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ShareAug. 6, 2010 — Researchers led by Dr. Catherine Chaussain of the University of Paris Descartes implicate a novel peptide in impaired dentin mineralization in rickets. They report their data in the August 2010 issue of the American Journal of Pathology.
Rickets, the softening of bones in children, is often caused by vitamin D deficiency due to severe malnutrition. Rickets is one of the most frequent childhood diseases in developing countries and is associated with severe bone deformities, including dental ailments due to impaired dentin mineralization.
Some cases of rickets, such as familial hypophosphatemic rickets, have a genetic basis. These cases are often caused by a mutation in the protein PHEX. Boukpessi et al hypothesized that PHEX impairment resulted in the release of a peptide, ASARM, which is known to inhibit dentin mineralization. They observed that ASARM was abnormally produced in patients with familial rickets, and that both symptoms and ASARM production could be attenuated by a diet high in vitamin D and phosphate during growth. The presence of the ASARM peptide may thus contribute to impaired dentin mineralization in rickets, in a manner compensated for by vitamin D and phosphate.
Dr. Chaussain and colleagues suggest that "the release of this peptide may partially explain the impaired dentin mineralization associated with the disease in teeth from hypophosphatemic patients with mutation of the PHEX gene. However, treatment during growth may limit the clinical consequences of this anomaly in the dentin of permanent teeth. This observation highlights the importance of improving phosphate and vitamin D environment on dentin mineralization, which compensates the adverse effect of PHEX mutation."
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The above story is reprinted from materials provided by American Journal of Pathology, via EurekAlert!, a service of AAAS.
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Journal Reference:
- Boukpessi T, Gaucher C, Léger T, Salmon B, Le Faouder J, Willig C, Rowe PS, Garabédian M, Meilhac O, Chaussain C. Abnormal presence of the MEPE-derived ASARM peptide in human hypophosphatemic dentin. Am J Pathol, 2010; 177: 803-812
Note: If no author is given, the source is cited instead.
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