Mechanical loading: biphasic osteocyte survival and targeting of osteoclasts for bone destruction in rat cortical bone

Author:

Noble Brendon S.12,Peet Nicky3,Stevens Hazel Y.12,Brabbs Alex3,Mosley John R.1,Reilly Gwendolen C.3,Reeve Jonathan2,Skerry Timothy M.3,Lanyon Lance E.1

Affiliation:

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

Abstract

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.

Publisher

American Physiological Society

Subject

Cell Biology,Physiology

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