UMMS Affiliation

Department of Medicine, Division of Rheumatology

Publication Date


Document Type



Animals; Bone Resorption; Carrier Proteins; Cell Differentiation; Glycoproteins; Humans; Membrane Glycoproteins; Osteoprotegerin; Proteins; RANK Ligand; Receptor Activator of Nuclear Factor-kappa B; Receptors, Cytoplasmic and Nuclear; Receptors, Tumor Necrosis Factor; Signal Transduction; TNF Receptor-Associated Factor 1; TNF Receptor-Associated Factor 2; TNF Receptor-Associated Factor 3; TNF Receptor-Associated Factor 4; TNF Receptor-Associated Factor 5; TNF Receptor-Associated Factor 6; Tumor Necrosis Factor Receptor-Associated Peptides and Proteins


Cellular and Molecular Physiology | Musculoskeletal Diseases | Rheumatology | Skin and Connective Tissue Diseases


The contribution of osteoclasts to the process of bone loss in inflammatory arthritis has recently been demonstrated. Studies in osteoclast biology have led to the identification of factors responsible for the differentiation and activation of osteoclasts, the most important of which is the receptor activator of NF-kappa B ligand/osteoclast differentiation factor (RANKL/ODF), a tumor necrosis factor (TNF)-like protein. The RANKL/ODF receptor, receptor activator of NF-kappa B (RANK), is a TNF-receptor family member present on both osteoclast precursors and mature osteoclasts. Like other TNF-family receptors and the IL-1 receptor, RANK mediates its signal transduction via TNF receptor-associated factor (TRAF) proteins, suggesting that the signaling pathways activated by RANK and other inflammatory cytokines involved in osteoclast differentiation and activation are interconnected.


osteoclasts, RANK, RANKL, TNF-α, TRAF

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DOI of Published Version



Arthritis Res. 2001;3(1):6-12. Epub 2000 Nov 2. doi:10.1186/ar134. Link to article on publisher's site

Journal/Book/Conference Title

Arthritis research


At the time of publication, Ellen Gravallese was not yet affiliated with the University of Massachusetts Medical School.

Related Resources

Link to Article in PubMed

PubMed ID