Available at: https://digitalcommons.calpoly.edu/theses/205
Date of Award
Biomedical and General Engineering
The onset of osteoporosis caused by aging, disease states, and post-menopausal conditions significantly impacts patient quality of life, required healthcare funding, personal autonomy losses from increased fracture risk and the subsequent corrective surgery. Research has indicated that osteocyte apoptosis may be a key parameter in bone remodeling, raising the possibility of remodeling rate modulation for the mitigation of bone mass resorption. By developing therapies that target osteocyte apoptosis, it may be possible to prevent undesired bone remodeling activity while maintaining a healthy balance between damage formation in the form of microcracks induced by the strain environment and the removal of damaged bone facilitated by resorbing BMUs, resulting in the preservation of bone mass. This preservation in turn results in a decreased risk of bone fracture.
The purpose of the current study was to develop a computational model to predict bone density changes from empirical osteocyte apoptosis data. This was achieved by developing a simulation that correlates osteocyte apoptosis with activation frequency and mechanical stimulus, two key bone remodeling parameters. The results of the simulation show that it is possible to use osteocyte apoptosis to predict remodeling and the resulting bone porosity changes. Instances of increased osteocyte apoptosis occurred simultaneously with increases in porosity, and under-loaded force conditions were more deleterious to bone porosity then overload associated with heavy exercise, which agrees with previous models.