英语文献学习.pptx

Currentconceptsonosteonecrosisofthefemoralhead,Itisestimatedthat20000to30000newpatientsarediagnosedwithosteonecrosis（股骨头坏死）annuallyaccountingforapproximately10%ofthe250000totalhiparthroplasties(THA)doneannuallyintheUnitedStates.Thelackoflevel1evidenceintheliteraturemakesitdifficulttoidentifyoptimaltreatmentprotocols（协议）tomanagepatientswithpre-collapseavascularnecrosisofthefemoralhead,andearlyinterventionpriortocollapseiscriticaltosuccessfuloutcomesinjointpreservingprocedures.Therehavebeenavarietyoftraumaticandatraumaticfactorsthathavebeenidentifiedasriskfactorsforosteonecrosis,buttheetiologyandpathogenesisstillremainsunclear.,Abstract,（whichare）,Generally,thefirstradiographicchangesseenbyradiographwillbecysticandscleroticchangesinthefemoralhead.Althoughthediagnosismaybemadebyradiograph,plainradiographsaregenerallyinsufficientforearlydiagnosis,thereforeMRIisconsideredthemostaccuratebenchmark（标准）.Treatmentoptionsincludepharmacologicagents（药剂）suchasbisphosphonates（磷酸盐）andstatins,biophysicaltreatments,aswellasjoint-preservingandjoint-replacing.Ingeneral,FHSP(femoralheadsparingprocedures)areindicatedatpre-collapsestageswithminimalsymptomswhereasFHRP(femoralheadreplacementprocedures)arepreferredatpost-collapsesymptomaticstages.,Currentosteonecrosisdiagnosisisdependentuponplainanteroposteriorandfrog-leglateralradiographsofthehip,followedbymagneticresonanceimaging(MRI).Itisdifficulttoknowwhetheranytreatmentmodalitychangesthenaturalhistoryofcoredecompressionsincethetruenaturalhistoryofcoredecompressionhasnotbeendelineated,Introduction,Osteonecrosis(ON)ofthefemoralhead(ONFH)isthefinalcommonpathwayofaseriesofderangements（混乱）thatresultinadecreaseinbloodflowtothefemoralhead(FH)leadingtocellulardeath,fracture,andcollapseofthearticularsurface.Ittypicallyaffectsrelativelyyoung,activepeoplebetween20and40yearsandregularlyfollowsanunrelenting（不松懈的、无情的）courseresultinginsubstantiallossoffunction.,ETIOLOGYANDPATHOGENESIS,TherehavebeenavarietyoftraumaticandatraumaticfactorsthathavebeenidentifiedasriskfactorsforON,buttheetiologyandpathogenesisstillremainsunclear.TheestimatedfrequencyofthemostfrequentriskfactorsforONFHintheUnitedStatesis:alcohol(20%-40%),corticosteroidtherapy(35%-40%),andidiopathic（特发性的）(20%-40%).,Moststudieshaveattributedthediseaseprocesstothecombinedeffectsofgeneticpredisposition（遗传易感性）,metabolicfactors（代谢因素）,andlocalfactorsaffectingbloodsupplysuchasvasculardamage,increasedintraosseouspressure,andmechanicalstress.Thisresultsinboneischemiaandinfarctionleadingtobonedeath.Theprecipitatingmechanismwhichleadstothispathwayisvariablethough.Ischemiacanresultfromexternalorinternalvascularinsult（血管损伤）typicallycausedbydirecttrauma,vascularocclusion（闭塞）,directcellulartoxicity,oralteredmesenchymalstemcelldifferentiation.,Severalmechanismsleadingtovascularocclusionhavebeenproposedaspossibleunderlyingcausesofnecrosis.Highdosesofglucocorticoidsprevalentinsystemicdiseasessuchassystemiclupuserythematosusaswellasexcessivealcoholintakehavebeenassociatedwithalterationsincirculatinglipidswithresultantmicroemboliinthearteriessupplyingthebone.Inadditionincreasedriskoffatemboli（脂肪栓赛）hasalsobeenattributedtotheincreaseinbonemarrowfatcellsizewhichblocksvenousflow.Therefore,fatemboli,adipocytehypertrophy（脂肪细胞肥大）,andvenousstasishaveallbeenimplicatedasetiologic（病因学的）factorsinthisdiseaseprocess.,Vascularocclusioncanalsoresultfromdiseaseprocessesthatincreaseintravascularcoagulation（血管内凝血）andthrombusformation（血栓形成）.Antiphospholipidantibodies（抗心磷脂抗体）,inheritedthrombophilia,andhypofibrinolysis（低纤维蛋白溶解）haveallbeenassociatedwithalteredmechanismsinboththecoagulationandfibrinolyticpathways.Traumaduetofractureordislocationcanleadtodamagetotheextraosseous（骨外的）bloodsupply.,Thisisespeciallyspecifictofracturesinthesubcapitalregionofthefemoralneck.Traumaatthislocationinterruptstheanastomosisbetweenthelateralepiphysealvessels（骺外侧动脉）,whicharebranchesfromthemedialfemoralcircumflexartery（旋股内侧动脉）supplying,andthearteryoftheligamentumteresleadingtocompromisedbloodflowtotheFH.,DIAGNOSISANDASSESSMENT,EarlydiagnosisiscrucialforoptimaltreatmentofON,astreatmentsuccessisrelatedtothestageatwhichthecareisinitiated.ClinicalpresentationofONtypicallyisasymptomaticinearlystages,althoughpatientsmaydevelopgroinpainthatcanradiatetothekneeoripsilateralbuttock.Onphysicalexamination,patientsusuallypresentwithalimitedrangeofmotionatthehipandcomplainofpainparticularlywithforcedinternalrotation（强制内旋）.,Ficatclassificationconsistsoffourstages,basedonstandardradiographs.Stageindicatesnormalimaging.StageindicatesnormalFHcontour（轮廓）,butwithevidenceofbone-remodeling,suchascysticorosteoscleroticregions.Stageindicatesevidenceofsubchondralcollapse,orflatteningoftheFH.Stageindicatesanarrowingofthejointspacewithsecondarydegenerativechanges（退行性改变）intheacetabulum,suchascysts,osteophytes（骨刺）,andcartilagedestruction.,Subtleosteoscleroticorcysticchangesinthesubchondralregions（软骨下区域）maybemissedbecausetheanteriorandposterioracetabularmarginsoverlapthesuperiorFH,thereforelateralfrog-legradiographsoftheFHarenecessary.Earlydelaminationofthecartilagefromtheunderlyingbonewillmostlikelybedemonstratedbythecrescentsign(Figures2and3)FlatteningoftheFHcanalsobeviewedbyradiograph,butmayonlybevisibleinoneview.,Figure3Bilateralosteonecrosisofthefemoralheadwithflatteningofthesurfaceandearlysingsofosteoarthritis.,Figure2LefthipanteriorposteriorandcrossleglateralX-raysshowing(arrows)thecrescentsing.,Althoughthediagnosismaybemadebyradiograph,plainradiographsaregenerallyinsufficientforearlydiagnosis;thereforeMRIisconsideredthemostaccuratebenchmark.Asingle-densitylineonT1-weightedimagesandahighsignalintensitylineonT2-weightedimagesrepresenttheearlynecrotic-viableboneinterfaceandthehypervascular（富血管性）granulationtissue（肉芽组织）characterizingON.However,recentlysubchondralin