Steroid-induced osteoporosis (SIOP) is osteoporosis arising due to use of glucocorticoids (steroid hormones) - analogous to Cushing's syndrome and involving mainly the axial skeleton. The synthetic glucocorticoid prescription drug prednisone is a main candidate after prolonged intake. Bisphosphonates are beneficial in reducing the risk of vertebral fractures.  Some professional guidelines recommend prophylactic calcium and vitamin D supplementation in patients who take the equivalent of more than 30 mg hydrocortisone ( mg of prednisolone), especially when this is in excess of three months.   The use of thiazide diuretics, and gonadal hormone replacement has also been recommended, with the use of calcitonin, bisphosphonates, sodium fluoride or anabolic steroids also suggested in refractory cases.  Alternate day use may not prevent this complication. 
The first isolation and structure identifications of prednisone and prednisolone were done in 1950 by Arthur Nobile .    The first commercially feasible synthesis of prednisone was carried out in 1955 in the laboratories of Schering Corporation, which later became Schering-Plough Corporation , by Arthur Nobile and coworkers.  They discovered that cortisone could be microbiologically oxidized to prednisone by the bacterium Corynebacterium simplex. The same process was used to prepare prednisolone from hydrocortisone . 
An attempt was made to reproduce in the experimental animal the clinical condition of steroid induced avascular necrosis of bone. There was a decrease in the ability of subchondral osteocytes to metabolize H3 cytidine and an increased amount of cell death as indicated by the number of empty subchondral lacunae. Oil red O stain for intravascular fat demonstrated large accumulations of fat in subchondral vessels. Much of this fat was deformed and was surrounded by reticulin, leading to the conclusion that it was embolic. A study of human material showed intravascular fat and diminished number of osteocytes in patients on systemic steroids who had died without clinical evidence of avascular necrosis. In addition, intravascular fat was demonstrated in avascular femoral heads and humeral heads both from transplant patients and patients receiving steroids for other reasons. The most tenable explanation for this series of events involves steroid-induced fatty liver with subsequent showeres of fatty emboli, which lodge in the subchondral region owing to the microvascular anatomy. Cell death ensues, and the necrotic bone is partially removed by the normal resorptive mechanism, but steroids retard osteogenesis, lead to microfractures, and eventually sequester the involved area.