Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/95431
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Type: Journal article
Title: Vitamin-D regulation of bone mineralization and remodelling during growth
Author: Morris, H.
Turner, A.
Anderson, P.
Citation: Frontiers in Bioscience, 2012; E4(2):677-689
Publisher: Frontiers in Bioscience
Issue Date: 2012
ISSN: 1945-0494
1945-0508
Statement of
Responsibility: 
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
RMID: 0030037018
DOI: 10.2741/409
Published version: https://www.bioscience.org/2012/v4e/af/409/fulltext.htm
Appears in Collections:Medicine publications

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