RANKL-RANK-OPG信号通路对类风湿关节炎骨破坏作用的研究进展

Research Progress of RANKL-RANK-OPG Signaling Pathway in the Pathogenesis of Bone Destruction in Rheumatoid Arthritis

类风湿关节炎(RA)是一种以对称性、多关节的慢性炎症为主要特征的全身性自体免疫病,可导致软骨和骨骼的结构破坏。延缓甚至抑制RA患者骨破坏发生是临床治疗的主要目标。现有研究表明,在RA发病过程中,破骨细胞生成、分化和活化的改变在RA骨破坏的发病机制中起着至关重要的作用,RANKL-RANK-OPG信号系统是RA炎症导致继发性骨丢失的主要通路。但是,在RA骨破坏的过程中,RANKL-RANK-OPG系统与骨代谢系统间复杂的交互作用仍然有待进一步阐明。本文主要综述目前RANKL-RANK-OPG信号通路在RA骨破坏发生机制中的研究进展,以期为RA骨破坏的研究提供更系统的思路和新的方向。

Rheumatoid arthritis（ RA） is a systemic autoimmune disease characterized by symmetrical,multi joint chronic inflammation,leading to destruction of cartilage and skeleton. The key objective of treatment is to postpone or even inhibit the occurrence of bone destruction in RA patients. It is well known that the modification of osteoclast formation,differentiation and activation plays a crucial role in the pathogenesis of RA bone destruction and RANKL-RANK-OPG signal pathway is the main pathway for RA inflammation to cause secondary bone loss. However,the precise underlying mechanism of interaction between complex RANKL-RANK-OPG system and bone metabolism system in RA remains to be explored. In this paper,we focus on the most updated advances in the mechanism of RANKL-RANK-OPG signal pathway in the pathogenesis of RA bone destruction and hope to provide more systematic thinking and new direction for the research of RA bone destruction.