Abstract
Osteoclasts are the only cells that destroy and resorb bone. Calcitonin, a calcium regulatory hormone, strongly inhibits bone-resorbing activity of osteoclasts. The calcitonin-induced inhibition of osteoclast function is believed to be due to disruption of cytoskeletal organization (distraction of actin rings) and disappearance of the cellular polarity of osteoclasts. Calcitonin receptors are coupled to both cAMP-PKA- and Ca(2+)-PKC (protein kinase C)-mediated signaling pathways. Using mouse osteoclasts formed in vitro, it is shown that inhibitory effects of calcitonin on bone resorption is mainly mediated by the cAMP-PKA signal. This article describes the mechanism of calcitonin action in the suppression of osteoclast function.
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