ABSTRACT

Vitamin D de„ciency causes rickets in children and osteomalacia in adults. It also can precipitate and exacerbate osteoporosis including risk of fracture (Holick, 2007). Rickets/osteomalacia by de„nition means that osteoblasts have laid down a collagen matrix, but a defect exists in its ability to be mineralized. In children, a defect in the mineralization of the osteoid in the long bones and the failure or delay in the mineralization of endochrondal bone formation at the growth plate leads to the classic skeletal deformities of rickets (Holick, 2006) (Figure 10.1). However, in adults, the mineralization defect takes on a different character because of the failure of mineralization of newly formed osteoid at sites of bone turnover of periosteal or endosteal apposition. Several possible causes of poor or absent skeletal mineralization may lead to both rickets and osteomalacia. Although the major cause of rickets/osteomalacia is a de„ciency of vitamin D, rare causes include a defect in vitamin D metabolism or in its recognition by calcium-regulating tissues.