PAGE1PAGE3UnitNineETIOLOGYANDCLASSIFICATIONOFPULPITISFormerlyitwasthoughtthatthepulprespondedinitiallybyacuteinflammation,followedbychronicinflammation,regardlessoftheetiologicfactor.However,Brannstr8mandLindandSeltzershowedthattheinitialresponsetocariesmightbechronicinflammationbecauseoftherelativelyslowprogressionoftheirritant.Operativeprocedures,becauseoftheirrapideffect,probablyresultinatransientacuteinflammation.Almostanyinsulttothetooth(dependingonitsseverityanddurationcansettheinflammatoryprocessinmotion.Threepathwaystothepulpareusuallydescribed:l.Directextensionthroughthedentinaltubules,asincariesorchemicalsplacedonthedentin.2.Extensionbytheprocessofanachoresis,thelocalizationofblood-bornebacteriawithinthepulp(StudieshaveshownthatorganismstendtolocateinareasthatarealreadyinflamedorpreviouslyinjuredGrossmanwasabletorecovertestorganismsinteeththatweretraumatized,buthewasnotabletorecoverthemfromthecirculatingbloodstream.Thismayhelptoexplainwhysomepulpsbecomenecroticwhenthereisnoapparentetiologicfactor.)3.Extensionofperiodontaldiseaseintothepulp.(Recentworkhasshownthatinjuryordiseaseintheperiodontalligamentcanhaveapulpaleffect.Langelandetal.demonstratedlocalizedareasofinflammationinthepulptobearesultofperiodontaldisease;buttheybelievetotalnecrosiswillresultonlyifthelateralcanalsorapicalforamen,orboth,areexposedtotheoralenvironment.)EtiologicfactorsTheetiologicfactorsinvolvedininflammationofthepulpcanbegroupedintofourgeneralcategories:bacterial,iatrogenic,traumatic,andidiopathic.Bacterialfactor.Bacteriaandtheirproductsarethemostcommoncauseofendodonticdisease.Inworkonbothconventionalandgnotobioticrats,Kakehashietal.graphicallyshowedtheimportanceofbacteria-specificallythatexposedpulpswoulddegenerateandbecometotallynecroticwithabscessformationonlyifbacteriawerepresent.Iatrogenicfactor.Thesecondmostcommoncauseofendodonticdiseaseoccursasaresultofattemptstocorrecttheravagesofdentaldisease.Theeffectsofoperativeproceduresresultinginexcessiveheatordrying,orboth,arewelldocumented.Pulpalchangeshavealsobeenreportedinresponsetoimpressiontechniqueswherebybacteriawereforcedthroughthedentinaltubulesintothepulp.Manymaterialsandchemicalsusedindentistryhavebeenfoundtocauseirritationinthepulp.NyborgandTullinreportedontheunpredictabilityof.thepathogicstatusofthepulpstumpaftervitalextirpation.Accordingtotheseauthorsthepulpstumpcanremainvitalorbecomeinflamedornecrotic,leadingtoperiapicaldisease.Thus,inthetreatmentofdisease,furtherdiseasecanbecreated.Traumaticfactor.Theresponsetotraumaappearstobeparticularlydependentontheseverityofthetrauma.Forexample,relativelylighttraumafromocclusionmaycauselittleornoeffect.However,heaviertraumafromocclusionmayhaveasignificantpulpaleffect.Inglereportedacaseofpulpalnecrosis,apparentlytheresultofbruxism.Theresponsetotraumafromblowsoraccidentscanbevaried.SomepulpsapparentlyhealWithnoadverseeffects,whereasothersbecomenecrotic.Thereappearstobeamiddleground(i.e.,someteethrespondtotraumabyincreasedpulpalcalcification).Thismaybesoextensivethatradiographicallytheentirecanalappearscalcified.Traumacausingacrackedorfracturedtoothsecondarilyprovidesapathwayfortheoralfloratoreachthepulp.Oncethepulpisexposedtotheoralenvironment,inflammationisapredictablecomplication.Thesecrackedteethcanresultinbizarreclinicalsymptoms,makingdiagnosisverydifficult.Idiopathicfactor.Pulpalchangesalsooccurforreasonsthatareasyetunknown(idiopathic).Acommonexampleisinternalresorption.Althoughtraumahasbeenimplicatedtoanextentin.internalresorption,thisdoesnotexplainthewholephenomenon.Theseteetharefrequentlyasymptomaticandarediscoveredonroutinedentalradiographs.Microscopicallymacrophagesandmultinucleatedgiantcellsarefoundclosetotheresorbingdentin.Thetissuereplacingthelostdentinusuallyischronicallyinflamed.Alsoaperiapicalradiolucencymaybeassociatedwithinternalresorption,signifyingpulpalnecrosisasasequelatothereaction.ClassificationBecauseonreliablecorrelationhasbeendemonstratedbetweentheclinicalstatusandthehistologicstatusofthepulp,manyclassificationshavebeenbasedononeortheotherfinding.Themostdifficultaspecttoacceptisthatthereisnocorrelationbetweentheseverityofpainandtheextentofpulpalinvolvement.Thecriticaldecisionfortheclinicianiswhethertotreatthepulpendodonticallyorattemptpreventivemeasures.Oncethedecisionismadetoinstituteendodontictherapy,theprecisehistologicstateofthepulpisacademicbecausethetreatmentistotalextirpation.However,intheearlystagesofpulpalpathologythepulppassesfromareversibletoanirreversiblepulpitis.Thisdiagnosisisnotalwaysaneasyonetomakebecausethedividinglinecanbeveryobscure.Reversibleandirreversiblepulpitis.Todecidewhetherapulpitisisreversibleorirreversible.Wedependontestresults,clinicalsymptoms,andclinicaljudgment.Thepatient'shistoryofpainandthepresenceorabsenceofspontaneouspainisofcriticalimportance.Bythiswemeanpainthatisnotbroughtonbyaspecificstimulus(i.e.,heatorcold).Forexample,apatientwhohashadarestorationreplacedlmonthpreviousnowappearswithacomplaintofpain.Afteraperiodofquiescencethepainiscomingandgoingatnospecifictime.Duringthepastyeartherehavebeenseveralepisodesofspontaneouspain.Irreversiblepulpitisisimmediatelysuspected.ThermaltestsmaybevaluableatthisstagebecausepainusuallyI-ingersafterthermalstimuliareappliedandwithdrawn.Thepulptestermayshowahigherreadingonadjacentandcontralateralteeth.ChiltonandFertigdemonstratedthestatisticalvalidityofthethermaltest.Ontheonehand,ifthepainiselicitedonlybyhotcoffeeoricecreamandgoesawayimmediatelywhenthestimulusisremoved,reversiblepulpitisissuspected.Nohistoryofpreviouspainwouldaddtothisdiagnosis.However,ifamoreacuteorprolongedpainfulsensationexists,irreversiblepulpitisisusuallydiagnosed.Seltzebelievesthatthemostdefinitivefactorinirreversiblepulpitisisthepresenceofanintrapulpalabscess.Thisdiagnosisisbasedonahistoryofpreviouspain(moderatetosevere),noresponsetopulptests,orvitalometertestsdifferingmarkedlyfromthoseoncontrolteeth.Inaddition,thepresenceofspontaneousseverepainoraprolongedresponseafterthermaltestingusuallyindicatesirreversiblepulpitis.Inthepresenceoftwoormorefindings,irreversiblepulpitisisfairlyeasytodiagnose.Therealdiagnosticchallengeisthegrayareaprecedingthisstage.Mistakesindiagnosiscanbemade;however,goodclinicaljudgmentandunderstandingofthebasicpathologicprocesseskeepthesetoaminimum.Seltzersummeduptheentirespectrumofpulpalhistopathologybythefollowingclassification:AtrophicpulpTransitionalstageAcutepartialpulpitisChronicpartialpulpitisChronicpartialpulpitiswithliquefactionnecrosisChronictotalpulpitisTotalpulpnecrosisEachofthesestagescanbeseenasastepinthespectrumoftheinflammatoryprocess.Thestagesarefixedandstaticonlyinmicroscopictissuesections.Invivotheinflammatoryprocessisdynamicandeverchanging.PeriapicalextensionofpulpalinflammationPeriapicalinflammationisanextensionofthepulpalinflammatoryprocess.Atsometimeduringthespectrumofpulpitis,theperiodontalligamentbecomesinvolvedininflammation.Bythetimethepulpbecomestotallynecrotic,periapicalinflammationiswellunderway.Thisexplainswhyitispossibletohaveaperiapicalradiolucencyandstillsomevitaltissueremainingintherootcanalsystem.MitchellandTarpleyreportedthatteethsensitivetopercussionclinicallyhadonlylocalizedinflammationitthepulpchamberwhenstudiedhistologically.Althoughtheperiapicalinflammatoryresponseisthesameasthepulpalresponse,therearetwoenvironmentaldifferencesthataffectit:l.Theharddentinwallsnolongerexertadirectinfluence.Bone,anotherhardtissuesurroundingthereaction,ispresentbutissusceptibletomorerapidresorptionduringinflammation.2.Uniikethepulp,theperiodontalligamentisendowedwithavascularnetworkprovidingrichcollateralcirculationthatgreatlyenhancestheabilityofperiapicaltissuetoheal.Thebasicmicrovascularresponseoftheperiodontalligamentissimilartothatwhichoccursinthepulp.