The structural integrity of bone is maintained by the coordinated actions of two cell types, the bone forming osteoblast and the bone resorbing osteoclast. In rheumatoid arthritis (RA), there is an imbalance in the activities of these two cells, with osteoclast resorption predominating. This results in bone loss within the joints leading to joint deformity and pain. The exact mechanisms mediating this imbalance have not been fully explained. White blood cells such as T cells not only contribute to inflammation within the RA joint, but have also been implicated in mediating the formation of osteoclasts. There is also evidence to suggest that T cells may modulate osteoblast formation and function. Therefore, T cells represent a potential target for therapeutic intervention to prevent arthritis-induced bone loss.

Dr. Nicole Walsh’s study will assess the potential for the T cells to modulate osteoblast formation and function in arthritis, using experimental animal models of arthritis. A clearer understanding of the role of T cells in mediating arthritis-induced bone loss may lead to the development of novel therapeutic strategies to prevent bone loss in this disease.