骨搬移技术治疗骨不连的分子机制研究初探  

Exploration of Molecular Mechanism of Removal Technology Treatment of Nonunion Bone

作　　者：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》2014年第7期1156-1158,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,在骨科领域中如何利用骨搬移技术治疗骨不连成为医学界广泛瞩目的焦点。该文阐释骨保护素/核因子κB受体活化因子配基/核因子κB受体活化因子系统对破骨细胞分化、激活和凋亡的调节机制,并探讨在骨搬移技术治疗中压应力如何抑制破骨细胞的分化,从而为进一步研究Ilizarov的骨搬移技术通过压应力刺激骨不连组织及其骨不连细胞治疗骨不连的机制打下基础。In recent years, the use of bone removal technology in the treatment of bone non-union become the focus of widespread attention of the orthopedics medical field. Here is to illustrate the regulating mechanisms of OPG/RANKL/RANK signaling pathway on osteoclast differentiation, activation and apoptosis from the molecular level, and explore how the compressive stress in the bone removal technique for inhibition of osteoclast differentiation, to lay the foundation for further study of the mechanisms of the Ilizarov bone removal technique by compressive stress stimulation of bone non-union tissue and cells.

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受体活化因子信号通路 

分 类 号：R68[医药卫生—骨科学]