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The molecular mechanism of osteoclastogenesis in rheumatoid arthritis

Nobuyuki Udagawa1*, Shigeru Kotake2, Naoyuki Kamatani2, Naoyuki Takahashi3 and Tatsuo Suda4

Author affiliations

1 Department of Biochemistry, Matsumoto Dental University, Nagano, Japan

2 Institute of Rheumatology, Tokyo Women's Medical University, Tokyo, Japan

3 Institute for Dental Science, Matsumoto Dental University, Nagano, Japan

4 Research Center for Genomic Medicine, Saitama Medical School, Saitama, Japan

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Citation and License

Arthritis Res 2002, 4:281-289  doi:10.1186/ar431

Published: 12 April 2002


Bone-resorbing osteoclasts are formed from hemopoietic cells of the monocyte–macrophage lineage under the control of bone-forming osteoblasts. We have cloned an osteoblast-derived factor essential for osteoclastogenesis, the receptor activator of NF-κB ligand (RANKL). Synovial fibroblasts and activated T lymphocytes from patients with rheumatoid arthritis also express RANKL, which appears to trigger bone destruction in rheumatoid arthritis as well. Recent studies have shown that T lymphocytes produce cytokines other than RANKL such as IL-17, granulocyte–macrophage colony-stimulating factor and IFN-γ, which have powerful regulatory effects on osteoclastogenesis. The possible roles of RANKL and other cytokines produced by T lymphocytes in bone destruction are described.

granulocyte–macrophage colony-stimulating factor; IFN-γ; IL-17; IL-18; RANKL