The main cause of femoral head osteonecrosis (SIONFH) is resulted from low osteogenesis and high adipogenesis of bone marrow mesenchymal stem cells (BMSCs) stimulated by excess glucocorticoid-used, the mechanisms are not elucidated completely. Studies had found that glucocorticoid can induced the increase of 11 beta-hydroxysteroid dehydrogenase 1 (11β-HSD1) activity in bone tissue, leading to endogenous glucocorticoid accumulation and inhibiting bone formation. Inhibition 11β-HSD1 activity can promote osteoblasts differentiation, inhibit fat differentiation and formation of atherosclerotic plaque in mice. It is peculated that there is glucocorticoid metabolism in bone tissue regulated by 11β-HSD1 in patients with steroid-induced osteonecrosis of the femoral head (SIONFH), and there may be an endogenous hormone metabolic pathway regulated by 11β-HSD1 in the process of the pathogenesis of SIONFH between the changes of hormone and BMSCs activity. Therefore, it is important that researching the roles of 11β-HSD1-Mediated endogenous hormone metabolic pathway in SIONFH will help us further understand the pathogenesis of SIONFH.