Abstract
This chapter highlights various abnormal metabolism including vitamin D and phosphate that results osteomalacia. Osteomalacia can occur locally in pagetic lesions because bone of high turnover either needs more vitamin D or permits the more rapid development of the histological expression of impaired mineralization; the opposite probably applies to bone of low turnover. Pregnancy depletes vitamin D stores because calcidiol is transferred preferentially to the fetus, which produces biochemical deterioration and can precipitate overt osteomalacia. It can be inferred that all patients with impaired mineralization because of hypophosphatemia evolve through a stage of atypical osteomalacia, in which a reduction in the rate of mineral apposition is accompanied by a parallel reduction in the rate of matrix apposition or looked at from a different viewpoint by an inversely proportional prolongation of mineralization lag time. Osteomalacia, according to reasonable criteria, has also resulted from chronic phosphorus depletion.
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