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Bone. 2010 Apr;46(4):911-9. doi: 10.1016/j.bone.2009.08.050. Epub 2009 Aug 27.

Control of RANKL gene expression.

Author information

  • Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences, and Central Arkansas Veterans Healthcare System, Little Rock, AR 72205, USA. caobrien@uams.edu

Abstract

Osteoclasts are highly specialized cells capable of degrading mineralized tissue and form at different regions of bone to meet different physiological needs, such as mobilization of calcium, modeling of bone structure, and remodeling of bone matrix. Osteoclast production is elevated in a number of pathological conditions, many of which lead to loss of bone mass. Whether normal or pathological, osteoclastogenesis strictly depends upon support from accessory cells which supply cytokines required for osteoclast differentiation. Only one of these cytokines, receptor activator of NFkappaB ligand (RANKL), is absolutely essential for osteoclast formation throughout life and is thus expressed by all cell types that support osteoclast differentiation. The central role of RANKL in bone resorption is highlighted by the fact that it is the basis for a new therapy to inhibit bone loss. This review will discuss mechanisms that control RANKL gene expression in different osteoclast-support cells and how the study of such mechanisms may lead to a better understanding of the cellular interactions that drive normal and pathological bone resorption.

Published by Elsevier Inc.

PMID:
19716455
[PubMed - indexed for MEDLINE]
PMCID:
PMC2842447
Free PMC Article

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