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1: Arthritis Res. 2002;4(5):281-9. Epub 2002 Apr 12.Click here to read Click here to read Links

The molecular mechanism of osteoclastogenesis in rheumatoid arthritis.

Udagawa N, Kotake S, Kamatani N, Takahashi N, Suda T.

Department of Biochemistry, Matsumoto Dental University, Nagano, Japan. udagawa@po.mdu.ac.jp

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-kappaB 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-gamma, which have powerful regulatory effects on osteoclastogenesis. The possible roles of RANKL and other cytokines produced by T lymphocytes in bone destruction are described.

PMID: 12223101 [PubMed - indexed for MEDLINE]

PMCID: PMC128939