Glucocorticoid activity, inactivity and the osteoblast

Glucocorticoids clearly regulate several crucial determinants of osteoblast differentiation, proliferation and function. These effects are complex and at times opposing, depending upon dose and stage of osteoblast differentiation. In addition to improving our understanding of glucocorticoid action, we are now increasingly aware of important factors that regulate glucocorticoid 'inactivity' within osteoblasts. In keeping with other peripheral target tissues, the expression of 11β-HSD isozymes within human bone suggests that corticosteroid hormone action is modulated at a pre-receptor level. Further studies are required to define the regulation of 11β-HSD within human osteoblasts at varying stages of differentiation, but the manipulation of 11β-HSD within bone itself may, in the future, offer a novel therapeutic approach in modulating glucocorticoid 'activity' or 'inactivity' in bone.