Abstract
Exposure to high levels of fluoride (F-) can result in dental fluorosis in different individuals, but the mechanism of dental fluorosis remains unclear. Autophagy is a highly conserved intracellular digestion process that degrades damaged organelles and protein aggregates. This study examined the effect of sodium fluoride (NaF) on the expression of Beclin1 and mTOR to elucidate the development mechanisms of dental fluorosis. HAT-7 cells were incubated with various concentrations of NaF, and autophagic vacuoles were studied by transmission electron microscopy. At both mRNA and protein level, expression of Beclin1, which is required for autophagosome formation and decreases the expression of mTOR, an autophagy-related complex, was increased at 1.2 mmol/l NaF compared to baseline (0 mmol/l NaF). Additionally, immunohistochemical analysis was performed on paraffin-embedded rat incisor sections to identify the expression of Beclin1 and mTOR proteins in vitro. Highly significant differences were detected compared to controls. In summary, our results demonstrate unequivocally that excessive amounts of fluoride cause autophagy of HAT-7 cells, indicating that autophagy is involved in dental fluorosis.
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Utilization of ( 3 H)-serine by ameloblasts of rats receiving sub-mottling doses of fluoride.
Five-day-old Wistar rats were given three intraperitoneal injections at 2-hourly intervals of a solution of sodium fluoride in 0.9 per cent sodium chloride. Three fluoride levels were used: a mottling dose of 3 mgF/kg body weight; and two sub-mottling doses, 0.05 mg and 0.01 mgF/kg body weight. Thirty minutes after
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ENAM Gene Variation in Students Exposed to Different Fluoride Concentrations.
The ENAM gene is important in the formation of tooth enamel; an alteration can affect the lengthening of the crystals, and the thickness in enamel. The objective was to determine the presence of the single nucleotide variant (SNV) rs12640848 of the ENAM gene in students exposed to different concentrations of
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Fluoride Alters Klk4 Expression in Maturation Ameloblasts through Androgen and Progesterone Receptor Signaling.
Fluorosed maturation stage enamel is hypomineralized in part due to a delay in the removal of matrix proteins to inhibit final crystal growth. The delay in protein removal is likely related to reduced expression of kallikrein-related peptidase 4 (KLK4), resulting in a reduced matrix proteinase activity that found in fluorosed
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The effects of chronic high fluoride levels on forming enamel in the rat.
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
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Appropriate real-time PCR reference genes for fluoride treatment studies performed in vitro or in vivo
OBJECTIVE: Quantitative real-time PCR (qPCR) is routinely performed for experiments designed to identify the molecular mechanisms involved in the pathogenesis of dental fluorosis. Expression of reference gene(s) is expected to remain unchanged in fluoride-treated cells or in rodents relative to the corresponding untreated controls. The aim of this study was
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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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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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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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Racial Disparities in Dental Fluorosis
In 2005, the Centers for Disease Control published the results of a national survey of dental fluorosis conducted between 1999 and 2002. According to the CDC, black children in the United States have significantly higher rates of dental fluorosis than either white or Hispanic children. This was not the first time that black children were found to suffer higher rates of dental fluorosis. At least five other studies -- dating as far back as the 1960s -- have found black children in the United States are disproportionately impacted by dental fluorosis.
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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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