Trabecular bone remodelling involves the continual resorption and formation of bone along the surface of a strut. Experimental studies have shown that mechanical stimuli, such as strain and damage, initiate and regulate this biological process. The aim of this thesis is to develop a mechanoregulation algorithm, based on both strain and damage stimuli, and to investigate whether such an algorithm is capable of simulating the bone remodelling cycle along a trabecular strut. Following on from this, the changes occurring to the process that lead to rapid and irreversible loss of bone, as observed in skeletal diseases such as osteoporosis, were investigated. Generally, this bone loss is attributed to an imbalance in the bone remodelling process, with more bone being resorbed than refilled. It is the contention of this thesis that a change in the mechanotransduction of the sensor cells to their loading environment is an alternative mechanism. Two causes of rapid loss of bone trabeculae are hypothesised:​ firstly that increases in the bone tissue elastic modulus lead to an increased propensity for trabecular perforation and secondly, that decreases in the mechanosensitivity of the bone tissue result in under-refilling of cavities and perforation by osteoclastic resorption.

A mechanobiological algorithm was developed which was based on two premises, (i) that bone remodelling is a turnover process that repairs damaged bone tissue by resorbing it and returning it to a homeostatic strain level, and (ii) that the local and spatial behaviour of osteoblasts is under biochemical control. It was found that this algorithm could simulate the normal remodelling cycle in a trabecular strut where damaged bone is resorbed to form a pit which is subsequently refilled with new bone. The simulation also predicts that increases in the elastic modulus of the bone tissue result in an altered mechanical environment. This perceived change in stimulus was found to lead to easier trabecular perforation. Changes in the mechanosensitivity of the bone tissue were examined by varying the threshold for bone formation, ϵ_max. Results show that ϵ_max is a critical threshold parameter:​ if it is higher in an individual (genetics) or increases (with age) the remodelling mass deficit in a remodelling cycle increases. Furthermore there is a value of ϵ_max above which remodelling to repair microdamage in trabecular tissue is impossible because trabecular perforation occurs.

As increased minerahzation has been previously measured in osteoporotic bone, this change in m aterial property may contribute to the rapid loss of trabecular bone mass observed in osteoporotic patients. It may also be concluded that if cells become less mechanosensitive with age then bone loss per remodelling cycle increases, and the likelihood of trabecular perforation and rapid loss of bone mass increases. Therefore, preserving the bone mineral content in bone tissue or maintaining bone cell mechanosensitivity could be therapeutic targets for the prevention of osteoporosis.