Glucocorticoid therapy is the most common cause of secondary iatrogenic osteoporosis. The bone loss occurs predominantly due to a decrease in bone formation, although increased bone resorption also occurs. Glucocorticoids induce osteoblast apoptosis and increase osteoclast survival and activity. Most of these effects are mediated through the RANKL-OPG system but perturbations in gonadal hormone activity and calcium balance may also contribute significantly to bone loss. Future therapies in the treatment and prevention of glucocorticoid-induced osteoporosis may be targeted at restoring the hormonal and cytokine balance to nullify the apoptotic effect of glucocorticoids on bone forming cells.
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Rehman et al. (2003) studied this question.
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