破骨细胞及其分化调节机制的研究进展  

Research progress on osteoclast and its differentiation regulation mechanism

作　　者：蒋鹏[1] 宋科官[1] JIANG Peng SONG Ke-guan.(The first Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, 150001, China)

机构地区：[1]哈尔滨医科大学附属第一医院,黑龙江150001

出　　处：《中国骨与关节杂志》2017年第3期223-227,共5页Chinese Journal of Bone and Joint

基　　金：国家自然科学基金资助项目(81270635)

摘　　要：人体骨骼是一个动态的、不断更新的组织,据调查,成年人每年大约有10%的骨骼会发生骨重建[1],骨重建主要涉及骨吸收和骨形成两个方面,二者保持动态平衡维系着骨的正常代谢,如果二者失去平衡将会引起相应的骨骼疾病[2-5]。骨质疏松症和关节假体周围骨溶解均是常见的骨代谢性疾病,主要原因就是由骨吸收功能强于骨形成,二者失去平衡引起。破骨细胞是人体惟一的具有骨吸收功能的细胞,因此研究破骨细胞的分化机制具有重要意义。Osteoclasts derive from mononuclear hematopoietic stem cells in the bone marrow, which are the major bone resorption cells in the human body and play an important role in the reconstruction of bone. The differentiation and maturation of osteoclasts are regulated by many factors, such as receptor activator tbr nuclear factor-κB ligand （ RANKL ）, macrophage colony-stimulating factor （ MCSF ）, interleukin-1 （ IL-1 ）, interleukin-6 （ IL-6 ） and tumor necrosis factor-alpha （ TNF-α ）, which can promote osteoclast differentiation and increase osteoclast formation. And there are some other factors, such as osteoprotegerin （ OPG ） and interleukin-10 （ IL-10 ）, which can inhibit osteoclast differentiation and thereby prevent excessive growth of osteoclasts. RANK / RANKL / OPG pathway is the hub of signal transduction in the process of osteoclast mobilization and differentiation. Most cytokines play roles in osteoclast differentiation through this transduction pathway. To explore its mechanism and make feasible and effective measures to prevent the impact which is caused by the increase or reduction of osteoclasts on the organism has become an important research field in recent years.

关 键 词：破骨细胞 细胞分化 核因子ΚB受体活化因子配体 巨噬细胞集落刺激因子 信号传导 

分 类 号：R68[医药卫生—骨科学]