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Cited by 259

The DOI matches its Crossref record; 14 of the 14 references it cites were found in a registry or an index.

TNF.ALPHA. and pathologic bone resorption

Open access
Boyce, Brendan E, Li, Ping, Yao, Zhenqiang, Zhang, Qian, Badell, I. Raul, Schwarz, Edward M., O’Keefe, Regis J., Xing, Lianping·2005·The Keio Journal of Medicine

Abstract

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 (TNFa). These cytokines may induce resorption indirectly by affecting the production of the essential osteoclast differentiation factor, receptor activator of NF-kB 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 TNFa in the pathogenesis of various forms of bone loss is supported by both experimental and clinical evidence. However, TNFa is not absolutely required for osteoclastogenesis, erosive arthritis, or osteolysis, as all these events could occur in the absence of TNFa and whether TNFa promotes osteoclast formation independently of RANK signaling is still a topic of debate. Here we review our current understanding of the mechanisms whereby TNFa increases osteoclastogenesis in vitro and in vivo.

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Crossref · 10.2302/kjm.54.127

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Metadata

Authors
Boyce, B. E., Li, P., Yao, Z., Zhang, Q., Badell, I. R., Schwarz, E. M., O’Keefe, R. J., & Xing, L.
Venue
The Keio Journal of Medicine
Published
2005
Volume
54
Issue
3
Pages
127-131
ISSN
  • 0022-9717 (ISSN-L)
  • 1880-1293
OpenAlex
W1984721683
Cited by
259
References
14
FWCI
2.77
Type
journal article
Language
en
Open access
bronze

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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