压应力对骨愈合过程中破骨细胞的作用机制研究进展  

The Compressive Stress on the Mechanism of Osteoclasts during Bone Healing

作　　者：郑未来 于大淼[1] 廉永云[1] 

机构地区：[1]哈尔滨医科大学附属第四医院骨科,哈尔滨150001

出　　处：《医学综述》2015年第17期3095-3097,共3页Medical Recapitulate

基　　金：黑龙江省教育厅科学技术研究项目(12521182)

摘　　要：近年来运用力学技术治疗骨不愈合成为骨科领域的重点,尤其是压应力学对骨细胞作用的分子机制研究更是临床医师和广大科研工作者研究的热点。该文通过分析引起骨不连的力学因素以及骨保护素/细胞核因子κB受体活化因子配基信号系统的组成和相互作用,进一步探讨压应力抑制破骨细胞分化的内在机制,从而为更深一步拓宽医学与工程学尤其是力学领域的通力合作打下坚实的基础。Over the last period the use of mechanical treatment of bone nonunion, especially study on the molecular mechanism of compressive stress on the bone cells has become the focus of the orthopedic field. Here analyzes the factors causing the composition of nonunion mechanics and osteoprotegerin/receptor activa- tor of nuclear factor KB ligand signaling system, and further explores the intrinsic mechanisms of how stress suppresses osteoclast differentiation, so as to lay a solid foundation for deeper cooperation between medicine and engineering, especially mechanics.

关 键 词：破骨细胞 压应力 骨保护素/细胞核因子κB受体活化因子配基/细胞核因子κB受体活化因子 

分 类 号：R68[医药卫生—骨科学]