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Osteocyte RANKL in bone homeostasis: a paradigm shift?

Nature Reviews Rheumatology volume 7, page 619 (2011)Cite this article

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Receptor activator of nuclear factor-κB ligand (RANKL) regulates osteoclast function, and its expression by osteoblasts is postulated to link bone resorption and formation. However, two independent studies, led by Hiroshi Takayanagi of the Tokyo Medical and Dental University and Charles O'Brien of the University of Arkansas for Medical Sciences, now challenge this paradigm by providing evidence that osteocytes are a major source of RANKL, and are essential for bone remodeling—a process that is defective in many rheumatic diseases.

“Many different cell types express RANKL and it remained unclear which ones were providing the RANKL involved in osteoclast formation in vivo,” states O'Brien. His group and Takayanagi's initially took different approaches to attempt to fill this gap in our knowledge; Takayanagi et al. purified osteoblast and osteocyte populations, analysis of which revealed that RANKL levels were considerably higher in the latter, and the isolated osteocytes were more effective at driving the differentation of osteoclast precursors in vitro.

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ORIGINAL RESEARCH PAPERS

  1. Xiong, J. et al. Matrix-embedded cells control osteoclast formation. Nat. Med. doi:10.1038/nm.2448

  2. Nakashima, T. et al. Evidence for osteocyte regulation of bone homeostasis through RANKL expression. Nat. Med. doi:10.1038/nm.2452.

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  1. David Killock
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Killock, D. Osteocyte RANKL in bone homeostasis: a paradigm shift?. Nat Rev Rheumatol 7, 619 (2011). https://doi.org/10.1038/nrrheum.2011.151

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  • DOI: https://doi.org/10.1038/nrrheum.2011.151

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