Musculoskeletal tissues, such as bone, cartilage and tendon, evolve in response to the mechanical stimuli experienced throughout the lifetime of the individual, producing structures that are uniquely suited to bear functional loads. In the skeleton, dynamic mechanical stimuli are important regulators of both cortical and cancellous bone mass and structure. Controlled mechanical loading holds promise as an agent to inhibit bone loss and maintain bone mass and strength following hormonal compromise and aging.
Our knowledge of controlled mechanical loads and bone formation is based primarily on cortical bone in healthy animals and may not be directly relevant to corticocancellous sites in osteoporotic women, who are hormonally-compromised aging individuals and experience fractures clinically. Therefore, we study in vivo loading at predominantly cancellous sites in the skeleton with altered metabolic and hormonal status.
In the process of understanding skeletal adaptation to loading, we discovered the the adverse effects of loading on other joint tissues, particularly cartilage. We have developed an in vivo model of load-induced osteoarthritis. We are now studying the role of bone stiffness and turnover in the development of joint damage and osteoarthritis pathology.
• Modulating subchondral bone properties to inhibit OA development
• Enhancing adaptation to loading with PTH in osteoporosis
• Enhancement of implant osseointegration
• Role of cartilage matrix in a model of load-induced OA
• Loading overcomes osteopenia from sex hormone withdrawal