Fukumoto S
Department of Medicine, Tokyo University Branch Hospital.
Nihon Rinsho. 1998 Jun;56(6):1419-24.
Elevation of extracellular calcium has been shown to inhibit osteoclastic bone resorption and stimulate proliferation and chemotaxis of osteoblasts. Therefore, calcium released by bone resorption may have important roles in the coupling of bone resorption and bone formation. Although both osteoclasts and osteoblasts have calcium-sensing mechanisms, the responsible molecule in these cells seems to be different. Functional and histological studies show that calcium-sensing mechanism in osteoclasts is a ryanodine receptor-like molecule in plasma membrane. In contrast, calcium-sensing mechanism in osteoblasts has similar functional property to parathyroid calcium-sensing receptor (CaSR), but is a different molecule from CaSR. In addition, several bone marrow cells express CaSR. The elucidation of the identity and the physiological roles of these calcium-sensing mechanisms would give us a more clear view of bone remodeling.
细胞外钙升高已被证明可抑制破骨细胞的骨吸收，并刺激成骨细胞的增殖和趋化性。因此，骨吸收释放的钙可能在骨吸收与骨形成的偶联中发挥重要作用。虽然破骨细胞和成骨细胞都有钙感知机制，但这些细胞中的相关分子似乎有所不同。功能和组织学研究表明，破骨细胞中的钙感知机制是质膜上一种类兰尼碱受体分子。相比之下，成骨细胞中的钙感知机制与甲状旁腺钙敏感受体（CaSR）具有相似的功能特性，但却是一种与CaSR不同的分子。此外，几种骨髓细胞表达CaSR。阐明这些钙感知机制的特性和生理作用将使我们对骨重塑有更清晰的认识。
