Bone quality is maintained by the concerted action of osteoclasts (bone-resorbing cells), osteoblasts (bone-forming cells), and osteocytes, which appear to have a mechanosensory function and respond to microdamage. Glucocorticoid treatment causes an increase in apoptosis of osteoblasts and osteocytes, which may contribute to increased bone fragility and the higher incidence of fractures in glucocorticoid-treated patients. Bisphosphonates are currently the most important class of antiresorptive drugs used in the treatment of such metabolic bone disorders. As well as inhibiting bone resorption by osteoclasts and decreasing the risk of fractures, long-term treatment with bisphosphonates can modestly increase bone mass, suggesting that these drugs may have effects in addition to their antiresorptive action. To determine whether bisphosphonates and calcitonin could help to reduce fracture risk and increase bone mass in vivoby preventing apoptosis of osteocytes and osteoblasts, thereby preserving the osteocytic network in bone and causing a net increase in bone density.