Effect of RANKL inhibition on fibrous dysplasia lesions (mouse)

we investigated mechanisms underlying RANKL inhibition with the monoclonal antibody denosumab on FD tissue, and its likely indirect effects on osteoprogenitors, by evaluating human FD tissue pre and post-treatment and in murine in vivo pre-clinical models. Results from this study demonstrate that, beyond its expected anti-osteoclastic effects, denosumab reduces FD lesion activity by decreasing FD cell proliferation and increasing osteogenic maturation, leading to increased bone formation within lesions For human analysis :6 pairs of human samples (FD patients) before and after denosumab treatment. For Mouse model: 6 uninduced mice (WT), 5 mice induced for FD and treated with Isotype control and 6 mice induced for FD and treated with αRANKL antibody