Computational models for osteocyte-interstitial-fluid interaction in bone
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Osteocytes are bone cells responsible for sensing mechanical cues and directing bone remodeling. They reside in lacunae (cavities) deep within bone and have numerous dendritic structures (processes) that reach out through canaliculi (canals) to connect with other osteocytes. Between the cell and the lacuna-canalicular wall lies salt-water-like fluid and pericellular matrix (PCM; a “cell coating”). If the bone is mechanically loaded, the interstitial fluid is driven through the PCM around the cell. The flow generates stress and strain on the cell and the cell can perceive the stimuli. Past studies show that the stress and strain that can cause significant response in osteocytes are approximately 10X greater than those typically experienced during normal activity. How macroscale stress is magnified tenfold before each reaches osteocytes is not yet fully understood. Because of the complexity of the osteocyte-fluid-lacuna-canalicular network, in vivo studies are challenging. Computational modeling provides a viable alternative to complement in vitro studies for producing insights into the amplification mechanism. We have developed three computational models in two and three dimensions to investigate the influences of the number and geometry of the canaliculi, the interactions among fluid, osteocyte body, and its processes on the fluid wall shear stress (WSS) and normal stress (WNS) on an osteocyte, using the lattice Boltzmann methods (D2Q9 and D3Q19 models) and the immersed boundary framework. Our major findings include 1) the average magnitudes of the stresses on the osteocyte are not significantly altered by the number and geometry of the canaliculi despite some quantitative influence of the latter on overall variation and distribution of those stresses; 2) the stress and strain tend to attain their local maxima near the regions where the processes meet the cell body; 3) our 3D model is a useful numerical tool capable of providing insights into the mechanism of stress and strain amplification of the osteocyte-fluid-lacuna-canaliculi system. Our results may lead to a greater understanding of the mechanism and may inspire novel therapeutics for bone diseases such as osteoporosis.
