类风湿关节炎（rheumatoid arthritis，RA）是一种系统性自身免疫病，以关节损害和病理性骨量丢失为特征。近年来研究表明，核因子κB受体激活蛋白（receptor activator of nuclear factor κB，RANK）配体（RANK ligand，RANKL）-RANK通路在RA骨损害中起关键作用。人源化单克隆抗体狄诺塞麦（Denosumab，DMab）可特异性结合RANKL，阻断RANKL-RANK通路，起到骨保护作用。DMab作为一种新的治疗手段，对RA患者的局部骨侵蚀和全身性骨质疏松治疗具有明确的理论基础。此文对近5年国内外使用DMab治疗RA的研究进展做一综述。

Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by damage joint and pathologic bone mass loss  . Recent studies have shown that receptor activator of nuclear factor κB (RANK) ligand (RANKL)-RANK pathway plays a vital role in the bone damage by RA. Denosumab (DMab), a humanized monoclonal antibody, can specifically bind RANKL and block RANKL-RANK pathway, thereby protecting the bone. DMab, as a new therapeutic strategy, has a clear theoretical basis for the treatment of local bone erosion and systemic osteoporosis in RA patients. This article reviews the research progress in DMab use for the treatment of RA at home and abroad in the past 5 years.