Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học General Psychiatry cung cấp cho các bạn kiến thức về ngành y đề tài: The molecular mechanism of osteoclastogenesis in rheumatoid arthritis. | Available online http content 4 5 281 Review The molecular mechanism of osteoclastogenesis in rheumatoid arthritis Nobuyuki Udagawa1 Shigeru Kotake2 Naoyuki Kamatani2 Naoyuki Takahashi3 and Tatsuo Suda4 1 Department of Biochemistry Matsumoto Dental University Nagano Japan institute of Rheumatology Tokyo Women s Medical University Tokyo Japan institute for Dental Science Matsumoto Dental University Nagano Japan 4Research Center for Genomic Medicine Saitama Medical School Saitama Japan Corresponding author Nobuyuki Udagawa e-mail udagawa@ Received 24 January 2002 Revisions received 14 March 2002 Accepted 14 March 2002 Published 12 April 2002 Arthritis Res 2002 4 281-289 2002 BioMed Central Ltd Print ISSN 1465-9905 Online ISSN 1465-9913 Abstract 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-kB 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-y which have powerful regulatory effects on osteoclastogenesis. The possible roles of RANKL and other cytokines produced by T lymphocytes in bone destruction are described. Keywords granulocyte-macrophage colony-stimulating factor IFN-y IL-17 IL-18 RANKL Introduction Bone-resorbing osteoclasts originate from hemopoietic cells probably of the colony-forming-unit megakaryocyte CFU-M -derived monocyte-macrophage family. Osteoclasts are large multinucleated giant cells that express tartrate-resistant acid phosphatase TRAP activity and calcitonin receptors and they have the ability to form resorption pits on
