Glucocorticoid induced osteoporosis (GIO) is the most frequent form of drug induced osteoporosis. Glucocorticoids affect osteoblastogenesis, osteoclastogenesis and promote the apoptosis of osteoblasts and osteocytes. A decrease of bone mineral density has been described in several pediatric diseases that require glucocorticoids, both as long-term replacement therapy, such as Congenital Adrenal Hyperplasia, and as treatment of acute phase or relapses, such as asthma, juvenile rheumatoid arthritis, inflammatory bowel diseases, systemic lupus erythematosus, organ transplantation and Steroid Sensitive Nephrotic Syndrome. The increasing number of children with GIO and at risk of fractures reflects the complex nature of this condition, and the need of development of anti-osteoporotic drugs. In this review, we focus on the mechanisms of GIO in some pediatric diseases and on treatment of osteoporosis. We also report data on new signaling pathways as potential targets for future anti-osteoporotic drugs.
Keywords: bisphosphonates; bone mineral density; children; congenital adrenal hyperplasia; glucocorticoid; glucocorticoid sensitive nephrotic syndrome; osteoporosis.