牙体牙髓病学课件

EtiologyofDentalCariesThefourcirclesdiagrammaticallyrepresentthefactorsinvolvedinthecariousprocess.allfourfactorsmustactconcurrently(overlappingofthecircles)forcariestooccurMicro-organismshost&toothSub-stratecariestimenocariesnocariesnocariesnocariesHostfactor:salivaWhatissalivaheremean? a.majorsalivaglandsSaliva parotid,submandibular,sublingual b.minorgland c.gingivalexudateWhySaliva?AnimalexperimentsClinicalobservationsAnimalexperimentGroup No.hamstersAvg.no.Avg.caries cariousteethscoreIntactsalivaryglands202.34.0Desalivated* 10 10.5 39.0*Parotid,submandibular,andsublingualglands.EffectofdesalivationoncariesinhamstersClinicalobservationsXerostomia: decreasedorlackofsalivarysecretionCause:therapeuticradiation salivaryglandsdisorder(e.g.sjogrensyndrome) takingmedicineClinicalobservationCariesinapatientwithimpairedsalivaryfunctionasresultofradiationtherapy(courtesyofDrsJansmaandVissink,RUG,theNetherlands.Thecariesisdifferentfromcommon.Decayofferseenincervicalarea,arapiddemineralizationoverbroadsurfaceswithnocavity.thehugechangeinquantityofsalivaisresponsible.InxerostomiaTheamountofbacteriaThequalityofplaquechangeS.mutans,Lactobacillus,Yeast,ActinomyceS.sanguis,Veillonella,NeisseriaAcasereportDecayed,missing,andfilledteethpriortotheanticholinergictherapyobtainedfromthepatient’sdentalrecordsandroentgenographsFull-mouthroentgenographsofpatientshowingrampantcariesandpulpalinvolvementofmandibularanteriorteethDecayed,missing,andfilledteethofapatientwhoreceivedprolongedanticholinergictherapyforaduodenalulcer.Notethesteepcariesincrement(DMFT27)thatoccurredduringthetimeofxerostomiaSalivarycompositionandcariesRelationshipbetweensalivarycharacteristicsandcariesprevalencePropertyRelationshipPropertyRelationshipFlowrate±pH -Buffercapacity + Ca - PO4 - NH3 - Amylase Viscosity - Urea -+positiverelation;±somerelation;-norelation.Whyflowrate?Flushingandneutralizingeffectreferedas“SalivaryClearance”or“OralClearanceCapacity”TheDawes(1983)modeloforalclearance.Salivaisproducedataratedependentontheconcentrationofsugarinthesaliva.Whenamaximumvolumeofsaliva(Vmax)isreached,aswallowoccursandthesalivaryvolumedecreasestoaresidualvolume(Resid),therebyeliminatingsomeofthesugarFlowrateofsalivaUnstimulated 0.3ml/min 0.7~1.5L/daySeverexerostomia 0.05ml/minAcomputersimulationoftheeffectofchangesintheunstimulatedflowrateontheclearanceofsucroseaftera10%sucrosemouthrinse.ThesimulationassumedaveragevaluesforResid(0.8ml),andVmax(1.1ml)Sucroseconcentrationsinsalivaatdifferentsitesandtimesaftera10%sucrosemouthrinseWS=wholesaliva;FUM=facialuppermolarsFUI=facialpalatalupperincisorsLLM=linguallowermolarsFLM=faciallowermolarshighflowratehighbuffercapacityflowratebicarbonateconcentrationNa+Electrolyteconcentrationasafunctionofsalivaryflowrate.Seealsochapter3Salivarycompositionandcaries:contradictoryresults,becauseofthedifficultiesinstudyRelationshipbetweensalivarycharacteristicsandcariesprevalencePropertyRelationshipPropertyRelationshipFlowrate±pH -Buffercapacity + Ca - PO4 - NH3 - Amylase Viscosity - Urea -+positiverelation;±somerelation;-norelation.SalivarybuffersInsaliva,twochiefbuffersystem,bicarbonate-carbonicacid(HCO3-/H2CO3,PK1=6.1)ANDphosphate(HPO4=/H2PO4-,PK2=6.8)BicarbonateismostimportantbuffersystemDialysisofsaliva,removeallion,keepprotein,nobuffercapacityremained.DiagramofaStephancurve–theplaquepHresponsetoa10%glucosesolution(RedrawnfromJenkins,Thephysiologyandbiochemistryofthemouth.Blackwell,London,1978).TheeffectofrestrictingtheaccessofsalivatoplaqueupontheshapeoftheStephancurve(Reproducedfrom)Jenkins,thephysiologyandbiocbemistryofthemouth.Blackwell,London,1978)MeanStephancurvedfollowingrinsingwithsucrosealoneandfollowingparafilmchewingorcheesechewing.ReproducedfromHighamandEdgar;CariesRes1989;23:42-48Conceptof“CriticalpH”Innormalconcentrationofcalciumandphosphate,thecriticalpHis5.5.AntibacterialfactorofglandularoriginLysozyme（溶菌酶）Hydrolyticenzyme,cleavesthe1-4linkagebetweenN-acetylglucosamineand(N-乙醯葡糖胺）,N-acetylmuramicacid(N-乙醯胞壁酸）astructureofcellwallofbacteria.lysozyme,existinmanytissuefluidsuchastear,egg,salivaetc.Manybacteriaisresistanttolysozymebycapsuleandextracellularpolymers.Animaltestshowlysozymealonecouldnotpreventcaries.Lysozymefunctionbyaffectingtheecologicalbalancebetweenmicroorganism.SalivaryperoxidaseThiocyanateion(SCN-) fromsalivaryglands硫氰酸鹽HydrogenperoxidefrombacteriaSalivaryperoxidasesystem

(唾液過氧化物酶系統）H2O+SCN- OSCN-+H2OOSCN-硫氰酸鹽中間產物，包括二氰代硫、氰亞磺酸、氰磺酸等PeroxidaseOSCN-inactivatevariousenzymeoftheglycolyticpathwayandthereforeinhibitgrowth,respirationandmetabolismofmanybacteria.Lactoferrin（乳鐵蛋白）Ferriciron(Fe3+)isanessentialmicrobialnutrientLactoferrinbindsferriciron,makeitunavailableformicrobialuse.UnboundlactoferrinmayalsohavebactericidaleffectonsomemicroorganismssuchasS.mutansMicroorganism’spolicyagainstLFSomebacteriaproduceaprotein(enterochelins)bindingFe++moreeffectivelySomebacteriadegradedLFandusethereleasedFe++Amylase（澱粉酶）Acalciummetalloenzymehydrolysesthealpha1-4bondofstarchAmylasemayhelpcleantheteethofcarbohydratedebris.Butwhyappearintears,serum,brohchial(支氣管）,maleandfemaleurogenitalsecretions?Recentdiscovery:amylasemayspecificallybindstosomeoralmicro-organism.Histatins（富組蛋白）Agroupofsmallhistidin-richprotein.Inhibitorofcandidaalbicans(白色念珠菌）andS.mutans.Unstimulatesaliva:2~30nmol/mlStatherins（富酪蛋白）a43residueprotein,producedbyacinarcellInhibitprimaryprecipitationofcalciumphosphate,entiremoleculeisneeded.Inhibitsecondaryprecipitation(crystalgrowth).Onlyfirstsixresiduesareneeded.Statherins

InagivenpH,onlysupersaturatedsalivawouldpreventdemineralization(脫礦)andpromoteremineralization(再礦化).However,supersaturatedwithcalciumphosphatewillpromotecrystallizationofcalciumphosphatesaltsontotoothsurface.Whyinhibitingprecipitation?Proline-richproteins(PRPs,富脯蛋白)3PRPswasidentified,witharound150aminoacidresidues.Inhibitionofcrystalgrowthcalculusformation,remineralizationandcalciumphosphateprecipitation

thefirstby30residuesattheamino-terminalpart

ImportantconstituentofacquiredpellicleInteractionwithoralbacteria,modulationofadhesionofselectedbacteriatotoothsurfaceThePRPsmoleculeisthoughttobindtotoothsurfaceviaitsamino-terminalsegment.toothBindingofthissegmentissufficienttofulfilltheprimaryrole(inhibitionofcrystalgrowth),andleavesthecarboxy-terminalregionofthemolecule,whichhasadifferentcomposition,directedtotheoralcavity,andfreetointeractwithoralbacteria.NCCariesImmunologyImmunologicalpreventionofinfectiondiseaseachievedvastsuccessinthiscentury.smallpox,poliomyelitisetc.Howaboutdentalcaries?inhibitcolonization,surfaceprotein（表面蛋白）,glucosyltransferase（葡糖基轉移酶GTF）Opsonize（調理）bacteria,permittingphagocytosisTheoretically,antibodymaycontrolcariogenicbacteriabyHumoralandcellularfactorsattheplaque/toothinterface.SalivaprovidessecretoryIgA,whichcanreachplaquebothatthegingivaandatocclusalfissures.Gingivalexudateprovidesbothhumoral(IgG,IgM,andIgA)antibodiesandcellularcomponents(neutrophils,lymphocytes),butonlytoplaqueinthegingivalregion.PolypeptidechainstructureofhumanIgAElectronmicrographofahumandimericIgAmyelomaproteinStructureofhumansecretoryIgA1(sIgA1)AnimalstudiesrodentorprimatesDietcontainingsucrose(diet2000)InfectedtestcariogenicbacteriaControlgroupCariesdevelopmentisdeterminedbyKeyesmethodAnimialcariesmodel取唾液取靜脈血本課題獲國家自然科學基金重點專案資助WholecellWholeproteinorpeptidePartofpeptide,onemoredormainCheramicpeptide--AgI/II~GTFDNAvaccinCandidateantigenSIgA,locallyorviagutserumantibody,viasystematicPassiveimmunizationActiveimmunization

MonoclonalantibodyagainstS.mutans

MonoclonalantibodyagainstthesurfaceproteinantigenofS.sobrinus(Pag)PassiveimmunizationA重組質粒pCIA-PB重組質粒pCIA-PC重組質粒pCIA-PD空載體制裁粒pCIE生理鹽水茸毛鏈球菌占總的可培養細菌的百分數A單抗處理組B腹水對照組CPBS處理組ABC012345Series1Series2Series3Series4Series5Series6Series7Series8Series9Series10C.PBS處理組ImmunoelectronmicroscopyofPcAbagainstS.sobrinus6715wholecellsreactedwiththethreebacteriaS.sobrinusS.mutansS.rattusImmunoeletornmicroscopyofMcAbZS2/286reacted

withthethreebacteriaS.sobrinusS.mutansS.rattusImmunoeletornmicroscopyofnon-specificmiceascitesreacted

withS.sobrinus6715

PolyclonalantibodyagainstaS.mutans

GTase-IoverexpressionstrainPolyclonalantibodyagainstcariesinmilkIgYagainstcariesinhenegg-yolkWesternblotofoverexpressGTase-IstrainEffectofspecificbovinemilkantibodiesagainstdentalcaries

constructionofGTase-IoverexpressingstrainB29-33

intramuscularimmunization

specificcowmilkantibodies

mouserinsing

colonizationlevelofS.mutanonteethsurface

TwocowsbothimmunizedwiththeGTaseover-expressionstraindevelopedgoodIgGinmilk.SpecificIgGlevelinbovinemilkbyELISA3255060759500.10.20.30.4Series1OD(405nm)daysafterparturitionOD405temperature（℃）TheeffectsoftemperatureonIgGinmilk

EffectofspecificIgYonpreventionofdentalcarieskilledS.mutans,S.sobrinuswholecells

eggyolkIgY

effectofspecificIgYonS.mutansinvitro

effectofspecificIgYoncaries preventioninanimalmodelsintramuscularimmunizationHostfactors:toothToothmorphologyandarchformClinicalObservationPitandfissureareaofposteriorteetharehighlysusceptibletocaries.Fooddebrisandmicrooganismsreadilyimpactinthefissures.Insametooth,differencesinsurfacesregardingtosusceptibletocariesInmandibularfirstmolarsocclusal>buccal>mesial>distal>lingualInmaxillaryfirstmolarocclusal>mesial>lingual(palatal)>distal>buccalReason:Partlyduetotoothmorphologypitandfissure>smoothfewcariesincuspalareaInfirstmolar,distalareaisfreetosalivafor4-5year,whereasthemesiaareareadilyformdentalplaquein4~5dayaftereruption.DefectintoothPlaquegrowth24hoursaftercleaning,onacentralmaxillaryincisorofapatientwhoisan“abundant”plaqueformer.Notethespreadalongthegingivalmargin,thecrack,andothersurfacedefects.Extensivedentalcariesontheleftsideofmaxillaandmandibleinapatientwhohasreceived>40GyradiationdosetotheareaoftheleftparotidglandWheredentalplaquelikelytoform?Stagnationarea(滯留區）Photographofplaqueaccumulationinstagnationareasafteromissionoftoothbrushingfor3days.NotethataccumulationspreferentiallyoccuralongthegingivalmarginandinterproximalspaceswhereasnoplaqueaccumulatesincuspalandincisalareasduetocontinuousmechanicalwearontheseareasIrregularitiesinarchform,crowdingandoverlappingoftheteethalsofavorthedevelopmentofcariouslesions.BecauseofmorestagnationareasClinicalfeaturesimmediatelyafterremovaloforthodonticappliancesandcleaning.Theorthodontictreatrmenthadlastedfor2years.Noethemarkedgingivalreactionandthecharacteristicchalkysurfaceappearanceoftheactiveenamellesion.After3monthswithcarefuloralhygienethegingivaltissueshaverecoveredandtheactivelesionhasbeencompletelyarrested.ThewhiteappearanceofthelesionhasdiminishedmarkedlyduetopolishingawayoftheerodedoutermostenamelsurfaceToothcompositionEnamalsurfaceismorecaries-resistantthanthesubsurfaceMicroradiographofwhitespotlesionofenamel.Comparetheextensivedemineralizationofthesubsurfaceenamelwiththebettermineralizedsurfacelayer(originalmagnificaiton100)Thesurfaceenamelhasmoremineralandorganicmatterbutrelativelylesswater.Inaddition,certainelements,includingfluoride,chloride,zincaccumulateintheenamelsurface.A-CConcentrationgradientsofdifferentelementsinenamelfromthesurfacetowardstheenamel-dentinaljunctionChangesoftheenamel,suchasadecreaseindensityandpermeabilityandaincreaseinnitrogenandfluoridecontentoccurwithage.This“maturation”makerthetoothmoreresistanttocaries.Fluorideconcentrationsinsurfaceenamelofdeciduouscaninesasafunctionofdentalcariesprevalenceinthedeciduousdentitionattheageof6years.Nostraightforwardrelationshiptoillustratethatahighfluorideconcentrationshouldbelinkedtoalowcariesprevalenceisseen.However,whenthecariesexperienceishigh,thefluorideconcentrationinenamelbecomeshighaswell.Substrate:DietandCariesDiet:foodanddrinktakenbyanypersonfromdaytoday.Function:locallysystemicLocally:reactwiththeenamelsurfaceandbyservingasasubstrateforcariogenicmicrooganisms.Systemically:Nutrition,onmelabolicprocessesDifficultiesinidentifydietroleininfluencingcariesReason:difficultiesincontroldietforalongtimeinformationonlyfromdiethistoryManyresearchesindicatethesucroseinthe“archcriminal”intheetiologyofcaries.Cumulativedentaldecayprevalence,expressedasDMFpermanentteeth,inchildrenages11to12.Correspondingannual1959percapitasucroseutilizationdatafor18countriesandthestateofHawaii,fromthefoodandAgricultureOrganizationoftheUnitedations.(CourtesyofDr.T.Marthaler.)Relationshipbetweendentalcariesandmeansugarintake(g/day)forSouthAfricanmales(16to17yearsold)offourdifferentethnicgroups.Thereisadirectrelationshipbetweenpercentpopulationcaries-freeandsugarintake.(DrawnfromthedataofRetiefetal.)InterventionalhumanstudiesVipeholmstudyHopewoodHousestudyPlotofthemeannumberofDMFteethperchildversuschronologicalageinstateschoolsofAustraliaandinchildrenofHopewoodHouse(withstandarderrorofmeans).Notetheextremelylowcariesincrementoftheinstitutionalizedchildrenwhileunderstrictdietarycontrolandthesteepincreaseincariesexperiencewhendietarysupervisionwasnolongerineffect–atabove13yearsofage.(CourtesyofT.Marthaler)Specialpopulationgroups

hereditaryfructoseintolerance(HFI)AssessmentofcariogenicpotentialoffoodsuffsInvitromodelofcariesadhesivenessoffoodenameldemineralizationproductionoftitratableacidMonitoringofplaquepHchangesacidogenicityismeasuredAnimaltestingAdhesivenessoffoods

adhesiveness:

attacmentbetweenfoodandthetoothsurface,stickyfoodDeterminingsucrosecontentPlaque-pHcurvesfollowingtheapplicationofA:lactose,glucose,maltose,fructoreandsucrose,andB:rawstarch,cookedstarch,maltoseandsucrose.TelemetricallyrecordedpHofinterdentalplaque(5daysold)inasubjectduringand17minafterrinsingwith15mlof10percenttestsolutionsofLycasin,xylitol,sorbitol,sorboseandsucrose.PC=3minparaffinchewing;U=2minurearinse.OtherdietarycomponentsandcariesPhosphates

cariostaticactivityanimalexperimentsupportthataddingphosphateindietreducecariesinanimal,bylocaleffect.Humanstudy:notconvincingReason:differenceinanimalandhumanandinexperiment.TraceelementsRelationshipofmineralelementstocariesFrequencyofeatingandcaries

VipeholmstudyResultsoftheVipeholmdentalcariesstudy.Sugarinvariousformswasgiveneitherbetweenorwithmealsoverseveralyears,andtherateofcariesincreasewasstudied.Thecariesincrementwasmuchlowerwensugarwasgivenwithmealscomparedwithsugarbetweenmeals.(courtesyofB.E.Gustafsson.)Theeffectofbetween–mealeatingoncariesactivityin5-to6-year-oldchildren.Themoresnackschildreneat,thehigheristhecariesincrement.(def)Decayed,extracted,filled(teeth).(CourtesyofWeissandTrithart.)AnimalstudiesEarlytheoriesofcariesetiologyWorms:

蟲牙學說Humors體液學說:

ancientgreek;fourfluidofbodyarenotinbalanceVitaltheory(活體學說)18century,diseaseoriginatetoothitself.Chemiealtheory(化學酸學說)parmly(1819)suggestacidmayinducecaries.Parasiticorseptictheory(寄生腐敗學說)microorganismmayplayrole,bymicroscope,manybacteriaontoothwerefound.proteolysis-chelationtheoryFirstorganicmatterdissolved,degraded,then,theendproductmayhavechelatingeffectandtherebydissolvethemineralsintheenamel.ThisprocessmayhappenatneutraloralkalinepHMillerchemico-parasitictheoryacidwaspresentincariesmanyfoodmixedwithsaliveandincubateat37℃coulddecalcifytoothSeveraloralbacteriacouldproduceacidtocausecariesDifferentbacteriainvadecarieslesionCurrentconceptsofcariesetiologyMicro-organismshost&toothSub-stratecariestimenocariesnocariesnocariesnocariesClinicalclassificationofcariesRateofcariesprogression1950’sstudy:ittookoneyeartheenamelfissurecariesdevelopintodentine.1989’sstudy:only50%fissuredevelopedintodentinewithin2years.FluorideapplicationmayretardcariesprogressionTheprogressionratesofproximalcarieslesionsfrominitialenamelcariestodentinalcariesinpermanentdentitionwasestimateto68(2yearsatage7,4yearsatage12).ClassificationaccordingtoprogressionrateAcutecaries:progressfast,ofteninchildrenandteenagers,lightcoloredcavity.Rampantcaries,manytoothinvolvedatsametimeacutecariesfeatureoftenaccompaniedbysystematicdisorder.Suchassjogrensyndromeorsalivareductionafterradiation.Cariesinapatientwithimpairedsalivaryfunctionasresultofradiationtherapy(courtesyofDrsJansmaandVissink,RUG,theNetherlands).Chroniccaries

progressslowly,blackorbrowncoloredcavityhardremainingdentineArrestedcaries

cariesstopprogressingbecauseofthelocaletiologicalchangeSecondarycaries(recurrentcaries)

cariesrecurredaftertreatment.OftenatthemarginthefillingmaterialsrestorationorbeneathTheshadowlocatedonthemesiolingualcuspadjacenttothelargerocclusalamalgamrestorationonthemaxillaryrightfirstmolarindicatesthepresenceofcariousdentinClassificationaccordingtotheinvolvingsiteOcclusalcariesRootcariesSmoothsurfacecariesClassificationaccordingtothedeepnessSuperfacialcaries(淺齲)

whitespotlesions,visiblyfrostedsurfacebrownspotDentincaries(中齲)

cavitatedlesioninvolvingtheuppartofdentinDeepcaries(深齲)

cavitatedlesioninvolvingthepupalthirdofdentinDiagnosis

VisualchangeProbing:roughsurfaceortrappingpointpainuponprobingTemperaturetestX-rayexaminationTransilluminationVisualchangeMatte,white,activecervicallesionsProbing:roughsurfaceortrappingpointpainuponprobingTheexplorertipcaneasilydamagewhitespotlesionsTemperaturetestX-rayexaminationtransilluminationProximalcarieslesionisdetectedinananteriortoothwiththeuseoftransilluminationSuperfacialcaries(淺齲)Whitespotorbrown,darklesion,roughuponprobingNocomplaint,nohypersensitivityDentincaries(中齲)Cavity,hypersensitivityuponprobing,hotorcoldstimulus.CurrentconceptsofCariesDentalcariesisaspecificinfectiousmicrobiologicaldiseaseoftheteeththatresultsinlocalizeddissolutionanddestructionofthecalcifiedtissues.Germfreeanimalsdonotgetcaries.CurrentconceptsofcariesetiologyMicro-organismshost&toothSub-stratecariestimenocariesnocariesnocariesnocariesCurrentconceptsofCariesThediseaseprocessbeginswiththeconcentrationofmutansstreptococcusatspecifiedtoothsurfacesandmayleadtowhitespotformationorevencavitation.

CurrentconceptsofCariesThedevelopmentofdentalcariesisadynamicprocessofdemineralizationof

thedentalhardtissuesbytheproductsofbacterialmetabolism,alternating

withperiodsofremineralization.

HarrisandChristen《PrimaryPreventiveDentistry》,1995ClassificationaccordingtotheprogressionrateaccordingtotheinvolvingsiteaccordingtotheseverityaccordingtotheprevioustreatmentClassification

accordingtotheprogressionrateAcutecariesRampantcariesChroniccariesArrestedcariesSecondarycariesActivecariesArrestedcariesAcuteCariesprogressfast,ofteninchildrenandteenagers,lightcoloredcavity.RampantCariesCariesinapatientwithimpairedsalivaryfunctionasresultofradiationtherapy

(DrsJansmaandVissink)Rampantcaries,manytoothinvolvedatsametimewithacutecariesfeatureoftenaccompaniedbysystematicdisorder,suchasSjogrensyndromeorsalivareductionafterradiation.ChronicCariesprogressslowly,blackorbrowncoloredcavityhardremainingdentineArrestedCariescariesstopprogressingbecauseofthelocaletiologicalchangeClassification

accordingtothetreatmenthistoryPrimarycariesSecondarycariesorRecurrentcariesSecondaryCariesClassification

accordingtotheinvolvingsitePits&fissurescariesSmoothsurfacecariesRootsurfacecariesThefirstandmostsusceptiblesiteisthedevelopmentalpitsandfissuresofenamel.Theshapeofthepitsandfissurescontributetotheirhighsusceptibilitytocaries.Howmanytypesofthefits&fissuresinyourtextbook?Pits&FissuresCariesThesecondsiteisoncertainareasofthesmoothsurfaceofenamel.Theseinclude:1.theareasofcontactingproximalsurfaceand2.areasgingivaltotheheightofcontourofthefacialandlingualsurface.Couldyouexplainwhytheproximalsurfacesareparticularlysusceptibletocaries?SmoothSurfaceCariesThethirdsitewherecariesmayattackistherootsurface.Therootsurfaceisrougherthanenamelandreadilyallowsplaqueformationintheabsenceofgoodoralhygiene.Theanotherreason?RootSurfaceCariesClassification

accordingtotheSeverityIncipientcariesModeratecariesSeverecariesAdvancedcariesSuperfacialcariesMiddlecariesDeepcariesIncipientCariesModerateCariesAdvancedCariesSevereCariesANewClassificationRecommendedbyDr.GrahamMount&Dr.RoryHumeInUCLA/pic/members/caries/index.htmlDiagnosisEarlydetectionofincipientcariesandlimitationofcariesactivitypriortosignificanttoothdestructionareprimarygoalsofaneffectivediagnosisandtreatmentprogram.DiagnosisClinicalsigns

visual-location,cavitationtactile-textureClinicalsymptomsDiagnostictestDiagnosisTestRadiographs(filmanddigital)Transillumination(FOTI/DFOTI)Electricalconductivity(EC)Optical(fluorescence)methods(QLF)FluorescentdyeDiagnosticTestOnlyacceptablegoldstandardpresentlyishistologicalassessment.Mostdiagnostictestsarelimitedtospecificapplications.Visual-tactilemethodremainsthemostaccurateandreproduciblemethodofdiagnosisofdentalcaries.VisualClassifications

(occlusalsurfaces)0.Noorslightchangesinenameltranslucencyafterprolongedair-drying1.Opacity(whiteoryellow)hardlyvisibleonthewetsurfacebutdistinctlyvisibleafterair-drying2.Opacity(whiteoryellow)distinctlyvisiblewithoutair-dryingVisualClassifications(continued)3.Localizedenamelbreakdowninopaqueordiscolouredenameland/orgreyishdiscolourationfromtheunderlyingenamel4.cavitationinopaqueordiscolouredenamelexposingthedentinebeneathEkstrandetal,1997ProximalcarieslesionisdetectedwiththeuseoftransilluminationQuantitativeLightFluorescence(QLF)ProgressionofDentalCariesdemineralizationofenamelsurfacesub-surfaceenamellesiondemineralizationofdentinecavitationofenamelsurfacecavitationintothedentineTreatmentProgramNon-surgical-remineralizationSurgical-restorationNon-cavitatedlesionsdeservemoreattentionbecausethey:–aremoreprevalentthancavitatedlesionsineconomicallydevelopedcountries–canvalidlyserveasindicatorsofcariessusceptibility–appropriatelyshouldbetreatednonsurgicallywhichispreferable.TwoDifficultiesWhentoplaceaninitialrestoration?BreakdownoftheouterenamelisanimportantclinicalindicatoroftreatmentManagementofFissuredSurfaceNoCariesorArrestedCariesinFissureswithSusceptibleMorphologyEnamelDemineralizationorQuestionableCariesinDentinCavitationorCariesinDentinCariesRisk?NotreatmentSealantEnamelPRRRestorationCariesRisk?LowHighLowOpenfissureswithroundburHighDemineralizationinvolveenameldentinUniversityofTexasHealthScienceCenteratSanAntonio,UTHSCSALinkingdiagnosistoclinicalmanagementTwoDifficultiesWhentoplaceaninitialrestoration?BreakdownoftheouterenamelisanimportantclinicalindicatoroftreatmentHowtodealwithseverecaries?ProtectionofdentalpulpistheprimarygoalReference/pic/members/caries/index.html/classe