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lüll Calcium signaling in osteoclast differentiation and bone resorption Kajiya HAdv Exp Med Biol 2012[]; 740 (ä): 917-32Calcium (Ca(2+)) signaling controls multiple cellular functions and is regulated by the release of Ca(2+) from internal stores and its entry from the extracellular fluid. Ca(2+) signals in osteoclasts are essential for diverse cellular functions including differentiation, bone resorption and gene transcription. Recent studies have highlighted the importance of intracellular Ca(2+) signaling for osteoclast differentiation. Receptor activator of NF-kappaB ligand (RANKL) signaling induces oscillatory changes in intracellular Ca(2+) concentrations, resulting in Ca(2+)/calcineurin-dependent dephosphorylation and activation of nuclear factor of activated T cells c1 (NFATc1), which translocates to the nucleus and induces osteoclast-specific gene transcription to allow differentiation of osteoclasts. Recently, some reports indicated that RANKL-induced Ca(2+) oscillation involved not only repetitive intracellular Ca(2+) release from inositol 1, 4, 5-triphosphate channels in Ca(2+) store sites, but also via store-operated Ca(2+) entry and Ca(2+) entry via transient receptor potential V channels during osteoclast differentiation. Ca(2+)-regulatory cytokines and elevation of extracellular Ca(2+) concentrations have been shown to increase intracellular Ca(2+) concentrations ([Ca(2+)](i)) in mature osteoclasts, regulating diverse cellular functions. RANKL-induced [Ca(2+)](i) increase has been reported to inhibit cell motility and the resorption of cytoskeletal structures in mature osteoclasts, resulting in suppression of bone-resorption activity. In conclusion, Ca(2+) signaling activates differentiation in osteoclast precursors but suppresses resorption in mature osteoclasts. This chapter focuses on the roles of long-term Ca(2+) oscillations in differentiation and of short-term Ca(2+) increase in osteoclastic bone resorption activity.|Animals[MESH]|Bone Resorption/*etiology[MESH]|Calcium Channels/physiology[MESH]|Calcium Signaling/*physiology[MESH]|Calcium/metabolism[MESH]|Cell Differentiation[MESH]|Cell Movement[MESH]|Humans[MESH]|NFATC Transcription Factors/physiology[MESH]|Osteoclasts/*cytology[MESH]|TRPV Cation Channels/physiology[MESH] |