Original Article

Tumor Necrosis Factor Stimulates Osteoclast Differentiation by a Mechanism Independent of the ODF/RANKL–RANK Interaction

Correspondence to: Tatsuo Suda, Department of Biochemistry, School of Dentistry, Showa University, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan. Tel:81-3-3784-8162 Fax:81-3-3784-5555 E-mail:suda{at}showa-u.ac.jp.

Osteoclast differentiation factor (ODF, also called RANKL/TRANCE/OPGL) stimulates the differentiation of osteoclast progenitors of the monocyte/macrophage lineage into osteoclasts in the presence of macrophage colony-stimulating factor (M-CSF, also called CSF-1). When mouse bone marrow cells were cultured with M-CSF, M-CSF–dependent bone marrow macrophages (M-BMM) appeared within 3 d. Tartrate-resistant acid phosphatase–positive osteoclasts were also formed when M-BMM were further cultured for 3 d with mouse tumor necrosis factor (TNF-) in the presence of M-CSF. Osteoclast formation induced by TNF- was inhibited by the addition of respective antibodies against TNF receptor 1 (TNFR1) or TNFR2, but not by osteoclastogenesis inhibitory factor (OCIF, also called OPG, a decoy receptor of ODF/RANKL), nor the Fab fragment of anti–RANK (ODF/RANKL receptor) antibody. Experiments using M-BMM prepared from TNFR1- or TNFR2-deficient mice showed that both TNFR1- and TNFR2-induced signals were important for osteoclast formation induced by TNF-. Osteoclasts induced by TNF- formed resorption pits on dentine slices only in the presence of IL-1. These results demonstrate that TNF- stimulates osteoclast differentiation in the presence of M-CSF through a mechanism independent of the ODF/RANKL–RANK system. TNF- together with IL-1 may play an important role in bone resorption of inflammatory bone diseases.

Key Words: bone resorption, tumor necrosis factor receptor, nuclear factor-B, macrophage colony-stimulating factor, interleukin-1

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• Jiang, Y., Mehta, C. K., Hsu, T.-Y., Alsulaimani, F. F. H. (2002). Bacteria Induce Osteoclastogenesis via an Osteoblast-Independent Pathway. Infect. Immun. 70: 3143-3148 [Abstract] [Full Text]  
• Matsumoto, Y., Tanaka, K., Hirata, G., Hanada, M., Matsuda, S., Shuto, T., Iwamoto, Y. (2002). Possible Involvement of the Vascular Endothelial Growth Factor-Flt-1-Focal Adhesion Kinase Pathway in Chemotaxis and the Cell Proliferation of Osteoclast Precursor Cells in Arthritic Joints. J. Immunol. 168: 5824-5831 [Abstract] [Full Text]  
• Nakamura, I., Kadono, Y., Takayanagi, H., Jimi, E., Miyazaki, T., Oda, H., Nakamura, K., Tanaka, S., Rodan, G. A., Duong, L. T. (2002). IL-1 Regulates Cytoskeletal Organization in Osteoclasts Via TNF Receptor-Associated Factor 6/c-Src Complex. J. Immunol. 168: 5103-5109 [Abstract] [Full Text]  
• Neale, S.D., Schulze, E., Smith, R., Athanasou, N.A. (2002). The influence of serum cytokines and growth factors on osteoclast formation in Paget's disease. QJM 95: 233-240 [Abstract] [Full Text]  
• Fuller, K., Murphy, C., Kirstein, B., Fox, S. W., Chambers, T. J. (2002). TNF{alpha} Potently Activates Osteoclasts, through a Direct Action Independent of and Strongly Synergistic with RANKL. Endocrinology 143: 1108-1118 [Abstract] [Full Text]  
• Wei, S., Wang, M. W.-H., Teitelbaum, S. L., Ross, F. P. (2002). Interleukin-4 Reversibly Inhibits Osteoclastogenesis via Inhibition of NF-kappa B and Mitogen-activated Protein Kinase Signaling. J. Biol. Chem. 277: 6622-6630 [Abstract] [Full Text]  
• Pfeilschifter, J., Koditz, R., Pfohl, M., Schatz, H. (2002). Changes in Proinflammatory Cytokine Activity after Menopause. Endocr. Rev. 23: 90-119 [Abstract] [Full Text]  
• Mansky, K. C., Sulzbacher, S., Purdom, G., Nelsen, L., Hume, D. A., Rehli, M., Ostrowski, M. C. (2002). The microphthalmia transcription factor and the related helix-loop-helix zipper factors TFE-3 and TFE-C collaborate to activate the tartrate-resistant acid phosphatase promoter. J. Leukoc. Biol. 71: 304-310 [Abstract] [Full Text]  
• Nosaka, K., Miyamoto, T., Sakai, T., Mitsuya, H., Suda, T., Matsuoka, M. (2002). Mechanism of hypercalcemia in adult T-cell leukemia: overexpression of receptor activator of nuclear factor kappa B ligand on adult T-cell leukemia cells. Blood 99: 634-640 [Abstract] [Full Text]  
• Childs, L. M., Goater, J. J., O'Keefe, R. J., Schwarz, E. M. (2001). Effect of Anti-Tumor Necrosis Factor-{alpha} Gene Therapy on Wear Debris-Induced Osteolysis. JBJS 83: 1789-1797 [Abstract] [Full Text]  
• Roggia, C., Gao, Y., Cenci, S., Weitzmann, M. N., Toraldo, G., Isaia, G., Pacifici, R. (2001). Up-regulation of TNF-producing T cells in the bone marrow: A key mechanism by which estrogen deficiency induces bone loss in vivo. Proc. Natl. Acad. Sci. USA 98: 13960-13965 [Abstract] [Full Text]  
• Miyamoto, T., Ohneda, O., Arai, F., Iwamoto, K., Okada, S., Takagi, K., Anderson, D. M., Suda, T. (2001). Bifurcation of osteoclasts and dendritic cells from common progenitors. Blood 98: 2544-2554 [Abstract] [Full Text]  
• Lubberts, E., Joosten, L. A. B., Oppers, B., van den Bersselaar, L., Coenen-de Roo, C. J. J., Kolls, J. K., Schwarzenberger, P., van de Loo, F. A. J., van den Berg, W. B. (2001). IL-1-Independent Role of IL-17 in Synovial Inflammation and Joint Destruction During Collagen-Induced Arthritis. J. Immunol. 167: 1004-1013 [Abstract] [Full Text]  
• Ikeda, T., Kasai, M., Utsuyama, M., Hirokawa, K. (2001). Determination of Three Isoforms of the Receptor Activator of Nuclear Factor-{{kappa}}B Ligand and Their Differential Expression in Bone and Thymus. Endocrinology 142: 1419-1426 [Abstract] [Full Text]  

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