The response of the osteocyte to disuse

Summary form only. In bone, the osteocyte is an ideal cellular candidate to initiate biochemical responses culminating in tissue adaptation. We summarize our recent data suggesting that osteocyte hypoxia may act as a novel mechanotransduction pathway within bone. Our approach to detect osteocyte hypoxia has coupled immunohistochemistry with the avian ulna model of disuse osteopenia. We have found that acute deprivation of bone loading (24 hr) induces significant osteocyte hypoxia compared to intact contralateral bones from the same animals (8.4 i: 1.8% vs 1.1 10.5%; p=0.03). Next, we have supplemented 24 hr of disuse with a single brief external loading protocol that induced physiologic strains within the bone. The brief 4 min regimen completely rescued osteocytes from disuse induced hypoxia. Though preliminary, these data strengthen our hypothesis by supporting a cause and effect relation between disuse and the induction of osteocyte hypoxia. These data suggest that the fundamental physiologic process of oxygen metabolism may have an additional parallel role as a mechanotransducer within the skeleton. In a broader perspective, the integral role of oxygen metabolism in the normal functioning of cells, tissues, organs, and organisms suggests the potential for this pathway to function outside the skeleton.