Osteocyte apoptosis

被引：185

作者：

Jilka, Robert L. ^{[1
]}

Noble, Brendon ^{[2
]}

Weinstein, Robert S. ^{[1
]}

机构：

[1] Univ Arkansas Med Sci, Div Endocrinol & Metab, Ctr Osteoporosis & Metab Bone Dis, Cent Arkansas Vet Healthcare Syst, Little Rock, AR 72205 USA

[2] Sch Sci Technol & Hlth, Ipswich IP4 1QJ, Suffolk, England

来源：

BONE | 2013年 / 54卷 / 02期

基金：

美国国家卫生研究院; 英国医学研究理事会;

关键词：

Osteocytes; Apoptosis; RANKL; Mechanical force; Ovariectomy; Glucocorticoid excess; MECHANICAL STIMULATION; BONE-RESORPTION; DEATH; GLUCOCORTICOIDS; FATIGUE; CELLS; OSTEONECROSIS; ACTIVATION; OSTEOBLAST; INTEGRINS;

D O I：

10.1016/j.bone.2012.11.038

中图分类号：

R5 [内科学];

学科分类号：

100201 [内科学];

摘要：

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.

引用

页码：264 / 271

页数：8

共 86 条

[1]

Adler RA, 2008, OSTEOPOROSIS, VOLS I AND II, 3RD EDITION, P1135

[2]

Osteocyte apoptosis is induced by weightlessness in mice and precedes osteoclast recruitment and bone loss [J].