Finally, in mouse cortical bone, glucocorticoids repress MMP13 and other PLR enzymes, resulting in canalicular degeneration, collagen disorganization, and hypermineralization of subchondral bone,27 all of which mimic the signs of PLR suppression in the subchondral bone from another human joint disease, glucocorticoid-induced osteonecrosis.25,26,54 Nevertheless, it is possible that osteocytic MMP13 supports joint homeostasis through PLR-independent mechanisms, such as activation of latent growth factors55–57 or control of osteocyte differentiation or embedding. Here, MMP13 is linked to osteonecrosis.