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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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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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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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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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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Dental fluorosis and a polymorphism in the COL1A2 gene in Mexican children.
Highlights Dental fluorosis is a public health problem in the communities evaluated. The rs 412777 polymorphism in the COL1A2 gene was found in Mexican children. An association between the COL1A2 gene polymorphism and dental fluorosis was found. The genetic variant evaluated represents a risk factor to develop dental fluorosis. OBJECTIVE:
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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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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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Annapolis: Water Fluoridation Linked to Death of Dialysis Patient
EVENING CAPITAL (Annapolis, Maryland) November 29, 1979 Fluoride Linked to Death by Mary Ann Kryzankowicz Staff Writer Fluoride poisoning has been definitely linked to the death of a 65-year-old kidney dialysis patient who became ill during a blood cleaning process Nov 11. State Medical Examiner Dr. (illegible) Guard has ruled that Lawrence Blake, 65, of Arundel
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Community Fluorosis Index (CFI)
The current Community Fluorosis Index for U.S. adolescents as a whole (from both fluoridated and non-fluoridated areas) is roughly 5 times higher than the CFI health authorities predicted for fluoridated areas when fluoridation first began. It is also higher than the CFI that the NIDR found in fluoridated areas back in the 1980s. It is readily apparent, therefore, that children are ingesting far more fluoride than was the case in the 1950s, and even as recently as the 1980s.
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