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Advances in dental research. 1996;10(2):270-274; discussion 275.Abstract
The ability of ameloblasts and the enamel organ to control the influx of ions into the developing enamel is of considerable interest. The development of transgenic mice lacking a cAMP-regulated chloride channel, the cystic fibrosis transmembrane conductance regulator (CFTR), provides a model that may prove valuable for the study of ion regulation in developing teeth. The purpose of this investigation was to characterize the mineral content of normal and CF mice. Five homozygous and five heterozygous adult mice having the CFTR knockout transgene were evaluated. The mice were killed with CO2 and their mandibular incisors removed, embedded in methacrylate, and sectioned, and enamel particles from the incisal region were then dissected for analysis. Each particle was analyzed for its calcium, phosphorus, and magnesium content. The normal mice had a mean mineral content of 80.5%, in contrast to the CF mice, that had markedly hypomineralized enamel (mean = 51.5%). The calcium/phosphorus ratios were similar for both groups of mice and were compatible with the enamel consisting primarily of hydroxyapatite mineral. The enamel magnesium content was significantly elevated in the CF mice (mean = 3560 ppm) compared with the normal mice (mean = 2280 ppm). Normal mouse enamel was highly mineralized, while the CF mouse enamel mineral content was significantly reduced and had an elevated level of magnesium. The altered mineral content of CF mouse enamel indicates that CFTR could play an important role in ion regulation and consequently mineralization of mouse enamel.
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