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The influence of fluoride on tooth germ development, especially mineralised tissue, is well documented in numerous dental publications, but there are few reports concerning the influence of fluoride on enamel organ and dental papilla cells. The aim of the study was to assess histologically the development of tooth germs of 20-day-old rat foetuses whose mothers drank water without fluoride or with low (10 mg) and high (110 mg) contents of natrium fluoride, starting from the 12th day of the pregnancy. The fluoride contained in drinking water in low as well as high concentration accelerated the development of enamel organ and dental papilla structures in rat foetuses. The acceleration was proportional to the content of fluoride in drinking water. No disturbances caused by high concentration of natrium fluoride were observed.
Fluoride alters the expression and post-translational modifications of extracellular matrix proteins in dentin. The aim of our study was to determine the effects of fluoride on type I collagen expression during the early stages of tooth germ development in rats. Pregnant dams were divided into three groups and fed a standard diet. From the fifth day of pregnancy the three groups received tap water with, respectively, trace amounts of fluoride (C), a low fluoride concentration (FL) or and a high fluoride concentration (FH). Changes in type I collagen expression and distribution were evaluated. The expression of type I collagen was restricted to the extracellular spaces of cells of mesenchymal origin. In the youngest animals the most intense immunoreactivity for type I collagen was detected in predentin of the FL group. Although the intensity of immunostaining increased in proportion to the age of the animals, the largest increase in the groups investigated was detected in the FL group. We concluded that a low concentration of fluoride can act as a stimulator of type I collagen deposition in the extracellular matrix of dentin, while high concentrations of fluoride have an opposite effect, acting as an inhibitor of type I collagen formation in dentin.
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