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Oestrogen deficiency modulates particle-induced osteolysis 英文参考文献
Nichetal.ArthritisResearchTherapy2011,13:R100
/content/13/3/R100
RESEARCH ARTICLE
OpenAccess
Oestrogendeficiencymodulatesparticle-induced
osteolysis
ChristopheNich1*,JeanLanglois1,ArnaudMarchadier2,3,CatherineVidal3,MartineCohen-Solal4,HervéPetite1and
MoussaHamadouche1
Abstract
Introduction:Postmenopausalosteoporosismaymodulateboneresponsetoweardebris.Inthisarticle,we
evaluatetheinfluenceofoestrogendeficiencyonexperimentalparticle-inducedosteolysis.
Methods:Polyethylene(PE)particleswereimplantedontothecalvariaofnormalcontrols,sham-ovariectomized
(OVX),OVXmiceandOVXmicesupplementedwithoestrogen(OVX+E).After14days,sevenskullspergroupwere
analyzedusingahigh-resolutionmicro-computedtomography(micro-CT)andhistomorphometry,andfortartrate-
specificalkalinephosphatase.FivecalvariaepergroupwereculturedfortheassayofIL-1b,IL-6,TNF-aandreceptor
activatorofthenuclearfactorB(RANKL)secretionusingquantitativeELISA.SerumIL-6concentrationswere
obtained.TheexpressionofRANKLandosteoprotegerin(OPG)mRNAwereevaluatedusingreal-timePCR.
Results:AsassessedbyμCTandbyhistomorphometry,PEparticlesinducedextensiveboneresorptionandan
intenseinflammatoryreactioninnormalcontrols,sham-OVXandOVX+Emice,butnotintheOVXmicegroup.In
normalcontrols,sham-OVXandOVX+Emice,PEparticlesinducedanincreaseinserumIL-6,inTNF-aandRANKL
localconcentrations,andresultedinasignificantincreaseinRANKL/OPGmessengerRNA(mRNA)ratio.Conversely,
theseparametersremainedunchangedinOVXmiceafterPEimplantation.
Conclusions:OestrogenprivationintheosteolysismurinemodelultimatelyattenuatedosteolyticresponsetoPE
particles,suggestingaprotectiveeffect.Thisparadoxicalphenomenonwasassociatedwithadown-regulationof
pro-resorptivecytokines.Itishypothesizedthatexcessiveinflammatoryresponsewascontrolled,illustratedbythe
absenceofincreaseofserumIL-6inOVXmiceafterPEimplantation.
Introduction
recentwork,weevaluatedtheboneresponsetoparticu-
Asepticlooseningoftotaljointreplacementsdevelopsas late debris in an ovariectomized mice model [6]. We
a
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