Glucocorticoid-induced osteoporosis (GIO) is the most common form of secondary osteoporosis. Bisphosphonates are considered the first-line treatment option for the majority of glucocorticoid-treated patients at increased risk of fractures. However, the anti-resorptive mechanism of bisphosphonates does not address the major pathophysiological mechanisms of impaired bone formation during chronic glucocorticoid treatment. PTH, when administered intermittently and at low doses, has effects on bone formation opposite to those of glucocorticoids and therefore is conceptually a more attractive approach. Teriparatide (1-34PTH) has been studied in patients with GIO with effects on bone mineral density and on fracture risk which were shown to be superior to those obtained with alendronate.
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