Osteocyte RANKL: New insights into the control of bone remodeling
Open Access
- 21 February 2012
- journal article
- review article
- Published by Oxford University Press (OUP) in Journal of Bone and Mineral Research
- Vol. 27 (3), 499-505
- https://doi.org/10.1002/jbmr.1547
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. © 2012 American Society for Bone and Mineral ResearchKeywords
This publication has 78 references indexed in Scilit:
- Matrix-embedded cells control osteoclast formationNature Medicine, 2011
- The amazing osteocyteJournal of Bone and Mineral Research, 2010
- Continuous elevation of PTH increases the number of osteoblasts via both osteoclast-dependent and -independent mechanismsJournal of Bone and Mineral Research, 2010
- Osteocyte apoptosis and control of bone resorption following ovariectomy in miceBone, 2010
- Commitment to the Osteoblast Lineage Is Not Required for RANKL Gene ExpressionJournal of Biological Chemistry, 2009
- Targeted Deletion of a Distant Transcriptional Enhancer of the Receptor Activator of Nuclear Factor-κB Ligand Gene Reduces Bone Remodeling and Increases Bone MassEndocrinology, 2007
- Loss of DMP1 causes rickets and osteomalacia and identifies a role for osteocytes in mineral metabolismNature Genetics, 2006
- Parathyroid Hormone Controls Receptor Activator of NF-κB Ligand Gene Expression via a Distant Transcriptional EnhancerMolecular and Cellular Biology, 2006
- Detection of osteoprotegerin (OPG) and its ligand (RANKL) mRNA and protein in femur and tibia of the ratJournal of Molecular Histology, 2005
- Expression of Cre recombinase in the developing mouse limb bud driven by a Prxl enhancergenesis, 2002