We are currently investigating the underlying mechanisms IL-33, a key factor shown to act on bone inhibiting osteoclasts, as well as boost production of factors known to stimulate bone formation. We aim to translate these findings to develop new therapies to treat bone loss and destruction resulting from cancer, osteoporosis, and inflammatory diseases such as arthritis.
Many common diseases cause loss of bone, either locally in focal lesions, or more generally throughout the skeleton. Bone destruction is a common feature of cancers that invade bone (e.g. breast cancer) but is also seen in inflammatory diseases both chronic (e.g. rheumatoid arthritis) and in acute bacterial infections.
Central to all bone destruction in health and disease is the osteoclast cell, which is related to macrophages but is specialized to resorb (destroy) bone. Both in inflammation and in cancer, the number of osteoclasts increase greatly, resulting in bone loss. It is critical to block this bone destruction, and to do so in a way that does not impair bone formation as many current anti-osteoclastic therapies do.
Our research has focused upon the identification of novel factors that influence osteoclast formation and activity as well as understanding the processes that control how osteoclasts form and activate.
We continue to investigate the underlying mechanisms of IL-33 with the hope of applying these to the development of new therapies to protect against bone loss. In particular, we have found that IL-33 assists bone formation by acting on osteocytes to suppress sclerostin, a factor that inhibits bone formation.