[Frontiers in Bioscience E4, 677-689, January 1, 2012]
Vitamin-D regulation of bone mineralization and remodelling during growth
Howard A Morris1, Andrew G Turner1, Paul H Anderson1
1School of Pharmacy and Medical Sciences, University of South Australia and Endocrine Bone Laboratory, Hanson Institute, SA Pathology, Adelaide, South Australia 5000
TABLE OF CONTENTS
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.