I. Introduction CALCITONIN (CT) was first discovered in 1962 and named because of its ability to lower plasma calcium concentrations (1). In 1964, the thyroid was established as its major source (2). Since then, extensive investigation has greatly enhanced our understanding of the structure, biosynthesis, physiology, and pharmacology of the hormone (3–9). Despite this progress, the physiological function of CT remains uncertain, although current theories include a role as one of several hormones involved in the chronic regulation of skeletal homeostasis and calcium balance. There has also been a great deal of interest in the relationship of CT to osteoporosis, both as a possible pathogenetic factor and as a potential therapeutic agent. In order to carefully examine this important area of investigation, we have undertaken a critical assessment of the published literature concerning the role of CT in the development and treatment of osteoporosis. II. CT Physiology CT is a 32-amino acid peptide hormone with a 1–7 disulfide bridge at the amino terminus and a carboxyterminal proline amide (9).