has demonstrated the role of oxygen tension in the regulation of skeletal cell function and viability, the microenvironmental oxemic status of bone cells remains unknown. In this study, we have employed the Krogh cylinder model of oxygen diffusion to predict the oxygen distribution profiles in cortical and cancellous bone. Under the assumption of saturation-type Michaelis-Menten kinetics, our numerical modeling has indicated that, under steady-state conditions, there would be oxygen gradients across mature osteons and trabeculae. In Haversian bone, the calculated oxygen tension decrement ranges from 15 to 60%. For trabecular bone, a much shallower gradient is predicted. We note that, in Haversian bone, the gradient is largely dependent on osteocyte oxygen utilization and tissue oxygen diffusivity; in trabecular bone, the gradient is dependent on oxygen utilization by cells lining the bone surface. The Krogh model also predicts dramatic differences in oxygen availability during bone development. Thus, during osteon formation, the modeling equations predict a steep oxygen gradient at the initial stage of development, with the gradient becoming lesser as osteonal layers are added. In contrast, during trabeculum formation, the oxygen gradient is steepest when the diameter of the trabeculum is maximal. Based on these results, it is concluded that significant oxygen gradients exist within cortical and cancellous bone and that the oxygen tension may regulate the physical dimensions of both osteons and bone trabeculae. osteon; bone trabeculum; kinetics; Krogh; H; aversian OXYGEN DELIVERY governs the form and function of both soft and hard tissues (25). In the bone, a decrease in the rate of oxygen transport can severely impact skeletal health causing delays in bone healing, a change in the rate of bone turnover, and a raised incidence of vertebral and cranial malformations (7,26,31,33,40). Most commonly, oxemic stress is thought to be caused by a decrease in fluid flow during biomechanical unloading (8,13,22,34); when this occurs, there is a reduction in the oxygen transport rate in the lacunocanalicular system and impaired osteocyte function (29). While it is clear that the local oxygen tension (PO 2 ) is a potent regulator of skeletal cell metabolism and viability (1, 38, 41, 43), the oxygen distribution profile in the bone is currently unknown.The viability and function of cells in complex tissues is dependent on the delivery of oxygen and nutrients. Several numerical studies have attempted to model nutrient exchange by stress-induced fluid flow and diffusion within the lacunocanalicular system of the bone (22,29,34,45). While these studies have provided values for low-molecular-weight solutes, oxygen transport in the bone has not been addressed. In an earlier investigation, we have employed the Krogh cylinder assumption to model the oxygen supply to avian femoral growth cartilage (16); this same model has been used to predict the oxygen tension in skeletal muscle (24), brain (21), and bone marrow (3, 4).The Krogh cy...