股骨頭壞死

股骨頭壞死是引起髖關節(jié)疼痛，活動受限的常見原因，很多是因為激素、酗酒、外傷等原因造成的。股骨頭壞死早期很多人癥狀不明顯，有時候感覺坐著起來的幾步疼，然后接著走就不疼了。很多時候是休息的時候不疼，變換姿勢起身走路就有點疼，有時候還疼得有點明顯，但是再走就又不疼了。那么這樣是不是就可以多走？盡量站著，不坐下變換體位不就不疼了嗎？這樣理解是不對的！股骨頭壞死以后股骨頭因為有壞死，股骨頭強度就會有下降。尤其是負重區(qū)的壞死，在負重情況下會引起股骨頭局部壓力增加，會加速股骨頭壞死的進展。負重不是說自己扛什么重東西，站立時候的體重壓在股骨頭上就是在增加股骨頭的負重了。所以這樣就可以理解，為什么股骨頭壞死早期，即使不疼或者疼痛不嚴重，醫(yī)生也是建議一定要扶拐保護。扶拐保護的目的就是盡量減輕體重對股骨頭的壓力，避免壞死的股骨頭由于局部壓力的增加，使得早期壞死治療的效果大打折扣。所以股骨頭壞死早期一定要重視，好好扶拐保護，減輕股骨頭負重，保護好自己的股骨頭

激素使用對股骨頭骨壞死發(fā)生和進展的影響:一項全國性巢式病例對照研究（2024）EffectofCorticosteroidUseontheOccurrenceandProgressionofOsteonecrosisoftheFemoralHead:ANationwideNestedCase-ControlStudy?KwonHM,HanM,LeeTS,JungI,SongJJ,YangHM,LeeJ,LeeSH,LeeYH,ParkKK.EffectofCorticosteroidUseontheOccurrenceandProgressionofOsteonecrosisoftheFemoralHead:ANationwideNestedCase-ControlStudy[J].JArthroplasty,2024轉載文章的原鏈接1：https://pubmed.ncbi.nlm.nih.gov/38830431/轉載文章的原鏈接2：https://www-clinicalkey-com-443.vpnm.ccmu.edu.cn/#!/content/journal/1-s2.0-S0883540324004595?AbstractBackgroundAlthoughitisverywellknownthatcorticosteroidscauseosteonecrosisofthefemoralhead(ONFH),itisunclearastowhichpatientsdevelopONFH.Additionally,therearenostudiesontheassociationbetweencorticosteroiduseandfemoralheadcollapseinONFHpatients.WeaimedtoinvestigatetheassociationbetweencorticosteroiduseandtheriskofONFHamongthegeneralpopulationandwhatfactorsaffectONFHoccurrence.Additionally,weaimedtodemonstratewhichfactorsaffectfemoralheadcollapseandtotalhiparthroplasty(THA)afterONFHoccurrence.雖然眾所周知，皮質類固醇會導致股骨頭骨壞死(ONFH)，但目前尚不清楚哪些患者會發(fā)生ONFH。此外，沒有關于皮質類固醇使用與ONFH患者股骨頭塌陷之間關系的研究。我們的目的是調查普通人群中皮質類固醇使用與ONFH風險之間的關系，以及影響ONFH發(fā)生的因素。此外，我們旨在證明哪些因素影響ONFH發(fā)生后股骨頭塌陷和全髖關節(jié)置換術(THA)。?MethodsAnationwide,nestedcase-controlstudywasconductedwithdatafromtheNationalHealthInsuranceServicePhysicalHealthExaminationCohort(2002to2019)intheRepublicofKorea.WedefinedONFH(N=3,500)usingdiagnosisandtreatmentcodes.PatientswhohadONFHwerematched1:5toformacontrolgroupbasedonthevariablesofbirthyear,sex,andfollow-upduration.Additionally,inpatientswhohaveONFH,welookedforriskfactorsforprogressiontoTHA.使用韓國國民健康保險服務機構身體健康檢查隊列(2002年至2019年)的數(shù)據(jù)進行了一項全國性的巢式病例對照研究。我們使用診斷和治療代碼定義ONFH(N=3,500)。根據(jù)出生年份、性別、隨訪時間等變量對ONFH患者進行1:5匹配，形成對照組。此外，在患有ONFH的患者中，我們尋找進展為THA的危險因素。?ResultsComparedwiththecontrolgroup,ONFHpatientshadalowhouseholdincomeandhadmorediabetes,hypertension,dyslipidemia,andheavyalcoholuse(drinkingmorethan3to7drinksperweek).Systemiccorticosteroiduse(≥1,800mg)wassignificantlyassociatedwithanincreasedriskofONFHincidence.However,lipidprofiles,corticosteroidprescription,andcumulativedosesofcorticosteroiddidnotaffecttheprogressiontoTHA.與對照組相比，ONFH患者家庭收入較低，糖尿病、高血壓、血脂異常和重度飲酒(每周飲酒超過3至7天)的發(fā)生率更高。全身使用皮質類固醇(≥1800mg)與ONFH發(fā)生率增加顯著相關。然而，脂質譜、皮質類固醇處方和皮質類固醇累積劑量對進展到THA沒有影響。?ConclusionsTheONFHriskincreasedrapidlywhencumulativeprednisoloneusewas≥1,800mg.However,oralorhigh-doseintravenouscorticosteroiduseandcumulativedosedidnotaffecttheprognosisofONFH.SincetheoccurrenceandprognosisofONFHarecomplexandmultifactorialprocesses,furtherstudyisneeded.當累積使用潑尼松龍≥1800mg時，ONFH風險迅速增加。然而，口服或大劑量靜脈注射皮質類固醇和累積劑量不影響股骨頭壞死的預后。由于股骨頭壞死的發(fā)生和預后是一個復雜的多因素過程，需要進一步研究。?Osteonecrosisofthefemoralhead(ONFH)maycauseseverehippain,andcanultimatelyleadtocollapseofthefemoralheadandsubsequentrapiddestructionofthehipjointinrelativelyyoungpatients[1-3].Intractablepaincausedbyfemoralheadcollapseeventuallyleadstototalhiparthroplasty(THA)atayoungage[4,5].Althoughtrauma,theuseofcorticosteroid,andexcessivealcoholintakearewell-knownriskfactorsforONFH,theetiologyofONFHremainsmultifactorial,andnoconsensusexistsonthecommonpathophysiology[6-9].Impairedperfusionofbloodtobone,abnormalcellularreparativeprocesses,andgeneticpointmutationsarepresumedtoaffectONFHoccurrence,butithasnotyetbeenclarified[10-12].股骨頭壞死(Osteonecrosisoffemoralhead,ONFH)可引起嚴重的髖關節(jié)疼痛，在相對年輕的患者中，最終可導致股骨頭塌陷并隨后迅速破壞髖關節(jié)[1-3]。股骨頭塌陷引起的頑固性疼痛最終導致在年輕時進行全髖關節(jié)置換術(THA)[4,5]。雖然創(chuàng)傷、皮質類固醇的使用和過量飲酒是眾所周知的ONFH的危險因素，但ONFH的病因仍然是多因素的，對共同的病理生理尚未達成共識[6-9]。據(jù)推測，骨血流灌注受損、細胞修復過程異常以及基因點突變可能影響ONFH的發(fā)生，但尚未明確[10-12]。AlthoughitisverywellknownthatcorticosteroidscauseONFH,itisunclearastowhichpatientsdevelopONFH.Thereareseveralstudiesreportingthathigh-dosecorticosteroiduseof2grams(g)ormorewithin3monthsisassociatedwithONFHdevelopment[8,13-15].However,thesewerestudieswitharelativelysmallnumberofpatients,andthereareheterogeneitiesinpatientdemographicsandepidemiologicvariabilities.OnceONFHoccurs,theprognosisisknowntobepoor,andtherearestudiesstatingthatfemoralheadcollapseprogressesfromabout24.6to42.8%withnaturalevolutionwithin2years[16,17].Inparticular,whenfemoralheadcollapseoccurs,manypatientsoftenreceiveTHAatayoungage,sopredictingtheprognosisforfemoralheadcollapseisasimportantaspredictingtheoccurrenceofONFH.SeveralstudieshavedemonstratedthatfemoralheadcollapseinONFHpatientsisassociatedwithsize,volume,locationofnecroticlesions,andanatomicalparameters[1,2,18,19].However,therearenostudiesontheassociationbetweencorticosteroiduseandfemoralheadcollapseinONFHpatients.雖然眾所周知，皮質類固醇會引起ONFH，但尚不清楚哪些患者會發(fā)生ONFH。有幾項研究報道，在3個月內使用2克或更多的高劑量皮質類固醇與ONFH的發(fā)生有關[8,13-15]。然而，這些研究的患者數(shù)量相對較少，并且在患者人口統(tǒng)計學和流行病學變異方面存在異質性。一旦發(fā)生ONFH，預后很差，有研究表明股骨頭塌陷在2年內自然演化，從24.6%發(fā)展到42.8%[16,17]。特別是股骨頭塌陷發(fā)生時，許多患者往往在年輕時接受THA，因此預測股骨頭塌陷的預后與預測ONFH的發(fā)生同樣重要。多項研究表明，ONFH患者股骨頭塌陷與壞死灶的大小、體積、位置和解剖學參數(shù)有關[1,2,18,19]。然而，目前還沒有關于ONFH患者使用皮質類固醇與股骨頭塌陷之間關系的研究。TheNationalHealthInsuranceService(NHIS)ofSouthKoreaisanationalinsurancecoverageservicethatcoversabout97%ofcitizensinSouthKorea,includingdemographicdataandaclaimdatabaseincludingdiagnosesandprescriptions[20].Additionally,theNHISoffershealthscreeningexaminationsforinsuredKoreansaged40yearsorolder,includingbasicbloodtests,smoking,drinking,andphysicalactivitiesusingself-reportedquestionnaires.BecausetheNationalHealthInsuranceService–NationalSampleCohort(NHIS-NSC)isahighlyrepresentativepopulation-basedcohortoftheentireKoreanpopulation,itcanbeusedasapopulation-based,nationwidestudyforepidemiologicresearchonvariousdiseases[20-22].韓國國民健康保險服務(NationalHealthInsuranceService,NHIS)是一項覆蓋韓國約97%公民的國民保險服務，包括人口統(tǒng)計數(shù)據(jù)和包括診斷和處方在內的索賠數(shù)據(jù)庫[20]。此外，國民健康保險制度還為40歲或40歲以上的參保韓國人提供健康檢查，包括基本的血液檢查、吸煙、飲酒和使用自我報告問卷的體育活動。由于國民健康保險服務-國民樣本隊列(NationalHealthInsuranceService-NationalSampleCohort,NHIS-NSC)是韓國人口中極具代表性的基于人群的隊列，因此可以作為一項基于人群的全國性研究，用于各種疾病的流行病學研究[20-22]。Therefore,inthepresentstudy,weaimedtoinvestigatetheassociationbetweencorticosteroiduseandtheriskofONFHdevelopmentamongthewholegeneralpopulationandwhatfactorsaffectONFHdevelopmentusinganationwidelargesamplefromlongitudinalnestedcase-controldatainalong-termcohortstudy.Inaddition,weaimedtodemonstratewhichfactorsaffectTHAafterthedevelopmentofONFH.因此，在本研究中，我們旨在通過一項長期隊列研究，在全國范圍內采用縱向嵌套病例對照數(shù)據(jù)的大樣本，調查皮質類固醇使用與整個普通人群中ONFH發(fā)生風險之間的關系，以及影響ONFH發(fā)生的因素。此外，我們旨在證明哪些因素會影響ONFH發(fā)展后的THA。?MaterialsandMethodsStudyPopulationWeuseda2002to2019datasetfromtheNHISPhysicalHealthExaminationCohort(NHIS-NSC)2.0databaseintheRepublicofKorea[23].TheNHIS-NSC2.0databasewascomprisedofatotalof1,137,861participantswhowerestratifiedandrandomlysampledsuchthattheage,sex,region,healthinsurancetype,andhouseholdincomesofthesamplesremainedproportionaltothoseofthe2006Koreanpopulationof50million.Weexcluded223,474participantswhowerealreadyprescribedintravenous(IV)ororalcorticosteroidstoreducethebiasintheanalysisoftheeffectoftheprescribedcorticosteroiddoseonONFH.Fromtheremainingcohort,weexcluded241participantswhowerealreadydiagnosedwithONFHin2002toobtainthenewdevelopmentofONFH(washoutperiod).Therefore,theindexdatewasthedatethatthepatientwasdiagnosedwithONFH.Weincluded914,146participantsinthefinalanalysis.Theinformationinthedatasetincludedallinpatientandoutpatientmedicalclaimsdata,includingprescriptiondruguse,diagnosticandtreatmentcodes,primaryandsecondarydiagnosticcodes,andhealthexaminationdata.AlltheindividualsincludedintheNHIS-NSCwerefolloweduntil2019,unlesstherewasadeathordisqualificationforNationalHealthInsurance,suchasemigration.TheprotocolofthisstudywasapprovedbytheInstitutionalReviewBoardofourinstitution(4-2022-0304)andtheNHIS(NHIS-2022-2-232).我們使用了2002年至2019年的數(shù)據(jù)集，這些數(shù)據(jù)集來自韓國NHIS身體健康檢查隊列(NHIS-nsc)2.0數(shù)據(jù)庫[23]。國民健康保險制度-國家安全保障制度2.0數(shù)據(jù)庫共包括1137861名參與者，這些參與者的年齡、性別、地區(qū)、健康保險類型和家庭收入與2006年韓國5000萬人口的比例保持一致，并進行了分層和隨機抽樣。我們排除了223,474名已經(jīng)靜脈注射或口服皮質類固醇的參與者，以減少處方皮質類固醇劑量對ONFH影響分析的偏倚。從剩余隊列中，我們排除了241名在2002年已經(jīng)診斷為ONFH的參與者，以獲得ONFH的新進展(洗脫期)。因此，索引日期為患者被診斷為ONFH的日期。我們在最終分析中納入了914146名參與者。數(shù)據(jù)集中的信息包括所有住院和門診醫(yī)療索賠數(shù)據(jù)，包括處方藥使用、診斷和治療代碼、初級和二級診斷代碼以及健康檢查數(shù)據(jù)。納入國家健康保險制度-國家安全保障制度的所有個人都被跟蹤到2019年，除非死亡或喪失參加國家健康保險的資格，例如移民。本研究的方案經(jīng)我院機構審查委員會(4-2022-0304)和NHIS(NHIS-2022-2-232)批準。?CaseandControlSelectionWeusedtheInternationalStatisticalClassificationofDiseasesandRelatedHealthProblems,10thRevision(ICD-10)toidentifycasepatients.WedefinedONFH(N=3,500)usingthediagnosticcodeandtreatmentcodeICD-10codesforosteonecrosisofthefemur(SupplementaryTable1).Toavoidlengthbias,anestedcase-controlanalysiswasdesignedtoinvestigatetheeffectoftheprescribedcorticosteroiddoseonONFH.PatientswhohadONFHwerematched1:5toformacontrolgroupbasedonthevariablesofbirthyear,sex,andfollow-upduration.Identicalexclusioncriteriawereappliedtothecontrolgroup(N=12).Finally,casepatients(N=3,488)andcontrolpatients(N=17,440)werematchedbasedonsexandageattheindexdateandcompared(Figure1).我們使用國際疾病和相關健康問題統(tǒng)計分類第十次修訂版(ICD-10)來確定病例患者。我們使用股骨骨壞死的診斷代碼和治療代碼ICD-10來定義ONFH(N=3,500)(補充表1)。為避免長度偏倚，設計了巢式病例對照分析，以調查處方皮質類固醇劑量對ONFH的影響。根據(jù)出生年份、性別、隨訪時間等變量對ONFH患者進行1:5匹配，形成對照組。對照組(N=12)采用相同的排除標準。最后，根據(jù)索引日期的性別和年齡對病例患者(N=3,488)和對照患者(N=17,440)進行匹配和比較(圖1)。??Fig.1Studyflow:selectionofparticipantsofcasesandmatchedcontrolsONFH,osteonecrosisoffemoralhead.??DefinitionofParametersFromthehealthexaminations,participantswereclassifiedinto4groupsbasedonthebodymassindex(BMI)accordingtotheWorldHealthOrganizationWesternPacificRegionguidelineandtheKoreanpracticalguidelineasfollows:low(<18.5),normal(18.5to23),overweight(23to25),andobese(>25).UnderlyingcomorbiditiesweredefinedbyatleastoneadmissionoroutpatienttreatmentupontheprimaryorfirstsecondarydiagnosisusingtheICD-10codeforthepastyear(hypertension:I10-I15,diabetesmellitus:E10-E14,dyslipidemia:E78).Thefrequencyofdrinkingalcoholwascategorizedas“non-alcoholuse”(drinkinglessthan1drinkperweek),“mildalcoholuse”(drinking1to2drinksperweek),or“heavyalcoholuse”(drinkingmorethan3to7drinksperweek).Smokingstatuswascategorizedasnonsmoker,pastsmoker,orcurrentsmoker.Afterovernightfasting,bloodsampleswereobtained,andserumhigh-densitylipoproteincholesterol,low-densitylipoprotein(LDL)cholesterol,andtriglyceride(TG)resultscouldbeobtained.根據(jù)健康檢查結果，根據(jù)世界衛(wèi)生組織西太平洋地區(qū)指南和韓國實踐指南，將參與者的身體質量指數(shù)(BMI)分為4組:低(<18.5)、正常(18.5~23)、超重(23~25)和肥胖(>25)。潛在的合并癥是在過去一年中使用ICD-10代碼進行原發(fā)性或首次繼發(fā)性診斷時至少進行一次住院或門診治療(高血壓:I10-I15，糖尿病:E10-E14，血脂異常:E78)。飲酒頻率分為“不飲酒”(每周飲酒少于1杯)、“輕度飲酒”(每周飲酒1至2杯)或“重度飲酒”(每周飲酒超過3至7杯)。吸煙狀況分為不吸煙者、過去吸煙者和現(xiàn)在吸煙者。禁食過夜后采集血樣，得到血清高密度脂蛋白膽固醇、低密度脂蛋白膽固醇和甘油三酯(TG)結果。?SystemicCorticosteroidPrescriptionWedefinedsystemiccorticosteroidprescriptionsasoralcorticosteroidprescriptionsandIVcorticosteroidprescription.Systemiccorticosteroidusewasdefinedastheprescriptionofmedicationcodesduringadmissionsandoutpatientvisitsfrom2003totheindexdate(Table1).Bothgroupshadidenticalobservationperiods.Allcorticosteroidformulationswereconvertedintoadailydosebasedonprednisoneequivalentdoses[24](1mgprednisolone=4mghydrocortisone=0.8mgmethylprednisolone=0.8mgtriamcinolone=0.16mgbetamethasone=1.2mgdeflazacort),andwecalculatedcumulativedosesofexposureforcorticosteroidswiththesumofthedosesforalltheprescribeddays,whichwasexpressedasthecumulativedefineddailydose(cDDD)accordingtotheWorldHealthOrganizationdefinition.我們將系統(tǒng)性糖皮質激素處方定義為口服糖皮質激素處方和靜脈糖皮質激素處方。系統(tǒng)性糖皮質激素使用定義為從2003年到基線日期（見表1）的住院和門診就診期間的藥物代碼處方。兩組觀察期相同。將所有糖皮質激素制劑轉換為基于潑尼松等效劑量（1毫克潑尼松龍等于4毫克氫化可的松等于0.8毫克甲基潑尼松龍等于0.8毫克曲安奈德等于0.16毫克倍他米松等于1.2毫克德夫氯喹）的每日劑量，并根據(jù)世界衛(wèi)生組織的定義計算糖皮質激素的累積暴露劑量（累積定義每日劑量，cDDD），即將所有處方天數(shù)的劑量相加。?Table1PrescriptionDrugCodesandDosageofSystemicCorticosteroidBasedontheHealthInsuranceClaimsPaymentCodingSystem.Drug???????Code??????CorticosteroidandDosageOralcorticosteroids116401ATB???betamethasone0.5mg116501ATB???betamethasonesodiumphosphate0.5mg296900ATB???betamethasone0.25mg140801ATB???deflazacort6mg140802ATB???deflazacort30mg141901ATB???dexamethasone0.5mg141903ATB???dexamethasone0.75mg141904ATB???dexamethasone4mg170901ATB???hydrocortisone10mg170905ATB???hydrocortisone20mg170906ATB???hydrocortisone5mg193301ATB???methylprednisolone16mg193302ATB???methylprednisolone4mg193303ATB???methylprednisolone8mg193304ATB???methylprednisolone2mg193305ATB???methylprednisolone1mg217001ATB???prednisolone5mg243201ATB???triamcinolone1mg243202ATB???triamcinolone2mg243203ATB???triamcinolone4mgHigh-doseIVcorticosteroids?171201BIJ???????hydrocortisonesodiumsuccinate100mg171202BIJ?????hydrocortisonesodiumsuccinate250mg171203BIJ?????hydrocortisonesodiumsuccinate40mg193601BIJ?????methylprednisolonesodiumsuccinate125mg193602BIJ?????methylprednisolonesodiumsuccinate250mg193603BIJ?????methylprednisolonesodiumsuccinate40mgmethylprednisolonesodiumsuccinate500mg193604BIJ?????methylprednisolonesodiumsuccinate1000mg193605BIJ?????prednisolonesodiumsuccinate1000mg217301BIJ?????prednisolonesodiumsuccinate250mg217302BIJ???????SubgroupAnalysisATHAafteranONFHdiagnosiswasusedasasurrogateforfemoralheadcollapse.Therefore,wedividedallcasesinto2groups:agroupthatreceivedTHAandanothergroupthatdidnotreceiveTHAusingtreatmentcodes(N0711.N7020).Amongatotalof3,430patients,weexcluded70patientswhohadaTHAtreatmentcodepriortodiagnosis,1,175patientswhoreceivedTHAduringtheobservationperiod,and2,255patientswhodidnot.Wecomparedthe2groupsandanalyzedthemusingtheCoxproportionalhazardsmodel,whichfactorsaffectdiseaseprogressionleadingtoTHA(Figure2).診斷為ONFH后進行THA作為股骨頭塌陷的替代。因此，我們使用治療代碼(N0711)將所有病例分為兩組:接受THA治療的組和未接受THA治療的組。N7020)。在總共3430例患者中，我們排除了70例在診斷前有THA治療代碼的患者，1175例在觀察期間接受THA治療的患者和2255例未接受THA治療的患者。我們對兩組患者進行比較，并使用Cox比例風險模型進行分析，分析影響THA病情進展的因素(圖2)。??Fig.2Studyflow:comparisonofpatientswhoreceivedanddidnotreceivetotalhiparthroplastyafterdiagnosisONFH,osteonecrosisoffemoralhead;THA,totalhiparthroplasty.??DataAnalysisChi-squaredtestsforcategoricalvariableswereperformedtocomparethebaselinecharacteristicsbetweencaseandcontrolpatients.AconditionallogisticregressionanalysiswasperformedtoevaluatetheassociationbetweensystemiccorticosteroiduseandtheriskofONFH.Forsubgroupanalysis,weusedCoxproportionalhazardmodelstoestimateadjustedhazardratios(aHRs)and95%confidenceintervals(CIs).APvalue<.05wasconsideredsignificant.AllstatisticalanalyseswereperformedusingSASEnterpriseGuideversion7.1(SASInstitute,Cary,NorthCarolina).?ResultsDemographicDataforONFHCasesandMatchedControlsTable2showsthebaselinecharacteristicsofcasesandmatchedcontrols.The2groupshadevendistributionsinthematchingvariables,includingsexandbirthyear.Subjectswerepredominantlymen(61.1%),andthemostcommonagegroupwasthoseborninthe1950s(age63to72asof2022).Comparedwiththecontrolgroup,ONFHcasepatientshadlowhouseholdincomeandhadmorediabetes,hypertension,dyslipidemia,andheavyalcoholuse(drinkingmorethan3to7drinksperweek).Inaddition,thecasepatientshadnormalserumLDLlevels(<100mg/dL),butconversely,thereweremanycasesofhypertriglyceridemiawithserumTGlevelsof200mg/dLormore.??Table2BaselineCharacteristicofOsteonecrosisofFemoralHeadCasesandMatchedControls.totalN=20,928(%)?????CasesN=3,488(%)ControlsN=17,440(%)?????PSex????????????????????????Men12,792(61.1)?2,132(61.1)???10,660(61.1)?Women???8,136(38.9)???1,356(38.9)???6,780(38.9)???????Birthyear??????????????????????????????<1930????852(4.1)142(4.1)710(4.1)1930to1939?3,024(14.4)???504(14.4)??????2,520(14.4)?????1940to1949?4,074(19.5)???679(19.5)??????3,395(19.5)?????1950to1959?5,112(24.4)???852(24.4)??????4,260(24.4)?????1960to1969?3,786(18.1)???631(18.1)??????3,155(18.1)?????1970to1979?2,184(10.4)???364(10.4)??????1,820(10.4)?????1980to1989?1,080(5.2)?????180(5.2)900(5.2)1990to1999?558(2.7)93(2.7)??465(2.7)2000to2009?210(1.0)35(1.0)??175(1.0)2010to2019?48(0.2)??8(0.2)????40(0.2)??Age(atindexdate)55.2±16.9????55.2±16.9???????55.2±16.9????Householdincome????????????????????????Low4,535(21.7)???896(25.7)??????3,639(20.9)???????<.001Middle???6,500(31.0)???1,090(31.2)???5,410(31.0)???????High???????9,893(26.5)???1,502(43.1)???8,391(48.1)???????Comorbidities????????????????????????Hypertension?6,631(31.7)???1,301(37.3)???5,330(30.6)?????<.001Diabetesmellitus???4,567(21.8)???908(26.0)???????3,659(21.0)???<.001Dyslipidemia??5,555(26.5)???1,120(32.1)???4,435(25.4)?????<.001Frequencyofdrinkingalcohol??????????????????????????????<1d/wk??10,044(48.0)?1,613(46.2)???8,431(48.3)???????<.0011to2d/wk?????3,987(19.1)???560(16.1)??????3,427(19.7)?????3to7d/wk?????2,794(13.3)???621(17.8)??????2,173(12.5)?????Missing??4,103(19.6)???694(19.9)??????3,409(19.5)???????Smokingstatus?????????????????????????????Non-smoker???9,455(45.2)???1,539(44.1)???7,916(45.4)?????.199Ex-smoker?????2,865(13.7)???462(13.3)??????2,403(13.8)?????Currentsmoker??????4,488(21.4)???790(22.6)???????3,698(21.2)???Missing??4,120(19.7)???697(20.0)??????3,423(19.6)???????BMI,kg/m2??24.0±3.3??????23.9±3.4??????24.0±3.3??.547<18·5?????608(2.9)113(3.2)495(2.8).09018·5to22·9???6,126(29.3)???1,029(29.5)???5,097(29.2)?????23·0to24·9???4,239(20.3)???651(18.7)??????3,588(20.6)?????≥25·0?6,113(29.2)???1,049(30.1)???5,064(29.0)???????Missing??3,842(25.1)???646(18.5)??????3,196(18.3)???????HDL,mg/dL??54.2±20.5????55.2±22.7????54.0±20.0.015<40?2,113(10.1)???339(9.7)1,774(10.2%).03340to59??8,856(42.3)???1,411(40.5)???7,445(42.7%)??≥60???????4,700(22.5)???830(23.8)????3870(22.2%)???????Missing??5,259(25.1)???908(26.0)??????4,351(24.9%)??LDL,mg/dL???114.8±77.2??110.6±56.9??115.7±80.6<.001<100??????5,627(26.9)???1,045(30.0)???4,582(26.3)???????<.001100to159?????8,493(40.6)???1,297(37.2)???7,196(41.3)?????≥160?????1,528(7.3)?????234(6.7)1,294(7.4)?????Missing??5,280(25.2)???912(26.1)??????4,368(25.0)???????TG,mg/dL?????144.5±108.7154.8±125.0142.5±105.1??????<.001<150??????10,395(49.7)?1,651(47.3)???8,744(50.1)???????<.001150to199?????2,447(11.7)???390(11.2)??????2,057(11.8)?????≥200?????2,829(13.5)???540(15.5)??????2,289(13.1)???????Missing??5,257(25.1)???907(26.0)??????4,350(24.9)???????BMI,bodymassindex;HDL,highdensitylipoprotein;LDL,lowdensitylipoprotein;TG,triglyceride.??Table3showsthecomparisonofprescribedsystemiccorticosteroidsincasepatientsandcontrolpatients.Bothgroupshadidenticalobservationperiods(meanobservationperiodwas8.26years).Systemiccorticosteroidwasprescribedatleastoncemoreinthecasegroupthaninthecontrolgroup(71.8versus62.9%,P<.001).EvenwhenoralcorticosteroidsandIVcorticosteroidswerecompared,respectively,thenumberofcasesprescribedcorticosteroidsatleastoncewashigherinthepatientswhohadONFH(oralcorticosteroids:71.2versus62.4%,P<.001/IVcorticosteroids:10.7versus4.9%,P<.001).??Table3DifferenceinCorticosteroidUseBetweenCasesandMatchedControlsFrom2003UntilDiagnosis.TotalN=20,928(%)?????CasesN=3,488(%)ControlsN=17,440(%)?????PCorticosteroid(oralorhigh-doseIV)???????????????????????????Neveruse???????7,453(35.6)???983(28.2)??????6,470(37.1)?????<.001Everuse?13,475(64.4)?2,505(71.8)?10,970(62.9)???????Oralcorticosteroid????????????????????????Neveruse???????7,562(36.1)???1,004(18.8)???6,558(37.6)?????<.001Everuse?13,366(63.9)?2,484(71.2)?10,882(62.4)???????Neveruse???????7,562(36.1)???1,004(18.8)???6,558(37.6)?????<.001<180cDDDs??12,667(60.5)?2,192(62.8)???10,475(60.1)?????180to364cDDDs?397(1.9)146(4.2)251(1.4)365to729cDDDs?179(0.9)84(2.4)??95(0.5)??≥730cDDDs123(0.6)62(1.8)??61(0.4)??High-doseIVcorticosteroid??????????????????????????Neveruse???????19,703(94.2)?3,116(89.3)???16,587(95.1)?????<.001Everuse?1,225(5.8)?????372(10.7)??????853(4.9)Neveruse???????19,703(94.2)?3,116(89.3)???16,587(95.1)?????<.001<180cDDDs??988(4.7)266(7.6)722(4.1)180to364cDDDs?120(0.6)46(1.3)??74(0.4)??365to729cDDDs?77(0.4)??40(1.2)??37(0.2)??≥730cDDDs40(0.2)??20(0.6)??20(0.1)??cDDDs,cumulativedefineddailydoses(prednisolone10mg);IV,intravenous.??CumulativeCorticosteroidDoseandONFHDevelopmentConditionallogisticregressionanalysiswasperformedtoanalyzetheeffectofthecumulativedoseofsystemiccorticosteroidsfor1yearbeforediagnosisontheincidenceofONFH(Table4).SystemiccorticosteroidusewassignificantlyassociatedwithanincreasedriskofONFHincidencecomparedtothatofnonusers.Specifically,higherdosesoforalcorticosteroidwereassociatedwithincreasedriskofONFH(oddsratiosof1.61(95%CI1.47to1.78,P<.001),4.39(95%CI3.47to5.56,P<.001),6.42(95%CI4.65to8.87,P<.001),and5.44(95%CI3.65to8.13,P<.001)forpatientswhohavecorticosteroiduseof<180,180to365,365to720,and>720cDDDs(valuesconvertedtodailyprednisolone10mg),respectively.TheriskofONFHincreasedrapidlywhenthecDDDwas180ormore,thatis,whencumulativeprednisoloneusewas1,800mgormore.Inaddition,atrendtowardriskincreasewithcumulativedosesofIVcorticosteroidusewasshownwithadjustedoddsratio(AOR)of1.63(95%CI1.39to1.90,P<.001),2.34(95%CI1.57to3.49,P<.001),3.77(95%CI2.33to6.10,P<.001),and2.76(95%CI1.41to5.39,P=.003)forpatientswhohavecorticosteroiduseof<180,180to365,365to720,and>720cDDDs(valuesconvertedtodailyprednisolone10mg),respectively.??Table4AdjustedRiskofOsteonecrosisofFemoralHeadOccurrence.ConditionalLogisticRegressionAnalysisforONFHDevelopmentCrudeOR??????95%CI???P?????AdjustedOR??95%CI???????PHouseholdincome????????????????????????????????????????Low1.381.26to1.52???<.001?????1.381.25to1.51???????<.001Middle???1.131.03to1.23???.0071.131.03to1.23???????.008High???????1.00ref.?????????1.00ref.??Comorbidities???????????????????????????????????????Hypertension?1.471.35to1.60???<.001?????1.21???????1.06to1.37???.004Diabetesmellitus???1.381.26to1.51???<.001???????1.070.95to1.20???.289Dyslipidemia??1.471.35to1.60???<.001?????1.18???????1.04to1.34???.012Frequencyofdrinkingalcohol?????????????????????????????????????????????<1d/wk??1.00ref.?????????1.00ref.??1to2d/wk?????0.870.78to0.97???.0150.900.80to1.01.0713to7d/wk?????1.541.38to1.73???<.001?????1.54???????1.36to1.74???<.001Missing??1.080.97to1.20???.1801.120.59to2.14???????.731Smokingstatus?????????????????????????????????????????????Non–smoker??1.00ref.?????????1.00ref.??Ex–smoker?????1.010.89to1.15???.8670.930.82to1.07.314Currentsmoker??????1.131.01to1.26???.0321.01???????0.90to1.14???.855Missing??1.060.95to1.18???.2791.030.55to1.94???????.923BMI,kg/m2?????????????????????????????????????????<18·5?????1.130.91to1.41???.2621.150.92to1.44???????.23218·5to22·9???1.00ref.?????????1.00ref.??23·0to24·9???0.900.81to0.99???.0490.900.80to1.01.062≥25·0?1.020.93to1.13???.6280.990.89to1.09???????.784Missing??1.000.90to1.13???.9450.800.55to1.17???????.254HDL,mg/dL?????????????????????????????????????????<40?1.010.88to1.15???.9250.950.83to1.09???????.44740to59??1.00ref.?????????1.00ref.??≥60???????1.131.03to1.25???.0091.100.99to1.21???????.069Missing??1.121.01to1.23???.0312.910.14to60.46???????.490LDL,mg/dL??????????????????????????????????????????<100??????1.00ref.?????????1.00ref.??100to159?????0.790.72to0.86???<.001?????0.86???????0.78to0.94???.001≥160?????0.790.67to0.92???.0030.84071to0.98???????.031Missing??0.930.83to1.03???.1520.840.28to2.56???????.762TG,mg/dL????????????????????????????????????????????<150??????1.00ref.?????????1.00ref.??150to199?????1.010.89to1.14???.9170.990.88to1.13.970≥200?????1.261.13to1.40???<.001?????1.171.04to1.32.009Missing??1.121.01to1.23???.0250.460.03to7.70???????.585Medication????????????????????????????????????????????Steroid(oralorhigh–doseIV)?????????????????????????????????????????????Neveruse???????1.00ref.?????????1.00ref.??Everuse?1.751.59to1.92???<.001?????1.771.60to1.94<.001POsteroid?????????????????????????????????????????????Neveruse???????1.00ref.?????????1.00ref.??Everuse?1.731.57to1.90???<.001?????1.681.53to1.85<.001Neveruse???????1.00ref.?????????1.00ref.??<180cDDDs??1.631.49to1.79???<.001?????1.61???????1.47to1.78???<.001180to364cDDDs?4.983.96to6.25???<.001???????4.393.47to5.56???<.001365to729cDDDs?7.515.50to10.27?<.001???????6.424.65to8.87???<.001≥730cDDDs8.966.16to13.02?<.001?????5.44???????3.65to8.13???<.001High–doseIVsteroid????????????????????????????????????????????Neveruse???????1.00ref.?????????1.00ref.??Everuse?2.422.12to2.76???<.001?????2.201.92to2.51<.001Neveruse???????1.00ref.?????????1·00?????ref.??<180cDDDs??2.041.76to2.38???<.001?????1.63???????1.39to1.90???<.001180to364cDDDs?3.402.35to4.92???<.001???????2.341.57to3.49???<.001365to729cDDDs?5.863.74to9.18???<.001???????3.772.33to6.10???<.001≥730cDDDs5.232.81to9.73???<.001?????2.76???????1.41to5.39???.003BMI,bodymassindex;cDDDs,cumulativedefineddailydoses(prednisolone10mg);CI,confidenceinterval;HDL,highdensitylipoprotein;IV,intravenous;LDL,lowdensitylipoprotein;ONFH,osteonecrosisoffemoralhead;OR,oddsratio;PO,peroral;TG,triglyceride.??RiskFactorsforTHAinPatientswhoHaveONFHFortheONFHcasepatients,asubgroupanalysiswasperformedon1,175patientsintheTHAgroupand2,255patientsinthenon-THAgroupduringtheobservationperiod.Thefollow-updurationoftheTHAgroup(1,175patients)was1.03±2.25years,andthefollow-updurationofthenon-THAgroup(2,255patients)was7.93±5.15years.Table5showsthebaselinecharacteristicsofTHAcasesandnon-THAcases.IntheTHAgroup,therewasagreaterproportionofmen(63.9versus60.0%,P=.028),higherBMI(24.1versus23.8,P=.027),heavyalcoholuseofthosewhoconsumedalcoholmorethan3to7daysaweek(22.9versus15.2%,P<.001),currentsmokers(26.4versus20.8%,P<.001),andhigherTG(162.3mg/dLversus150.0,P≤.001).However,whentheeffectondiseaseprogressionwasanalyzedusingCoxproportionalhazardsmodelforsurvivalanalysisafterONFHdiagnosis,heavyalcoholuseandlongercorticosteroidusesweretheriskfactorsaffectingdiseaseprogression,anddiabeteswasafactorthatslowedprogression.Moreover,otherlipidprofilesaswellascorticosteroidsusedandcumulativedosesofcorticosteroidsdidnotaffecttheincidenceofTHA(Table6).Inaddition,whenthesurvivalanalysiswasperformedafterthediagnosisofONFHbydividingthepatientgroupintomalesandfemales,heavyalcoholuseinvolvingthosewhoconsumedalcoholmorethan3to7daysaweekincreasedtheriskofdiseaseprogressionafterONFHdiagnosisinmalesonly(aHR:1.38,95%CI1.16to1.65,P<.001),andaBMIof25orhigherinfemalesonlyincreasedtheriskofincidenceofTHAafterONFHdiagnosis(aHR:1.52,95%CI1.18to1.96,P<.001).??Table5Comparisonofthe2GroupsAccordingtoWhetherorNotTotalHipArthroplastywasPerformedDuringtheFollow-UpPeriodAfterOsteonecrosisofFemoralHeadDiagnosis.TotalN=3,430(%)??????THAafterDiagnosisN=1,175(%)?????NoTHAafterDiagnosisN=2,255(%)???????PSex????????????????????????Men2,104(61.3)???751(63.9)??????10,660(61.1)???????.028Women???1,326(38.7)???424(36.1)??????6,780(38.9)???????Birthyear??????????????????????????????<1930????141(4.1)16(1.4)??125(5.5)<.0011930to1939?492(14.3)??????153(13.0)??????339(15.0)?????1940to1949?665(19.4)??????246(20.9)??????419(18.6)?????1950to1959?837(24.4)??????344(29.3)??????493(21.9)?????1960to1969?621(18.1)??????229(19.5)??????392(17.4)?????1970to1979?359(10.5)??????118(10.0)??????241(10.4)?????1980to1989?180(5.3)56(4.8)??124(5.2)1990to1999?92(2.7)??13(1.1)??79(3.5)??2000to2009?35(1.0)??0(0.0)????35(1.6)??2010to2019?8(0.2)????0(0.0)????8(0.3)????Age(atindexdate)55.1±17.0????56.41±13.8???????54.6±18.4????.007Householdincome????????????????????????Low880(25.7)??????283(24.1)??????597(26.5)???????.008Middle???1,077(31.4)???409(34.8)??????668(29.6)???????High???????1,473(42.9)???483(41.1)??????990(43.9)???????Comorbidities????????????????????????Hypertension?1,269(37.0)???445(37.9)??????824(36.5)?????.466Diabetesmellitus???888(25.9)??????285(24.3)???????603(26.7)??????.125Dyslipidemia??1,095(31.9)???383(32.6)??????712(31.6)?????.568Frequencyofdrinkingalcohol??????????????????????????????<1d/wk??1,581(46.1)???504(42.9)??????1,077(47.8)???????<.0011to2d/wk?????549(16.0)??????207(17.6)??????342(15.2)?????3to7d/wk?????613(17.9)??????269(22.9)??????344(15.2)?????Missing??687(20.0)??????195(16.6)??????492(21.8)???????Smokingstatus?????????????????????????????Nonsmoker????1,507(43.9)???491(41.8)??????1,016(45.1)?????.199Ex-smoker?????454(13.2)??????180(15.3)??????274(12.2)?????Currentsmoker??????780(22.7)??????310(26.4)???????470(20.8)??????Missing??689(20.1)??????194(16.5)??????495(21.9)???????BMI,kg/m2???23.9±3.4??????24.1±3.4??????23.8±3.3??.027<18·5?????112(3.3)37(3.2)??75(3.3)??<.00118·5-22·9??????1,014(29.3)???355(30.2)??????659(29.2)?????23·0-24·9??????640(18.7)??????218(18.5)??????422(18.7)?????≥25·0?1,024(29.8)???388(33.0)??????636(28.2)???????Missing??640(18.7)??????177(15.1)??????463(20.5)???????HDL,mg/dL??55.3±22.9????55.7±16.0????55.1±26.1.015<40?331(9.6)110(9.4)221(9.8).03340-59?????1,379(40.2)???494(42.0)??????885(39.2)???????≥60???????822(24.0%)??322(27.4%)??500(22.2%)???????Missing??898(26.2%)??248(21.2%)??649(28.8%)???????LDL,mg/dL???110.6±57.1??111.4±80.9??110.1±37.0.668<100??????1,023(29.8%)378(32.2%)??645(28.6%)???????<.001100-159?1,277(37.2%)464(39.5%)??813(36.1%)???????≥160?????229(6.7%)????81(6.9%)??????148(6.5%)???????Missing??901(26.3%)??252(21.4%)??649(28.8%)???????TG,mg/dL?????154.5±125.1162.3±141.3150.0±114.5??????.024<150??????1,626(47.4%)576(19.0%)??1,050(46.6%)??<.001150-199?378(11.0%)???140(11.9%)???238(10.5%)???????≥200?????530(15.5%)??211(18.0%)???319(14.2%)???????Missing??896(26.1)??????248(21.1)??????648(28.7)???????Systemiccorticosteroid(Oralorhigh-doseIV)???????????????????????????Neveruse???????2,090(60.9)???710(60.4)??????1,380(61.2)?????.687Everuse?1,340(39.1)???465(39.6)??????875(38.8)???????Oralcorticosteroid????????????????????????Neveruse???????2,119(61.8)???718(61.1)??????1,401(62.1)?????.584Everuse?1,311(38.2)???457(38.9)??????854(37.9)???????.690Neveruse???????2,119(61.8)???718(61.1)??????1,401(62.1)?????<180cDDDs??1,240(36.1)???434(36.9)??????806(35.7)?????180-364cDDDs????47(1.4)??15(1.3)??32(1.4)??365-729cDDDs????21(0.6)??8(0.7)????13(0.6)??≥730cDDDs3(0.1)????0(0.0)????3(0.1)????High-doseIVcorticosteroid??????????????????????????Neveruse???????3,322(96.9)???1,142(97.2)???2,180(96.7)?????.471Everuse?108(3.1)33(2.8)??75(3.3)??.858Neveruse???????3,322(96.9)???1,142(97.2)???2,180(96.7)?????<180cDDDs??84(2.4)??26(2.2)??58(2.5)??180-364cDDDs????9(0.3)????2(0.2)????7(0.3)????365-729cDDDs????10(0.3)??4(0.3)????6(0.3)????≥730cDDDs5(0.1)????1(0.1)????4(0.2)????BMI,bodymassindex;cDDDs,cumulativedefineddailydoses(prednisolone10mg);CI,confidenceinterval;HDL,highdensitylipoprotein;IV,intravenous;LDL,lowdensitylipoprotein;ONFH,osteonecrosisoffemoralhead;OR,oddsratio;TG,triglyceride;THA,totalhiparthroplasty.??Table6AdjustedRiskofTotalHipArthroplastyofOsteonecrosisofFemoralHeadPatients.ConditionalLogisticRegressionAnalysisforONFHDevelopmentCrudeOR??????95%CI???P?????AdjustedOR??95%CI???????PSex????????????????????????????????????????Men1.00ref.?????????1.00ref.??Women???0.890.79to1.01???.0601.030.88to1.20???????.731Age?1.011.00to1.01???<.001?????1.011.01to1.02???????<.001Householdincome????????????????????????????????????????Low1.000.86to1.16???.9891.020.88to1.19???????.786Middle???1.201.05to1.37???.0081.211.06to1.38???????.006High???????1.00ref.?????????1.00ref.??Comorbidities???????????????????????????????????????Hypertension?1.120.99to1.26???.0581.100.91to1.32.340Diabetesmellitus???0.950.83to1.09???.4460.80???????0.68to0.96???.013Dyslipidemia??1.090.97to1.23???.1570.980.81to1.19.842Frequencyofdrinkingalcohol?????????????????????????????????????????????<1d/wk??1.00ref.?????????1.00ref.??1to2d/wk?????1.231.05to1.45???.0111.231.02to1.47.0263to7d/wk?????1.501.30to1.74???<.001?????1.38???????1.16to1.65???<.001Missing??0.900.76to1.06???.2043.120.80to12.23???????.103Smokingstatus?????????????????????????????????????????????Nonsmoker????1.00ref.?????????1.00ref.??Ex-smoker?????1.311.11to1.56???.0020.251.03to1.52.027Currentsmoker??????1.261.09to1.45???.0021.17???????0.98to1.41???.085Missing??0.860.73to1.02???.0850.400.10to1.64???????.203BMI,kg/m2?????????????????????????????????????????<18·5?????0.940.67to1.31???.6980.890.63to1.25???????.51018·5to22·9???1.00ref.?????????1.00ref.??23·0to24·9???0.940.80to1.12???.4940.950.80to1.12.519≥25·0?1.090.95to1.26???.2321.110.96to1.29???????.176Missing??0.770.65to0.93???.0051.040.61to1.77???????.880HDL,mg/dL?????????????????????????????????????????<40?0.930.76to1.15???.5170.910.74to1.12???????.37640to59??1.00ref.?????????1.00ref.??≥60???????1.130.98to1.30???.0941.161.01to1.34???????.043Missing??0.770.66to0.90???<.001?????0.320.03to3.11.325LDL,mg/dL??????????????????????????????????????????<100??????1.00ref.?????????1.00ref.??100to159?????0.970.84to1.11???.6140.990.86to1.13.844≥160?????0.930.73to1.18???.5610.960.75to1.23???????.728Missing??0.740.63to0.87???<.001?????5.091.59to16.28??????.006TG,mg/dL????????????????????????????????????????????<150??????1.00ref.?????????1.00ref.??150to199?????1.070.89to1.29???.4471.050.87to1.27.583≥200?????1.191.02to1.39???.0301.110.94to1.31???????.231Missing??0.780.67to0.91???.0010.490.07to3.60???????.485Medication????????????????????????????????????????????Steroid(oralorhigh–doseIV)?????????????????????????????????????????????Neveruse???????1.00ref.?????????1.00ref.??Everuse?1.090.97to1.22???.1721.070.95to1.21???????.268POsteroid?????????????????????????????????????????????Neveruse???????1.00ref.?????????1.00ref.??Everuse?1.090.97to1.23???.1341.070.95to1.21???????.268Neveruse???????1.00ref.?????????1.00ref.??<180cDDDs??1.090.97to1.23???.1421.080.95to1.21.247180to364cDDDs?1.100.66to1.83???.7161.22???????0.73to2.06???.449365to729cDDDs?1.280.64to2.58???.4821.62???????0.79to3.36???.191≥730cDDDs<0.001???<0.001to999.944<0.001???????<0.001to999.943High–doseIVsteroid????????????????????????????????????????????Neveruse???????1.00ref.?????????1.00ref.??Everuse?0.910.64to1.29???.5920.900.63to1.28???????.552Neveruse???????1.00ref.?????????1.00ref.??<180cDDDs??0.950.64to1.39???.7760.870.59to1.30.504180to364cDDDs?0.600.15to2.41???.4740.71???????0.17to2.87???.626365to729cDDDs?1.200.45to3.20???.7191.35???????0.50to3.64???.554≥730cDDDs0.480.07to3.38???.4580.540.07to4.01.545Steroiduseduration?????????????????????????????????????????????Neveruse???????1.00ref.?????????1.00ref.??<3mobeforediagnosis?1.601.45-1.76<.001???????1.621.47-1.78<.0013-6mobeforediagnosis3.863.22-4.63<.001???????3.913.25-4.70<.0016-12mobeforediagnosis??????5.284.16-6.71<.001???????5.234.10-6.67<.001>12mobeforediagnosis7.575.98-9.59<.001???????7.405.82-9.42<.001?查看原圖BMI,bodymassindex;cDDDs,cumulativedefineddailydoses(prednisolone10mg);CI,confidenceinterval;HDL,highdensitylipoprotein;IV,intravenous;LDL,lowdensitylipoprotein;ONFH,osteonecrosisoffemoralhead;OR,oddsratio;PO,peroral;TG,triglyceride;THA,totalhiparthroplasty.??DiscussionWeevaluated3,488ONFHcasesand17,440controlcaseswithmatchingvariablesincludingage,sex,andthetimeofthefollow-upata1:5ratiofromtheNHIS-NSC,includingthefollow-updatafrom2002to2019of1,137,861participantsinanationwidelongitudinalnestedcase-controlstudy.Wedemonstratedthatalowhouseholdincome,diabetes,hypertension,dyslipidemia,heavyalcoholicswhoconsumedalcoholmorethan3daysaweek,andserumTGlevelsof200mg/dLormorewereassociatedwiththedevelopmentofONFH.Inaddition,systemiccorticosteroidusewassignificantlyassociatedwithanincreasedriskofONFHincidencecomparedtothatofnonusers.Specifically,theriskofONFHincreasedrapidlywhenthecDDDswere180ormorecumulativedosesofcorticosteroiduse.WeanalyzedthefactorsaffectingtheprogressionofthediseasebycomparingpatientswhounderwentTHAwiththosewhodidnotundergoTHAduringthefollow-upperiodafterONFHdiagnosis.Men,whohadahigherBMI,heavyalcoholicswhoconsumedalcoholmorethan3daysaweek,currentsmokers,andserumTGlevelsof200mg/dLormorewereassociatedwithTHAafterONFHdiagnosis.However,afteradjustingforcompoundfactors,heavyalcoholicsweretheonlyfactoraffectingtheincidenceofTHAafterONFHdiagnosis,anditmaybeusedtocounselONFHpatients.Otherlipidprofiles,corticosteroidsused,andcumulativedosesofcorticosteroidsdidnotaffecttheincidenceofTHA.我們評估了3488例ONFH病例和17440例對照病例，匹配變量包括年齡、性別和隨訪時間，比例為1:5，來自NHIS-NSC，包括2002年至2019年全國縱向巢式病例對照研究中1137861名參與者的隨訪數(shù)據(jù)。研究表明，家庭收入低、糖尿病、高血壓、血脂異常、每周飲酒超過3天的重度酗酒者以及血清TG水平≥200mg/dL與ONFH的發(fā)生有關。此外，與不使用皮質類固醇的患者相比，全身性使用皮質類固醇與ONFH發(fā)生率增加顯著相關。特別是，當皮質類固醇的累積使用劑量達到180或更高時，ONFH的風險迅速增加。我們通過比較ONFH診斷后隨訪期間接受THA和未接受THA的患者來分析影響疾病進展的因素。BMI較高的男性、每周飲酒超過3天的重度酗酒者、當前吸煙者、血清TG水平≥200mg/dL的男性在ONFH診斷后與THA相關。然而，在調整復合因素后，重度酗酒者是ONFH診斷后唯一影響THA發(fā)生率的因素，可用于指導ONFH患者。其他脂質特征、使用的皮質類固醇和皮質類固醇的累積劑量對THA的發(fā)生率沒有影響。TherelationshipbetweencorticosteroiduseandONFHdevelopmenthasbeenrevealedinseveralstudies[8,25,26],andtherearealsosomestudiesthathavesuggestedspecificdosesanddurationsofcorticosteroiduse,suchastheassociationwiththedevelopmentofdiseasewhenusingmorethan2gwithin3months[27]orthemeancorticosteroiduseofpatientswhohaveONFHdevelopmentof3,314mg[28].Inthecurrentlargecohortstudyofthegeneralpopulation,weanalyzedvariousfactorsthatcanaffectthedevelopmentofONFH.Asinpreviousstudies,thecaseofcorticosteroiduseatleastonceandadditionalcumulativecorticosteroiddosewereassociatedwiththeincreasedriskofONFHdevelopment,andwhencumulativeprednisoloneusewas1,800mg(180cDDDs)ormore,theriskofONFHdevelopmentincreasedrapidly.Surely,thedevelopmentofONFHrelatedtocorticosteroiduseisthoughttobecausedbyacombinationofnotonlycorticosteroidusebutalsoseveralfactorssuchascomorbidities,alcohol,smoking,andgeneticfactors.Sincecorticosteroidtreatmentisoftenessentialformanydiseases,itisnecessarytobeawareofthecumulativedoseatwhichtheriskofONFHincreasesrapidlywhencontinuouscorticosteroidtreatmentisrequired.?一些研究已經(jīng)揭示了皮質類固醇的使用與ONFH發(fā)展之間的關系[8,25,26]，也有一些研究提出了皮質類固醇使用的特定劑量和持續(xù)時間，如在3個月內使用超過2g與疾病發(fā)展的關系[27]，或ONFH發(fā)展患者的平均皮質類固醇使用量為3,314mg[28]。在目前針對普通人群的大型隊列研究中，我們分析了影響ONFH發(fā)展的各種因素。與之前的研究一樣，至少使用一次皮質類固醇和額外的皮質類固醇累積劑量與ONFH發(fā)展的風險增加有關，當潑尼松龍累積使用1800毫克(180cDDDs)或更多時，ONFH發(fā)展的風險迅速增加。當然，與皮質類固醇使用相關的ONFH的發(fā)展被認為不僅是由皮質類固醇使用引起的，還包括合并癥、酒精、吸煙和遺傳因素等多種因素。由于皮質類固醇治療通常對許多疾病至關重要，因此有必要了解在需要持續(xù)皮質類固醇治療時ONFH風險迅速增加的累積劑量。Tothebestofourknowledge,nostudyhascomparedtheincidenceofONFHwithhigh-doseIVandoralcorticosteroidsatthesamecumulativedose.Inthepresentstudy,bothoralcorticosteroidandhigh-doseIVcorticosteroidsincreasedtheriskofdevelopingONFH,andwhencomparingtheoralandhigh-doseIVatthesamecumulativedose,oralcorticosteroidhadahigherrisk;totheAORsoforalcorticosteroidwere1.61(<180cDDDs),4.39(180to365cDDDs),6.42(365to720cDDDs),and5.44(>720cDDDs).TheAORsofhigh-doseIVcorticosteroidwere1.63(<180cDDDs),2.34(180to365cDDDs),3.77(365to720cDDDs),and2.76(>720cDDDs),respectively.Ingeneral,sincetheprednisolonepotencyoforalcorticosteroidsismuchlowerthanthatofhigh-doseIV,thedurationoforalcorticosteroidusewouldhavebeenlongerifthesamecumulativedosewasused.Montetal.reportedthatONFHoccurrencewasassociatedwithmeandailycorticosteroiddose,cumulativedose,andtreatmentduration[8].Ofcourse,ONFHoccurrenceswouldbeaffectedbygeneticsusceptibilityandexposuretovariousriskfactors,butinourstudy,weconfirmedthatmoreONFHoccurredinoralcorticosteroidswitharelativelysmalldailydoseatthesamecumulativedosecomparedtohigh-doseIVcorticosteroid,soitisassumedthatthelongertreatmentperiodofcorticosteroidisalsoassociatedwithdevelopingONFH.據(jù)我們所知，沒有研究比較相同累積劑量的高劑量靜脈注射和口服皮質類固醇對ONFH的發(fā)生率。在本研究中，口服皮質類固醇和高劑量靜脈注射皮質類固醇都增加了發(fā)生ONFH的風險，并且在相同累積劑量下，口服皮質類固醇與高劑量靜脈注射皮質類固醇相比，風險更高;口服皮質類固醇的AORs分別為1.61(<180cDDDs)、4.39(180~365cDDDs)、6.42(365~720cDDDs)和5.44(>720cDDDs)。高劑量靜脈注射皮質類固醇的AORs分別為1.63(<180cDDDs)、2.34(180~365cDDDs)、3.77(365~720cDDDs)和2.76(>720cDDDs)。一般來說，由于口服皮質類固醇的強的松龍效力遠低于高劑量靜脈注射，如果使用相同的累積劑量，口服皮質類固醇的使用時間會更長。Mont等人報道ONFH的發(fā)生與皮質類固醇的平均每日劑量、累積劑量和治療時間有關[8]。當然，ONFH的發(fā)生會受到遺傳易感性和暴露于各種危險因素的影響，但在我們的研究中，我們證實在相同累積劑量下，相對于高劑量靜脈注射皮質類固醇，日劑量相對較小的口服皮質類固醇更易發(fā)生ONFH，因此我們假設皮質類固醇治療時間越長也與ONFH的發(fā)生有關。ItiswellknownthatahigherTGlevel,orLDLcholesterol,isanimportantriskfactorforischemicheartdiseaseandstrokebyinhibitingbloodflow,andONFHispresumedtoberelatedtoinhibitionofbloodflowtothefemoralheadinasimilarmechanism[29].Similartopreviousstudies[7,30],higherTGwasariskfactorforONFHinourstudy.Inaddition,itwasconfirmedthatLDLatlessthan100mg/dLhasaprotectiveeffectontheoccurrenceofONFH.眾所周知，較高的TG或LDL膽固醇水平通過抑制血流是缺血性心臟病和中風的重要危險因素，而ONFH被認為與股骨頭血流的抑制有類似的機制[29]。與以往的研究相似[7,30]，在我們的研究中，高TG是ONFH的危險因素。此外，還證實了低于100mg/dL的LDL對ONFH的發(fā)生有保護作用。SinceONFHoccurspredominantlyinyoungerpatientsandpreservationofthenativejointasmuchaspossibleistheprincipleoftreatment,thediseaseprogressionandprognosisareasimportantastheoccurrenceofthedisease.WeoftenseecasesofbilateralONFHdevelopmentwhereonesidehasfemoralcollapseandtheothersideremainsasymptomaticwithoutfemoralheadcollapse.Alternatively,somecaseswereasymptomaticwithoutfemoralheadcollapse,butreceivedTHA.ItisknownthattheprognosisafterONFHdevelopmentisinfluencedbyvariousfactors,anduntilnow,therehavebeenstudiesshowingthatradiologicfactorssuchasthesizeorlocationofnecrosisoracetabularanatomicalfactorshaveaneffect[1,19,31].Montetal.reportedthattheprevalenceoffemoralheadcollapsewas38%(106of282hips)inameta-analysisandvariedfrom17to73%dependingontheriskfactor[16].Inourstudy,34.3%ofpatientsunderwentTHA,anaverageof1.03±2.25yearsafterdiagnosis,similartothepreviousstudy.Althoughradiologicassessmentcouldnotbeperformed,casesthatmayhaveseengreaterphysicalloads,suchasmen,whohadahigherBMI,excessivedrinking,smoking,andahigherserumTGlevelover200mg/dL,wereassociatedwithdiseaseprogression.Inparticular,thefactorsthatincreasedtheriskofdiseaseprogressionweredifferentinmenandwomen.Wefoundthatcorticosteroidsprescribedornotandcumulativedosesofcorticosteroidswereunlikelytoaffectdiseaseprogression.由于ONFH主要發(fā)生在年輕患者中，治療原則是盡可能保留原有關節(jié)，因此疾病的進展和預后與疾病的發(fā)生同樣重要。我們經(jīng)常看到雙側ONFH發(fā)展的病例，其中一側有股骨頭塌陷，另一側無股骨頭塌陷癥狀。另外，一些病例無股骨頭塌陷癥狀，但接受了THA。眾所周知，ONFH發(fā)生后的預后受多種因素影響，迄今已有研究表明，壞死的大小或位置等放射學因素或髖臼解剖因素對ONFH的預后有影響[1,19,31]。Mont等人在一項薈萃分析中報道，股骨頭塌陷的患病率為38%(282髖中的106髖)，根據(jù)危險因素的不同，患病率從17%到73%不等[16]。在我們的研究中，34.3%的患者接受了THA，平均診斷后1.03±2.25年，與之前的研究相似。雖然無法進行放射學評估，但可能出現(xiàn)較大身體負荷的病例，如男性，BMI較高，過度飲酒，吸煙，血清TG水平高于200mg/dL，與疾病進展相關。特別是，增加疾病進展風險的因素在男性和女性中是不同的。我們發(fā)現(xiàn)，開具或不開具皮質類固醇以及皮質類固醇的累積劑量不太可能影響疾病進展。Ourstudyhasseveralpotentiallimitationsthatshouldbeaddressedinfurtherstudies.TheONFHwasassessedbyanoperationaldefinitionusingadiagnosiscode,notbyaradiologicevaluationsuchasanx-rayorMRI.However,theincidenceofONFHinthisstudywassimilartothatinapreviousAsiangeneralpopulationstudythatdefineditusinghipjointx-raysand/orMRI[32].BecauseanaccurateselectionofONFHpatientsmaynothavebeenmade,anestedcase-controlanalysisfromapopulation-basedcohortwasperformedtoincreasetheaccuracyoftheanalysis.Additionally,usingtheNHIS-NSCdatabase,prescriptionrecordsforcorticosteroidscouldbeaccessed.However,theactualintakeofcorticosteroidsinsubjectsmightbedifferentfromtheprescriptionrecords.Fortunately,severalstudieshaveshownagoodcorrelationbetweenprescriptionsandrealexposuretodrugs[33,34].Also,wecouldnotobtaininformationabouttraumaticONFH,whichmayhaveinfluencedtheresultsofthecurrentstudy.Inaddition,wecouldnotassessotherinterventionsthatcouldaffectdyslipidemia,microvascularbloodflow,andosteogenesis,suchastheuseoflipid-loweringmedication,aspirin,antiplatelets,andanticoagulantmedication.Thisshouldbeevaluatedinfuturestudies.Furthermore,ananalysisofmultiplecomorbiditiessuchasrheumaticdisease,sicklecelldisease,humanimmunodeficiencyvirus,organtransplantation,andsoonthatcouldaffecttheoccurrenceandprognosisofONFHwasnotperformed.Inparticular,sincetheprognosisofONFHisdifferentforeachdisease,subgroupanalysisaccordingtocomorbidityisabsolutelynecessaryforfuturestudies.Additionally,weanalyzedtheassociationbetweencumulativedoseofcorticosteroidanddiseaseprogressionafterONFHdiagnosisusingcDDD,andweconfirmedthatcumulativedoseofcorticosteroiddidnotaffectdiseaseprogression.However,sincethenumberofpatientswhohave180cDDDormorewassmall,additionalanalysiswithalargernumberofpatientsmaybeneededtoobtainmoreaccurateresults.我們的研究有幾個潛在的局限性，應該在進一步的研究中加以解決。ONFH通過使用診斷代碼的操作定義進行評估，而不是通過x射線或MRI等放射學評估。然而，本研究中ONFH的發(fā)生率與先前的亞洲普通人群研究相似，該研究使用髖關節(jié)X光片和/或MRI來定義ONFH[32]。由于可能沒有對ONFH患者進行準確的選擇，因此進行了基于人群的隊列嵌套病例對照分析，以提高分析的準確性。此外，使用NHIS-NSC數(shù)據(jù)庫，可以訪問皮質類固醇的處方記錄。然而，受試者的實際皮質類固醇攝入量可能與處方記錄不同。幸運的是，有幾項研究表明，處方與實際接觸藥物之間存在良好的相關性[33,34]。此外，我們無法獲得有關創(chuàng)傷性ONFH的信息，這可能影響了當前研究的結果。此外，我們無法評估其他可能影響血脂異常、微血管血流和成骨的干預措施，如使用降脂藥物、阿司匹林、抗血小板和抗凝藥物。這應該在未來的研究中進行評估。此外，對風濕病、鐮狀細胞病、人類免疫缺陷病毒、器官移植等可能影響ONFH發(fā)生和預后的多重合并癥未進行分析。特別是，由于每種疾病的預后不同，因此根據(jù)合并癥進行亞組分析對于未來的研究是絕對必要的。此外，我們分析了使用cDDD診斷ONFH后皮質類固醇累積劑量與疾病進展之間的關系，我們證實皮質類固醇累積劑量不影響疾病進展。然而，由于cDDD≥180的患者數(shù)量較少，因此可能需要對更多患者進行額外分析，以獲得更準確的結果。?ConclusionLowhouseholdincome,diabetes,hypertension,dyslipidemia,heavyalcoholicswhoconsumedalcoholmorethan3daysaweek,serumTGlevelsof200mg/dLormore,andoralorhigh-doseIVcorticosteroiduseareassociatedwithONFHdevelopment.Specifically,theriskofONFHincreasedrapidlywhencumulativeprednisoloneusewas1,800mgormore.However,oralorhigh-doseIVcorticosteroiduseandcumulativedosedidnotaffecttheprognosisofONFH.SincethedevelopmentandprognosisofONFHarecomplexandmultifactorialprocesses,furtherstudyisneeded.低收入家庭、糖尿病、高血壓、血脂異常、每周飲酒超過3天的重度酗酒者、血清TG水平≥200mg/dL、口服或高劑量靜脈注射皮質類固醇與ONFH的發(fā)生有關。具體來說，當累積使用強的松龍超過1800毫克時，ONFH的風險迅速增加。然而，口服或高劑量靜脈注射皮質類固醇和累積劑量對ONFH的預后沒有影響。由于ONFH的發(fā)展和預后是一個復雜的多因素過程，需要進一步研究。

CORR深刻見解?:股骨頭壞死患者股骨頭塌陷和髖臼覆蓋之間是否存在關聯(lián)?（2023）CORRInsights?:IsThereanAssociationBetweenFemoralHeadCollapseand?AcetabularCoverageinPatientsWithOsteonecrosis??PrasadK.CORRInsights?:IsThereanAssociationBetweenFemoralHeadCollapseand?AcetabularCoverageinPatientsWithOsteonecrosis?[J].ClinOrthopRelatRes,2023,481(1):60-62.?轉載文章的原鏈接1：https://pubmed.ncbi.nlm.nih.gov/36441115/?轉載文章的原鏈接2：https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9750567/?WhereAreWeNow?我們現(xiàn)在在哪里?Nontraumaticosteonecrosisofthefemoralhead(ONFH)isadevastatingdiseasethatdisproportionatelyaffectsyoungpatientsandcarriesarealriskoffemoralheadcollapse,resultinginprematureend-stagearthritisandTHA.Thisputstheseyoungpeopleonacoursethatoftenincludesmultiplerevisionsandsometimesseverecomplications.ClassificationsystemsofONFHbasedonsize,extent,volume,andlocationscanhelpsurgeonsanticipatewhichpatientsareatthegreatestriskoffemoralheadcollapse[1,10-12].However,thesesystemsdonotperfectlycapturethemanyfactorsthatcanmodifythisrisk(whetherthesebehost-relatedfactorsorinterventions),andovertime,clinician-scientistsareuncoveringnewriskfactorsthatarenotincludedintheoldclassificationsystems.Suchfactorsmayincludepelvicincidenceandacetabularcoverage,whichcanresultingreatercontactstressesonthefemoralheadandmayinfluencetheriskofprogressioninpatientswithONFH.非創(chuàng)傷性股骨頭壞死（ONFH）是一種破壞性疾病，主要影響年輕患者，并具有股骨頭塌陷的real風險，導致早期終末期關節(jié)炎和THA。這讓這些年輕人經(jīng)歷了一個經(jīng)常需要多次revisions的過程，有時還會出現(xiàn)嚴重的并發(fā)癥?；贠NFH的大小、范圍、體積和位置的分類系統(tǒng)可以幫助外科醫(yī)生預測哪些患者股骨頭塌陷的風險最大[1,10-12]。然而，這些系統(tǒng)并不能完美地捕捉到許多可以改變這種風險的因素（無論這些因素是與宿主相關的因素還是干預措施），隨著時間的推移，臨床科學家正在發(fā)現(xiàn)舊分類系統(tǒng)中未包括的新風險因素。這些因素可能包括骨盆入射角和髖臼覆蓋范圍，這可能導致股骨頭上更大的接觸應力，并可能影響ONFH患者進展的風險。Patientswithhighpelvicincidence,conceptualizedasthesumofpelvictiltandsacralslopeanddefinedastheanglebetweenalineperpendiculartothemidpointofthesacralplateauandalinefromthispointtothecenterofthefemoralhead,reportedlyhaveinadequateanteriorcoverageofthefemoralhead,whichmaybeassociatedwithacceleratedfemoralheadcollapseinpatientswithONFH[6].However,anotherstudydiffered,withnoassociationfoundbetweenpelvicincidenceandacetabularcoverage[3].InthecurrentstudyinClinicalOrthopaedicsandRelatedResearch?,therewerenodifferencesinpelvicincidencebetweenthecollapseandnoncollapsegroupswithin1yearafterpresentation[4].Basedonthis,theassociationbetweenpelvicincidenceandfemoralheadcollapseinpatientswithONFHremainsuncertain.6.KwonHM,YangI-H,ParkKK,etal.Highpelvicincidenceisassociatedwithdiseaseprogressioninnontraumaticosteonecrosisofthefemoralhead.ClinOrthopRelatRes.2020;478:1870-1876.3.IwasaM,AndoW,UemuraK,HamadaH,TakaoM,SuganoN.Pelvicincidenceisnotassociatedwiththedevelopmentofhiposteoarthritis.BoneJointJ.2021;103-B:1656-1661.4.IwasaM,AndoW,UemuraK,HamadaH,TakaoM,SuganoN.Isthereanassociationbetweenfemoralheadcollapseandacetabularcoverageinpatientswithosteonecrosis?ClinOrthopRelatRes.2023;481:51-59.高骨盆入射角的患者，被定義為骨盆傾斜和骶骨傾斜的總和，并被定義為垂直于骶骨平臺中點的線與從該點到股骨頭中心的線之間的夾角，據(jù)報道，股骨頭前部覆蓋不足，這可能與ONFH患者股骨頭加速塌陷有關[6]。然而，另一項研究卻有所不同，沒有發(fā)現(xiàn)骨盆發(fā)病率與髖臼覆蓋率之間的關聯(lián)[3]。在臨床骨科及相關研究?中，塌陷組和非塌陷組在發(fā)病后1年內盆腔發(fā)病率沒有差異[4]?；诖?，ONFH患者盆腔發(fā)生率與股骨頭塌陷之間的關系仍不確定。Inaddition,thecurrentstudyfoundtherewasaslightlysmallerlateralcenter-edgeangleof28°inthecoronalplanewithahigheroddsofcollapseinpatientswithseveregradesofONFH,buttherewasadifferentialeffectsizeofjust4°betweenthecollapseandnoncollapsegroupsandnodifferencesinfouradditionalangularparametersinthesagittalandaxialplanesoftridemensionalacetabularcoverage[4,8].Thus,thecontributiontoandclinicalsignificanceofthelateralcenter-edgeangleandacetabularcoverageregardingcollapseinpatientswithONFHisquestionable.Thus,factorsotherthanacetabularcoveragemaybepredominant,particularlybecause35patientswithONFH(35%),allwithsymptomsinitially,experiencedrapidlyprogressivecollapsewithin1year(potentiallyrisingto71%in24months[6]).Ontheotherhand,anassociationbetweensurgicaltreatmentoutcomesandlateralcenter-edgeangleinpatientswithONFHhasbeendocumented;asmallerangleentailsasubstantialriskofcollapseandhipsurvivalleadingtoTHAafterfreevascularizedfibulargraftingforONFH[9],whichdiffersfromthenaturalhistorythecurrentstudy[4]investigated.此外，目前的研究發(fā)現(xiàn)，嚴重程度的ONFH患者的冠狀面外側中心邊緣角略小，為28°，塌陷的幾率更高，但塌陷組和非塌陷組之間的差異效應大小僅為4°，并且在髖臼三維覆蓋的矢狀面和軸向面四個額外的角度參數(shù)沒有差異[4,8]。因此，外側中心邊緣角和髖臼覆蓋范圍對ONFH患者塌陷的貢獻和臨床意義值得懷疑。因此，髖臼覆蓋范圍以外的因素可能占主導地位，特別是35例ONFH患者(35%)，最初都有癥狀，在1年內經(jīng)歷了快速進行性塌陷（24個月內可能上升到71%[6]）。另一方面，ONFH患者的手術治療結果與外側中心邊緣角之間的關聯(lián)已被記錄；較小的角度會帶來很大的塌陷和髖關節(jié)存活風險，從而導致ONFH游離帶血管腓骨移植術后的THA[9]，這與當前研究[4]所調查的自然病史不同。ThekeymessageofthisstudyinCORR?[4]isthatmorethanone-thirdofpatientswithsymptomaticONFHoninitialpresentationexperiencedacceleratedcollapseofthefemoralheadwithin1year,andthatacetabularcoveragewasnotasstronganassociatedfactorinthenaturalhistoryofONFHasonemighthaveexpectedittobe.Basedonthesefindings,surgeonsshouldfocusonsymptomaticONFHandmonitorsusceptiblevascularityandearlycollapsecloselywithin2yearsafterpresentationforappropriatejoint-preservinginterventions,withconservationandpromotionofvascularity.CORR?[4]這項研究的關鍵信息是，超過三分之一的首發(fā)癥狀性ONFH患者在1年內股骨頭加速塌陷，并且髖臼覆蓋在ONFH自然病史中的相關因素并不像人們預期的那樣強?；谶@些發(fā)現(xiàn)，外科醫(yī)生應關注有癥狀的ONFH，并在就診后2年內密切監(jiān)測易感血管和早期塌陷，以采取適當?shù)谋ｊP節(jié)干預措施，保護和促進血管。?WhereDoWeNeedtoGo?我們需要去哪里?Althoughthevascularenvironmentandmechanicalenvironmentarenotalwaysentirelyindependentofoneanother,IbelievenontraumaticONFHpredominantlyreflectsdeteriorationofthevascularityofthefemoralhead,whetherasaprimaryphenomenon,asecondaryone,orboth.盡管血管環(huán)境和機械環(huán)境并不總是完全獨立的，但我認為非創(chuàng)傷性ONFH主要反映了股骨頭血管的惡化，無論是作為原發(fā)性現(xiàn)象，繼發(fā)性現(xiàn)象，還是兩者兼而有之。EveninaninnovativecenterinJapangearedtosuccessfullyperformosteotomiesfornontraumaticONFH,only9%ofpatientsyoungerthan30yearswereselectedforfemoralosteotomiesbasedonstringentcriteria,whilethosewhoweresignificantlysymptomatic(83%)underwentTHAwithinadecade[4].Ideally,anomaliesofthevascularsupply(includingvariationsinmicrocirculatorypatternsandcollateralcirculationintheheadofthefemur)andmechanicalvariantsandvariationsofhipmorphologymeritapreciseinvestigationbeforesurgicalplanningwhenjoint-preservingproceduressuchasosteotomiesareconsidered,inordertopreservethefemoralhead’sbloodsupply.4.IwasaM,AndoW,UemuraK,HamadaH,TakaoM,SuganoN.Isthereanassociationbetweenfemoralheadcollapseandacetabularcoverageinpatientswithosteonecrosis?ClinOrthopRelatRes.2023;481:51-59.即使在日本的一個創(chuàng)新中心，針對非創(chuàng)傷性ONFH成功實施截骨術，根據(jù)嚴格的標準，30歲以下的患者中只有9%被選中進行股骨截骨術，而那些有明顯癥狀的患者（83%）在十年內接受了THA[4]。理想情況下，血管供應的異常（包括股骨頭微循環(huán)模式和側支循環(huán)的變化）、機械變異和髖關節(jié)形態(tài)的變化值得在手術計劃之前進行精確的調查，當考慮進行關節(jié)保護手術（如截骨）時，為了保持股骨頭的血液供應。Futurestudiesshouldalsoassessthedegreeandrateofcollapse.Inthecurrentstudy[4],femoralheadcollapsewasdeemedprogressivewhentheamountofcollapseincreasedby>1mmcomparedwithpreviousradiographs;thisincrementmightbetoosmalltomatter.AnotherstudyreportedthatinasmallproportionofpatientswithJapaneseInvestigationCommitteeTypeBandcollapseoflessthan2mm,thecollapsemaystopandpatientsmaybecomeasymptomaticforanindeterminateperiod[8].Rapidlyprogressiveandstaticcollapsedemandsclosemonitoringbasedonprecisecriteria.8.NishiiT,SuganoN,OhzonoK,SakaiT,SatoY,YoshikawaH.Signi?canceoflesionsizeandlocationinthepredictionofcollapseofosteonecrosisofthefemoralhead:anewthree-dimensionalquan-ti?cationusingmagneticresonanceimaging.JOrthopRes.2002;20:130-136.未來的研究還應評估坍塌的程度和速度。在目前的研究中[4]，當股骨頭塌陷的數(shù)量比之前的X線片增加>1mm時，股骨頭塌陷被認為是進行性的；這個增量可能太小而無關緊要。另一項研究報道，在一小部分日本調查委員會B型塌陷小于2mm的患者中，塌陷可能停止，患者可能在不確定的時間內無癥狀[8]?？焖贊u進和靜態(tài)坍塌需要基于精確標準的密切監(jiān)測。Otherfundamentalquestionsrelatetojointpreservationthroughnonoperativeoptionsincludingmedicationssuchastransientbisphosphonatesforprecollapselesionsorpotentiallyforsmall,mediallesions;directsurgicaloptionsrelatedtopreservationofandimprovementinvascularityincludingcoredecompression,adjunctivebonegrafting,andvascularizedbonegrafting;selectiveredirectionalosteotomiestoreducemechanicalstressesandfacilitatevascularimprovement;andtheadditionofnoveladjunctivetherapiesincludingstemcelltherapiesinisolationorincombination.其他基本問題涉及到通過非手術選擇來保護關節(jié)，包括藥物治療，如用于塌陷前病變或潛在的小的、內側病變的短暫性雙膦酸鹽；與保存和改善血管性相關的直接手術選擇包括髓芯減壓、輔助植骨和帶血管的植骨；選擇性定向截骨術減少機械應力，促進血管改善;以及新的輔助療法的加入，包括分離或聯(lián)合的干細胞療法。FuturestudiesmustevaluatepatientswithsymptomaticprecollapselesionscausedbynontraumaticONFHtoidentifyanomaliesofthevascularsupplyandvariationsinmicrocirculatorypatternsandcollateralcirculation.Thiswillhelpguidesurgicalplanningtopreserve,promote,andrestorethatvascularsupply.Whetherthatmightbethroughprecisesurgicaltargetingofcoredecompressionorvascularizedbonegraftingisyettobedetermined.未來的研究必須評估非創(chuàng)傷性ONFH引起的癥狀性塌陷前病變患者，以確定血管供應異常、微循環(huán)模式和側枝循環(huán)的變化。這將有助于指導手術計劃，以保護、促進和恢復血管供應。這是否可能是通過精確的手術靶向髓芯減壓或血管化骨移植尚未確定。?HowDoWeGetThere?我們如何到達那里?Theannualincidenceofnew-onsetONFHwasreportedtobe1.91per100,000personsinJapan[2],whichmakesaccumulatingpatientsdifficultforsingle-centerstudies,especiallyforasubgroupanalysis.Obviously,studieswithmorepatientsareneededinthefutureforcomprehensiveanalyses.Multicenterstudieswithsuperiorstatisticalpowerincludingsubgroupsarelikelytocontributemore-robustdataandconclusionswithwiderimplicationsforprecisetimingofadvancingmodalitiesofinvestigationsanddifferentialmanagementoptionsofONFH.據(jù)報道，日本新發(fā)ONFH的年發(fā)病率為每10萬人1.91例[2]，這使得單中心研究難以積累患者，尤其是亞組分析。顯然，未來需要更多患者的研究來進行全面分析。包括亞組在內的具有卓越統(tǒng)計能力的多中心研究可能會提供更可靠的數(shù)據(jù)和結論，對ONFH的先進調查模式的精確時間和不同的管理選擇具有更廣泛的意義。Nationalandmultinationalstudiesandlarge-databasestudiesthatevaluateregionalandethnicvariations,guidedbytheAssociationofResearchCirculationosseousstagingsystemofosteonecrosisofthefemoralheadandJapaneseInvestigationCommittee,aredesirablebutaresubjecttologisticandresourceimplications.在研究循環(huán)協(xié)會股骨頭壞死骨分期系統(tǒng)和日本調查委員會的指導下，評估地區(qū)和種族差異的國家和多國研究和大型數(shù)據(jù)庫研究是可取的，但受后勤和資源影響。Contrast-enhancedMRarteriographydeservesmoreattention.Itcanbeusedtoevaluatehipswithprecollapsetodeterminevascularcompromiseandmayhelpusanticipatewhichhipsareatthegreatestriskofcollapse.Prognosticstudiesusingthistechniqueseemplausible,giventheconstraintsofsmallpatientnumbersandhowoftencollapseoccursinpatientswiththisdiagnosis.Dependingonthefindings,thisimagingtoolmayproveclinicallyusefulinthiscontext.增強磁共振動脈造影值得更多關注。它可以用來評估髖關節(jié)塌陷前的血管損傷，并幫助我們預測哪些髖關節(jié)塌陷的風險最大?？紤]到患者數(shù)量少的限制以及這種診斷的患者發(fā)生崩潰的頻率，使用這種技術進行預后研究似乎是合理的。根據(jù)結果，這種成像工具可能在臨床上證明是有用的。MRIuseinreal-timethree-dimensionalguidanceforcoredecompressionistechnicallyfeasible,safe,andaccurate[5].EvolutionofMRI-guided(withMR-compatibleinstrumentation)[5,7]robot-assistedsurgicalapproachesmaybethenextfrontierinjointpreservationinpatientswithONFH.Evaluatingit,though,wouldprobablyrequirethecooperationofseverallike-mindedcentersthattreatalargenumberofpatientswiththiscondition.GivenitsrelativefrequencyinsomeregionsofAsia(comparedwithEuropeortheUnitedStates),Isuspectmoreofthisresearchwillcomefromthosegeographiclocationswithworldwidetechnologicalinnovation,andIlookforwardtoreadingitwhenitappears.5.KerimaaP,VaananenM,OjalaR,etal.MRI-guidanceinpercutaneouscoredecompressionofosteonecrosisofthefemoralhead.EurRadiol.2016;26:1180-1185.7.MontMA,SalemHS,PiuzziNS,GoodmanSB,JonesLC.Nontraumaticosteonecrosisofthefemoralhead:wheredowestandtoday?:A5-yearupdate.JBoneJointSurgAm.2020;102:1084-1099.MRI用于實時三維指導髓芯減壓在技術上是可行的、安全的、準確的[5]。MRI引導（與MRI兼容的儀器）[5,7]機器人輔助手術入路的發(fā)展可能是ONFH患者關節(jié)保護的下一個前沿。然而，評估它可能需要幾個志同道合的中心的合作，這些中心治療了大量患有這種疾病的患者?？紤]到它在亞洲某些地區(qū)的相對頻率（與歐洲或美國相比），我猜想更多的這類研究將來自那些具有全球技術創(chuàng)新的地理位置，我期待著它出現(xiàn)時的閱讀。

近日，從國家中醫(yī)藥管理局官方網(wǎng)站獲悉，韋標方教授團隊榮獲國家級中醫(yī)藥項目1項。股骨頭壞死是骨科難治疾病之一。中西醫(yī)結合治療骨科疾病是當前學術熱點方向。臨沂市人民醫(yī)院韋標方教授團隊歷經(jīng)30余年臨床實踐，在取得了眾多科研成績的基礎上，再次獲得國家級中醫(yī)藥項目，標志著團隊在中西醫(yī)結合治療股骨頭壞死領域再上新臺階！?韋標方教授帶領團隊刻苦攻關，采用中西醫(yī)結合方法破解股骨頭壞死醫(yī)療難題，形成了一套成熟的診療方案。堅持個性化分期治療原則，對股骨頭壞死早、中、晚期患者采用階梯治療，診療各類患者20余萬例，深受全國各地患者好評。學科從無到有，經(jīng)過20余年的努力，成功邁入“國家隊”——國家級中西醫(yī)協(xié)同旗艦科室。相信團隊會在此基礎上更加努力，更好地服務于患者。?項目負責人簡介韋標方，臨沂市人民醫(yī)院骨科主任醫(yī)師，二級教授，博士生導師，博士后導師。國家級中西醫(yī)協(xié)同旗艦科室學術帶頭人，享受政府特殊津貼專家，山東省中醫(yī)藥臨床重點?？茖W術帶頭人。作者簡介于浩，廣州中醫(yī)藥大學博士研究生，師從韋標方教授，研究方向：中西醫(yī)結合治療股骨頭壞死。

骨質疏松癥在初期通常沒有明顯的臨床表現(xiàn)，但是隨著發(fā)展，可能會出現(xiàn)脊柱變形、疼痛、和輕微外力下的骨折。因此稱它為寂靜的疾病或者靜悄悄的疾病?！?骨質疏松主要有以下4個表現(xiàn)：（1）疼痛。疼痛是原發(fā)性骨質疏松癥最為常見的癥狀。患者表現(xiàn)為不明原因的腰背疼痛，沿著脊柱兩側彌漫性癥布，平臥休息以后，疼痛可以稍微緩解，直立后仰、久站久坐后疼痛會非常明顯。（2）變矮駝背。許多老年朋友感覺自己身高跟年輕時相比明顯“縮水”了，腰也伸不直了。骨質疏松的脊柱椎體骨量明顯減少、骨強度差，容易壓縮變形，尤其是彎腰等動作容易導致椎體前部分壓縮變扁，這種原因導致的身高短縮通常超過3厘米且有駝背的表現(xiàn)。（3）骨折。骨折是最嚴重的骨質疏松并發(fā)癥，輕則影響機體功能，重則致殘甚至致死。嚴重骨質疏松的患者，輕微受傷甚至日常做家務，如從沙發(fā)上坐地跌倒、彎腰拖地、崴腳就可導致相應部位的骨折，常見的骨折部位是腰背部、髖部和手臂。（4）心肺功能受損。骨質疏松的患者如發(fā)生胸、腰椎壓縮性骨折，可出現(xiàn)脊椎后凸畸形（駝背），胸腔容量變小且胸廓活動范圍受限，導致肺活量和最大換氣量顯著減少，患者往往感覺心慌、憋氣、氣不夠用等，以爬樓、擰重物時較為明顯。為什么會出現(xiàn)骨質疏松？老年人容易得骨質疏松主要是由于性激素的減少、臟器功能的減弱，刺激了破骨細胞，同時也抑制了成骨細胞的增生，造成了骨量減少。在臨床上骨質疏松是非常常見的一種疾病。有研究表明，六十歲以上的老年人得骨質疏松的幾率可以達到百分之三十五以上，并且隨著年齡的增長幾率逐漸增加。隨著老年人年齡的增長，其臟器的功能會下降，吸收營養(yǎng)的效率也會減退。導致維生素D的缺乏、鈣流失等，從而引起骨質疏松。女性由于絕經(jīng)以后，雌激素水平降低，無法有效的抑制破骨細胞，導致破骨細胞過度的增生和活躍，也會導致骨的分解和吸收而形成骨質疏松?？梢酝ㄟ^口服藥物以及在日常生活中增加鈣含量的食物來改善骨質疏松。什么是腰間盤突出？骨質疏松會導致骨頭強度下降，椎間盤承受壓力會過高，椎間盤纖維環(huán)發(fā)生破損的幾率就會變高。纖維環(huán)一旦破損就出現(xiàn)腰間盤突出，骨質疏松跟腰間盤突出是有一定的關系的。骨質疏松跟腰間盤突出是兩種不同的疾病，骨質疏松使骨的強度下降，椎間盤突出是椎間盤破壞以后或椎間盤前塊損傷以后，導致神經(jīng)卡壓的一種表現(xiàn)。骨質疏松如何引起股骨頭壞死？導致股骨頭壞死的常見因素，有長期服用激素類藥物，外傷以及大量飲酒，強制性的脊柱炎，先天性的髖臼發(fā)育不良等。骨質疏松是股骨頭壞死的病因之一。骨質疏松的患者骨骼中，蛋白鈣、磷的比例減少，骨的脆性增加，容易發(fā)生骨折。如果骨折發(fā)生在股骨頭部位，就會引發(fā)股骨頭的血運受到損害，造成股骨頭局部的血液循環(huán)障礙，進而引發(fā)股骨頭壞死。此外，由于骨質疏松造成骨吸收增加，疏松的股骨頭強度會降低，股骨頭局部會出現(xiàn)壓縮塌陷，導致流經(jīng)股骨頭部的骨流量減少，股骨頭的骨細胞和骨髓成分會引發(fā)股骨頭壞死。骨質疏松應該如何進行治療？對于骨質疏松首先要注意是骨質疏松還是骨質疏松癥，因為骨質疏松是一個慢性的蛻變性信號。骨質疏松治療方法：首先要強調非藥物的治療為主。比如采用平衡的飲食，適當?shù)难a充鈣劑、維生素D，適當?shù)幕顒?，戒煙，預防摔倒，這個是骨質疏松一個基本的治療前提和方案。

臀中肌鍛煉(2)：漸進式臀中肌抗阻力康復訓練，髖臼發(fā)育不良DDH/股骨頭壞死——保髖截骨術后康復指導作者：JayREbert,PeterKEdwards,DanielPFick,GregoryCJanes.作者單位:SchoolofSportScience,ExerciseandHealth,UniversityofWesternAustralia,Crawley,Perth,WesternAustralia.譯者：陶可（北京大學人民醫(yī)院骨關節(jié)科）摘要背景：鑒于臀中肌在骨盆和下肢穩(wěn)定性中的作用，以及臀中肌無力與許多下肢疾病之間已知的聯(lián)系，臀中肌康復至關重要。目的：系統(tǒng)地回顧文獻并提出一系列循證的漸進式臀中肌負荷練習。證據(jù)獲取：2016年1月進行了系統(tǒng)文獻檢索，以確定報告康復鍛煉期間臀中肌活動占最大等長收縮(MVIC)百分比的研究。其中包括調查無受傷參與者的研究。對鍛煉的類型或方式?jīng)]有限制，但排除了無法在獨立環(huán)境中準確復制或進行的鍛煉。未將肌電活動標準化為側臥MVIC的研究被排除。根據(jù)運動類型和%MVIC對運動進行分層：低（0%至20%）、中（21%至40%）、高（41%至60%）和極高（＞61%）。證據(jù)綜合：本次綜述納入了20項研究，報告了33項練習（以及同一練習的一系列變體）的結果。俯臥、四足和雙側橋式練習通常產(chǎn)生低或中等負荷。據(jù)報告，特定的髖部外展/旋轉練習為中等、高或極高負荷。存在對側肢體運動的單側站立練習通常是高負荷或極高負荷的活動，而一系列功能性負重練習則存在高變異性。結論：這篇綜述概述了康復環(huán)境中常用的一系列練習，根據(jù)運動類型和臀中肌激活程度進行分層。這將有助于臨床醫(yī)生從術后早期到康復后期為患者量身定制臀中肌負荷方案。ASystematicReviewofRehabilitationExercisestoProgressivelyLoadtheGluteusMediusAbstractContext:Gluteusmediusrehabilitationisofcriticalimportancegivenitsroleinpelvicandlowerlimbstability,andtheknownlinkbetweengluteusmediusweaknessandmanylowerlimbconditions.Objective:Tosystematicallyreviewtheliteratureandpresentanevidence-basedgraduatedseriesofexercisestoprogressivelyloadgluteusmedius.Evidenceacquisition:AsystematicliteraturesearchwasconductedinJanuary2016toidentifystudiesreportinggluteusmediusmuscleactivityasapercentageofmaximalvolitionalisometriccontraction(MVIC),duringrehabilitationexercises.Studiesthatinvestigatedinjuryfreeparticipantswereincluded.Norestrictionswereplacedonthetypeormodeofexercise,thoughexercisesthatcouldnotbeaccuratelyreplicatedorperformedwithinanindependentsettingwereexcluded.StudiesthatdidnotnormalizeelectromyographicactivitytoasidelyingMVICwereexcluded.Exerciseswerestratifiedbasedonexercisetypeand%MVIC:low(0%to20%),moderate(21%to40%),high(41%to60%),andveryhigh(＞61%).Evidencesynthesis:20studieswereincludedinthisreview,reportingoutcomesin33exercises(andarangeofvariationsofthesameexercise).Prone,quadruped,andbilateralbridgeexercisesgenerallyproducedlowormoderateload.Specifichipabduction/rotationexerciseswerereportedasmoderate,high,orveryhighload.Unilateralstanceexercisesinthepresenceofcontralaterallimbmovementwereoftenhighorveryhighloadactivities,whilehighvariabilityexistedacrossarangeoffunctionalweight-bearingexercises.Conclusions:Thisreviewoutlinedaseriesofexercisescommonlyemployedinarehabilitationsetting,stratifiedbasedonexercisetypeandthemagnitudeofgluteusmediusmuscularactivation.Thiswillassistcliniciansintailoringgluteusmediusloadingregimenstopatients,fromtheearlypostoperativethroughtolaterstagesofrehabilitation.Jiànjìnshìtúnzhōngjīfùhèkāngfùxùnliàn文獻出處：JayREbert,PeterKEdwards,DanielPFick,GregoryCJanes.ASystematicReviewofRehabilitationExercisestoProgressivelyLoadtheGluteusMedius.ReviewJSportRehabil.2017Sep;26(5):418-436.doi:10.1123/jsr.2016-0088.視頻資料來源:Youtube，Googleimage.

股骨頭壞死（Avascularnecrosisofthefemoralhead.AVN）是一種常見的骨科疾病，指的是由于各種原因導致股骨頭的血液供應不足，從而引起骨細胞和骨髓細胞的死亡，進而導致股骨頭的結構破壞和塌陷，最終形成髖關節(jié)炎。股骨頭壞死多發(fā)生在中青年人群，主要表現(xiàn)為髖關節(jié)疼痛和活動受限，嚴重影響生活質量和工作能力，被稱為“不死的癌癥”。股骨頭壞死的原因可以分為原發(fā)性和繼發(fā)性兩大類。原發(fā)性股骨頭壞死又稱為特發(fā)性股骨頭壞死：顧名思義，主要是指股骨頭壞死的原因不明確。對于有明確原因的股骨頭壞死，稱為繼發(fā)性股骨頭壞死，可分為創(chuàng)傷性和非創(chuàng)傷性兩大類。創(chuàng)傷性股骨頭壞死：是指由于髖部外傷，如股骨頸骨折、髖臼骨折、髖關節(jié)脫位等，導致股骨頭的血管受損或中斷，造成股骨頭的缺血壞死。非創(chuàng)傷性股骨頭壞死：是指由于其他原因，如長期使用或濫用糖皮質激素、長期過量飲酒、減壓病、血液病、自身免疫病、感染、放射治療等，導致股骨頭的血管痙攣、狹窄、栓塞或閉塞，造成股骨頭的缺血壞死。我國非創(chuàng)傷性股骨頭壞死最常見的原因是飲酒和糖皮質激素導致的壞死。因此，我們應該避免長期大量飲酒，在醫(yī)生指導下應用糖皮質激素，預防出現(xiàn)股骨頭壞死。股骨頭壞死的癥狀因病變的部位、范圍和程度不同而異。早期，股骨頭壞死可能沒有明顯的癥狀，或者只有輕微的髖關節(jié)不適，難以引起注意。隨著病情的發(fā)展，股骨頭壞死會出現(xiàn)以下的癥狀：?髖關節(jié)疼痛：這是股骨頭壞死的最常見和最主要的癥狀，通常表現(xiàn)為病變側的髖部、臀部或腹股溝部位的疼痛，有時也會放射到大腿內側或膝關節(jié)。疼痛的性質可以是鈍痛、隱痛、刺痛或劇痛，疼痛的程度可以是輕微、中等或嚴重，疼痛的時間可以是間歇性、持續(xù)性或加重性。一般來說，疼痛會隨著活動的增加而加重，隨著休息的延長而減輕，但在病變嚴重時，即使在靜止或夜間也會出現(xiàn)疼痛。?髖關節(jié)活動受限：這是股骨頭壞死的另一個常見的癥狀，通常表現(xiàn)為病變側的髖關節(jié)的活動范圍減少，特別是內旋、屈曲和外展等方向的活動受限。髖關節(jié)活動受限會影響患者的正常行走、下蹲、上下樓梯等日?；顒樱踔翆е迈诵谢蛐枰褂幂o助器具。?髖關節(jié)畸形：這是股骨頭壞死的晚期癥狀，通常表現(xiàn)為病變側的髖關節(jié)的外形發(fā)生改變，如股骨頭塌陷、髖關節(jié)間隙狹窄、下肢短縮等。髖關節(jié)畸形會進一步加重髖關節(jié)的疼痛和活動受限，甚至導致髖關節(jié)的功能喪失。股骨頭壞死的分型和分期有多種方法，常用的有以下幾種：?根據(jù)病變的程度，分為Ficat分期和ARCO分期。Ficat分期是最常用的分期方法，根據(jù)X線片的表現(xiàn)，分為0期、I期、II期、III期和IV期。0期：無疼痛，X線片正常，MRI或骨掃描出現(xiàn)異常；I期：有疼痛，X線片正常，MRI或骨掃描出現(xiàn)異常；II期：有疼痛，X線片出現(xiàn)囊性變或硬化，沒有軟骨下骨折；III期：有疼痛，X線片出現(xiàn)股骨頭塌陷，有新月征或臺階征；IV期：有疼痛，X線片出現(xiàn)髖臼病變，有關節(jié)間隙狹窄和骨關節(jié)炎。ARCO分型是在FICAT分期的基礎之上，根據(jù)X光片上股骨頭壞死的范圍，將每一期進一步分為ABC三個亞型，并發(fā)現(xiàn)ARCO1/2C型的患者股骨頭塌陷率高達70-90%。這是因為C型患者股骨頭壞死區(qū)域超出了髖臼邊緣以外，整個壞死區(qū)域都在髖臼應力集中區(qū)域，因而更加容易發(fā)生塌陷。?A型：壞死區(qū)位于股骨頭的中心部，占據(jù)股骨頭的1/4至1/2。?B型：壞死區(qū)位于股骨頭的邊緣部，占據(jù)股骨頭的1/4至1/2，但仍在髖臼邊緣外側負重區(qū)以內。?C型：壞死區(qū)位于股骨頭的整個部位，占據(jù)股骨頭的1/2以上，超過了髖臼邊緣外側負重區(qū)。ARCO分型的意義在于，由于不同類型患者的塌陷風險不同，該分型可以指導治療方案和預后：A型的患者可以采用保髖治療，如髓心減壓、骨移植等；B型的患者可以采用保髖或置換治療，如髖臼成形術、表面置換術等；C型的患者則需要采用置換治療，如全髖關節(jié)置換術。股骨頭壞死的治療方法主要有非手術治療和手術治療兩種。非手術治療適用于ARCO1/2A型患者，或者已塌陷患者置換前的對癥治療：?藥物治療：目前常用藥物包括降脂藥（如阿托伐他?。?、參與骨代謝藥物（如雙膦酸鹽）、抗凝藥（如阿司匹林）、血管擴張劑（如尼可地爾）、抗炎藥（如非甾體抗炎藥）等，可以改善股骨頭的血液循環(huán)，減輕炎癥反應，促進骨組織修復。?物理治療：包括體外高能震波、高壓氧、電磁場、超聲波等，可以刺激股骨頭的血管生成，增加骨髓血流，抑制骨吸收，增強骨形成。非手術治療的優(yōu)點是無創(chuàng)、安全、經(jīng)濟，但缺點是效果不穩(wěn)定、不可預測，需要長期堅持，且不能根本解決股骨頭的壞死問題，只能延緩病情的進展。因此，非手術治療需要嚴格遵循醫(yī)囑，定期復查，及時評估療效，一旦發(fā)現(xiàn)股骨頭有塌陷的跡象，應及時轉為手術治療。?保髖手術：保髖手術是指通過保留患者自身的股骨頭為主的修復重建術，來延緩或避免行人工髖關節(jié)置換術。保髖手術的種類很多，常用術式包括髓芯減壓術、截骨術、帶或不帶血運的骨移植術、鉭棒植入手術、介入手術、股骨頭自體干細胞移植等。保髖手術適用于股骨頭壞死早期（FICATⅠ期和Ⅱ期），且壞死體積在15%以上者。保髖手術的優(yōu)點是可以最大限度地保留患者自身的骨組織和關節(jié)功能，避免人工關節(jié)置換術的并發(fā)癥和修復術。但缺點是有一定的失敗率和復發(fā)率，需要嚴格掌握適應癥和手術時機。對塌陷前的ARCO1-2A/B型的患者，積水潭醫(yī)院矯形骨科周一新教授領銜研發(fā)了一種新的股骨頭壞死保髖治療術式——多孔AVNCage（3D打印籠形鈦金屬假體）支撐術，可避免既往鉭棒、人工骨、異體骨等植入材料的局限性（如導致后續(xù)治療困難和粗隆區(qū)骨折的并發(fā)癥、不能長時間維持壞死區(qū)減壓、阻礙粗隆區(qū)向壞死區(qū)的修復通道、不能形成長期有效力學支撐等）。自2018年開始，我們采用AVNCAGE這一新型假體，并改良手術工具及手術方式，可避免牽引床手術，可有效避免術中股骨頭穿透等并發(fā)癥。該項創(chuàng)新術式將手術時間從1-2小時縮短為平均0.5小時，使2年股骨頭生存率從平均70-75%(髓心減壓術）提高至88%，使很多中青年病人避免了致殘及人工關節(jié)置換術，降低了醫(yī)療費用，獲批多項專利，獲NMPA3類注冊證1項，目前已經(jīng)在國內臨床應用400余例。針對股骨頭壞死已經(jīng)塌陷，但仍未發(fā)生髖關節(jié)骨關節(jié)炎的FICAT3期患者，傳統(tǒng)保髖手術就無能為力了。針對這一部分患者的臨床需求，積水潭醫(yī)院矯形骨科周一新教授領銜研發(fā)了一種新型3D打印個性化定制部分髖關節(jié)假體，采用不損傷旋股動脈的外科脫位入路，進行塌陷區(qū)域股骨頭的部分置換，恢復關節(jié)面平滑度，延緩關節(jié)炎進展，延后或避免全髖置換術。自2021年，我中心已開始以定制化手術開展3D打印定制部分髖關節(jié)置換術，適應證為塌陷早期且壞死面積相對局限的股骨頭壞死病例，采用外科脫位入路，術中不切斷任何髖關節(jié)肌肉，保留髖臼側所有正常結構，可極大保留髖關節(jié)功能，臨床隨訪使得傳統(tǒng)100需要髖關節(jié)置換的FICAT3期患者，有75%病例獲得明顯延緩甚至避免行全髖置換術。該手術填補了FICAT3期股骨頭壞死的手術治療空白，為因股骨頭塌陷致殘的中青年病人帶來了新的治療選擇。當股骨頭壞死進展為髖關節(jié)炎（FICAT4期），就失去了保髖治療機會了，需要進行人工髖關節(jié)置換術。人工髖關節(jié)置換術的種類也很多，常用術式包括全髖關節(jié)置換術、表面置換術、半髖關節(jié)置換術等。人工髖關節(jié)置換術適用于股骨頭壞死晚期（FICAT3-4期）且癥狀嚴重、保髖手術失敗或不適合者。人工髖關節(jié)置換術的優(yōu)點是可以徹底解決股骨頭壞死引起的疼痛和功能障礙，療效顯著、穩(wěn)定，但缺點是有一定的手術風險和并發(fā)癥，如感染、血栓、脫位、松動等，且人工關節(jié)有一定的使用壽命，對于年輕患者，存在可能需要進行二次翻修的風險。

股骨頭壞死早中期經(jīng)常面臨兩個問題：一、容易誤診、漏診，以至于失治誤治；二、治療方法選擇困難，對手術與否、何時手術心存疑慮，甚至錯過最佳治療時機。希望本案例可提供一點借鑒。男性，41歲，2016年12月主訴“不明原因右臀部疼痛”以雙側股骨頭壞死為診斷住院治療。在當?shù)蒯t(yī)院磁共振檢查確診，左側壞死尚無癥狀。在我院CT檢查示：X線檢查：術中所見：我們采用外科脫位技術，充分暴露股骨頭，經(jīng)圓韌帶窩窗口挖出死骨并進行植骨。術中見關節(jié)面軟骨發(fā)生退變，死骨松軟如豆腐渣。術后復查：術后1年復查：術后3.5年復查：骨吸收是股骨頭壞死修復過程中非常棘手的問題，必須采取積極措施阻止進一步惡化。通常會采取多種方法，包括藥物治療、高能聚焦沖擊波治療等。半年后再次復查：又過了1年，術后第5年復查：術后7年復查：術后8年復查：至于左側股骨頭壞死，因為面積較小，簡單采用中藥、沖擊波治療，一直情況穩(wěn)定，這次就不展開贅述。如下：幾句話總結1.年輕股骨頭壞死保頭要趁早，切莫沉醉在所謂“秘方”的幻想中，建議通過全面檢查評估制定周全的治療方案；2.大約2/5的早中期病例可通過保守治療控制病情，但需要手術的情況也不能視而不見，理性、客觀對待病情；3.股骨頭壞死的病情轉歸十分復雜，別人成功的經(jīng)驗一定不是放之四海而皆準，除了因人而異進行治療之外，必須堅持定期復查、長期觀察，以準確掌握病情變化，在關鍵節(jié)點調整治療措施；4.任何一種單一治療措施發(fā)揮的作用總是有限的，就如做飯放調料，某一種佐料看似不起眼，缺一樣就少一種味道，和諧搭配才能取得最佳效果。同樣，藥物治療、物理治療，甚或手術治療需要有機結合，切莫盲目相信某一種方法的“神奇”效果。

治療前股骨頭壞死對于年輕患者來說往往比較麻煩，如果可能的情況下，盡量對患者行保頭治療，給股骨頭一個能自我修復的機會，如果成功了，還是自己原裝的好。治療中術前透視下精確定位好壞死位置，使用專用工具對病灶徹底刮除，沖洗，再行打壓植骨填充壞死區(qū)治療后治療后7天患者創(chuàng)傷小，術后恢復快。7天出院，出院前拍片復查。最后一張為術后一個月