Abstract
Rickets is a complex syndrome with a variety of causes. One common feature of all patients with rickets is impaired mineralization at the epiphyseal growth plate, resulting in defective growth of long bones. Classically, deficiency of vitamin D, essential for absorption of dietary calcium, has been the major cause. Vitamin D deficiency is now rare, except in certain ethnic groups, but should not be overlooked. Advances in molecular genetics have enabled defects to be identified in the rarer inherited forms of rickets often associated with resistance to vitamin D and are leading to an increased understanding of the structure and function of the vitamin D receptor and the 25-hydroxyvitamin D-1α-hydroxylase and also of the PHEX gene, associated with X-linked hypophosphatemia. Curr Opin Orthop 1999, 10:354–360 © Lippincott Williams & Wilkins, Inc.
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