granules ontain 0eparin( 0istamine and 0ydro+y tryptamine an &e distinguis!ed &y

granules )!i ! usually fill t!e

and )!en t!ese granules are stimulated &y tissue in,ury or antigen t!ey degranulate and release t!ese su&stan es( )!i ! an initiate an inflammatory or a allergi response' 2' 3asop!ils and masts ells are onsidered similar system and mast ells e+ ept t!at ells in tissues'

3asop!ils are found in !emopoeti

Fun tions of &ot! t!ese ells are same' Macro%!ages: 5' T!ese ells are deri*ed from ir ulating mono ytes' Immature

mono ytes in e+tra*as ular areas of inflammation differentiate into ma rop!ages' a' Ma rop!ages are p!ago yte ells t!at ingest - Cellular de&ris

- Mi roorganisms - "arti ulate matter &' T!ey release mediation of inflammation su ! as lysosomal en:ymes( omplement proteins and prostaglandins' ' T!ey en!an e t!e immunologi al rea tion &y ingesting pro essing and degrading t!e antigen &efore presenting it to t!e lymp!o ytes' d' e' T!en apa ity to remo*e de&ris from area fa ilitates repair' Ma rop!ages are mononu leated a ti*ity( may fuse into ot!er multinu leated giant ell' T!ey release en:ymes li-e 5' 7' 8' 2' A id !ydrolases' Neutral proteases( t!ese en:ymes result in digestion of dead ells' Collagenase' #lastase' ells t!at( in periods of great ma rop!ages to produ e a

L"m%!oc"te: 5' T!ese ells appear in t!e !roni stage of inflammation' T!ey are

intimately related to t!e immunologi al system of t!e organism' 7' It is seen t!at immune system also fig!ts infe tion along )it! t!e inflammatory pro ess' 8' If t!e normal inflammatory pro ess fails to sum up )it! t!e infe tion t!en t!e &ody mounts up a more massi*e !ig!ly effi ient response t!at is apa&le of memory as )ell as spe ifi ity . *i:'( t!e immune system' T!e immune system is omprised of t)o &asi ' 56 3 ells 76 T ells

3ot! deri*ed from t!e !aemopoiti ytoplasm ontaining small granules' T!e stem differentiate as T 1 Cells 5' In t!ymus t!ey &e ome immuno omp' T ells' 7' Most ommon ells of lymp!o ytes 8' Responsi&le for ell mediated immunity E immuno sur*eillan e of t!e !uman organisms 2' Cir ulate t!roug! t!e lymp!oid tissues and ot!er organs of &ody e+ ept t!ymus' A' Found in para orti al area of lymp! nodes' C' F!en stimulated &y foreign &ody t!ey form sensiti:ed T' lymp!o ytes ells are

system' T!ese

ells !a*e a

large sp!eri al or slig!tly indented nu leus surrounded &y a t!in &and of

arried &y t!e &lood to t!e t!ymus )!ere t!ey

0 1 Cells 5' 3e ome immuno ompetent in &one manner 7' Lesser in num&er t!an T ells' 8' Responsi&le for !umoral immunity'

2'

@' Types a6 Memory T- ells . Speed up immunologi al rea tion )!en in onta t )it! same antigen' &6 0elper or suppressor ells. )!i ! stimulate or suppress t!e de*elopment of effe ts T or 3 ells' 6 #ffe tor T ells . "rodu e ell mediated immune rea tion su ! as delayed !ypersensiti*ity

A' Found in orti al areas of lymp! nodes' C' F!en stimulated &y foreign &ody t!ey &e ome large ells alled plasma &lasts' "lasma &lasts di*ide into ' "lasma ells d' Memory 3 Cells @' Types a6 "lasma ells . Large oral round ells )it! !romati nu leus( )!i ! ontains !romati net)or- in art)!eel form' T!ese ells produ e immunologlo&ulin or anti&odies' &6 Memory 3 ells . speed up t!e immunologi rea tion in su&se;uent en ounters )it! same antigen'

G6 Cells release !emi al mediations -no)n as lymp!o-ines H6 Lymp!o-ines- may a ti*ate a6 Ma rop!ages &6 "MNS 6 Non-sensiti:ed T ells or d6 "rodu e interferron )!i ! in!i&its *iral repli ation Anti&odies in !umoral immunity

G6

H6 Immunoglo&ulin or anti&odies of )!i ! !a*e fi*e lasses IgM( Ig=( IgA( I;D I Ig#'

IgM: In t!e first anti&ody to &e produ ed )!en !ost is stimulated &y an antigen' "lasma ells t!en produ e Ig=' Ig2 , Igm: are t!e ir ulatory anti&odies and one t!e most important of t!e serum anti&odies' Ig= E IgM &ase t!e apa ity to &ind to t!e antigen on spe ifi re eptor sites' T!is pro ess is termed as Opsoni:ation and t!e anti&odies are alled opsonins' IgA: Is found in sali*a( tears et ' IgE: In on,un tion )it! eosinop!il ser*es a fun tion of prote tion against parasiti infe tion' IgD: Fun tion is not yet -no)n &ut is onsidered to &e a surfa e on 3lymp!o ytes !en e triggering antigen related lymp!o ytes differentiation' T!ese anti&odies om&ine )it! spe ifi antigen to form a omple+ t!at a ti*ates t!e ompliment system' T!e omplement system t!en release !romati fa tors t!at attra t p!ago yti ells to t!e area t!at eugenol t!e antigen and destroy it' Inflammatory "ro ess Acute inflammation: T!is pro ess an &e studied as a' 4as ular !anges &' #s ape of ells from &lood *essels into tissues ' Tissue !anges

3ascular C!anges: In any -ind of in,ury 7 types of *as ular appre iated a' 4asodilatation' &' In rease in *as ular permea&ility Immediate response to in,ury results in transient *aso onstri tion of &lood *essels( )!i ! lasts for fe) se onds' T!is is follo)ed &y *asodilatation of &lood *essels t!at persists for day to )ee-s t!at is as long as t!e inflammation persists' T!is *asodilatation of arterioles is aused &y t!e rela+ation of anterior and apillary sp!in ters' As a result of *asodilatation t!ere is in reased rate of &lood flo)( )!i ! also results in opening of dormant apillary &eds t!at in reases t!e &lood supply to t!e affe ted area' T!is !eat' Simultaneously &e ause of release of proteolyti en:ymes from in,ured ells( &a terial to+ins and traumati me !ani al for es( !istamine is triggered off from t!e mast ells' T!is !istamine ontra ts t!e endot!elial ells and in reases t!e intra ellular gaps &et)een t!em' T!ese gaps along )it! t!e intra *as ular pressure results in some plasma fluid to lea*e t!e *essels' T!is fluid is less in protein and is termed as inflammatory transudate' T!is transudate is soon o*er s!ado)ed &y t!e &lood plasma )!i ! ontains ri ! plasma proteins su ! as al&umin( fi&rinogen( immunoglo&ulin( )!i ! is alled as inflammatory e+udates' 5' 7' 8' T!is &lood plasma !elps in &ringing t!e !emi al mediation and ells of inflammation to start t!e inflammatory rea tion' It also dilutes &a terial to+ins' It !elps to form fi&rin to ontain t!e inflammatory rea tion' T!is e+udate a umulates in t!e tissue produ ing edema' auses rise in intra *as ular pressure leading to redness and !anges an &e

As t!e in reased &lood flo) t!roug! t!e *essels fills up t!e apillary &eds( t!e *olume of apillary &ed in reases so t!ere is slo)ing do)n of &lood flo)' T!is alteration in t!e ali&er of &lood flo) results in stru tural !anges in t!e mi ro *as ulature i'e'(

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5' 7'

T!e R3Cs ome in t!e enter Leu-o ytes mo*e to)ards t!e *essel )all' T!is pro ess is alled margination of leu-o ytes'

After margination t!e leu-o ytes ad!ere to t!e *essel )all( )!i ! is termed as pa*ementation' After t!e pro edure t!e ne+t step is #migration of Leu-o ytes' At t!e site of inflammation t!ese leu-o ytes are attra ted &y Compliment system "rostaglandins Jalli-rein

F!i ! a ts a !emota ti agent' T!is is alled as K !emoto+is> )!ere t!e leu-o ytes migrate t!roug! t!e *essel )all &y amoe&oid mo*ements' T!e "MN>s migrate 5 s t follo)ed &y mono ytes and lymp!o ytes' Simultaneously K0eggman fa tor> or fa tor LII is also released into t!e tissue in t!e inflammatory e+udates' T!is fa tor is a ti*ated &y A& omple+es' ollagenD damaged &lood *esselsD Ag-

Rea ts )it! "reJalli-rien . Jinin' Jinin produ ed 56 0elps in dilatation of &lood *essels(

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76 permea&ility of &lood *essels' T!e 0eggman fa tor also a ti*ates t!e fi&rinolyti aggulating systems' Fi&rinogen LII---- Fi&rin ---. to a limited area' "lasminogen LII----- plasmin --- a ti*ates t!e omplement system T!is --- digests fi&rin to remo*e &lood lots' ---A ti*ates -inin system' omplement system in turn releases t!e !emota ti fa tors( onfines t!e inflammatory rea tion and &lood o-

)!i ! aid in !emoto+is' T!e *as ular response ontinues )it! t!e aggregating of R3C in

t!e *essel ausing resistan e of &lood flo)' T!is resistan e along )it! t!e in rease in &lood *is osity produ ed &y t!e loss of plasma auses meta&oli 5' De rease in o+ygen on entration' 7' In rease in ar&on dio+ide' 8' Lo) p0' Relating t!ese !anges to pulpal tissues as else)!ere in t!e &ody losed are detrimental as t!ey pre*ent t!e remo*al of )aste produ ts' T!e spread of inflammation is faster in pulp tissue as it is in a !am&er( )!i ! may lead to total ne rosis of t!e pulp' a immunologi rea tion' T!e ma rop!ages( plasma Also t!e !anges su ! as

migration of mono ytes and lymp!o ytes at t!e inflammatory sites start ells deri*ed &y 3lymp!o ytes and lymp!o ytes mediators of t!e immune response are also found at t!e site' #+tra *as ular immunoglo&ulins found are predominantly Ig= apart from Ig#( IgA( IgM'

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T!e re o*ery of pulp responses'

an &e e+plained &y some uni;ue *as ular

Anterior *enous anastamoses and U turn loops open in t!e pulpal *as ulature to redu e t!e flo) to t!e area of inflammation t!ere &y de rease in t!e *as ular pressure' T!e in reased tissue pressure plays an important role in t!e re o*ery of pulp &y allo)ing return of ma romole ules and fluids to t!e *enules' T!erefore t!ese 7 !agoc"tosis: T!is is defined as pro ess of engulfment of solid parti ulate material &y t!e mainly 5' "MN>sD 7' Cir ulating mono ytes or Ma rop!ages' "!ago ytosis ta-es pla e in 8 stages &. Attac!ment stage: T!e serum at t!e in,ury site o urring opsonins' T!ese opsonins get mi roorganisms' Main opsonins are: 56 Ig= opsonin 76 C 8 3 opsonin ). Engulfment stage: T!e p!ago yte gets attra ted to t!is opsonised mi roorganism and sends out en losing t!e p!ago yti ytoplasmi pseudopods t!at en*elop and en loses t!e organism forming a *a uole' T!e plasma mem&rane *a uole &rea-s' T!e lysosomes fuse to t!e p!ago yti *a uole to form a p!agolysosome' +. Degranulation anti&a terial stage: Degranulation )!i ! -ills ta-es t!e pla e releasing T!e ontains naturally oated on t!e ells' T!is is arried out &y ells alled as "!ago ytes !anges return t!e *as ular pressure and tissue pressure to normal and stimulate t!e repair'

su&stan es(

mi roorganisms'

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en:yme released !elp in digestion and li;uefying of t!e dead and damaged tissues' Tissue !anges follo)ing inflammation< Can &e eit!er 5' Degenerati*e 7' "roliferati*e &. Degenerati4e c!anges: Degenerati*e !anges in t!e pulp may &e i' ii' iii' i*' *' Fi&rous Resorpti*e Cal ifi Ne rosis Supporti*e

ells

Suppuration o formation' A

urs due to release of proteolyti en:ymes from t!e

"MN resulting in li;uifa tion of dead tissue resulting in to pus

umulation of t!is pus forms an a&s ess'

Re;uirements for pus formation a' &' ' ). Ne rosis of tissue ells Suffi ient num&er of "MN>s and Leu-o ytes Digestion of t!e dead material &y protolyti en:ymes'

roliferati4e c!anges: T!ese are produ ed &y irritants mild enoug! to a t as a stimulatant' Fit!in an area( a su&stan e may &e &ot! irritant and a stimulant' For e'g' Ca9O06 7 in t!e enter of inflammatory area may a t as an

irritant strong enoug! t!e produ e regeneration or distru tion )!ere as at t!e perip!ery it may &e mild enoug! to stimulate proliferation' F!en a gap is present &et)een tissue parts( repair is made &y granulation tissue' eriradicular manifestations:

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If t!e inflammatory response o*er )!elms t!e pulp t!ere is partial or total ne rosis of t!e pulp in t!e root antigeni agents' T!e inflammatory and immunologi periradi ular area as in pulp In t!e periradi ular area t!e no+ious produ ts ause' 3one resorption and resor&ed &one is repla ed &y granulation tissue' T!e affe ted tissue ells( ma rop!ages( mast IgM( Ig# and omplement' Some re ent reports indi ate t!at some endodonti lymp!o-ine alled ostoelasti flare -ups are mediated &y Ig# rea tions and t!at !a*e &one resorption is mediated &y a ti*ating fa tor' T!ese findings tells us t!e important role t!at immunology plays in t!e p!ysiology( and pat!ology of t!e periradi ular tissue' Re%air: Repair is t!e return of tissue to normal stru ture and fun tion and it &egins as t!e tissue &e omes in*ol*ed in t!e inflammatory pro ess' Repair of t!e tissue depends on 5' 7' Se*erity of in,ury 0ost resistan e ontains neutrop!ils( lymp!o yte( plasma ells along )it! immunoglo&ulins Ig=( IgA( rea tion ontinue in t!e anal( t!is ser*es as a pat!)ay to t!e periradi ular area for t!e no+ious produ ts of tissues ne rosis and

Re*ersi&le damage Repair Irre*ersi&le damage Ne rosis $tages of Re%air: 5' After organi:ation of t!e &lood lot t!ere is formation of

granulation tissue' During t!is stage t!e endot!elial loops &e ome pressure of t!e &lood allo)ing ne) &lood' anali:ed &y t!e ir ulation of

!annels for

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Anastomasis of t!ese loops o &lood *essels' 7'

ur forming a ri ! net)or- of small

In t!e soft tissues( de*elopment of s ar tissue &egins fi&ro&lasts gro) along fi&rin strands and !elp to form t!e protein matri+ &y laying do)n ollagen fi&res' After t!is &ot! t!e fi&ro&last and t!e apillaries &e ome fe)er in num&er and an a*as ular fi&rous tissue i'e' s ar tissue is formed'

8'

In &one t!e pro ess is more on*erted into !ard matri+' 3one is

omple+ as soft tissue( !as to get al ium salts

omposed of protein matri+ infiltrated &y al ium

li-e

al ium p!osp!ate Ca9"O 2 6 7 and

ar&onate Ca9CO 8 6 8 ' T!is al ium salts'

protein matri+ is formed &y osteo&lasts' Surrounding t!e matri+ is a fluid su&saturated )it! Ca9"O 2 6 7 )!i ! gets pre ipitated as matri+' T!ere areas or islands in )!i ! t!e Ca9"O 2 6 7 is pre ipitated unite to form spongy tra&e ular' Repair al)ays pro eeds from perip!ery to)ards t!e enter T!erefore to summarise' =ranulation tissue------fi&rous onne ti*e tissue ----- &one' T!e osteo&lasts produ e al-aline p!osp!atase )!i ! !elp in forming

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Endodontic Im%lications < Fis! des ri&ed t!e rea tion of periradi ular tissues to no+ious produ ts of tissue ne rosis( &a terial produ ts( and antigeni from t!e root anal and esta&lis!ed an e+perimental fo )!i ! !e des ri&ed as 2 :ones' Four :ones of rea tion are 5' 1one of infe tion 7' 1one of ontamination 8' 1one of irritation 2' 1one of stimulation Zone of infection : 5' 7' 8' Infe tion is present in t!e enter of t!e lesion' Mi ro-organisms are also present only in t!at area' It ontains pus fluid( )!i ! ontains i' ii' iii' 2' A' C' Dead ells' Destru ti*e omponents released from p!ago yts' Intermediate 9"roteolysis6' Main ells are polymorphoneuclear leukocytes Mi ro-organisms are atta -ed &y t!ese leu-o ytes' T!e mi roorganisms not atta -ed &y leu-o ytes are found in t!e 0a*ersian anals or in t!e fissures of &one matri+ made &y &ur' Zone of contamination: 5' 7' 8' 2' T!e prin ipal differen e ells are t!e round ells mainly lymphocytes. Ma rop!ages are less in num&er' T!ese appear later &e ause t!ey are less motile and sur*i*e longer t!an neutrop!ils or lymp!o ytes' Dilution of to+i elements ta-es pla e' Fis! o&ser*ed :one' ellular distortion around t!e entral :one( not from entral &a teria t!emsel*es &ut from to+ins dis !arged from t!e and end produ ts of protein de omposition agents i of in,e tion(

17

A'

3one

ells die and undergo Autolysis' T!erefore t!e la unae appear

empty as opposed to t!at of t!e entral :one' Zone of irritation: To+i ity diminis!es as distan e in reases from entral :one' 1. Principal cells a. Macrophages. b. Osteoclass. 7' 8' 2' Undifferentiated ells ,oin to form osteo last )!i ! resor& t!e ollagen net)or- &y ma rop!ages and ontaminated &one' "!ago ytosis ta-es pla e of ells' T!e a ti*ity of osteo lasts on &one open up gap in t!e &one all around t!e enter of lesion' T!is spa e gets filled )it! leu-o ytes 3e ause in t!isD -0ealing starts to ta-e pla e -Repair' A' C' Capillary proliferation' Cells li-e plasma ells( lymp!o ytes( ma rop!ages et '( starts de*eloping more from undifferentiated ells' Zone of stimulation: To+i ity redu ed to mild stimulatant 1) Cells a. Fibroblasts b. Osteoblasts T!is :one ta-es are of perip!ery i'e' perip!eral orientation ta-es pla e' 76 Collagen fi&res are laid do)n &y fi&ro&last )!i ! a t as a' Fall of differen e around :one of irritation' &' S affolding on )!i ! osteo&lasts lays ne) &one'

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Ne) &one is irregular in pattern' 3y t!is e+periment fis! 0o)e*er t!ey on luded t!at root anal is a seat of

infe tion' T!e mi roorganisms from t!e root anal or t!e meta&oli

anal are rarely motile' produ ts of

an multiply suffi iently enoug! to gro) out of t!e root produ ts of mi roorganisms or to+i

tissue ne rosis may diffuse into t!e periradi ular tissue' As t!e mi roorganisms gain entry into t!e periradi ular area t!ey are destroyed &y t!e leu-o ytes' If t!e num&er of mi roorganisms is less a stalemate o more( !roni a& ess o urs' urs' If it is

T!e to+i produ ts of mi roorganisms and t!e ne roti pulp in t!e root anal a ts as irritants and destroy t!e periradi ular tissues along )it! proteolyti en:ymes resulting in pus formation' At t!e perip!ery of t!e lesion t!ere is stimulation of fi&ro&lasts to &uild t!e fi&rous tissues and osteo&lasts to limit t!e area )it! a )all of s leroti &one' T!is !appens &e ause of dilution of to+i yst de*elops' On e t!e root produ ts( ell rests of anal !as &een )!i ! a ts as a stimulant' If in addition t!e epit!elial mallese: are stimulated a eliminated and t!e root

treated and t!e reser*oir of &a teria or no+ious produ ts !as &een anal t!oroug!ly o&turated t!e destroyed periapi al &one undergoes repair'

REFERENCE$: =rossman . #ndodonti "ra ti e' Ro&&ins . 3asi "at!ology'

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