RANKL: A therapeutic target for bone destruction in rheumatoid arthritis

被引：70

作者：

Tanaka, Sakae ^{[1
]}

Tanaka, Yoshiya ^{[2
]}

Ishiguro, Naoki ^{[3
]}

Yamanaka, Hisashi ^{[4
]}

Takeuchi, Tsutomu ^{[5
]}

机构：

[1] Univ Tokyo, Dept Orthopaed Surg, Fac Med, Tokyo, Japan

[2] Univ Occupat & Environm Hlth, Dept Internal Med 1, Fukuoka, Japan

[3] Nagoya Univ, Dept Orthopaed Surg, Grad Sch Med, Nagoya, Aichi, Japan

[4] Tokyo Womens Med Univ, Inst Rheumatol, Tokyo, Japan

[5] Keio Univ, Sch Med, Dept Internal Med, Div Rheumatol, Tokyo, Japan

来源：

MODERN RHEUMATOLOGY | 2018年 / 28卷 / 01期

关键词：

Denosumab; osteoclast; RANKL; rheumatoid arthritis; MODIFYING ANTIRHEUMATIC DRUGS; OSTEOCLAST DIFFERENTIATION; ZOLEDRONIC ACID; DOUBLE-BLIND; EULAR RECOMMENDATIONS; SYNOVIAL FIBROBLASTS; JAPANESE PATIENTS; MINERAL DENSITY; TNF-ALPHA; T-CELLS;

D O I：

10.1080/14397595.2017.1369491

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Rheumatoid arthritis (RA) is a chronic inflammatory disorder characterized by progressive joint destruction. Recent studies have indicated the critical involvement of osteoclasts in bone destruction in RA. The osteoclast differentiation factor receptor activator of NF-kappa B ligand (RANKL), which belongs to the tumor necrosis factor superfamily, plays a critical role in osteoclast differentiation and bone destruction in RA. Denosumab, an antibody against human RANKL, efficiently suppressed the progression of bone erosion in RA patients in randomized controlled studies, and is considered as a putative therapeutic option for preventing bone destruction in RA.

引用

页码：9 / 16

页数：8

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