The pathophysiology of glucocorticoid-induced bone disease involve interactions with calcium and bone metabolism at 
multiple levels with both direct and indirect effects which impact on osteoblasts and osteoclasts. See informations about glucocorticoid-induced osteoporosis (the cellular changes, bone histomorphometry) in this journal.
The balance between bone resorption, bone formation and bone cell proliferation (as seen in the picture), which maintains adult skeletal mass, is controlled not only by changes in the production of osteoclasts and osteoblasts but also by alterations in the duration of the lifespan of these cells through programmed cell death, or apoptosis. See also explanation about decreased cell production, decreased cell lifespan and the effect of chronic prednisone treatment on human cancellous and cortical bone.
Further description about Bone Remodeling and Pathogenesis of Glucocorticoid-Induced Bone Disease can be seen completely here (source: clinexprheumatol.org).
