TRANSPORT PROCESSES AND CELLULAR METABOLISM IN BONE

INTRODUCTION Bone cells (osteocytes) are encased in calcified cavities (lacunae). These cells are interconnected to each other and to a nearby capillary (contained in a Haversian canal) via microchannels (canaliculi) permeating the calcified bone matrix. Molecular diffusion between osteocytes and the blood supply—the mechanism by which cells typically obtain nutrients and dispose of waste products—may be insufficient to maintain osteocytic metabolism. Consequently, osteocytes need a patent fluid pathway to the extracellular fluid in the osteonal canal, and the interconnected lacunocanalicular network has been suggested to provide such a pathway. This network is not only the largest reservoir for fluid within bone, but it is also the fluid space in closest proximity to osteocytes. Little, however, is known about bone microcirculation, as experimental quantification of intraosseous flow remains challenging. Alternatively, mathematical models can explain strain-derived fluid flow in the lacunocanalicular network. We are quantifying the effects of cyclic mechanical loading on fluid pressure and velocity, and nutrient transport in the lacunocanalicular network. Ostensibly, lack of microcirculation in the network may contribute to osteoporosis and bone resorption in regions of low fluid flow, where osteocytes are metabolically deficient. Thus, we tested two hypotheses: (1) tracer (simulated nutrient) transport is affected by particle size, and rate of cellular consumption, and (2) load-induced fluid flow through the canaliculi enhances transport efficiency and is dependent on mechanical loading frequency.