TNF.ALPHA. and pathologic bone resorption

DOI Web Site 被引用文献5件 参考文献41件
  • Boyce Brendan E
    Department of Pathology and Laboratory Medicine, University of Rochester Medical Center The Center for Musculoskeletal Research, University of Rochester Medical Center
  • Li Ping
    The Center for Musculoskeletal Research, University of Rochester Medical Center
  • Yao Zhenqiang
    Department of Pathology and Laboratory Medicine, University of Rochester Medical Center
  • Zhang Qian
    Department of Pathology and Laboratory Medicine, University of Rochester Medical Center
  • Badell I. Raul
    Department of Pathology and Laboratory Medicine, University of Rochester Medical Center
  • Schwarz Edward M.
    The Center for Musculoskeletal Research, University of Rochester Medical Center
  • O’Keefe Regis J.
    The Center for Musculoskeletal Research, University of Rochester Medical Center
  • Xing Lianping
    Department of Pathology and Laboratory Medicine, University of Rochester Medical Center The Center for Musculoskeletal Research, University of Rochester Medical Center

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Chronic inflammatory bone diseases, such as rheumatoid arthritis, periodontal disease and aseptic periprosthetic osteolysis, are characterized by bone loss around affected joints and teeth caused by increased osteoclastic bone resorption. This resorption is mediated largely by the increased local production of pro-inflammatory cytokines, such as tumor necrosis factor-alpha (TNFα). These cytokines may induce resorption indirectly by affecting the production of the essential osteoclast differentiation factor, receptor activator of NF-κB ligand, and/or its soluble decoy receptor, osteoprotegerin, by osteoblast/stromal cells or directly by enhancing proliferation and/or activity of cells in the osteoclast lineage. The importance of TNFα in the pathogenesis of various forms of bone loss is supported by both experimental and clinical evidence. However, TNFα is not absolutely required for osteoclastogenesis, erosive arthritis, or osteolysis, as all these events could occur in the absence of TNFα and whether TNFα promotes osteoclast formation independently of RANK signaling is still a topic of debate. Here we review our current understanding of the mechanisms whereby TNFα increases osteoclastogenesis in vitro and in vivo.

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