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|Title:||Vitamin-D regulation of bone mineralization and remodelling during growth|
|Citation:||Frontiers in Bioscience (Elite Edition), 2012; E4(2):677-689|
|Publisher:||Frontiers in Bioscience|
|Howard A Morris, Andrew G Turner, Paul H Anderson|
|Abstract:||Vitamin D status relates to two bone diseases, osteomalacia and osteoporosis which arise from distinct pathophysiogical pathways. They can occur in children as well as adults. Osteomalacia or rickets arises from a delay in mineralization and can be caused by severe vitamin D deficiency where the key to curing osteomalacia is the endocrine action of circulating 1,25-dihydroxyvitamin D to normalize the active intestinal transport of calcium and phosphate. Osteoporosis or sub-optimal bone mineral accretion during growth is a risk factor for fracture in children. Current evidence suggests serum 25- hydroxyvitamin D levels between 20 and 80 nmol/L are associated with decreased bone mineral content as a result, at least partly, of reduced vitamin D metabolism and activity within bone cells. The local synthesis of 1,25- dihydroxyvitamin D within bone is necessary to modulate bone resorption and promote bone formation. Thus an adequate vitamin D status is necessary for vitamin D activity within bone to establish a healthy skeleton.|
|Keywords:||Vitamin D metabolism; CYP27B1; CYP 24; bone cell activities; osteomalacia; osteoporosis; vitamin D actvities; review|
|Rights:||Copyright © Frontiers in Bioscience|
|Appears in Collections:||Aurora harvest 7|
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