title: Osteocyte RANKL: new insights into the control of bone remodeling.
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.
authors.affiliation: Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA.
authors.forename: Jinhu
authors.initials: J
authors.lastname: Xiong
authors.forename: Charles A
authors.initials: CA
authors.lastname: O'Brien
mesh_terms: D000818:Animals; D001696:Biomechanical Phenomena; D016723:Bone Remodeling / Q000502:physiology*; D006728:Hormones / Q000502:physiology; D006801:Humans; D010011:Osteocytes / Q000378:metabolism*; D053245:RANK Ligand / Q000502:physiology*
chemical_list: D006728:Hormones; D053245:RANK Ligand; C505688:TNFSF11 protein, human