Calcitonins and osteoporosis.

Abstract Calcitonin, a polypeptide hormone secreted by the parafollicular C cells of the thyroid gland, lowers serum calcium by decreasing bone resorption and tubular calcium reabsorption. An analgesic action, possibly mediated via beta-endorphins, is also evident. Parenteral calcitonin has been shown to stabilise and increase indices of cortical and trabecular bone mass and total body calcium when administered to patients with established osteoporosis. The routine use of this route of administration has been limited by poor patient compliance and tolerability. An intranasal preparation of calcitonin provided a more convenient means of administration. Several clinical trials have shown that intranasal calcitonin is effective and well tolerated both in prevention of postmenopausal bone loss and in established osteoporosis. Calcitonin therapy is particularly indicated for patients with high-turnover osteoporosis where results show a net gain of bone mineral in the axial skeleton and a slowing of bone loss in the appendicular bones. Due to receptor downregulation a resistance to the hormone may occur after 12-18 months of continuous treatment. This resistant can be avoided and delayed by the cyclical or discontinued administration of the hormone. Further research is needed to confirm longer-term efficacy and effects on fracture rate.