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Review
. 2012 Mar;27(3):499-505.
doi: 10.1002/jbmr.1547.

Osteocyte RANKL: new insights into the control of bone remodeling

Jinhu Xiong  1 , Charles A O'Brien
Affiliations
Review

Osteocyte RANKL: new insights into the control of bone remodeling

Jinhu Xiong et al. J Bone Miner Res. 2012 Mar.

Abstract

The idea that osteoblasts, or their progenitors, support osteoclast formation by expressing the cytokine receptor activator of NFkB ligand (RANKL) is a widely held tenet of skeletal biology. Two recent studies provide evidence that osteocytes, and not osteoblasts or their progenitors, are the major source of RANKL driving osteoclast formation in cancellous bone. The goal of this review is to highlight the results of these new studies and discuss their implications for our understanding of bone remodeling.

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Figures

Figure 1
Figure 1
Model depicting mechanisms by which osteocytes may independently control bone resorption and bone formation. Osteoclasts (OCs) and osteoblasts (OBs) within a cancellous BMU are shown as being derived from precursors (pOC and pOB). Osteocytes alter the rate of bone remodeling by controlling osteoclast formation via production of RANKL. On the other hand, osteocytes also control the balance between formation and resorption by regulating osteoblast formation via production of sclerostin. Sclerostin may have additional actions such as stimulation of RANKL expression by osteocytes.
See this image and copyright information in PMC

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