title: Osteocyte apoptosis.
abstract: Apoptotic death of osteocytes was recognized over 15 years ago, but its significance for bone homeostasis has remained elusive. A new paradigm has emerged that invokes osteocyte apoptosis as a critical event in the recruitment of osteoclasts to a specific site in response to skeletal unloading, fatigue damage, estrogen deficiency and perhaps in other states where bone must be removed. This is accomplished by yet to be defined signals emanating from dying osteocytes, which stimulate neighboring viable osteocytes to produce osteoclastogenic cytokines. The osteocyte apoptosis caused by chronic glucocorticoid administration does not increase osteoclasts; however, it does negatively impact maintenance of bone hydration, vascularity, and strength.
authors.affiliation: Division of Endocrinology & Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, Central Arkansas Veterans Healthcare System, 4301 W. Markham, Slot 587, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA. rljilka@uams.edu
authors.forename: Robert L
authors.initials: RL
authors.lastname: Jilka
authors.forename: Brendon
authors.initials: B
authors.lastname: Noble
authors.forename: Robert S
authors.initials: RS
authors.lastname: Weinstein
mesh_terms: D000818:Animals; D017209:Apoptosis; D016723:Bone Remodeling; D006801:Humans; D010011:Osteocytes / Q000166:cytology* / Q000378:metabolism / Q000648:ultrastructure; D053245:RANK Ligand / Q000378:metabolism; D015398:Signal Transduction; D016474:Weight-Bearing
chemical_list: D053245:RANK Ligand