Abstract
Calcium-sensing receptor (CaSR), whose expressions in the parathyroid and kidney are important for the homeostasis of extracellular calcium ion, is also expressed in chondrocytes and osteoblasts, in which the receptor suppression is linked to impaired mineralization. Unexpected observation of rickets in CaSR knockout mice amid a plenty of calcium ion under hyperparathyroidism seemed compatible with the above findings. On the other hand, constitutive activity of osteoblast CaSR enhances bone turnover and promotes loss of cancellous bone. These findings suggest that CaSR activation in chondrocytes and osteoblasts may stimulate bone remodeling in bone microenvironments.
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