The molecular mechanism of osteoclastogenesis in rheumatoid arthritis
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
Citation and License
Arthritis Res 2002, 4:281-289 doi:10.1186/ar431Published: 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.