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Calcium-sensing Receptor in Bone

  • Chapter
Calcium-Sensing Receptor

Part of the book series: Endocrine updates ((ENDO,volume 19))

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Abstract

Bone is intimately involved in systemic mineral ion homeostasis by virtue of its interplay with parathyroid gland and kidney (1). The extracellular calcium ion concentration (Ca2+ o) underneath actively resorbing osteoclasts can rise as high as 8–40 mM (2). Therefore, it is likely that Ca2+ o within the immediate microenvironment of such osteoclasts would change substantially when this calcium is released. Indeed, during uncontrolled osteoclastic release of skeletal Ca2+, as in cases where there is extensive skeletal metastases of certain malignancies promoting bone resorption via osteoclast-activating, hormonal factors, such as parathyroid hormone-related peptide (PTHrP) (e.g., breast), even the levels of systemic Ca2+ o can increase well above normal and become life-threatening (3). Ca2+ o in the local skeletal microenvironment is likely to be even higher in this setting. On the other hand, several hundred milligrams of Ca2+ o enter the skeleton owing to de novo formation of bone by osteoblasts on a daily basis. Local depletion of Ca2+ o will likely take place in the immediate vicinity of osteoblasts actively forming bone. Thus it is possible that the G protein-coupled, extracellular calcium (Ca2+ o)-sensing receptor (CaR) (4,5) may also play some role within the skeleton by sensing such local changes in Ca2+ o caused by bone remodeling.

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Yamaguchi, T. (2003). Calcium-sensing Receptor in Bone. In: Chattopadhyay, N., Brown, E.M. (eds) Calcium-Sensing Receptor. Endocrine updates, vol 19. Springer, Boston, MA. https://doi.org/10.1007/978-1-4419-9256-7_5

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