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Bone density after rigid plate fixation of tibial fractures. A dual-energy X-ray absorptiometry study

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Bone density after rigid plate fixation of tibial fractures. A dual-energy X-ray absorptiometry study
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  914THEJOURNALOFBONEANDJOINTSURGERY BONEDENSITYAFTERRIGIDPLATEFIXATIONOF TIBIALFRACTURES A DUAL-ENERGYX-RAYABSORPTIOMETRYSTUDY G.C.JANES,D.M.COLLOPY,R.PRICE,J.M.SIKORSKI FromtheUniversityofWesternAustraliaandtheSirCharlesGairdnerHospital,Perth,WesternAustralia We used dual-energyX-rayabsorptiometry  DEXA tomeasurethebonemineralcontent(BMC)ofbothtibiaein13patientswhohad been treatedforatibialfractureby rigidplatefixation.Within two weeks ofplateremovaltheBMCwassignificantly greater inthebonethathad been undertheplatethanatthesamesiteinthecontroltibia.An unplatedareaofbonenearthe ankle showed asignificant decreaseinBMCatthetimeofplateremovalwith subsequent return tothelevelofthecontroltibiaduringtheensuing18months.Weconcludethatosteoinductiveinfluencesoutweighthepotentialcausesofosteopenia,suchasstressshieldinganddisuse,andthat,contrarytoexpectation,demineralis-ationisnotafactorinthe diminished strengthofthetibia afterplatingforfracture.   oneJointSurg[ r] 1993 ; 75 B:914 7 Received26June1992;Acceptedafterrevision5May1993 Whendiaphyseal fracturesof thetibiaaretreatedbyopenreductionandapplicationofametalplate,utilising theprincipleofdynamiccompression,theimplantdivertsloadawayfromthebone(stress shielding)anditiswidely believed that thebonethenbecomesosteoporotic (Akeson etal1976).Inanimalexperimentsbonehasbeenshowntohavereducedstrengthcharacteristicsaftertheremovalofrigidinternalfixationdevices(Toninoet al 1976;L {226}ftmann, SigurdssonandStromberg1980;L {225}ftmannetal1989). Thecausesofthisweaknessarethoughttobeduetotwo G.C.Janes,MBBS,LecturerJ.M.Sikorski,MD,FRACS,ProfessorUniversityDepartmentofSurgery(Orthopaedics),2ndFloor,‘M’ Block,QueenElizabethIIMedicalCentre,Nedlands6009,Western Australia D.M.Collopy,MBBS,OrthopaedicRegistrarR.Price,PhD,ScientistinCharge,BoneStructuralUnit,Department ofEndocrinologySirCharlesGairdnerHospital,VerdunStreet,Nedlands6009,Western Australia CorrespondenceshouldbesenttoDrG.C.Janes.©l993BritishEditorialSocietyofBoneandJointSurgery0301-620X/93/6672 2.00 differentmechanisms,corticalatrophyandtheeffectoftheresidualscrewholes.UhthoffandDubuc(1971)platedosteotomisedcaninefemoraforperiodsrangingfrom2to30weeks. Theyfound thatthisresultedincorticalthinning,trabeculationofthecortexandpersistenceofdisorgan-isedwovenbone at theosteotomysite.Moststudieshaveshownthat thepreviouslyplated segmentofbonehasthincorticesandanenlargedmedullarycavityfromendostealresorption(Akesonetal1976;Moyenetal1978 ;Paavolainenet al1978 ;Sl {228}tistal1978;Stromberg andDalen1978;TerjesenandBenum1983;L {226}ftmann etal 1989).Carter,VasuandHarris(1981),however,inanimalstudiesreportedthickeningofthecorticalbone adjacenttotheplateduetonewboneformation. Twohypotheses, whicharenotmutuallyexclusive, areproposedto explain the phenomenonofcorticalatrophyobservedinanimalmodels.Thefirst,andmostwidely heldview,isthattherigidplatedivertscompres- sivebendingandtorsionalstressesawayfromthebone, whichreactsbyreducing itscorticalthicknessandbone massinaccordancewithWolff’slaw(Wolff1892;Carteretal1984;Perren1991).Thesecondhypothesisisthattherigidplatecompromisestheperiostealbloodsupply causingischaemiaandresorptionofthe underlyingbone.Thislatterconcepthasledtothedevelopmentofthe‘limited contact - dynamiccompressionplate’(Perren 1991).Theincreasedporosity(trabeculation)ofcorticalbonehasbeeninvestigatedbymicroscopy,microradiog- raphy(Paavolainenetal1978;Sl {228}tistal1978;Stromberg andDalen1978;Terjesen, NordbyandArnulf1985)cross-sectional pointcounting(StrombergandDalen 1978),singleanddualphotonabsorptiometry(Terjesen andBenum1983;Rosson,PetleyandShearer1991),and bygammarayabsorption (Toninoetal 1976). Allstudies foundanincreaseintheporosityofthecorticalboneundertheplate.Mostofthem,however,wereperformedonintactanimal longbones.L {225}ftmannetal(1989) combinedanosteotomywithplatingandreportedan initialincreaseinbonemineralisation,asmeasuredbyashweight,onlytofindthatitsoonreturnedtonormalandsubsequentlybecameatrophic.Somestudieshave  removal.Theaverageduration ofplatefixationwas 14.8 months(10 to24).Nopatientsuffered fromanymedicaldisorder,orwastakinganydrugs,suchasoralcontracep- tives,whichcouldaffectbonemetabolism.Alltheplates wereremovedundergeneralanaesthesiabyoneoftheauthors.Thepatientswereadvisedtoavoidcontactsports andheavymanualworkfor aperiod ofsixmonths.BonemineralcontentwasassessedusingDEXA (Hologic QDR - 1000/W,Waltham,Massachusetts).Weexaminedtheareabeneaththeplate(theregionofthefracture)and thetibiaabovetheankle(Fig.1). The regionbeneaththeplatewassubdividedintothearea undertheproximalportionoftheplate(P1),thatunderthemiddleofthe plate(P2) andthatunderthedistalendoftheplate(P3).Thesupramalleolarregionwas subdividedintothemid-distalregion(Dl)andthe ultra- distalregion(D2),6 mmproximal tothejointline,wellabovethesubchondralboneplate.TheDEXAresults areexpressed asgramsofhydroxyapatitepercentimetreofbone.Thefirstscanwasperformedwithintwoweeksof theremovaloftheplateinall13patients.Five patientsweresubsequentlylosttofollow-up.Theremainingeightwererescannedbetween12and18months later. Both tibiaewerescannedonbothoccasions. Toensurethat weusedequivalentareasofthetibia, thedistanceofthe fracturefromtheanklewasmeasuredandtheequivalentregiononthecontralateraltibiawasscanned. ThedataareexpressedasthemeanBMCateachlevelofthetibia±thestandarderror.Thesamedataare presentedasaratiooffracturedtocontrollimbsatthe equivalentsites ofthe tibia(TableI)toshowthedifferencesbetweenthelimbs.Itisnot possibleto comparedifferentareasofthetibiabecauseofthe Fig.1 comparedthe effectofplatesofdifferentrigidityand foundthat rigidplatesresulted inmorestressshielding andgreatersubsequentbone resorption(Akesonet al 1976;Moyenetal1978;Carteretal1984).Mostanimalstudieshavefoundadirectrelationshipbetweenosteopeniaandboneweakness.Thereductionofstrength ofrabbit tibiaeafter1 2 weeksofplating variedfrom 28%to 53 (L {225}ftmannetal1980;Terjesen and Benum1 983).Therewasanon-linearrecoverycurve,theperiodrequiredtoregainmaximumstrengthbeing approximatelyhalfthedurationoftheplatefixation. Onlyonestudyhasshownplate-inducedosteopenia inman.Terjesenetal(1985)usedquantitativeCTin previouslyfractured andplatedfemoraandfoundan 1 1 % reductioninbonemineralisationbutnoevidenceofdiminishedcorticalwidth.Rossonetal(1991),whoinvestigatedpreviouslyfracturedandplatedforearmbonesusingsinglephotonabsorptiometry,foundatrophic bonechangesonlywhenplateswereremovedpre-maturely(lessthan21months). Thepresence ofplate osteopeniathereforehasnotbeen conclusivelydemon- stratedinfractured, plated,human,longbonesafter the fracturehasunited. Tibialplatesremaininplacefor12to 1 8months on average.Whentheyare removed thereisaperiodofrelativeweaknessofthebonewhichissaidtobeassociatedwithanincreasedlikelihoodofrefracture(BuckwalterandCruess1991).Ithasbeenassumedthatthereisthenagradualreturntonormal bone strength.Thedurationofthisperiodofrelativeweaknessisunknown.Ourstudyaimed to testthefollowinghypotheses:1)that arelativeosteoporosisexistsin tibiaeafterthe applicationofrigidAOplatesforthemanagementoffractures ofthetibialdiaphysis; and(2)thatthisosteoporosisisreversedafterremovalofthe plate. Dual-energyX-rayabsorptiometry  DEXA is a minimallyinvasivetechniqueformeasuringboneden- sity.X-raysoftwoenergiesarepassedthroughacalibrator andsubsequentlythroughthesubject,andadetectorassessestheirdifferentialabsorptionbythetissues. DEXAhasseveraladvantagesoverexistingforms ofdensitometry.Itismoreprecisethansingleordualphotonabsorptiometry orquantified CTandits resultsaremorereproducible(Cullum,EllandRyder1989;SartorisandResnick1989;GlOeretal1990).Tiedemanetal(1990)showeda goodcorrelationbetweendensito- metricevaluationandbonerigidity.PATIENTSANDMETHODSWestudiedtenmenandthreewomenwithanaverage ageof26.2years  16.5 to42.4)allofwhomhadsustained afracture ofthetibialdiaphysiswhichhadbeenplatedwithanAONarrow DynamicCompressionPlate(AO International,Davos,Switzerland).Thefractureshadunitedclinically andradiologicallyatthetimeofplate Mid-distalDl 44mm Ultra-distal D220mm6mm proximal tojointline TheareasscannedbyDEXAafterremovaloftherigidplate. BONEDENSITYAFTERRIGIDPLATEFIXATIONOFTIBIALFRACTURES 915VOL.75-B,No.6,NOVEMBER1993 PLATEDREGION Proximal P1 20mm Middle P240mm Distal P3 20mm DISTAL REGION    4.5 04 000 > x 0 > E C.) a) 0 ProximalMiddle DistalSite onthetibia E Controltibia < 2weeks Controltibia > 12months .Fracturedtibia < 2 weeks {149}racturedtibia > 12months916G.C.JANES,D.M.COLLOPY,R.PRICE,J.M.SIKORSKITHEJOURNALOFBONEANDJOINTSURGERYTable I.BMC (g/cmhydroxyapatitecrystal ; mean± SEM) of13fracturedandcontroltibiaewithintwoweeksofremovaloftheplateFracturedtibiaeControltibiae Difference  per cent) RatioRegionnearfracture P1:proximal P2:middleP3:distal3.94±0.214.09±0.283.67±0.323.47±0.133.43±0.153.20±0.16  13.65 +19.38*  14.80 1.141.191.15RegionnearankleDl:mid-distalD2:ultra-distal3.04±0.213.76±0.332.94±0.164.07±0.22  3.42   7.5fl 1.030.92 * representsanincreaseinthefracturedlimbcomparedwiththecontrol,p < 0.05 t represents adecreaseinthefracturedlimbcomparedwiththecontrol,p < 0.05Table II.BMC (g/cmhydroxyapatitecrystal;mean±5EM)ofeightfracturedandcontroltibiae12toI8monthsafterremovaloftheplateFracturedtibiaeControltibiae Difference  per cent) Ratio Regionnearfracture Pl:proximal P2:middleP3:distal 4 14±0 24 4.32±0.373.84±0.44 3 30±0 14 3.27±0.I73.12±0.21 +25.45* + 32.JJ* + 23.07 1.25I.32I.23RegionnearankleDl:mid-distalD2:ultra-distal3.12±0.333.74±0.552.86±0.213.85±0.29  9.09 -2.85 1.090.97 * represents an increaseinthefracturedlimbcomparedwiththecontrol,p < 0.05 variationsinwidthandratioofcancelloustocortical bone. StatisticalanalysiswasperformedbytheWilcoxon matchedpairs signed-ranktest.RESULTSBMCtwoweeksafterplateremoval.In12ofthe13patientstheBMCwassignificantlygreater(p <0.05) at all sitesundertheplate(TableI);intheotheritwas slightlydiminished.Inthemid-distalregion(Dl)there wasalsoasmallbutnotstatisticallysignificantincrease.Bycontrast,theultra-distalregion(D2)ofthetibiashowed adecrease inmineralcontent(p < 0.05). Thebonewidthatthefracturesite,measuredatthetimeofthefirstscan,wasnotsignificantlydifferentfromthatofthecontroltibia.BMC18monthsafterplateremoval.TheBMCofeightofthe13patientswasmeasuredagain12to18monthsafterremovaloftheplate.TheincreaseinBMCintheareaoftheplatewasfoundtohavepersistedandwassignificantlygreaterinallareasthanimmediatelyafterplateremoval(TableII).Inthemid-distalregion(Dl)theincreasewasalsostatisticallysignificant.Intheultra- distal(D2)regiontherelativedemineralisationfound initiallyhadbeenreversed. Changesin BMCover18months.TheBMCofthecon- troltibiaedidnotchangesignificantlyduringthe18monthsofthestudy.Thevariationwas1.0%orlessinthecentraldiaphysis(p   0.96)and1.4%orlessatthedistalandultra-distalsites(p   0.38).Bycontrast,the previouslyplatedlimbsshowed a progressiveincreasein Fig 2 Comparisonofthemean BMC(g/cmhydroxyapatitecrystal)in fracturedandcontroltibiae. BMCwhich,whenusingmatchedpairs,was8%inP2 (p   0.005) and10%inP1(p < 0.001)(Fig.2);the6%increaseatP3wasnot significant.ThesiteDlshoweda smallerbut significantincreaseof 5.5 (p < 0.01).The area D2,whichhadinitiallyshownasignificantdecreaseinBMC,hadareversalofthistrendwithitsvalueapproachingthatofthecontroltibia.ThedifferencebetweenthecontrolandthefracturedtibiaeatD2was notsignificant. DISCUSSIONThisisthefirst studytohavedeterminedtheBMCin humanfracturedandplatedtibiaeand,asfarasweare  BONEDENSITYAFTERRIGIDPLATEFIXATIONOFTIBIALFRACTURES 917 VOL.75-B,No.6,NOVEMBER 1993 aware,itisthefirsttohaveusedDEXAinthiscontext. DEXA isnowestablishedasthemostaccuratemethod ofdeterminingthedegreeofmineralisationofbone. Theresultsshowthattherewasnoosteopeniabeneaththetibialplatesatthetimeoftheirremoval; contrarytoexpectationtherewasanincreasein BMCat thatsite.There was,however,a reduction inBMCabovetheankleprobablycausedbyrelativedisuse.Ourstudy did notdeterminetheBMC during thehealingphaseof thefracture, but after unionhadoccurred.Theincrease inbone densitybeneaththeplatesuggeststhatthereis an osteogenicstimulussufficient toovercometheeffects ofdisuseandstress shielding.Themostlikelycauseof theincreasedmineralcontentisthe formationofnew boneduringfracturerepair butwefinditsurprisingthat theinfluenceextendedalongtheentireareaofboneunderthe plate. Theprocessofinductionofbonecontinuedformorethanayearaftertheplatehadbeenremovedpossibly REFERENCES Akeson WH, WooS, RutherfordL,etal.Theeffectsofrigidityof internalfixationplatesonlongboneremodeling. ActaOrthop Scand 1976;47:241 9 BuckwalterJA, Cruess RL. 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ActaOrthop Scand 1989;60:718 22 MoyenBJ-L,LaheyPJJr,WeinbergEH,HarrisWH.Effectsonintact femoraofdogsoftheapplicationandremovalofmetalplates:ametabolicandstructuralstudycomparingstifferandmoreflexibleplates. JBoneJointSurg[Am] 1978 ;60-A:940-7. PaavolainenP,KaraharjuE,Sl {228}tis,Ahonen J, HolmstromT.Effectofrigidplatefixationonstructureandmineralcontentofcortical bone C inOrthop 1978;136:287 93 fromresumptionofnormalactivityandthecessationoftheeffectsofstressshielding. Theincreasein BMC was greaterin theareaunder theplate thanintheareaabovetheankle.ThefactthattheBMCishighafterremovaloftheplate does not meanthattheboneisstrong.Strength dependsnotonly uponmineral contentbutalsoupontheultrastructuralandbiochemicalorganisationofbone, andlocaliseddefectssuchasscrewholesareprobably important.Thisstudydoes nomorethan showthatoneofthe possibleoccurrencesofweaknessafterplate removal, namelydemineralisation,isnotafactor. 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