IMR Press / FBE / Volume 4 / Issue 2 / DOI: 10.2741/e409

Frontiers in Bioscience-Elite (FBE) is published by IMR Press from Volume 13 Issue 2 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.


Vitamin-D regulation of bone mineralization and remodelling during growth

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1 School of Pharmacy and Medical Sciences, University of South Australia and Endocrine Bone Laboratory, Hanson Institute, SA Pathology, Adelaide, South Australia 5000

*Author to whom correspondence should be addressed.

Academic Editor: Cory Xian

Front. Biosci. (Elite Ed) 2012, 4(2), 677–689;
Published: 1 January 2012
(This article belongs to the Special Issue Bone growth, regulation, injury and repair)

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.

Vitamin D metabolism
CYP 24
Bone Cell Activities
Vitamin D actvities
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