Calcium and bone disease

✍ Scribed by Harry C. Blair; Lisa J. Robinson; Christopher L.-H. Huang; Li Sun; Peter A. Friedman; Paul H. Schlesinger; Mone Zaidi

• Book ID: 112009955
• Publisher: IOS Press
• Year: 2011
• Tongue: English
• Weight: 232 KB
• Volume: 37
• Category: Article
• ISSN: 0951-6433
• DOI: 10.1002/biof.143

✦ Synopsis

Calcium transport and calcium signaling are of basic importance in bone cells. Bone is the major store of calcium and a key regulatory organ for calcium homeostasis. Bone, in major part, responds to calcium-dependent signals from the parathyroids and via vitamin D metabolites, although bone retains direct response to extracellular calcium if parathyroid regulation is lost. Improved understanding of calcium transporters and calcium-regulated cellular processes has resulted from analysis of genetic defects, including several defects with low or high bone mass. Osteoblasts deposit calcium by mechanisms including phosphate and calcium transport with alkalinization to absorb acid created by mineral deposition; cartilage calcium mineralization occurs by passive diffusion and phosphate production. Calcium mobilization by osteoclasts is mediated by acid secretion. Both bone forming and bone resorbing cells use calcium signals as regulators of differentiation and activity. This has been studied in more detail in osteoclasts, where both osteoclast differentiation and motility are regulated by calcium.