创伤性骨关节炎软骨细胞损坏与修复机制

Traumatic osteoarthritis chondrocytes damage and repair mechanism

背景:目前骨关节炎的发病机制在宏观及微观层次上虽然得到了很大的确证,但是仍然不甚清楚,甚至自相矛盾、顾此失彼、没能形成更加系统、全面、科学的理论体系。目的:对国内外创伤性骨关节炎软骨细胞损坏与修复机制的现状及新进展作一综述。方法:应用计算机检索CNKI和Pubmed数据库中1994年1月至2011年10月关于创伤性骨关节炎软骨细胞损坏与修复机制的文章,在标题和摘要中以"骨关节炎;细胞凋亡;基质金属蛋白酶;自由基"或"osteoarthritis,apoptosis,metalloprotease free radical"为检索词进行检索。选择文章内容与创伤性骨关节发病机制有关者,同一领域文献则选择近期发表或发表在权威杂志文章。初检得到140篇文献,根据纳入标准选择关于牙周局部缓释剂的31文献进行综述。结果与结论:创伤性骨关节炎的发生是在宏观生物力学改变的基础上,启动了细胞通讯系统中的细胞转导通路机制,激发了程序化的"破坏与修复"机制,其中软骨细胞凋亡、分解代谢酶、自由基以及相关细胞因子的免疫应答有可能就是其发病的"轴心"机制。

BACKGROUND：Although it has been confirmed in macro and micro level,the pathogenesis of osteoarthritis is still unclear,even self-contradictory and unable to form the more systematic,comprehensive,scientific theory system.OBJECTIVE：To review the progress in chondrocyte damage following traumatic osteoarthritis and repair mechanism.METHODS：A computer-based search of CNKI and the PubMed databases from January 1994 to October 2011 was performed for articles related to chondrocyte damage following traumatic osteoarthritis and repair mechanism.The keywords were ＂osteoarthritis,apoptosis,metalloprotease,free radical＂ in the title and abstract.Articles related to pathogenesis of traumatic osteoarthritis were selected,and articles published in the same field recently or in authorized journals were preferred.Totally 140 articles were checked,and finally 31 articles addressing periodontal local sustained release agent were reviewed.RESULTS AND CONCLUSION：Traumatic osteoarthritis occurs based on the macroscopic biomechanical changes,starting with cell transduction mechanism in cellular communication system,which inspires a programmed ＂destruction and repair＂ mechanism.Wherein,the chondrocyte apoptosis,catabolic enzymes,free radicals and related cytokine immune response may be the ＂axial＂ mechanism of traumatic osteoarthritis.