The pathogenesis of the osteoporosis that is a complication of glucocorticoid therapy centers around a negative bone balance that is due to a deficiency of formation relative to resorption. At a cellular level, glucocorticoids have an effect on the cytokine microenvironment that is mediated through hormone and growth-factor receptors, The importance of secondary hyperparathyroidism in pathogenesis is less certain. Many of the conditions for which glucocorticoids are prescribed are themselves associated with bone loss. Prevention and treatment depend on both an understanding of these complex interactions and on strategies to reverse this process. Treatment of the established condition is currently unsatisfactory because there is no effective treatment to reverse the primary inhibition of bone formation. Prevention of bone loss appears to be the best option, and several therapies, predominantly based on inhibition of bone resorption, have been shown to be of benefit.
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