2009
DOI: 10.1359/jbmr.081210
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Osteocyte Apoptosis Controls Activation of Intracortical Resorption in Response to Bone Fatigue

Abstract: Osteocyte apoptosis is spatially and temporally linked to bone fatigue-induced microdamage and to subsequent intracortical remodeling. Specifically, osteocytes surrounding fatigue microcracks in bone undergo apoptosis, and those regions containing apoptotic osteocytes co-localize exactly with areas subsequently resorbed by osteoclasts. Here we tested the hypothesis that osteocyte apoptosis is a key controlling step in the activation and/or targeting of osteoclastic resorption after bone fatigue. We carried out… Show more

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Cited by 303 publications
(295 citation statements)
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“…Microdamage is a well-known stimulus for the activation of new remodeling [59,60], mediated through the apoptosis of ostectyes in the vicinity of the damage [61,62]. The general suppression of remodeling certainly prevents the repair of some of this damage, but studies have also shown a more specific suppression of targeted remodeling by BPs [63].…”
Section: Accepted M Manuscriptmentioning
confidence: 99%
See 1 more Smart Citation
“…Microdamage is a well-known stimulus for the activation of new remodeling [59,60], mediated through the apoptosis of ostectyes in the vicinity of the damage [61,62]. The general suppression of remodeling certainly prevents the repair of some of this damage, but studies have also shown a more specific suppression of targeted remodeling by BPs [63].…”
Section: Accepted M Manuscriptmentioning
confidence: 99%
“…The likely reason for this suppression of targeted remodeling is the wellknown BP effect that prevents the apoptosis of osteocytes [65,66]. Because it is nearly certain now that osteocyte apoptosis is the critical signaling step to initiate new targeted remodeling events [61], any delay or prevention of this apoptosis will have the singular effect of suppressing targeted remodeling. This suggests that the suppression of bone remodeling by the BPs occurs not just through an interruption in the mevalonate pathway that prevents activation of fully differentiated osteoclasts, but also through a disruption of cell-level signaling pathways that impairs recruitment of new pre-osteoclasts to a site in need of repair.…”
Section: Accepted M Manuscriptmentioning
confidence: 99%
“…[7][8][9][10] The extensiveness of the lacunar-canalicular network provides support for the hypothesis that osteocytes function primarily as local sensors, triggering processes that allow bone to respond to surrounding environmental mechanical conditions or to hormonal signals during changing ion homeostasis demands. As the mechanosensors of bone, osteocytes detect local changes in strain in their vicinity, [11][12][13] and in response express membranebound proteins and release soluble factors that regulate and coordinate the function of bone surface cells (bone-forming osteoblasts and bone-resorbing osteoclasts 3,[14][15][16][17] ). The critical role of osteocytes in mechanosensing and bone tissue health is underlined for instance by Tatsumi et al's study, 18 where targeted ablation of osteocytes in a transgenic mouse model induced osteoporosis and a reduced response to changing mechanoenvironment.…”
mentioning
confidence: 99%
“…These descriptions by Frost [30] survive largely intact. Osteocytes function to regulate the work rules of the osteoblasts and osteoclasts [21]. Remodeling is the predominant bone cell activity during most of life, particularly adult life.…”
Section: Functions Of Bonementioning
confidence: 99%