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Previous Volume 338:681-682 March 5, 1998 Number 10 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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The typical clinical picture of rickets, first clearly described in the 17th century, includes growth-plate abnormalities and delayed growth, weakening and bowing of weight-bearing bones, hypoplasia of tooth enamel, and hypocalcemia with muscle hypotonia and even tetany. The basic skeletal lesion is impaired mineralization of the matrix produced by growth-plate chondrocytes or osteoblasts. The same disease in adults, osteomalacia, is much more silent, because the growth-plate effects, and therefore growth effects, are absent. In simple vitamin D deficiency, either small doses of vitamin D or exposure to ultraviolet radiation can correct all the bony abnormalities.

A few patients, however, are . . . [Full Text of this Article]

References

This article has been cited by other articles:

• Cheng, J. B., Levine, M. A., Bell, N. H., Mangelsdorf, D. J., Russell, D. W. (2004). Genetic evidence that the human CYP2R1 enzyme is a key vitamin D 25-hydroxylase. Proc. Natl. Acad. Sci. USA 101: 7711-7715 [Abstract] [Full Text]