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Effect of fluoride on growth and acid production by Streptococcus mutans in dental plaque.

The aim of this study was to measure the effect of fluoride on the production of organic acids by Streptococcus mutans in dental plaque. The effect was studied in a simplified model of dental plaque with gnotobiotic rats monoinfected with S. mutans Ny341. Adaptation of S. mutans to fluoride was induced by feeding one group of the rats on fluoride-containing diet and drinking water. No difference was found in the accumulation of S. mutans on the teeth between the fluoride-adapted and the control groups. However, there was a significant difference in the amount of lactic acid in metabolically resting plaque between the groups, lactic acid being lower in the fluoride-adapted plaque. At 5 min after a rinse containing 10% sucrose, a high level of lactic acid was found in plaque from animals not exposed to fluoride. Rinses containing 4 or 20 mM fluoride before the sucrose rinse significantly inhibited the lactic acid production in the control group. In the plaque from rats on fluoridated diet and drinking water the sucrose-induced production of lactic acid was not inhibited by a 4 mM fluoride rinse. Moreover, the production of lactic acid in the fluoride-adapted plaque was prolonged. The results indicate that due to fluoride adaptation the inhibition of acid production is unlikely to be important for the caries-preventive action of fluoride.

Acetates↗

Influence of pH and fluoride on properties of an oral strain of Lactobacillus casei grown in continuous culture.

A freshly isolated oral strain, Lactobacillus casei RB1014, was grown in continuous culture to compare the effects of pH and fluoride on growth and metabolism. The cells were grown at pH 7.0 to 3.2 in the absence of fluoride and from pH 7.0 to 5.4 with 20 mM NaF. Cell numbers varied from 3 X 10(9) to 30 X 10(9)/ml on blood agar during alterations in the growth pH from 7.0 to 4.27. Only when the culture was stressed by lowering the pH to 3.2 were cell numbers drastically reduced. Cells growing at pH 7.0 without fluoride were unable to grow when plated on fluoride agar (10.5 mM) at pH 5.5; however, when the growth pH was allowed to decrease to 4.94, cells grew on the fluoride plates in numbers equal to those growing on blood agar. This fluoride tolerance trait appeared rapidly once pH control was removed and was lost when the culture was returned to pH 7.0. The addition of 20 mM NaF to the culture medium did not adversely affect growth, provided that the pH was maintained at 6.0 or above; cells tolerant to 10.5 and 16 mM NaF appeared on pH 5.5 plates during this phase. In cells removed from the chemostat throughout the experiment and incubated at the pH of growth in a pH stat, glycolytic activity was optimum at pH 5.5 in the absence of NaF. Fluoride stimulated glycolytic activity by cells incubated at pH 7.0 and by cells growing with 20 mM NaF, provided that the pH of growth remained at or above 6.0. A more detailed examination of the adaptation to fluoride tolerance during shifts to acidic pH values revealed that cells capable of growth on acidic fluoride agar plates appeared within 2 h of the start of the fall in pH of the chemostat culture. Estimation of the intracellular pH during the period of the initial pH fall revealed that the intracellular pH was identical to the extracellular pH (i.e., no pH gradient [delta pH]), indicating that fluoride would not be transported into the cells to inhibit metabolism. However, once the pH of the medium was stabilized, delta pHs were generated, with the delta pH increasing as the pH declined. The inhibition of glycolysis by fluoride increased in proportion to the delta pH. Cells grown at pH 5.5 generated larger delta pHs than did cells grown at pH 7.0, although the values were normally small (approximately 0.9 U). The data suggest that the inherent fluoride tolerance of L. casei RB1014 was associated with relatively small delta pHs.

Fluorides↗

Fluoride inhibition of proton-translocating ATPases of oral bacteria.

The ATPases of isolated membranes of lactic acid bacteria were found to be inhibited by fluoride in a complex manner. Among the enzymes tested, that of Streptococcus mutans GS-5 was the most sensitive to fluoride, and the initial rate of hydrolysis of ATP was reduced 50% by approximately 3 mM fluoride. The enzyme of Lactobacillus casei ATCC 4646 was the most resistant, and about 25 mM fluoride was required for 50% inhibition. The response to fluoride appeared to involve reversible, noncompetitive inhibition during short exposure to low levels of fluoride and nonreversible inhibition at higher fluoride levels. In addition, kinetic studies of the effects of fluoride on the enzymes of membranes of S. mutans and L. casei indicated that reversible inhibition was at least partly overcome at high levels of either ATP or Mg. The effects of pH on fluoride inhibition of ATPases were markedly different from the effects of pH on inhibition of acid/base regulation of intact cells by fluoride. It appeared that formation of HF was not required for inhibition of the ATPases. F1 ATPases isolated from the membranes by washing with buffers of low ionic strength proved to be less sensitive to fluoride than the membrane-associated F1F0 holoenzymes, and it was concluded that the F0 or membrane sector of the holoenzyme is involved in fluoride inhibition.

Adenosine Triphosphatases↗

Water fluoridation, tooth decay in 5 year olds, and social deprivation measured by the Jarman score: analysis of data from British dental surveys.

OBJECTIVE: To examine the effect of water fluoridation, both artificial and natural, on dental decay, after socioeconomic deprivation was controlled for. DESIGN: Ecological study based on results from the NHS dental surveys in 5 year olds in 1991-2 and 1993-4 and Jarman underprivileged area scores from the 1991 census. SETTING: Electoral wards in three areas: Hartlepool (naturally fluoridated), Newcastle and North Tyneside (fluoridated), and Salford and Trafford (non-fluoridated). SUBJECTS: 5 year old children (n = 10,004). INTERVENTION: Water fluoridation (artificial and occurring naturally). MAIN OUTCOME MEASURE: Ward tooth decay score (score on the "decayed, missing, and filled tooth index" for each electoral ward). RESULTS: Multiple linear regression showed a significant interaction between Jarman score for ward, mean number of teeth affected by decay, and both types of water fluoridation. This confirms that the more deprived an area, the greater benefit derived from fluoridation, whether natural or artificial (R2 = 0.84, P < 0.001). At a Jarman score of zero (national mean score) there was a predicted 44% reduction in decay in fluoridated areas, increasing to a 54% reduction in wards with a Jarman score of 40 (very deprived). The area with natural fluoridation (at a level of 1.2 parts per million-higher than levels in artificially fluoridated areas) had a 66% reduction in decay, with a 74% reduction in wards with a Jarman score of 40. CONCLUSION: Tooth decay is confirmed as a disease associated with social deprivation, and the more socially deprived areas benefit more from fluoridation. Widespread water fluoridation is urgently needed to reduce the "dental health divide" by improving the dental health of the poorer people in Britain.

Child, Preschool↗

Inhibition of dentin demineralization by fluoride in vitro.

Compared with the knowledge accumulated on enamel-fluoride interactions, relatively little data is available regarding fluoride effects on dentin. This applies to both laboratory and clinical studies into the efficacy of fluoride schemes for the prevention of root surface caries. This study aimed to determine the effects of fluoride and pH on the demineralization of dentin, such as to provide information necessary to develop preventive programmes. Bovine dentin blocks were subjected to undersaturated calcium- and phosphate-containing solutions in the pH range 4.0-6.0 with fluoride added at concentrations between 0.5 and 10 ppm. Non-fluoride solutions served as controls. Mineral loss was assessed chemically and by transversal microradiography. Comparisons were made with similar studies on enamel demineralization. The results showed that demineralization of dentin depends on both pH and fluoride concentration in the demineralizing solution. Inhibition of demineralization that could be relevant from a clinical point of view was found at fluoride values 5-10 times the corresponding values for enamel. Also rapid depletion of fluoride from the solutions was observed, indicating the high uptake capacity of dentin for fluoride. Lesion depth depended on pH of the solution while the fluoride levels were associated with the surface layer, both in mineral content and depth. For dentin we propose a demineralization mechanism where acid penetrates rapidly into the tissue, presumably through the tubules, after which the released calcium and phosphate is partly trapped by the inward diffusing fluoride. This leads to the formation of a surface layer, which may even be hypermineralized compared to sound dentin.

Animals↗

Fluoride-dependent formation of mineralized layers in bovine dentin during demineralization in vitro.

Demineralization of dentin in the presence of fluoride produces lesions with a mineralized surface layer which becomes thicker and more mineralized with higher fluoride concentrations whereas the lesion depth is hardly affected. The aim of this study was to investigate the effects of the time of fluoride treatment and the amount of fluoride taken up on the properties of the mineralized layer. Discs of bovine dentin embedded in methylmethacrylate with one surface exposed were demineralized in 50 mM acetic acid, 2.2 mM CaCl2, 2.2 mM KH2PO4, pH 5.0. At the start and/or later during the demineralization period, the specimens were incubated individually for 1 or 2 days in 10 ml of the same demineralization solution supplemented with 0.5, 2.0 or 5.0 ppm fluoride, which was then assessed for changes in calcium and fluoride concentrations. After 2, 5 and 8 days, specimens were sectioned for microradiographic analysis so as to follow development of the lesions and the mineralized layers. The results were the following: While demineralization with fluoride present at the first day led to the formation of a surface layer, fluoride present only at a later day produced a subsurface layer, not at the lesion front but closer to the surface. This layer resulted from (re)precipitation and not from preservation of the original mineral. The 'integrated mineral content' of the surface layer increased linearly with the uptake of fluoride, which resulted in an apparent fluorapatite content of about 20 vol%. The profiles of the surface layers remained unchanged during continued demineralization in the absence of fluoride. It was concluded that in the presence of fluoride mineral loss is reduced as a result of the reprecipitation of dissolved mineral ions as a layer of fluoride-enriched apatite. This layer does not offer protection of underlying dentin against continued demineralization.

Acetic Acid↗

Maternal-fetal transfer of fluoride in pregnant women.

Gas chromatography was used to measure the maternal and fetal plasma inorganic fluoride values at term in 91 women. They were assigned to one of four groups: group A were untreated controls; group B received a single daily dose of 1.5 mg of fluoride (as calcium fluoride) during the final trimester of pregnancy; group C was given a single dose of 1.5 mg of fluoride (as sodium fluoride) and group D was given 2 daily doses of fluoride (as sodium fluoride) totaling 1.5 mg. There was a significant difference between the cord plasma fluoride levels of the newborns in the untreated group (mean: 27.8 micrograms/l) and that of the combined supplemented groups B, C and D (mean: 58.3 micrograms/l). There was no difference between the average fluoride levels in the three supplemented groups. There was no significant effect of maternal age, infant birth weight, gestation or diet during pregnancy on the cord plasma fluoride level. These results indicate that fluoride supplementation during the final trimester of pregnancy will significantly elevate cord plasma fluoride concentrations.

Adult↗

In vitro induced fluoride resistance of Streptococcus mutans and dental caries in rats.

The aim of this investigation was to study the effect of an in vitro acquired, stable, fluoride-resistant strain of Streptococcus mutans on dental caries in rats. Three groups (P0, P5 and P10) of SPF Osborne-Mendel rats were inoculated with the fluoride-sensitive S. mutans C180-2. Three other groups (FR0, FR5 and FR10) were inoculated with cultures of the fluoride-resistant S. mutans C180-2FR. Diet SSP 20/5 and tap water (less than 0.2 ppm fluoride) were available ad libitum to all groups. The drinking water of groups P5 and FR5 was supplemented with 5 mg F-/1 and the drinking water of groups P10 and FR10 with 10 mg F-/1. At the end of the caries experiment (days 58/59) there were no significant differences in the percentages and in the numbers of S. mutans in the total maxillary plaques of groups P0 to P10 and of groups FR0 to FR10, respectively. The fluoride tolerance of S. mutans cells re-isolated from rats, inoculated with the fluoride-sensitive strain, showed an unstable decrease compared to before inoculation. S. mutans cells re-isolated from rats, inoculated with the fluoride-resistant strain, showed both unstable and stable adaptation towards fluoride sensitivity. The animals superinfected with the fluoride-resistant strain developed less dentinal/fissure caries. Fluoride given in the drinking water at concentrations of 5 and 10 mg/l was effective in reducing caries irrespective of whether the animals were superinfected with the fluoride-sensitive or the fluoride-resistant strain.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

The physiological and toxicological characteristics of fluoride.

The metabolism and toxicity of fluoride are discussed with emphasis on new scientific findings. The gastric absorption, tissue distribution, and renal excretion of the ion are all influenced by the magnitude and direction of the pH gradient between adjacent body fluid compartments. This mechanism explains the asymmetric distribution of fluoride across cell membranes, and the manipulation of transmembrane pH gradients has proven efficacious in acute fluoride toxicity. The comparative metabolism and relative toxicities of ionic fluoride and monofluorophosphate are discussed. It is no longer certain that there is a difference between the acute toxic potentials of sodium fluoride and those of MFP. It is concluded that the "probably toxic dose" or PTD of fluoride--the dose which should trigger therapeutic intervention and hospitalization--is 5 mg/kg of body weight. As currently packaged, many dental products contain sufficient fluoride to exceed the PTD for young children. There is a need for additional research into the sources, effects, and fate of strongly bound or organic fluoride compounds. Attention is drawn to the fact that, while the metabolic characteristics and effects of fluoride in young and middle-aged adults have received considerable research attention, there is a paucity of such information for young children and the elderly. The increasing prevalence of dental fluorosis is addressed. It is concluded that nondietary sources of fluoride, mainly fluoride-containing dental products, are a major source of ingested fluoride. The article concludes with 12 recommendations for future research.

Absorption↗

Effects of fluoride on the microbial ecology of dental plaque.

In order to survive in a community such as dental plaque, bacteria must be able to resist changes in the environment. These changes may be the result of differences in the host or the activities of the bacteria within the community. Bacteria which cannot resist these environmental pressures may cease metabolism but survive, or be eliminated from the community. Fluoride is only one of numerous environmental pressures which impact on oral bacterial communities, yet its beneficial effect on caries is such that it could be proposed that in addition to its effects on enamel and remineralization, fluoride would affect the bacteria. It has been shown on many occasions that fluoride can affect bacterial carbohydrate fermentation; however, are there other effects of fluoride on the bacteriology of dental plaque? Although very high levels of fluoride (0.16-0.3 mol/L) will kill bacteria, there is little evidence that fluoride causes dramatic changes in the number of species found in plaque or their relative concentrations. The survival of the populations in the plaque community in the presence of fluoride could result from: (1) the fact that all the organisms are unaffected, (2) selection of mutant strains resistant to fluoride, or (3) adaptation of strains to fluoride resistance. Examples of these phenomena can be found among members of the oral flora. Some species are unaffected (Veillonella), but Streptococcus can be mutated to fluoride resistance and also adapt phenotypically to increasing levels of fluoride in the environment. Which of these mechanisms operates in vivo, and does resistance, mutation, or phenotypic adaptation of these bacteria reduce the effectiveness of fluoride, in controlling caries?(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗

Evaluation of topical fluoride preparations.

For practical reasons, evaluation of topical fluoride products must depend upon clinical and laboratory assessments. While not always a good predictor of clinical efficacy by itself, fluoride uptake is the most commonly used laboratory test. A consideration of the relationship between possible anticaries mechanisms of fluoride, different product types, and the meaning of various kinds of fluoride uptake data suggests that both the amount of fluoride taken up by early lesions and the amount of ambient fluoride present at a cariogenic site may play key roles in determining the efficacy of a product. While formulations applied annually or semi-annually probably depend on fluoride deposition, those used daily might not. There are no clear data supporting the superiority of one fluoride compound over another, even for infrequently used products, although there are significant differences among them in fluoride uptake by enamel. This suggests that fluoride uptake in vivo at a cariogenic site might actually be different from that suggested by in vitro data, or that larger differences are required for a clinical effect to be observable. Clinical data support the conclusion that a large increase in the fluoride concentration of a product will somewhat increase its anticaries effectiveness, although the increase will not be linearly related to concentration. There also are no obvious differences in clinical effectiveness caused by the addition of gelling agents to topical solutions. Fluoride varnishes are clinically effective but have not been shown to be superior to topical solutions or gels.(ABSTRACT TRUNCATED AT 250 WORDS)

Dentifrices↗

Fluoride reduces bone strength in older rats.

In response to recent concerns about the effect of water fluoridation on hip fracture rates, we studied the influence of fluoride intake on bone strength. Four groups of rats were fed a low-fluoride diet ad libitum and received 0, 5, 15, or 50 ppm of fluoride in their drinking water. Animals were euthanized after 3, 6, 12, or 18 months of treatment. Mechanical strength of the right femur was measured by three-point bending. Fluoride content for the left femur was measured, and static histomorphometric measurements were made on a lumbar vertebra. Femoral failure load was not significantly decreased in rats treated for 3 and 6 months, but was decreased as much as 23% in rats treated 12 and 18 months at 50 ppm fluoride. Extrapolation from regression equations predicted that older rats lose 36% of femoral bone strength when bone fluoride content is increased from 0 to 10,000 ppm, while younger rats will lose only 15%. Thus, the decreased strength appeared to be due to the combined effects of fluoride intake and age on bone tissue and was not associated with a decrease in bone density or mineralization defects. There were only small effects of fluoride on bone histomorphometry. Fluoride intake at high levels had no negative effects on bone mineralization. Fluoride intake was associated with slight increases in trabecular bone volume and trabecular thickness, but these effects could not be demonstrated consistently. The mechanism by which large amounts of fluoride affect bone strength more severely in older animals is unknown.

Aging↗

The effect of fluorhydroxyapatite-derived fluoride on acid production by streptococci.

The effect of fluoride derived from fluorhydroxyapatite (FHAp) minerals on bacterial glycolysis under aerobic and strictly anaerobic conditions was studied to validate the claims that this mineral could be used as a reservoir of fluoride in plaque. To isolate the direct effect of fluoride on bacterial glycolysis from that of an indirect pH-buffering effect of hydroxyl or phosphate ions which are also dissolved from the mineral, we equalized the pH-fall time course of reactions by manually adding KOH or HCl. This ensured that pH effects on glycolysis were minimized. Under controlled pH-fall and strictly anaerobic conditions, fluoride derived from the dissolution of FHAp containing more than 30,100 ppm fluoride (i.e., when the substitution of OH by F in the mineral was greater than 80%) had a direct inhibitory effect on lactic acid production in Streptococcus mutans. Under free pH-fall and strictly anaerobic conditions, increasing amounts of fluoride in FHAp (starting as low as 2000 ppm fluoride), appeared to have a pronounced indirect inhibitory effect on lactic acid production. This was probably mediated through a reducing pH buffer effect of the mineral. Even in the presence of high-fluoride FHAp, only 0.01 to 0.025 mmol/L fluoride was found in the reaction mixtures, a probable result of non-stoichiometric dissolution of FHAp. In spite of such low levels of fluoride, marked inhibitory effects on bacterial glycolysis were demonstrated. The results of this study suggest that high-fluoride FHAp may serve as a reservoir of fluoride for the inhibition of anaerobic acid production by S. mutans.

Anaerobiosis↗

Fluoride stimulates the accumulation of inositol phosphates, increases intracellular free calcium, and inhibits parathyroid hormone release in dispersed bovine parathyroid cells.

The stimulation of polyphosphoinositide (PPI) turnover is associated with cellular activation and hormone secretion in numerous systems. GTP-binding proteins appear to couple receptors to phospholipase-C-mediated PPI breakdown. We assessed the effects of fluoride, an activator of GTP-binding proteins, on inositol phosphate accumulation, intracellular free Ca2+ [(Ca2+)i], cAMP content, and PTH release in dispersed bovine parathyroid cells. Sodium fluoride (5-30 mM) produced marked dose-dependent increases in inositol phosphates. With anion exchange HPLC, we confirmed that 30 mM fluoride stimulated a rapid increase in 1,4,5-inositol trisphosphate, a potent Ca2+-mobilizing compound. Using the Ca2+-sensitive probe fura-2, we determined that 30 mM fluoride increased [Ca2+]i from 339 +/- 9 to 650 +/- 39 nM (n = 8) within 30-60 sec at 1 mM extracellular Ca2+. After the depletion of extracellular Ca2+ by the addition of 1 mM EGTA, 30 mM fluoride increased [Ca2+]i 45 +/- 9% (n = 4), indicating that fluoride can mobilize intracellular Ca2+ stores. Fluoride (1-30 mM) also inhibited PTH release in dose-dependent fashion. Fluoride (30 mM) produced 72.8 +/- 4.2% suppression of maximal low Ca2+-stimulated PTH release comparable to the 83.7 +/- 3.7% inhibition by 2.0 mM extracellular Ca2+. Since changes in both [Ca2+]i and cAMP regulate PTH release, we measured the effect of fluoride on intracellular cAMP. Fluoride did not detectably change basal cAMP content, but it reduced forskolin-stimulated increases in cAMP. We conclude that fluoride may activate at least two GTP-dependent processes in parathyroid cells, resulting in PPI breakdown and cAMP accumulation. While both may contribute to the fluoride-induced suppression of PTH release, our findings suggest that the stimulation of PPI turnover leads to inhibition of PTH secretion.

Animals↗

Fluoride at mitogenic doses induces a sustained activation of p44mapk, but not p42mapk, in human TE85 osteosarcoma cells.

Fluoride, at micromolar concentrations, stimulates bone cell proliferation in vitro. In this study, we sought to test whether fluoride at mitogenic doses increases the tyrosyl phosphorylation level and specific activity of a mitogen-activated protein kinase (MAPK) in human TE85 osteosarcoma cells. Analysis by immunoprecipitation with antiphosphotyrosine antibody followed by Western analysis using an anti-pan extracellular signal-regulated kinase antibody revealed that fluoride at the optimal mitogenic dose (i.e. 100 mumol/L) induced a time-dependent increase in the steady state tyrosyl phosphorylation level of p44mapk, but not p42mapk, with the maximal increase (4- to 13-fold) after 1-3 h fluoride treatment. The effect was sustained in that a 9-fold increase was seen after 12 h of the fluoride treatment. The sustained nature of the effect is consistent with an inhibition of dephosphorylation rather than a direct stimulation of phosphorylation. The fluoride effect on the tyrosyl phosphorylation level of p44mapk was dose dependent, with the optimal dose being 100 mumol/L fluoride. The mitogenic dose of fluoride also increased the specific activity and the in-gel kinase activity of p44mapk, but not that of p42mapk, in a time-dependent manner similar to the effect on the p44mapk tyrosyl phosphorylation level. Fluoride at the same micromolar doses did not increase cell proliferation, tyrosyl phosphorylation, or specific activity of any MAPK in human skin foreskin fibroblasts, which are fluoride-nonresponsive cells. Consistent with the interpretation that the effect of fluoride on the steady state tyrosyl phosphorylation level of p44mapk is a consequence of an inhibition of a phosphotyrosyl phosphatase (PTP), mitogenic doses of orthovanadate, a bone cell mitogen and a PTP inhibitor, also increased the steady state tyrosyl phosphorylation level of p44mapk, but not p42mapk, in a time-dependent sustained manner similar to that observed with fluoride. Together, these findings support the concept that inhibition of a PTP activity in bone cells could lead to an activation of MAPK activity.

Bone and Bones↗

Assessing fluoride levels of carbonated soft drinks.

BACKGROUND: Dental fluorosis occurs as a result of excessive total fluoride intake during tooth development. Some children may receive substantial intake from soft drinks, but few studies have reported fluoride levels in soft drinks. The authors examined the fluoride concentrations of 332 soft drinks. METHODS: Soft drinks were purchased from Iowa grocery stores. To identify production sites, the authors recorded product details and batch numbers. After decarbonating the drinks, the authors assayed samples for fluoride content using a fluoride ion-specific electrode, and reported the results in parts per million, or ppm, using appropriate standards and duplicate assessments. Descriptive statistics were used to summarize the findings. RESULTS: The fluoride levels of the products ranged from 0.02 to 1.28 ppm, with a mean level of 0.72 ppm. Fluoride levels exceeded 0.60 ppm for 71 percent of the products. Results varied substantially by production site, even within the same company and for the same product. There were no substantial differences between flavors or between diet and regular soft drinks. CONCLUSIONS: The majority of soft drinks had fluoride levels exceeding 0.60 ppm. Variation in fluoride levels probably is due largely to the different water sources used in production. CLINICAL IMPLICATIONS: With no fluoride levels marked on the soft drink products or easily available from the manufacturers, it is not possible for clinicians or consumers to directly estimate fluoride ingestion from carbonated beverages. Therefore, to reduce the risk of dental fluorosis, dental and medical practitioners should be cautious about prescribing dietary fluoride supplements to preschool-aged children in nonfluoridated areas who consume large quantities of carbonated soft drinks.

Carbonated Beverages↗

Fluoride dentifrice ingestion and fluorosis of the permanent incisors.

BACKGROUND: Fluoride dentifrice is a primary means of preventing childhood caries, but it is also an important risk factor for fluorosis. The authors examine the influence of fluoride dentifrice ingestion on fluorosis of the permanent incisors. METHODS: Participants in the Iowa Fluoride Study received questionnaires at regular intervals concerning fluoride sources. The authors assessed fluorosis using the fluorosis risk index. They estimated daily fluoride ingestion from dentifrice, diet and fluoride supplements and divided the amount by kilograms of body weight. The statistical analysis related fluoride ingestion to fluorosis in the permanent incisors. RESULTS: In bivariate analyses, mild fluorosis was significantly related to ingestion of fluoride dentifrice at ages 24 and 36 months (P = .02 for both). After the authors adjusted for fluoride ingested from dietary sources, logistic regression showed a significant association between fluorosis and dentifrice ingestion at age 24 months (P = .04). CONCLUSIONS: The study results suggest that fluorosis of the permanent incisors is influenced by ingestion of fluoride dentifrice during the first three years of life. Further research is needed to assess total intake of fluoride as a risk factor for fluorosis. CLINICAL IMPLICATIONS: These results support recommendations that young children use only a pea-sized amount of dentifrice. Parents should supervise young children as they brush their teeth with fluoride dentifrice.

Age Factors↗

[Estimation of exposure to fluoride in "Los Altos de Jalisco", México].

OBJECTIVE: To estimate the level of fluoride exposure and human health risks in Los Altos de Jalisco (Jalisco State Heights) region. MATERIAL AND METHODS: This study was conducted between May and July 2002. The fluoride concentrations of 105 water wells and six tap water samples were electrochemically measured. Exposure doses to fluoride and total intake of fluoride were estimated for babies (10 kg), children (20 kg), and adults (70 kg). RESULTS: The fluoride concentration of the water samples ranged from 0.1 to 17.7 mg/l. More than 45% of the water samples exceeded the national guideline value for fluoride of 1.5 mg/l. The estimated values of the exposure doses to fluoride and total intake of fluoride were in the range of 0.04-1.8 mg/kg/d and 0.5-18.4 mg/d, respectively. CONCLUSIONS: Dental fluorosis, skeletal fluorosis, and bone fractures are some of the potential health risks due to the intake of high doses of fluoride for the population of Los Altos de Jalisco. In order to reduce health risks, fluoridated salt,fluoridated toothpastes, and drinking water containing more than 0.7 mg/l of fluoride should be avoided.

Adult↗