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Since the classical epidemiological studies by Dean, it has been known that there should be an optimum level of exposure to fluoride that would be able to provide the maximum protection against caries, with minimum dental fluorosis. The "optimal" daily intake of fluoride for children (0.05-0.07 mg per kilogram bodyweight) that is still accepted worldwide was empirically determined. In the present review, we discuss the appropriateness of the current guidance for fluoride intake, in light of the windows of susceptibility to caries and fluorosis, the modern trends of fluoride intake from multiple sources, individual variations in fluoride metabolism, and recent epidemiological data. The main conclusion is that it is very difficult to think about a strict recommendation for an "optimal" range of fluoride intake at the individual level in light of existing knowledge of 1) the mechanisms of action of fluoride to control caries, 2) the mechanisms involved in dental fluorosis development, 3) the distinct factors that interfere in the metabolism of fluoride, and 4) the windows of susceptibility to both dental caries and fluorosis development. An "optimal" range of fluoride intake is, however, desirable at the population level to guide programs of community fluoridation, but further research is necessary to provide additional support for future decisions on guidance in this area. This list includes the effect of factors affecting fluoride metabolism, clinical trials on the effectiveness of low-fluoride dentifrices to prevent caries in the primary dentition, and validation of biomarkers of exposure to fluoride. [ABSTRACT FROM AUTHOR]

Cystatin B was recently identified as an acid-resistant protein in acquired enamel pellicle; it could therefore be included in oral products to protect against caries and erosion. However, human recombinant cystatin is very expensive, and alternatives to its use are necessary. Phytocystatins are reversible inhibitors of cysteine peptidases that are found naturally in plants. In plants, they have several biological and physiological functions, such as the regulation of endogenous processes, defense against pathogens, and response to abiotic stress. Previous studies performed by our research group have reported high inhibitory activity and potential agricultural and medical applications of several sugarcane cystatins, including CaneCPI-1, CaneCPI-2, CaneCPI-3, and CaneCPI-4. In the present study, we report the characterization of a novel sugarcane cystatin, named CaneCPI-5. This cystatin was efficiently expressed in Escherichia coli, and inhibitory assays demonstrated that it was a potent inhibitor of human cathepsins B, K, and L ( Ki = 6.87, 0.49, and 0.34 nM, respectively). The ability of CaneCPI-5 to bind to dental enamel was evaluated using atomic force microscopy. Its capacity to protect against initial enamel erosion was also tested in vitro via changes in surface hardness. CaneCPI-5 showed a very large force of interaction with enamel (e.g., compared with mucin and casein) and significantly reduced initial enamel erosion. These results suggest that the inclusion of CaneCPIs in dental products might confer protection against enamel erosion. [ABSTRACT FROM AUTHOR]

The effect of chronic fluoride (F) exposure from the drinking water on parameters related to glucose homeostasis was investigated. Wistar rats were randomly distributed into 2 groups (diabetic [D] and nondiabetic [ND]; n = 54 each). In D, diabetes was induced with streptozotocin. Each group was further divided into 3 subgroups (0, 10, or 50 mgF/L in drinking water). After 22 days of treatment, plasma and liver samples were collected. No alterations in glycemia, insulinemia, KITT, and HOMA2-IR (homeostasis model assessment 2 of insulin resistance) were seen for ND. F-exposure of D rats led to significantly lower insulinemia, without alterations in glycemia (increased %S). Proteomic analysis detected 19, 39, and 16 proteins differentially expressed for the comparisons D0 vs. D10, D0 vs. D50, and D10 vs. D50, respectively. Gene Ontology with the most significant terms in the comparisons D0 vs. D10, D0 vs. D50, and D50 vs. D10 were organic acid metabolic process and carboxylic acid metabolic process, organic acid metabolic process, and cellular ketone metabolic process. Analysis of subnetworks revealed that proteins with fold changes interacted with GLUT4 in comparison D0 vs. D10. Among these proteins, ERj3p was present in D10. Upregulation of this protein in the presence of F might help to explain the higher %S found in these animals. These data suggest that fluoride might enhance glucose homeostasis in diabetes and identify specific biological mechanisms that merit future studies. [ABSTRACT FROM AUTHOR]

Matrix metalloproteinase (MMP) inhibition has been shown to reduce dentin caries progression, but its role in dental erosion has not yet been assessed. This study tested the hypothesis that gels containing MMP inhibitors (epigallocatechin gallate-EGCG and chlorhexidine) can prevent dental erosion. Volunteers (n = 10) wore palatal devices containing bovine dentin blocks (n = 10/group) treated for 1 min with EGCG at 10 (EGCG10) or 400 µM (EGCG400), chlorhexidine at 0.012%, F at 1.23% (NaF), and no vehicle (placebo). Erosion was performed with Coca-Cola® (5 min) 4X/day during 5 days. The wear, assessed by profilometry (mean ± SD, µm), was significantly reduced by the gels containing MMP inhibitors (0.05 ± 0.02a, 0.04 ± 0.02a, and 0.05 ± 0.02a for EGCG10, EGCG400, and chlorhexidine, respectively) when compared with NaF (0.79 ± 0.35b) and placebo gels (1.77 ± 0.35b) (Friedman and Dunn's tests, p < 0.01). The use of gels delivering MMP inhibitors was shown to prevent erosion and opens a new perspective for protection against dental erosion. [ABSTRACT FROM AUTHOR]

A/J and 129P3/J mouse strains have different susceptibilities to dental fluorosis, due to their genetic backgrounds. This study tested whether these differences are due to variations in water intake and/or F metabolism. A/J (susceptible to dental fluorosis) and 129P3/J mice (resistant) received drinking water containing 0, 10, or 50 ppm F. Weekly F intake, excretion and retention, and terminal plasma and femur F levels were determined. Dental fluorosis was evaluated clinically and by quantitative fluorescence (QF). Data were tested by two-way ANOVA. Although F intakes by the strains were similar, excretion by A/J mice was significantly higher due to greater urinary F excretion, which resulted in lower plasma and femur F levels. Compared with 129P3/J mice given 50 ppm F, significantly higher QF scores were recorded for A/J mice. In conclusion, these strains differ with respect to several features of F metabolism, and amelogenesis in the 129P3/J strain seems to be unaffected by high F exposure. [ABSTRACT FROM AUTHOR]

There has been no comparison of fluoride (F) intake by pre-school children receiving more traditional sources of systemic F. The aim of this study was to estimate the dietary F intake by children receiving F from artificially fluoridated water (AFW-Brazil, 0.6-0.8 mg F/L), naturally fluoridated water (NFW-Brazil, 0.6-0.9 mg F/L), fluoridated salt (FS-Peru, 180-200 mg F/Kg), and fluoridated milk (FM-Peru, 0.25 mg F). Children (n = 21-26) aged 4-6 yrs old participated in each community. A non-fluoridated community (NoF) was evaluated as the control population. Dietary F intake was monitored by the "duplicate plate" method, with different constituents (water, other beverages, and solids). F was analyzed with an ionselective electrode. Data were tested by Kruskall- Wallis and Dunn's tests (p < 0.05). Mean (± SD) F intake (mg/Kg b.w./day) was 0.04 ± 0.01b, 0.06 ± 0.02a,b, 0.05 ± 0.02a,b, 0.06 ± 0.01a, and 0.01 ± 0.00c for AFW/NFW/FS/FM/NoF, respectively. The main dietary contributors for AFW/NFW and FS/FM/ NoF were water and solids, respectively. The results indicate that the dietary F intake must be considered before a systemic method of fluoridation is implemented. [ABSTRACT FROM AUTHOR]

It has been suggested that fluoride retention in plaque is limited by available binding sites. We determined the effects of fluoridated or placebo dentifrices on plaque and salivary fluoride concentrations [F]s in communities with different water fluoride concentrations (0.04, 0.85, 3.5 ppm). After one week of dentifrice use, samples were collected 1.0 and 12 hrs after the last use of dentifrices. After the use of fluoridated dentifrice, plaque fluoride concentrations were higher at both times, except at 12 hrs in the 3.5-ppm community. Plaque concentrations at 1.0 hr after the use of fluoridated dentifrice increased almost constantly (6.5 mmol/kg), but then decreased approximately 50% at 12 hrs in each community. Unlike previous studies, the present findings suggest that the use of fluoridated dentifrice is likely to increase plaque fluoride concentrations significantly for up to 12 hrs in areas where the water contains fluoride close to 1.0 ppm. As previously reported, plaque fluoride concentrations were directly related to calcium concentrations. [ABSTRACT FROM AUTHOR]