Clinica Chimica Acta. Available online 30 July 2013
Jackson W. Ryan, Paul H. Anderson, Andrew G. Turner, Howard A. Morris Howard.Morris at health.sa.gov.au
School of Pharmacy and Medical Sciences, University of South Australia, Adelaide, South Australia, Australia
Chemical Pathology Directorate and Hanson Institute, SA Pathology, Adelaide South Australia 5000, Australia
Bone mineral status depends on plasma calcium and phosphate homeostasis.
Vitamin D regulates bone remodelling via endocrine and intracrine activities.
Vitamin D stimulates or inhibits bone mineralisation under different circumstances.
Vitamin D activity requires an adequate vitamin D status as indicated by the serum level of 25-hydroxyvitamin D and appropriate expression of genes coding for vitamin D receptor and 25-hydroxyvitamin D 1α-hydroxylase, the enzyme which converts 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D. Vitamin D deficiency contributes to the aetiology of osteomalacia and osteoporosis. The key element of osteomalacia, or rickets in children, is a delay in mineralization. It can be resolved by normalisation of plasma calcium and phosphate homeostasis independently of vitamin D activity. The well characterised endocrine pathway of vitamin D metabolism generates plasma 1,25-dihydroxyvitamin D and these endocrine activities are solely responsible for vitamin D regulating plasma calcium and phosphate homeostasis and protection against osteomalacia. In contrast, a large body of clinical data indicate that an adequate serum 25-hydroxyvitamin D level improves bone mineral density protecting against osteoporosis and reducing fracture risk. Recent research demonstrates that the three major bone cell types have the capability to metabolise 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D to activate the vitamin D receptor and modulate gene expression. Dietary calcium intake 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 when calcium intake is inadequate or an anabolic action through a bone autocrine or paracrine system when calcium intake is sufficient.
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