FGF23 and Bone and Mineral Metabolism.

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Abstract

[Indexed for MEDLINE] 20. Scand J Clin Lab Invest Suppl. 2012;243:65-72. doi: 10.3109/00365513.2012.681963. Vitamin D and bone health. Turner AG(1), Anderson PH, Morris HA. Author information: (1)School of Pharmacy and Medical Sciences, University of South Australia, and Chemical Pathology Directorate, SA Pathology, Frome Road, Adelaide 5000 SA, Australia. Current data demonstrate that vitamin D deficiency contributes to the aetiology of at least two metabolic bone diseases, osteomalacia and osteoporosis. Osteomalacia, or rickets in children, results from a delay in mineralization and can be resolved by normalization of plasma calcium and phosphate homeostasis independently of vitamin D activity. The well characterized endocrine pathway of vitamin D metabolism and activities is solely responsible for vitamin D regulating plasma calcium and phosphate homeostasis and therefore for protecting against osteomalacia. In contrast a large body of clinical data indicate that an adequate vitamin D status as represented by the serum 25-hydroxyvitamin D concentration protects against osteoporosis by improving bone mineral density and reducing the risk of fracture. Interestingly adequate serum 1,25-dihydroxyvitamin D concentrations do not reduce the risk of fracture. In vitro human bone cell cultures and animal model studies indicate that 25-hydroxyvitamin D can be metabolised to 1,25-dihydroxyvitamin D by each of the major bone cells to activate VDR and modulate gene expression to reduce osteoblast proliferation and stimulate osteoblast and osteoclast maturation. These effects are associated with increased mineralization and decreased mineral resorption. Dietary calcium interacts with vitamin D metabolism at both the renal and bone tissue levels to direct either a catabolic action on bone through the endocrine system or an anabolic action through a bone tissue autocrine or paracrine system. DOI: 10.3109/00365513.2012.681963