CAJ | 학술논문

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,在标题和中以“骨关节炎;细胞凋亡;基质金属蛋白酶;自由基”或“osteoarthritis,apoptosis, metal oprotease 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.
배경:목전골관절염적발병궤제재굉관급미관층차상수연득도료흔대적학증,단시잉연불심청초,심지자상모순、고차실피、몰능형성경가계통、전면、과학적이론체계.목적:대국내외창상성골관절염연골세포손배여수복궤제적현상급신진전작일종술.방법:응용계산궤검색 CNKI 화 Pubmed 수거고중1994년1월지2011년10월관우창상성골관절염연골세포손배여수복궤제적문장,재표제화중이“골관절염;세포조망;기질금속단백매;자유기”혹“osteoarthritis,apoptosis, metal oprotease free radical”위검색사진행검색.선택문장내용여창상성골관절발병궤제유관자,동일영역문헌칙선택근기발표혹발표재권위잡지문장.초검득도140편문헌,근거납입표준선택관우아주국부완석제적31문헌진행종술.결과여결론:창상성골관절염적발생시재굉관생물역학개변적기출상,계동료세포통신계통중적세포전도통로궤제,격발료정서화적“파배여수복”궤제,기중연골세포조망、분해대사매、자유기이급상관세포인자적면역응답유가능취시기발병적“축심”궤제.
BACKGROUND: Although it has been confirmed in macro and micro level, the pathogenesis of osteoarthritis is stil unclear, even self-contradictory and unable to form the more systematic, comprehensive, scientific theory system. OBJECTIVE: To review the progress in chondrocyte damage fol owing 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 fol owing traumatic osteoarthritis and repair mechanism. The keywords were “osteoarthritis, apoptosis, metal oprotease, 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. Total y 140 articles were checked, and final y 31 articles addressing periodontal local sustained release agent were reviewed. RESULTS AND CONCLUSION: Traumatic osteoarthritis occurs based on the macroscopic biomechanical changes, starting with cel transduction mechanism in cel ular 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.