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1 Department of Veterinary Basic Science, Royal Veterinary College, London NW1 0TU; 2 University Department of Medicine, Addenbrooke's Hospital, Cambridge CB2 2QQ; and 3 Department of Biology, University of York, York YO10 5YW, United Kingdom
Bone is
removed or replaced in defined locations by targeting osteoclasts and
osteoblasts in response to its local history of mechanical loading.
There is increasing evidence that osteocytes modulate this targeting by
their apoptosis, which is associated with locally increased
bone resorption. To investigate the role of osteocytes in the control
of loading-related modeling or remodeling, we studied the effects on
osteocyte viability of short periods of mechanical loading applied to
the ulnae of rats. Loading, which produced peak compressive strains of
0.003 or 0.004, was associated with a 78% reduction in the
resorption surface at the midshaft. The same loading regimen resulted
in a 40% relative reduction in osteocyte apoptosis at the same
site 3 days after loading compared with the contralateral side
(P = 0.01). The proportion of osteocytes that were
apoptotic was inversely related to the estimated local strain
(P < 0.02). In contrast, a single short period of
loading resulting in strains of 0.008 engendered both tissue
microdamage and subsequent bone remodeling and was associated with an
eightfold increase in the proportion of apoptotic osteocytes
(P = 0.02) at 7 days. This increase in osteocyte
apoptosis was transient and preceded both intracortical
remodeling and death of half of the osteocytes (P < 0.01). The data suggest that osteocytes might use their U-shaped
survival response to strain as a mechanism to influence bone
remodeling. We hypothesize that this relationship reflects a causal
mechanism by which osteocyte apoptosis regulates bone's
structural architecture.
in vivo; rat ulnae; osteocytes; cell death
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