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Reflex sympathetic dystrophy (algodistrophy or Sudeck's disease)
Calcitonin, also called thyrocalcitonin, a protein hormone synthesized and secreted in humans and other mammals primarily by parafollicular cells (C cell) in the thyroid gland. At first it was believed that this hypocalcemic agent was produced by the parathyroid glands. Shortly thereafter, however, it was demonstrated that calcitonin was produced specifically within the parafollicular cells (C cells) of the thyroid gland giving rise to the name 'thyrocalcitonin'. More recent studies have shown calcitonin is also produced by the brain, breast, placenta and other neuroendocrine cells. >> Read More
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.
Inzerillo A M, Zaidi M, Huang C L H. Calcitonin: the other thyroid hormone[J]. Thyroid, 2002, 12(9): 791-798.
Calcitonin (CT), a 32 amino acid peptide hormone produced primarily by the thyroid, and its receptor (CTR) are well known for their ability to regulate osteoclast mediated bone resorption and enhance Ca2+ excretion by the kidney. However, recent studies now suggest that CT and CTRs may play an important role in a variety of processes as wide ranging as embryonic/foetal development and sperm function/physiology. In this review article, CT and CTR gene transcription, signal transduction and function are addressed. The effects of CT on the physiology of a variety of organ systems are discussed and the relationship between polymorphisms in the CTR gene and bone mineral density (BMD)/osteoporosis is examined. Recent studies demonstrating the ability of receptor activity modifying proteins (RAMPs) to post-translationally modify the calcitonin receptor-like receptor (CRLR) are detailed and studies employing transgenic mouse technology to determine the temporal and tissue specific transcriptional activity of the CTR gene in vivo are discussed.
Pondel M. Calcitonin and calcitonin receptors: bone and beyond[J]. International journal of experimental pathology, 2000, 81(6): 405-422.