Vitamin D deficiency and rickets.

Classical experimental rickets in the rat is a dual deficiency, resulting from both phosphate and vitamin D deficiency, with many of the features of rickets reproducible by simple phosphorus deficiency. Simple vitamin D deficiency differs markedly from experimental rickets, with only the absence of the vitamin D-dependent calcium-binding proteins common to both situations. The expression at the bone level of vitamin D deficiency differs in the two conditions, with rickets leading to profound structural and metabolic changes, whereas simple vitamin deficiency primarily compromises the regulatory function of bone, without obvious structural alterations. It is proposed that human nutritional rickets is the result of a nutritional vitamin D deficiency that aggravates the expression of a pre-existing metabolic defect in phosphate transport. Simple nutritional vitamin D deficiency, unaccompanied by rickets, may occur, but probably has always been rare.