Osteoarthritis (OA), which is characterized mainly by cartilage degradation, is the most prevalent joint disorder worldwide. Although OA is identified as a major cause of joint pain, disability, and socioeconomic burden, the etiology of OA is still not clearly known. Recently, gene microarray analysis has become an efficient method for the research of complex diseases and has been employed to determine what genes and pathways are involved in the pathological process of OA. In this review, OA study results over the last decade are summarized for gene expression profiling of various tissues, such as cartilage, subchondral bone, and synovium in human OA and mouse OA models. Many differentially expressed genes, which mainly involve matrix metabolism, bone turnover, and inflammation pathways, were identified in diseased compared with “normal” tissues. Nevertheless, rare common genes were reported from studies using different tissue sources, microarray chips, and research designs. Thus, future novel and carefully designed microarray studies are required to elucidate underlying genetic mechanisms in the pathogenesis of OA as well as new directions for potential OA-targeted pharmaceutical therapies.

骨关节炎（OA）的主要特征是软骨退化，是全世界最普遍的关节疾病。尽管OA被认为是导致关节疼痛，残疾和社会经济负担的主要原因，但OA的​​病因仍不清楚。近年来，基因芯片分析已成为研究复杂疾病的有效方法，并已被用于确定OA病理过程涉及哪些基因和途径。在这篇综述中，总结了过去十年的OA研究成果，以分析人OA和小鼠OA模型中各种组织的基因表达谱，例如软骨，软骨下骨和滑膜。与“正常”组织相比，在疾病中鉴定出许多差异表达基因，主要涉及基质代谢，骨骼更新和炎症途径。然而，使用不同组织来源，微阵列芯片和研究设计的研究报告了罕见的共有基因。因此，需要未来的新颖且经过精心设计的微阵列研究来阐明OA发病机理中的潜在遗传机制，以及可能针对OA的药物治疗的新方向。