Enamel and Dentin Fluoride Levels and Fluorosis following Single Fluoride Doses: A Nuclear Microprobe Study

Angmar‐Månsson, Birgit; Lindh, Ulf; Whitford, Gary M.

doi:10.1159/000261279

Cited by 22 publications

(12 citation statements)

References 9 publications

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“…Studies by Angmar-Mansson and Whitford (1985) and Angmar-Mansson et al (1990) showed that in a rat given a single injection of fluoride, the subsequently erupting enamel continued to show fluorosis after the period of time during which the serum fluoride levels would have reached baseline levels. This study supports the suggestion that fluoride accumulates locally in the surrounding tissues or bony environment of the developing tooth, and that higher than optimal levels may be released beyond the time at which the initial fluoride challenge occurred.…”

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confidence: 98%

“…Removal of fluoride from the blood stream may initially reduce the degree of enamel fluorosis by lowering the amount of fluoride available to the developing enamel. However, if fluoride does accumulate in the bone, a relatively large reservoir of fluoride may be present in the bones of the developing skeleton, which may be released locally (Pendrys and Stamm, 1990;Angmar-Mansson et al, 1990).…”

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confidence: 99%

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Dental Fluorosis: Its Use as a Biomarker

Besten

1994

Adv Dent Res.

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Several epidemiological studies, beginning with those of Dean and co-workers in the 1940's, clearly demonstrate the relationship between dental fluorosis in humans and the level of fluoride in water supplies. These studies and others have shown that, in a population, there is a direct relationship among the degree of enamel fluorosis, plasma and bone fluoride levels, and the concentration of fluoride in drinking water. However, dental fluorosis is a reflection of fluoride exposure only during the time of enamel formation, somewhat limiting its use as a biomarker. In addition, the degree of fluorosis is dependent not only on the total fluoride dose, but also on the timing and duration of fluoride exposure. At the level of an individual response to fluoride exposure, factors such as body weight, activity level, nutritional factors, and the rate of skeletal growth and remodeling are also important. These variables, along with an individual variability in response to similar doses of fluoride, indicate that enamel fluorosis cannot be used as a biological marker of the level of fluoride exposure for an individual.

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Dental Fluorosis: Its Use as a Biomarker

Besten

1994

Adv Dent Res.

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“…ingested vs. inhaled), renal function, rate of bone metabolism, metabolic activity, etc. [6]. In addition to these variables, genetic factors have been shown to dictate the severity of enamel fluorosis in mice [7].…”

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Chronic Fluoride Toxicity: Dental Fluorosis

DenBesten¹,

Li²

2011

Monographs in Oral Science

312

218

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Dental fluorosis occurs as a result of excess fluoride ingestion during tooth formation. Enamel fluorosis and primary dentin fluorosis can only occur when teeth are forming, and therefore fluoride exposure (as it relates to dental fluorosis) occurs during childhood. In the permanent dentition, this would begin with the lower incisors, which complete mineralization at approximately 2–3 years of age, and end after mineralization of the third molars. The white opaque appearance of fluorosed enamel is caused by a hypomineralized enamel subsurface; with more severe dental fluorosis, pitting and a loss of the enamel surface occurs, leading to secondary staining (appearing as a brown color). Many of the changes caused by fluoride are related to cell/matrix/mineral interactions as the teeth are forming. At the early maturation stage, the relative quantity of amelogenin protein is increased in fluorosed enamel in a dose-related manner. This appears to result from a delay in the removal of amelogenins as the enamel matures. In vitro, when fluoride is incorporated into the mineral, more protein binds to the forming mineral, and protein removal by proteinases is delayed. This suggests that altered protein/mineral interactions are in part responsible for retention of amelogenins and the resultant hypomineralization that occurs in fluorosed enamel. Fluoride also appears to enhance mineral precipitation in forming teeth, resulting in hypermineralized bands of enamel, which are then followed by hypomineralized bands. Enhanced mineral precipitation with local increases in matrix acidity may affect maturation stage ameloblast modulation, potentially explaining the doserelated decrease in cycles of ameloblast modulation from ruffleended to smooth-ended cells that occur with fluoride exposure in rodents. Specific cellular effects of fluoride have been implicated, but more research is needed to determine which of these changes are relevant to the formation of fluorosed teeth. As further studies are done, we will better understand the mechanisms responsible for dental fluorosis.

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“…11 Generally, evidence suggests that fluorosis is the result of peak fluoride in the plasma rather than the quantity absorbed. 12 Acute doses can result in sufficient fluoride being mobilized from the bone adjacent to the developing teeth to affect enamel development. 12 Thus, the use of fluoride varnishes is clinically appropriate.…”

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“…12 Acute doses can result in sufficient fluoride being mobilized from the bone adjacent to the developing teeth to affect enamel development. 12 Thus, the use of fluoride varnishes is clinically appropriate. 13,14 Other forms of fluoride, especially those used chronically, are swallowed and may increase risk for adverse effects.…”

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Pharmacokinetics of Fluoride in Toddlers After Application of 5% Sodium Fluoride Dental Varnish

et al. 2014

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The prevalence of dental caries (tooth decay) among preschool children is increasing, driven partially by an earlier age of onset of carious lesions. The American Academy of Pediatrics recommends application of 5% sodium fluoride varnish at intervals increasing with caries risk status, as soon as teeth are present. However, the varnishes are marketed for treatment of tooth sensitivity and are regulated as medical devices rather than approved by the US Food and Drug Administration for prevention of dental caries (tooth decay). The objective of this research is to examine the safety of use in toddlers by characterizing the absorption and distribution profile of a currently marketed fluoride varnish. We measured urinary fluoride for 5 hours after application of fluoride varnish to teeth in 6 toddlers aged 12 to 15 months. Baseline levels were measured on a separate day. The urine was extracted from disposable diapers, measured by rapid diffusion, and extrapolated to plasma levels. The mean estimated plasma fluoride concentration was 13 mg/L (SD, 9 mg/L) during the baseline visit and 21 mg/L (SD, 8 mg/L) during the 5 hours after treatment. Mean estimated peak plasma fluoride after treatment was 57 mg/L (SD, 22 mg/L), and 20 mg/kg (SD, 4 mg/L) was retained on average. Retained fluoride was 253 times lower than the acute toxic dose of 5 mg/kg. Mean plasma fluoride after placement of varnish was within an SD of control levels. Occasional application of fluoride varnish following American Academy of Pediatrics guidance is safe for toddlers. Pediatrics 2014;134:e870-e874 AUTHORS:

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Enamel and Dentin Fluoride Levels and Fluorosis following Single Fluoride Doses: A Nuclear Microprobe Study

Cited by 22 publications

References 9 publications

Dental Fluorosis: Its Use as a Biomarker

Dental Fluorosis: Its Use as a Biomarker

Chronic Fluoride Toxicity: Dental Fluorosis

Pharmacokinetics of Fluoride in Toddlers After Application of 5% Sodium Fluoride Dental Varnish

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