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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• 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]  
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