RANKL synthesized by articular chondrocytes contributes to juxta-articular bone loss in chronic arthritis 英文参考文献.docVIP

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RANKL synthesized by articular chondrocytes contributes to juxta-articular bone loss in chronic arthritis 英文参考文献.doc

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RANKL synthesized by articular chondrocytes contributes to juxta-articular bone loss in chronic arthritis 英文参考文献

Martínez-Calatravaetal.ArthritisResearchTherapy2012,14:R149 /content/14/3/R149 RESEARCH ARTICLE OpenAccess RANKLsynthesizedbyarticularchondrocytes contributestojuxta-articularbonelossinchronic arthritis MariaJMartínez-Calatrava,IvanPrieto-Potín,JorgeARoman-Blas,LidiaTardio,RaquelLargoand GabrielHerrero-Beaumont* Abstract Introduction:Thereceptoractivatornuclearfactor-kappaBligand(RANKL)diffusesfromarticularcartilageto subchondralbone.However,theroleofchondrocyte-synthesizedRANKLinrheumatoidarthritis-associatedjuxta- articularbonelosshasnotyetbeenexplored.ThisstudyaimedtodeterminewhetherRANKLproducedby chondrocytesinducesosteoclastogenesisandjuxta-articularbonelossassociatedwithchronicarthritis. Methods:Chronicantigen-inducedarthritis(AIA)wasinducedinNewZealand(NZ)rabbits.Osteoarthritis(OA)and controlgroupsweresimultaneouslystudied.DualX-rayabsorptiometryofsubchondralkneebonewasperformed beforesacrifice.HistologicalanalysisandproteinexpressionofRANKLandosteoprotegerin(OPG)wereevaluatedin jointtissues.Co-culturesofhumanOAarticularchondrocyteswithperipheralbloodmononuclearcells(PBMCs) fromhealthydonorswerestimulatedwithmacrophage-colonystimulatingfactor(M-CSF)andprostaglandinE2 (PGE2),thenfurtherstainedwithtartrate-resistantacidphosphatase. Results:SubchondralbonelosswasconfirmedinAIArabbitswhencomparedwithcontrols.Theexpressionof RANKL,OPGandRANKL/OPGratioincartilagewereincreasedinAIAcomparedtocontrolanimals,althoughthis patternwasnotseeninsynovium.Furthermore,RANKLexpressionandRANKL/OPGratiowereinverselyrelatedto subchondralbonemineraldensity.RANKLexpressionwasobservedthroughoutallcartilagezonesofrabbitsand wasspeciallyincreasedinthecalcifiedcartilageofAIAanimals.Co-culturesdemonstratedthatPGE2-stimulated humanchondrocytes,whichproduceRANKL,alsoinduceosteoclastsdifferentiationfromPBMCs. Conclusions:Chondrocyte-synthesizedRANKLmaycontributetothedevelopmentofjuxta-articularosteoporosis associatedwithchronicarthritis,byenhancingosteoclastogenesis.Theseresultspointout