Mechanical loading is the primary functional influence on bone mass and architecture. This influence is exerted by bone cells responding to the strains engendered by functional loading within bone tissue. Increased strain-related stimulation results in increased bone formation and decreased stimulation in bone resorption. With age this strain-related regulation fails, bone mass declines and fracture incidence increases. The lifetime risk of a fragility fracture in women is 53.2% and men 20.7%.

Working within the Price lab, which investigates the mechanisms linking functional strain to bone (re)modelling by assessing the osteo-regulatory responses to short periods of dynamic load in mouse bones in vivo and in cell culture models ex vivo, I am currently investigating the failure of aged bone's response to mechanical loading and the role of this mechanism in age-related osteoporosis.