Vitamin-D regulation of bone mineralization and remodelling during growth.

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.

• Authors: Howard A Morris, Andrew G Turner, Paul H Anderson
• Journal: Frontiers in bioscience (Elite edition) (Front Biosci (Elite Ed)) Vol. 4 Issue 2 Pg. 677-89 (01 01 2012) ISSN: 1945-0508 [Electronic] Singapore
• PMID: 22201904 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)

Chemical References

• Vitamin D

Topics

• Bone Remodeling
• Calcification, Physiologic
• Endocrine Glands (metabolism)
• Growth
• Humans
• Vitamin D (metabolism)