Abstract
Concurrent with the decline in dental caries has been an increase in the prevalence of dental fluorosis, a side-effect of exposure to greater than optimal levels of fluoride during amelogenesis. The mechanisms that underlie the pathogenesis of dental fluorosis are not known. We hypothesize that genetic determinants influence an individual’s susceptibility or resistance to develop dental fluorosis. We tested this hypothesis using a mouse model system (continuous eruption of the incisors) where genotype, age, gender, food, housing, and drinking water fluoride level can be rigorously controlled. Examination of 12 inbred strains of mice showed differences in dental fluorosis susceptibility/resistance. The A/J mouse strain is highly susceptible, with a rapid onset and severe development of dental fluorosis compared with that in the other strains tested, whereas the 129P3/J mouse strain is least affected, with minimal dental fluorosis. These observations support the contribution of a genetic component in the pathogenesis of dental fluorosis.
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Possible Association Between Polymorphisms in ESR1, COL1A2, BGLAP, SPARC, VDR, and MMP2 Genes and Dental Fluorosis in a Population from an Endemic Region of West Bengal.
Dental fluorosis (DF) is the most prevalent form of fluorosis in India affecting millions of people all over the country. As estrogen receptor 1 (ESR1), collagen type 1 alpha 2 (COL1A2), bone ?-carboxyglutamic acid protein (BGLAP), secreted protein acidic and cysteine-rich (SPARC), vitamin D receptor (VDR), and matrix metallopeptidase 2
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Evaluation of genetic polymorphisms in MMP2, MMP9 and MMP20 in Brazilian children with dental fluorosis.
Highlights MMP2, MMP9 and MMP20 were expressed in the enamel development of the animalmodels. Polymorphisms in MMP2, MMP9 and MMP2 were not associated with dental fluorosis. Afro-descendants had a higher risk of dental fluorosis than caucasian. Recent studies suggested that genetics contribute to differences in dental fluorosis (DF) susceptibility among individuals
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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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Effect of dietary protein or calcium supplement on the expression of collagen I and dentine phosphoprotein of rats with dental fluorosis.
This study aims to assess the roles of dietary protein (Pr) and calcium (Ca) levels associated with excessive fluoride (F) intake and the impact of Pr, Ca, and F on expression of collagen I (COL I) and dentine phosphoprotein (DPP) in rat incisors. Seventy-two rats were randomly allotted to six
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Enamel crystals of mice susceptible or resistant to dental fluorosis: an AFM study
Objective: This study aimed to assess the overall apatite crystals profile in the enamel matrix of mice susceptible (A/J strain) or resistant (129P3/J strain) to dental fluorosis through analyses by atomic force microscopy (AFM). Material and Methods: Samples from the enamel matrix in the early stages of secretion and maturation were obtained
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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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Factors which increase the risk for skeletal fluorosis
The risk for developing skeletal fluorosis, and the course the disease will take, is not solely dependent on the dose of fluoride ingested. Indeed, people exposed to similar doses of fluoride may experience markedly different effects. While the wide range in individual response to fluoride is not yet fully understood, the following are some of the factors that are believed to play a role.
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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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"Mild" Dental Fluorosis: Perceptions & Psychological Impact
The vast majority of research has found that patients, parents, and the general public alike view mild fluorosis (TF score 3) as a significant blemish of the teeth, one that is likely to embarrass the affected child to a degree that cosmetic treatment would be warranted.
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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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