Musculoskeletal Biology Research Laboratory
The laboratory focuses on strategies improve treatments for osteoporotic fractures and rare bone diseases. The group's research is focused on understanding of the nutritional and hormonal interactions on bone health, clinical studies related to fracture prevention, fracture healing, diabetes and poor bone health outcomes, and links between genetic mutations and poor bone health.
Link between vitamin D catabolism and Rickets-like bone disorder of X-linked Hypophosphatemia?
Vitamin D catabolism, by CYP24A1, opposes the beneficial effects of vitamin D in bone. This study will to determine whether Increased vitamin D catabolism is a major cause of X-linked Hypophosphatemic Rickets. The study will use using novel conditional KO mouse models, vitamin D catabolism inhibitor studies, and determine whether abolished CYP24A1 activity in osteocytes heals bone mineralisation in the hypophosphatemic rickets. For further information, contact Associate Professor Paul Anderson or Professor Howard Morris.
Synthesis of Vitamin D in Bone Cells: the fountain of bone youth?
Vitamin D is critical for bone health at all stages of life. We have shown the bone makes its own active vitamin D and that this is essential for bone mineralization. Artificially raising the synthesis of vitamin D in bone prevents age-related bone loss. This study will test whether advancing age results in impaired vitamin D metabolism and activity within osteoblasts and osteocytes resulting in cellular senescence and failure of formation. The study will establish the effects of impaired and/or enhanced vitamin D synthesis and activity in osteoblasts function, viability, osteogenesis, cell cycle regulation, respiration, apoptosis and autophagy. For more information, contact Ass. Professor Paul Anderson or Professor Howard Morris.
In Diabetes, do osteocytes become deranged and signal for bone loss, preventing bone healing, during a diabetic bone fracture?
Diabetics often have poorer quality bone and increased incidence of bone fracture. When Diabetics have a fracture, they frequently do not heal properly and sometimes do not heal at all, for reasons that nobody really understands. The osteocytes are key player in regulating mineralisation via producing a factor called Sclerostin. Whether inappropriately high sclerostin levels are the cause on the mal-union of fracture will be investigated. The study will establish the association between diabetes, poor, bone quality and high sclerostin levels, using a rat diabetes model. These data may lead on to establishing an anti-sclerostin treatment to promote healing of diabetic fractures. For more information, contact Associate Professor Paul Anderson or Professor Howard Morris.
Can vitamin D metabolism in the breast be modulated to reduce the risk and aggressiveness of breast cancer
Low vitamin D status is associated with an increased risk of breast cancer. In general, women with the lowest vitamin D status more than double their risk of breast cancer. Whilst vitamin D is an attractive preventative therapy to reduce breast cancer incidence, the evidence base for this approach is incomplete. A key question is whether vitamin D can directly influence breast development and the early stages of breast cancer. Studies include utilising novel models to assess the effects of abrogated vitamin D catabolism in mammary tissue during development and cancer initiation and progression and to test the therapeutic potential of vitamin D to inhibit tumour growth. For more information, contact Associate Professor Paul Anderson or Professor Howard Morris.