期刊
BONE
卷 54, 期 2, 页码 264-271出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.bone.2012.11.038
关键词
Osteocytes; Apoptosis; RANKL; Mechanical force; Ovariectomy; Glucocorticoid excess
资金
- Biomedical Laboratory Research and Development Service of the Veterans Affairs Office of Research and Development [I01 BX000514, I01 BX000436]
- National Institutes of Health [P01 AG013918]
- UAMS College of Medicine
- Medical Research Council [G9321536]
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. This article is part of a Special Issue entitled The Osteocyte. Published by Elsevier Inc.
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