Abstract
Sixty-gramme rats were given either 0, 75, 100 or 150 parts/10(6) fluoride in their drinking water. After five weeks, the fluoride, the phosphorus and the protein contents of the enamel were compared in control and experimental animals at three stages of enamel development. The mineral content was reduced in pigmented enamel from animals given 75 parts/10(6) or more fluoride in their drinking water. The fluoride content was elevated in all stages of fluorosed enamel development. At the lowest fluoride level (75 parts/10(6], a larger proline content was found in the proteins of the maturing, fluorosed enamel but there was no increase in the protein content. In animals given 100 parts/10(6) fluoride in their drinking water, the proline content of the protein was greater in maturing, fluorosed enamel, and the total protein content of the post-secretory enamel (maturing and pigmented) was greater than in the controls. These observations indicate that, with increasing levels of fluoride in drinking water, there was an initial delay in the loss of the amelogenin proteins followed by a decreased removal of total protein from the enamel. These results indicate that fluoride interfered with the normal post-secretory, pre-eruptive development of enamel.
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Collagenase 1A2 (COL1A2) gene A/C polymorphism in relation to severity of dental fluorosis
OBJECTIVES: The aim of this study was to evaluate the putative association between the presence of the COL1A2 gene A/C polymorphism and the severity of dental fluorosis in a sample exposed to high concentrations of fluoride. METHODS: A cross-sectional study was carried out that included 80 children residing in a community
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Fluorosed mouse ameloblasts have increased SATB1 retention and Gaq activity
Dental fluorosis is characterized by subsurface hypomineralization and increased porosity of enamel, associated with a delay in the removal of enamel matrix proteins. To investigate the effects of fluoride on ameloblasts, A/J mice were given 50 ppm sodium fluoride in drinking water for four weeks, resulting serum fluoride levels of
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Combined effect of amoxicillin and sodium fluoride on the structure of developing mouse enamel in vitro
OBJECTIVE: Excess fluoride intake during tooth development is known to cause dental fluorosis. It has also been suggested that amoxicillin use in early childhood is associated with enamel hypomineralization. The aim was to investigate separate and combined effects of sodium fluoride (NaF) and amoxicillin on enamel formation in vitro. DESIGN: Mandibular
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Mechanism of toxic action of fluoride in dental fluorosis: whether trimeric G proteins participate in the disturbance of intracellular transport of secretory ameloblast exposed to fluoride.
In enamel fluorosis model rats treated with sodium fluoride, secretory ameloblasts of incisor tooth germs exhibited disruption of intracellular trafficking. We examined whether heterotrimeric G proteins participated in the disruption of vesicular trafficking of the secretory ameloblast exposed to fluoride, using immunoblotting and pertussis toxin (IAP)-induced adenosyl diphosphate (ADP)-ribosylation for
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Short exposure to high levels of fluoride induces stage-dependent structural changes in ameloblasts and enamel mineralization.
We tested the hypothesis that the sensitivity of forming dental enamel to fluoride (F-) is ameloblast developmental stage-dependent and that enamel mineralization disturbances at the surface of fluorotic enamel are caused by damage to late-secretory- and transitional-stage ameloblasts. Four-day-old hamsters received a single intraperitoneal dose of 2.5-20 mg NaF/kg body
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Mechanisms by Which Fluoride Causes Dental Fluorosis Remain Unknown
When it comes to how fluoride impacts human health, no tissue in the body has been studied more than the teeth. Yet, despite over 50 years of research, the mechanism by which fluoride causes dental fluorosis (a hypo-mineralization of the enamel that results in significant staining of the teeth) is not
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Dental Fluorosis Is a "Hypo-mineralization" of Enamel
Teeth with fluorosis have an increase in porosity in the subsurface enamel ("hypomineralization"). The increased porosity of enamel found in fluorosis is a result of a fluoride-induced impairment in the clearance of proteins (amelogenins) from the developing teeth. Despite over 50 years of research, the exact mechanism by which fluoride impairs amelogin
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Diagnostic Criteria for Dental Fluorosis: The Thylstrup-Fejerskov (TF) Index
The traditional criteria (the "Dean Index") for diagnosing dental fluorosis was developed in the first half of the 20th century by H. Trendley Dean. While the Dean Index is still widely used in surveys of fluorosis -- including the CDC's national surveys of fluorosis in the United States -- dental
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Dental Fluorosis in the U.S. 1950-2004
Before the widespread use of fluoride in dentistry, dental fluorosis was rarely found in western countries. Today, with virtually every toothpaste now containing fluoride, and most U.S. water supplies containing fluoride chemicals, dental fluorosis rates have reached unprecedented levels. In the 1950s, it was estimated that only 10% of children in
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Moderate/Severe Dental Fluorosis
In its "moderate" and severe forms, fluoride causes a marked increase in the porosity of the enamel. After eruption into mouth, the porous enamel of moderate to severe fluorosis readily takes up stain, creating permanent brown and black discolorations of the teeth. In addition to extensive staining, teeth with moderate to severe fluorosis are more prone to attrition and wear - leading to pitting, chipping, and decay.
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