Aggressive periodontitis - Wikipedia

Aggressive periodontitis is often characterised by a rapid loss of periodontal attachment associated with highly pathogenic bacteria and an impaired immune ... Aggressiveperiodontitis FromWikipedia,thefreeencyclopedia Jumptonavigation Jumptosearch Aggressiveperiodontitisdescribesatypeofperiodontaldiseaseandincludestwoofthesevenclassificationsofperiodontitisasdefinedbythe1999classificationsystem:[1] Localizedaggressiveperiodontitis(LAP) Generalizedaggressiveperiodontitis(GAP) LAPislocalisedtofirstmolarorincisorinterproximalattachmentloss,whereasGAPistheinterproximalattachmentlossaffectingatleastthreepermanentteethotherthanincisorsandfirstmolar.[2]TheprevalenceofLAPislessthan1%andthatofGAPis0.13%.[2]Approximately0.1%ofwhiteCaucasians[3](with0.1%innorthernandincentralEurope,0.5%insouthernEurope,and0.1-0.2%inNorthAmerica[2])and2.6%ofblackAfricansmaysufferfromLAP.[3]Estimatesofthediseaseprevalenceare1-5%intheAfricanpopulationandingroupsofAfricandescent,2.6%inAfrican-Americans,0.5-1.0%inHispanicsinNorthAmerica,0.3-2.0%inSouthAmerica,and0.2-1.0%inAsia.[2]Ontheotherhand,inAsia,theprevalencerateof1.2%forLAPand0.6%forGAPinBaghdadandIranpopulation,and0.47%inJapanesepopulation.[2] Therefore,theprevalenceofLAPvariesconsiderablybetweencontinents,anddifferencesinraceorethnicityseemtobeamajorcontributingfactor.[2] Aggressiveperiodontitisismuchlesscommonthanchronicperiodontitisandgenerallyaffectsyoungerpatientsthandoesthechronicform.[2][3]Around1inevery1000patientssuffermorerapidlossofattachment.[4]MalesseemtobeathigherriskofGAPthanfemales[2] Thelocalizedandgeneralizedformsarenotmerelydifferentinextent;theydifferinetiologyandpathogenesis. Contents 1Etiology 1.1Microbiology 1.2Pathophysiology 2Features 2.1Primaryfeatures 2.2Secondaryfeatures 3Clinicalandradiographicfeatures 3.1Localizedaggressiveperiodontitis 3.1.1Clinicalfeatures 3.1.2Radiographicfeatures 3.2Generalizedaggressiveperiodontitis 3.2.1Clinicalfeatures 3.2.2Radiographicfeatures 4Screening 4.1Clinicalexamination 4.2Radiographs 4.3Strongfamilyassociation 5Treatment 5.1CauseRelatedTherapy 5.2Re-examination/ResponsetoTherapy 5.3DefinitiveTherapy 5.4Maintenance 6References Etiology[edit] Microbiology[edit] Ofthemicrofloracharacterisedinaggressiveperiodontitis,approximately65-75%ofbacteriaareGram-negativebacilli,withfewspirochaetesormotilerodspresent.[5]Aggressiveperiodontitisisoftencharacterisedbyarapidlossofperiodontalattachmentassociatedwithhighlypathogenicbacteriaandanimpairedimmuneresponse.VariousstudieshaveassociatedAggregatibacteractinomycetemcomitans,formerlyknownasActinobacillusactinomycetemcomitans,withaggressiveperiodontitis.Anearlystudydatingbackto1983explainsitsprevalenceanddocumentsitsroleinlocalisedaggressiveperiodontitis.[6] Virulencefactorsaretheattributesofmicroorganismsthatenableittocoloniseaparticularnicheinitshost,overcomethehostdefencesandinitiateadiseaseprocess.[7]FivesTayloretal.(2000)havecategorisedthevirulencefactorsofAggregatibacteractinomycetemcomitansasfollows.[7] Promotecolonizationandpersistenceintheoralcavity: Interferewithhostdefences: Destroyhosttissues: Inhibithostrepairoftissues: Adhesins Leukotoxin Cytotoxins Inhibitorsoffibroblastproliferation Invasins Chemotacticinhibitors Collagenase Bacteriocins Immunosuppressiveproteins Boneresorptionagents Inhibitorsofboneformation Antibioticresistance Fc-bindingproteins Stimulatorsofinflammatorymediators SamaranayakenotestheevidenceforthespecificinvolvementofAggregatibacteractinomycetemcomitansincludes:anincreasedincidenceofitfoundinsubgingivalplaqueobtainedfromlesionalsites,highlevelofitsantibodywhichtendstofallfollowingsuccessfultreatment,itspossessionofawiderangeofpotentiallypathogenicproductsanditseliminationwithconcordantdiseaseregression,followingtreatmentwithsuccessfulperiodontaltherapyandadjunctivetetracycline.[5] PorphyromonasgingivalisisaGram-negativeanaerobeassociatedwiththepathogenicityofperiodontaldisease,[8]andaggressiveperiodontitisisnoexception.GreaternumbersofbothPorphyromonasgingivalisandAggregatibacteractinomycetemcomitanswerefoundinactive,destructiveperiodontallesionsincomparisontonon-activesites.[8] Capnocytophagasppareimplicatedasprimeperiodontalpathogens,especiallyinlocalisedaggressiveperiodontitis.[5]BothCapnocytophagasppandPrevotellaintermediawerethemostfrequentlydetectedmicroorganismsinastudy,[9]whichalsonotedthatCapnocytophagasppwasthemostprominentbacteriainsubgingivalsamplesofaggressiveperiodontitissufferers.[9][10] Animpairedabilityofperipheralbloodlymphocytestoreacttochemotacticstimuliisfoundinthemajorityofpatientssufferingfromaggressiveperiodontitis.AswellasAggregatibacteractinomycetemcomitansbeingassociatedwiththis,thesynergismofthediseasealsoaccountsforbothCapnocytophagasppandPorphyromonasgingivalis.[5] Pathophysiology[edit] Aggressiveperiodontitisisamultifactorialdiseasewithmanycomplexinteractionsincludinghostfactors,microbiologyandgenetics. Hostdefencesinvolvemultiplefactors;saliva,epithelium,inflammatoryresponse,immuneresponseandchemicalmediators.TheinflammatoryexudateinthegingivaltissuesandgingivalcrevicularfluidismostlypolymorphneutrophilsbutalsoincludesBcellsandplasmacells.Theneutrophilsmayshowanintrinsicfunctionaldefectandrespondabnormallywhenchallengedbycertainpathogens.[11]Theplasmacellsproducespecificantibodiesinresponsetotheperiodontalpathogens,whichdiffuseintothegingivalcrevicularfluid.TheyproducemainlyIgG,withsomeIgA.[11]Ithasbeensuggestedthatthesegingivalcrevicularfluidantibodylevelscouldbepotentiallyusefulinthedevelopmentofavaccine.[12]PatientswithlocalisedaggressiveperiodontitishavelargeamountofAggregatibacteractinomycetemcomitansspecificIgG2.Thisissuggestedtobeprotectiveagainstwiderspreadperiodontalbreakdown.However,patientswithgeneralizedaggressiveperiodontitishavedecreasedabilitytomounthightitresofIgGtoPorphyromonasgingivalisandAggregatibacteractinomycetemcomitans. IthasalsobeenfoundthatalowT-helpertoT-suppressorratioisfoundinaggressiveperiodontitiswhichmayalterlocalimmuneregulation.Monocytesrespondtobacterialandinflammatorystimuliwithveryhighlevelsoflocalreleaseinflammatorymediatorsandinducehyper-inflammatoryreactionwithactivationoftissuedegradingmatrix-metalloproteinases.TheseisalsoevidencetheyproduceincreasedamountsIL-1αandIL-1βwhichcauseosteoclasticboneresorption.Theseamountsaregreatlyreducedfollowingtreatment.[11] Studiesoffamilies,twinsandsiblingpairshaveprovidedstrongevidenceforageneticbasisforaggressiveperiodontitis.[13]Aperson'sgeneticpredispositiontotheconditionisdeterminedbyasinglegeneofmajoreffect,inheritedasanautosomaldominanttrait.However,forthediseaseprocesstoinitiatethepersonmustbeexposedtothepresenceofperiodontalpathogensandpotentiallyalsovariousenvironmentalfactors. Smokingisageneralizedriskfactorforgeneralizedformsofaggressiveperiodontitis.Studiesfoundthatsmokershavemoreaffectedteeththannon-smokersandhighlevelsofattachmentloss.ThisisduetothesuppressionofserumIgG2andantibodyagainstAggregatibacteractinomycetemcomitansfoundinsmokers.[14] Features[edit] Accordingtothe1999InternationalWorkshopfortheClassificationofPeriodontalDiseases,aggressiveperiodontitiswasdefinedaccordingto3primaryfeatures,incontrasttochronicperiodontitis.[15]Thesefeaturesarecommonforbothlocalizedandgeneralizedformofdisease.[16][17] Primaryfeatures[edit] Patientsareclinicallyhealthy.[16] Patientsdonothaveanyunderlyingsystemicdiseasethatwouldcontributetoaggressiveperiodontitis.[18]Forinstance,diabetesisprovedtobeassociatedwithperiodontitis-itisamajorriskfactorwhenglycaemiccontrolispoor.[19] Therateoflossofattachmentandbonelossisrapid.[16] Lossofattachmentreferstothedestructionofperiodontiumwhereasthebonereferstothealveolarbonesupportingtheteeth.[20]Thelosscanbedeterminedbyusingacalibratedperiodontalprobeandtakingradiographsofthedentition.[21]Usuallythelossofattachmentisgreaterthan2mmperyear. Aggressiveperiodontitisrunsinthepatient'sfamily.[16] Familialaggregationofaggressiveperiodontitisisoftendiscoveredbytakingathoroughmedicalhistoryofthepatient.[22]Thepatientissaidtohaveahighgeneticsusceptibilitytoaggressiveperiodontitis.Manystudieshaveshownthatgeneticfactorscontributetothepathogenesisofthisdisease.[23]Inthiscase,themanifestationofaggressiveperiodontitisisbelievedtobetheresultofgeneticmutation,combinedwithenvironmentalfactors.[23] Secondaryfeatures[edit] Secondaryfeaturesarecharacteristicswhicharefrequentlyseenbutnotalwayspresentineverypatientdiagnosedwithaggressiveperiodontitis. Theseverityofperiodontaltissuedestructionisoutofproportiontoamountofbacteriapresent.[16] Theamountofbacteriaisoftenindicatedbythelevelofdentalplaque.[24]Thisfeatureimpliesthatwhenaggressiveperiodontitisispresent,lossofattachmentandbonelosstendtooccureveniftheplaquelevelislow. HighlevelsofAggregatibacter(orActinobacillus)actinomycetemcomitansand,insomepopulations,Porphyromonasgingivalis.[16] Thesegram-negativemicrobesareconsideredthechiefaetiologicalagentofaggressiveperiodontitis.Theyareimplicatedinthedevelopmentofaggressiveperiodontitisbytriggeringinflammatoryresponseinperiodontaltissue. Thereareabnormalitiesassociatedwithphagocytes.[16] Phagocytesareessentialinresolvinginflammation.Theimpairmentoftheirphagocyticactivityresultsinpersistentinflammationinperiodontaltissues.[25] Hyper-responsivemacrophagephenotype.[16] Duetotheincreasedresponsiveness,themacrophagesproduceexcessivelevelsofinflammatorymediatorandcytokine,suchasprostaglandinE2(PGE2)andinterleukin-1β(IL-1B).[16]Theirhyperactivityisassociatedwithperiodontaltissuedestructionandboneloss.[26] Progressionofattachmentlossandbonelossmaybeself-arresting.[16] Insomepatients,thediseasemayburnoutwithoutanycause-relatedtherapy.[27] Carieslevelshaveseentobelowerincasesofaggressiveperiodontitis[28][29] Staging CasesofaggressiveperiodontitishavebeenstagedintoStageI,IIandIIIbasedontheseverityofthecases.Thestagingindexwasproposedbasedonclinicalfeatures,radiologicalfeaturesandpossibleriskfactors.[22]Theproposedindexwasvalidatedwith10casesofaggressiveperiodontitisfollowedfor10years. Clinicalandradiographicfeatures[edit] Localizedaggressiveperiodontitis[edit] Clinicalfeatures[edit] LAPbeginsaroundtheageofpubertywherethereisinterproximallossofattachmentofthefirstmolar,andorincisors.[2]onatleasttwopermanentteeth(onewhichisafirstmolar)andnoinvolvementofmorethantwoteethotherthanthefirstmolarsandincisors,[2][30]lackofinflammationandevidenceofdeepperiodontalpocketwithadvancedboneloss.[2]Thereisalsoarelativelyfastprogressionofperiodontaltissueloss.[30] Withanincreaseintheageofthepatient,theremaybeprogressionofthediseaseinvolvingtheadjacentteethandleadtothepatientdevelopingGAP.[31][32]Theperiodontaltissuealsoexhibitsminimalsignsofinflammationclinically[33]andshowarobustresponsewithserumantibodiestopathogens.[30] Theamountofplaquepresentisinconsistentwiththeamountandseverityoftissuedestruction[2][30]butwithahighplaquepathogenicityduetothepresenceofincreasedlevelsofbacterialikeAggregatibacteractinomycetemcomitans(A.a)andPorphyromonasGingivalis(P.g).[2] SecondaryfeaturesofLAPmayalsobepresentincluding;[2] diastemaformationwithdisto-labialmigrationoftheincisors increasedmobilityoftheaffectedteeth,sensitivityduetoexposedroot, deepdullpainthatradiatestothejaw periodontalabscesswithlymphnodeenlargement Radiographicfeatures[edit] Radiographically,theperiodontallesionoftenpresentswithalveolarbonelossinahorizontalpatternattheinterproximalsurfaceofthepermanentfirstmolars[2][30][31]andusuallyhorizontalbonepatternofbonelossattheinterproximalsurfaceoftheincisorsastheboneisthinnerthanattheinterproximalsurfaceofthemolars.[30] Thealveolarbonelosspatternsareusuallybilateralandsimilaronbothsidesandhasbeenreferredtoasbeinga‘mirror-image’pattern.[31][30] Inadvancedcasesthealveolarbonelossmaybedepictedasahorizontalbonelosspatternradiographically.[30][31] Generalizedaggressiveperiodontitis[edit] Clinicalfeatures[edit] Mostlyinindividualsunder30yearsold[34] InGAP,theclinicalappearanceofthediseaseresembleschronicperiodontitis.ThedifferenceisthatindividualsaffectedbyGAParemuchyoungerandtheprogressionofdiseaseappearsmorerapid.[33] Thereisapoorserumresponseagainstinfectingagents[34]: Destructionispresentthatisnotinbalancewiththeamountoflocalirritantspresent[33] Generalizedinter-proximalattachmentlosson3ormorepermanentteeth,excludingthefirstmolarsorincisors[34]: ThemaindistinctionbetweenthelocalizedandgeneralizedformofAgPliesinthenumberofteethaffected.GAPbringsaboutattachmentlossinvolvingmorethan30%ofsitesonteeth;[1]effectivelybeingatleastthreepermanentteethotherthanthefirstmolarsorincisors.[17] Episodicnatureofattachmentloss:TwomaintissueresponseshavebeenfoundinGAPcases:[34] Tissuemayhavesevereacuteinflammationandoftenpresentswithanangryredappearanceandulceration.[35]Theremaybespontaneousbleedingorsuppuration.Thisresponseisknowntobepresentinthedestructivephase,wherethereispresenceofboneandattachmentloss. Theotherresponseisknownasaperiodofquiescence,wheregingivaltissuemayappearwithnoinflammation,pinkappearancewithsomepossiblestippling.Inadditiontothismildappearancetheremaybedeeppocketsuponprobing. Radiographicfeatures[edit] ThekeydiagnosticfeatureofAgPisverticalbonelossaroundteethincludingthefirstmolarsandincisors.Thistendstobeginaroundpubertyinotherwisehealthyindividuals.[34]Theremaybeanappearanceof“arc-shapedlossofalveolarboneextendingfromthedistalsurfaceofthesecondpremolartothemesialsurfaceofthesecondmolar”.[36] InGAP,generalizedbonedestructionispresentthatrangesfrommildcrestalboneresorptiontoseverealveolarbonedestruction,dependingontheseverityofthedisease.[36]Theremaybeacombinationofverticalandhorizontalbonelossdefects.[36] Screening[edit] Earlydiagnosisofaggressiveperiodontitisisimportantasitcancauserapidpermanentdestructionoftheperiodontaltissues.Itisessentialthatallpatientsundergoaroutineperiodontalexaminationtoscreenforanyformofperiodontaldiseaseduringadentalcheckup. Clinicalexamination[edit] Atthestartoftheclinicalexaminationofthegingivalandperiodontaltissues,thedentalpractitionerwouldlookattheappearanceofthegingivafirst.AhealthyperiodontiuminaCaucasianwouldappearstippledandpinkwithaknifeedgemarginwhereitabutsthetooth(pigmentationmaydifferinotherraces).[37]Afterthat,gingivalprobingdepthswouldbechecked.Thiswouldnormallybecarriedoutusingabasicperiodontalprobe(WHOCPI).[38]Onprobing,patientswithAgPshouldhaveevidenceofsignificantperiodontalpocketdepthsandlossofattachment(LOA).Dentalpractitionersshouldalsobeawareoffalsepocketingarounderupting/newlyeruptedteethinthemixeddentitionphaseandalsointhepresenceofgingivalinflammation.[38][39]Thepresenceofbleedingonprobing(BOP)shouldbenotedwhichisanindicatorofactivedisease. Radiographs[edit] RadiographicassessmentshouldbecarriedoutforpatientswithevidenceofperiodontitistoobservealveolarbonelevelswhichcanhelptoidentifysignsofAgP.[38]Inhealthyperiodontaltissues,thedistancefromtheamelocementaljunction(ACJ)tothealveolarbonecrestistypicallyintheorderof1mminyoungpeople.[40]IfthedistancebetweentheACJandalveolarbonecrestismorethan2-3mmthenthereisapossiblesuggestionofAgP.Inadditiontothat,presenceofangularorverticalboneloss(especiallyat6's)andarrowheadorfurcationlesionsarealsoastrongsuggestionofAgP. Strongfamilyassociation[edit] Itisalsoimportantforadentalpractitionertocheckforfamilyhistoryofperiodontaldiseaseforeachpatient.ThisisbecauseAgPmayhaveanautosomaldominantinheritancepatternwhichsuggeststhatupto50%ofsiblingscouldbeaffectedifoneparenthasthedisease.[41]CarefulinterpretationofthehistoryisrequiredbutitmayprovidevitalevidenceindiagnosingAgP.IfacaseofAgpisdiagnosed,itisimportanttoscreenthepatient'sfamilymembersaswellforAgP.[42][43]EarlydetectionofAgPallowsinterventiontobecarriedoutbeforeextensiveperiodontaldestructionhastakenplacewhichfurthersimplifiestreatment. Treatment[edit] FollowingtheinitialassessmentanddiagnosisofAgP,atreatmentplanisusuallydevelopedforeachindividualundergoingtherapy.AstheoveralltreatmentconceptsandgoalsforAgParenotsignificantlydifferentfromthatofchronicperiodontitis,thedifferenttreatmentphases(causerelatedtherapy;re-examinationforresponsetotherapy;definitivetherapy;andmaintenance)aresimilarforbothtypesofperiodontitis. Nevertheless,theconsiderableamountofbonelossrelativetotheyoungageoftheindividualinAgPnecessitatesanoftenmoreaggressivetreatmentapproach,tohaltfurtherperiodontaldestructionandregainasmuchperiodontalattachmentaspossible.Theobjectiveoftreatmentistocreateaconduciveclinicalconditionforretainingasmanyteeth,foraslongaspossible.[44] CauseRelatedTherapy[edit] Thisstageinvolvesdiscussionofthediseasewiththepatient. OralHygieneInstructions:Theclinicianshouldadvisethepatientofhisintrinsicsusceptibilitytoplaque,whichhisbodyinducesastrong,pro-inflammatoryresponseto.[45]Itisthusessentialtokeephisoralhygieneimmaculate.Thisinvolvegoingoverbothsmoothsurfaces(toothbrushinginstructions)andtheuseofinterproximalaids(e.g.floss). Smokingcessation(ifapplicable):SmokingisasignificantriskfactorforAgP,withpatientswhosmokehavingmoreaffectedteethwithlossofclinicalattachmentandmorebonelossthannon-smokingpatientswithAgP.[46]Non-smokersalsotendtohaveabetterresponsetoperiodontaltherapyascomparedtosmokers.Assuch,individualsmustbeadvisedofthebenefitsofsmokingcessationandtheotherwisepotentialrisksofaworseningperiodontalcondition.[36] Removalofplaqueretentivefactors:Localplaqueretentivefactorssuchasmal-positionedteeth,overhangingrestorations,crownandbridgework,partialdenturesandfixed/removableorthodonticappliancescanincreasetheriskofperiodontaldiseaseandpreventsuccessfultreatmentandresolutionofassociatedpockets.Priortostartingperiodontaltreatment,anyoverhangingorpoorlycontouredrestorationsshouldbemodifiedorreplaced.Instructionsshouldalsobegivenonhowtocleanadequatelyaroundfixedrestorationsandappliances,andhowtocleanremovableprostheses.Theseintra-oralappliancesshouldalsobewell-designedandfitting.[47] Theperiodontaltherapycarriedoutatthisstageisofanon-surgicalapproach,whichisaimedattheremovalofsupra-andsub-gingivalplaqueandcalculusdeposits,todecreasethemicrobialload,bacteriabiofilm,andcalculusfromtheperiodontallyinvolvedsites.[48] ScaleandPolish RootSurfaceDebridement(RSD) Antibiotics:Thereisevidencethattheadditionaluseofsystemicantibioticsinconjunctionwithnon-surgicalperiodontaltreatmentresultsinamorefavourableclinicalresponse,ascomparedtojustperiodontaltreatmentalone,asithelpstosuppresspathogenicbacteriaandcreateahealth-associatedbiofilm.[49]TherehavebeenmanyantibioticregimesproposedforthetreatmentofAgP.However,thecombinationofchoiceaccordingtocurrentresearchisacombinationofamoxicillin(500 mg,thrice/day)andmetronidazole(200 mg,thrice/day),for7days,startingonthedayofthefinaldebridement.Doxycycline(100 mg,once/day,withastartingfirstdoseof200 mg)isthechoiceofantibioticsforpatientsallergictopenicillin.[50] LightAmplificationbyStimulatedEmissionofRadiation(LASER)Therapy PhotodynamicTherapy(PDT):Thispotentiallyhasalltheadvantagesoflow-levelLASERtherapy,whichallowsthedisinfectionofperiodontalpocketandtheeradicationofbacteriainareasofdifficultaccess,withoutthethermaldamagetotissuesassociatedwiththehigh-poweredLASER.AsignificantreductionintheaggregatibacteractinomycetemcomitanscountfollowingPDTsuggeststhattheuseofPDTinconjunctionwithconventionalnon-surgicalperiodontaltreatmentcanpotentiallyresultinamoreeffectivetreatment.[51]Consideringtheglobalissueofantibioticresistance,furtherdevelopmentandresearchinPDTsuccessesmayprovetopresentitanidealadjuncttoconventionalnon-surgicalperiodontaltherapy,ascomparedtotheuseofsystemicantibiotics. Re-examination/ResponsetoTherapy[edit] Thisstageoftreatmentinvolvesthereassessmentoftheindividual'scompliance(i.e.leveloforalhygiene)andthetissueresponsetothetreatment.Thisiscarriedout10–12weeksfollowingRSD.Ifthediseaseisstabilised,thetreatmentprogressesontothemaintenancestage.Inthecasewherethediseaseisnotstabilised,thecauseoffailureshouldbeconsidered,andthetreatmentprogressesontothestageofdefinitivetherapy,ifthecauseiscorrectable. DefinitiveTherapy[edit] FurtherRSDatsiteswhichrequiretreatment UseofLocallyDeliveredAntimicrobials(LDA)asanadjuncttonon-surgicalperiodontaltreatment:Foruseindeeppocketswhichfailtorespondtorepeatednon-surgicaltreatmentinpatientswithadequateoralhygiene.Currently,theavailableLDAincludetetracycline,minocycline,chlorhexidinegluconateanddoxycycline,withthemodeofdeliverybeingintheformoffibers,chips,polymersandtrays.[52]TherehasyettobemuchresearchintotheeffectsofLDAinAgP,butcurrentstudiesreportaninsignificantdifferencetotheadjunctiveeffectofsystemicantibiotics.[44] Periodontalsurgery:Ifitisalocalisedproblemandifthecaseisnon-responsetonon-surgicaltreatmentdespitetheoralhygienebeingconsistentlyexcellent.Thiscouldinvolveanopenflapdebridementwithorwithoutregenerativeprocedures,withtheaimofgainingaccessandvisibilitytorootandfurcationareassothatathoroughinstrumentationanddebridementcanbecarriedout. Regenerativesurgicaltherapycurrentlyavailableincludetheuseofbonereplacementgrafts,barriermembranesorguidedtissueregeneration(GTR),biologicmodifierslikegrowthanddifferentiationfactors(GDF),andextracellularmatrixproteinslikeenamelmatrixproteins(EMD).[36][53]Thereishowever,agreatvariationinperiodontalgainsreportedintheliteratureavailable,signifyingthatresultsarenotentirelypredictable.[54] Maintenance[edit] Periodontaltreatmentmayhelptostabilisethedisease,butitdoesnotchangeone'ssusceptibilitytothedisease.GiventhehighsusceptibilityfordiseaseprogressionoftheindividualwithAgP,thereisahigherriskofdiseaserecurrence.[55]Itisthusnecessarytoattendfrequentreviewappointmentsatthedentisttoensurethereisnorelapseofthedisease,andthattheperiodontalhealthismaintainedafteractiveperiodontaltherapy.[44] References[edit] ^abArmitageGC(December1999)."Developmentofaclassificationsystemforperiodontaldiseasesandconditions".AnnalsofPeriodontology.4(1):1–6.doi:10.1902/annals.1999.4.1.1.PMID 10863370. 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vteDentistryinvolvingsupportingstructuresofteeth(Periodontology)Anatomy Periodontium Alveolarbone Biologicwidth Bundlebone Cementum Freegingivalmargin Gingiva Gingivalfibers Gingivalsulcus Junctionalepithelium Mucogingivaljunction Periodontalligament Sulcularepithelium Stippling DiseaseDiagnoses Chronicperiodontitis Localizedaggressiveperiodontitis Generalizedaggressiveperiodontitis Periodontitisasamanifestationofsystemicdisease Periodontosis Necrotizingperiodontaldiseases Abscessesoftheperiodontium Combinedperiodontic-endodonticlesions Infection A.actinomycetemcomitans Capnocytophagasp. F.nucleatum P.gingivalis P.intermedia T.forsythia T.denticola Redcomplex Entamoebagingivalis(amoebic) Trichomonastenax Other Calculus Clinicalattachmentloss Edentulism Fremitus Furcationdefect Gingivalenlargement Gingivalpocket Gingivalrecession Gingivitis Horizontalbonydefect Lineargingivalerythema Occlusaltrauma Periodontalpocket Periodontaldisease Periodontitis Plaque Verticalbonydefect Treatmentandprevention Periodontalexamination Ante'slaw Brushing Bleedingonprobing Chlorhexidinegluconate Flossing Hydrogenperoxide Mouthwash Oralhygiene Tetracycline Triclosan Hostmodulatorytherapy TreatmentConventionaltherapy Debridement Scalingandrootplaning Fullmouthdisinfection Fullmouthultrasonicdebridement Surgery Apicallypositionedflap Bonegraft Coronallypositionedflap Crownlengthening Freegingivalgraft Gingivalgrafting Gingivectomy Guidedboneregeneration Guidedtissueregeneration Enamelmatrixderivative Implantplacement Lateralpediclegraft Openflapdebridement Pocketreductionsurgery Socketpreservation Sinuslift Subepithelialconnectivetissuegraft Tools Curette Membrane Probe Scaler Importantpersonalities TomasAlbrektsson FrankBeube Per-IngvarBrånemark RobertGottsegen GaryGreenstein JanLindhe BrianMealey PrestonD.Miller WilloughbyD.Miller CarlE.Misch JohnMankeyRiggs JaySeibert JørgenSlots PaulRoscoeStillman DennisP.Tarnow Hom-LayWang JamesLeonWilliams W.J.Younger Otherspecialties Endodontology Orthodontology Prosthodontology vteDentistrySpecialties Endodontics Oralandmaxillofacialpathology Oralandmaxillofacialradiology Oralandmaxillofacialsurgery Orthodonticsanddentofacialorthopedics Pediatricdentistry Periodontics Prosthodontics Dentalpublichealth Cosmeticdentistry Dentalimplantology Geriatricdentistry Restorativedentistry Forensicodontology Dentaltraumatology Holisticdentistry Dentalsurgery Dentalextraction Toothfilling Rootcanaltherapy Rootendsurgery Scalingandrootplaning Teethcleaning Dentalbonding Toothpolishing Toothbleaching Socketpreservation Dentalimplant Organisations AmericanAssociationofOrthodontists BritishDentalAssociation BritishDentalHealthFoundation BritishOrthodonticSociety CanadianAssociationofOrthodontists DentalTechnologistsAssociation GeneralDentalCouncil IndianDentalAssociation NationalHealthService Seealso Indexoforalhealthanddentalarticles Outlineofdentistryandoralhealth Dentalfear Dentalinstruments Dentalmaterial Historyofdentaltreatments Infantoralmutilation Mouthassessment Oralhygiene Retrievedfrom"https://en.wikipedia.org/w/index.php?title=Aggressive_periodontitis&oldid=1070783209" Categories:PeriodontaldisordersHiddencategories:CS1errors:genericnameCS1Japanese-languagesources(ja)CS1:longvolumevalue Navigationmenu Personaltools NotloggedinTalkContributionsCreateaccountLogin Namespaces ArticleTalk English expanded collapsed Views ReadEditViewhistory More expanded collapsed Search Navigation MainpageContentsCurrenteventsRandomarticleAboutWikipediaContactusDonate Contribute HelpLearntoeditCommunityportalRecentchangesUploadfile Tools WhatlinkshereRelatedchangesUploadfileSpecialpagesPermanentlinkPageinformationCitethispageWikidataitem Print/export DownloadasPDFPrintableversion Languages العربية Editlinks