{"id":{"repo_id":"hull","oai_identifier":"oai:hull-repository.worktribe.com:4214562"},"canonical_url":"https://search.dev.ndltd.org/etd/hull/oai:hull-repository.worktribe.com:4214562","repository":{"repo_id":"hull","name":"University of Hull","base_url":"https://hull-repository.worktribe.com/oaiprovider"},"display":{"title":"Computer simulation of the osteocyte and bone lining cell network and the effect of normal physiological changes in cellular functions on that network","abstract":"Osteocytes play a critical role in the regulation of bone remodelling by translating strain due to mechanical loading into biochemical signals transmitted through the interconnecting lacuno-canalicular network to bone lining cells (BLCs) on the bone surface. This work aims to examine the effects of disruption of that intercellular communication by simulation of osteocyte apoptosis and microcrack in the bone matrix. A model of a uniformly distributed osteocyte network has been developed that stimulates the signalling through the network to the BLCs based on strain level. Bi-directional and asymmetric communication between neighbouring osteocytes and BLCs is included; with propagation of the signal through the network gradually decreasing by a calcium decay factor. The effect of osteocyte apoptosis and microcracks are then examined by preventing signalling at and through the affected cells. It is found that a small percentage of apoptotic cells and tiny microcracks both lead to a significant reduction in the peak signal at the BLCs. The simulation shows that either apoptosis of only 3% of the osteocyte cells or tiny microcrack of 42μm, 42μm below the surface leads to a significant reduction in the peak signal at the BLCs. Furthermore, experiments with the model confirm how important the location and density of the apoptotic osteocytes are to the signalling received at the bone surface. 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Bi-directional and asymmetric communication between neighbouring osteocytes and BLCs is included; with propagation of the signal through the network gradually decreasing by a calcium decay factor. The effect of osteocyte apoptosis and microcracks are then examined by preventing signalling at and through the affected cells. It is found that a small percentage of apoptotic cells and tiny microcracks both lead to a significant reduction in the peak signal at the BLCs. The simulation shows that either apoptosis of only 3% of the osteocyte cells or tiny microcrack of 42μm, 42μm below the surface leads to a significant reduction in the peak signal at the BLCs. Furthermore, experiments with the model confirm how important the location and density of the apoptotic osteocytes are to the signalling received at the bone surface. The result also shows the importance of the location and length of microcrack on the signalling of BLC. 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