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

1. Abstract

2. Introduction

3. Vitamin D metabolism - endocrine and autocrine/ paracrine activities

4. Endocrine activities of vitamin D

4.1. Intestine

4.2. Bone growth, mineralization and remodelling

4.3. Parathyroid glands

3.4. Kidney

4.5. Neuromuscular and other cellular functions

4. Vitamin D metabolism and activities within bone cells

5. Conclusion

6. Acknowledgments

7. References

1. 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.