Abstract
Calcitonin was originally discovered as a hypocalcemic factor synthesized by thyroid parafollicular C cells. Early experiments demonstrated that calcitonin inhibited bone resorption and decreased calcium efflux from isolated cat tibiae and subsequent histologic and culture studies confirmed the osteoclast as its major site of action. Its potent antiresorptive effect and analgesic action have led to its clinical use in treatment of Paget's bone disease, osteoporosis, and hypercalcemia of malignancy. This review surveys the cellular and molecular basis of these physiologic and clinical actions.
Get full access to this article
View all access options for this article.