Fluoride varnishes containing calcium glycerophosphate: fluoride uptake and the effect on in vitro enamel erosion

OBJECTIVES Calcium glycerophosphate (CaGP) was added to fluoride varnishes to analyze their preventive effect on initial enamel erosion and fluoride uptake: potassium hydroxide (KOH)-soluble and KOH-insoluble fluoride bound to enamel. MATERIALS AND METHODS This study was carried out in two parts. Part 1: 108 enamel samples were randomly distributed into six varnish groups: base varnish (no active ingredients); Duraphat® (2.26 %NaF); Duofluorid® (5.63 %NaF/CaF2); experimental varnish 1 (1 %CaGP/5.63 %NaF/CaF2); experimental varnish 2 (5 %CaGP/5.63 %NaF/CaF2); and no varnish. Cyclic demineralization (90 s; citric acid, pH = 3.6) and remineralization (4 h) was made once a day, for 3 days. Change in surface microhardness (SMH) was measured. Part 2: 60 enamel samples were cut in half and received no varnish (control) or a layer of varnish: Duraphat®, Duofluorid®, experimental varnishes 1 and 2. Then, KOH-soluble and KOH-insoluble fluoride were analyzed using an electrode. RESULTS After cyclic demineralization, SMH decreased in all samples, but Duraphat® caused less hardness loss. No difference was observed between varnishes containing CaGP and the other varnishes. Similar amounts of KOH-soluble and insoluble fluoride was found in experimental varnish 1 and Duofluorid®, while lower values were found for experimental varnish 2 and Duraphat®. CONCLUSION The addition of CaGP to fluoride varnishes did not increase fluoride bound to enamel and did not enhance their protection against initial enamel erosion. CLINICAL RELEVANCE We observe that the fluoride varnishes containing CaGP do not promote greater amounts of fluoride bound to enamel and that fluoride bound to enamel may not be closely related to erosion prevention

Bone Response to Fluoride Exposure Is Influenced by Genetics

Genetic factors influence the effects of fluoride (F) on amelogenesis and bone homeostasis but the underlying molecular mechanisms remain undefined. A label-free proteomics approach was employed to identify and evaluate changes in bone protein expression in two mouse strains having different susceptibilities to develop dental fluorosis and to alter bone quality. In vivo bone formation and histomorphometry after F intake were also evaluated and related to the proteome. Resistant 129P3/J and susceptible A/J mice were assigned to three groups given low-F food and water containing 0, 10 or 50 ppmF for 8 weeks. Plasma was evaluated for alkaline phosphatase activity. Femurs, tibiae and lumbar vertebrae were evaluated using micro-CT analysis and mineral apposition rate (MAR) was measured in cortical bone. For quantitative proteomic analysis, bone proteins were extracted and analyzed using liquid chromatography-electrospray ionization-tandem mass spectrometry (LC-ESI-MS/MS), followed by label-free semi-quantitative differential expression analysis. Alterations in several bone proteins were found among the F treatment groups within each mouse strain and between the strains for each F treatment group (ratio ≥1.5 or ≤0.5; p<0.05). Although F treatment had no significant effects on BMD or bone histomorphometry in either strain, MAR was higher in the 50 ppmF 129P3/J mice than in the 50 ppmF A/J mice treated with 50 ppmF showing that F increased bone formation in a strain-specific manner. Also, F exposure was associated with dose-specific and strain-specific alterations in expression of proteins involved in osteogenesis and osteoclastogenesis. In conclusion, our findings confirm a genetic influence in bone response to F exposure and point to several proteins that may act as targets for the differential F responses in this tissue

Fluoride modulates preosteoblasts viability and matrix metalloproteinases-2 and -9 activities

This study evaluated the influence of fluoride on cell viability and activity of matrix metalloproteinases (MMP) -2 and -9 secreted by preosteoblasts. Preosteoblasts (MC3T3-E1 murine cell line) were cultured in MEM medium supplement with 10% Fetal Bovine Serum (FBS) and nucleosides/ribonucleosides without ascorbic acid. Adherent cells were treated with different concentrations of F (as sodium fluoride-NaF) in medium (5 x 10-6 M, 10-5 M, 10-4 M and 10-3 M) for 24, 48, 72 and 96 h at 37ºC, 5% CO2. Control cells were cultivated in MEM only. After each period, preosteoblast viability was assessed by MTT assay. MMP-2 and -9 activities were performed by gel zymography. Also, alkaline phosphatase (ALP) activity was quantified by colorimetry in all experimental groups. It was shown that cultured cells with the highest dose of F (10-3 M) for 96 h decreased preosteoblast viability while lower doses of F did not alter it, when compared to untreated cells. No differences were observed in ALP activity among groups. Moreover, compared to control, the treatment of cells with F at low dose slightly increased MMP-2 and -9 activities after 24 h. It was concluded that F modulates preosteoblast viability in a dose-dependent manner and also may regulate extracellular matrix remodeling

Bone response to fluoride exposure is influenced by genetics.

Genetic factors influence the effects of fluoride (F) on amelogenesis and bone homeostasis but the underlying molecular mechanisms remain undefined. A label-free proteomics approach was employed to identify and evaluate changes in bone protein expression in two mouse strains having different susceptibilities to develop dental fluorosis and to alter bone quality. In vivo bone formation and histomorphometry after F intake were also evaluated and related to the proteome. Resistant 129P3/J and susceptible A/J mice were assigned to three groups given low-F food and water containing 0, 10 or 50 ppmF for 8 weeks. Plasma was evaluated for alkaline phosphatase activity. Femurs, tibiae and lumbar vertebrae were evaluated using micro-CT analysis and mineral apposition rate (MAR) was measured in cortical bone. For quantitative proteomic analysis, bone proteins were extracted and analyzed using liquid chromatography-electrospray ionization-tandem mass spectrometry (LC-ESI-MS/MS), followed by label-free semi-quantitative differential expression analysis. Alterations in several bone proteins were found among the F treatment groups within each mouse strain and between the strains for each F treatment group (ratio ≥1.5 or ≤0.5; p<0.05). Although F treatment had no significant effects on BMD or bone histomorphometry in either strain, MAR was higher in the 50 ppmF 129P3/J mice than in the 50 ppmF A/J mice treated with 50 ppmF showing that F increased bone formation in a strain-specific manner. Also, F exposure was associated with dose-specific and strain-specific alterations in expression of proteins involved in osteogenesis and osteoclastogenesis. In conclusion, our findings confirm a genetic influence in bone response to F exposure and point to several proteins that may act as targets for the differential F responses in this tissue

In situ effect of sodium fluoride or titanium tetrafluoride varnish and solution on carious demineralization of enamel

This study evaluated the effect of titanium tetrafluoride (TiF(4)) formulations on enamel carious demineralization in situ. Thirteen subjects took part in this cross-over, split-mouth, double-blind study performed in three phases of 14 d each. In each subject, two sound and two predemineralized specimens of bovine enamel were worn intra-orally and plaque accumulation was allowed. One sound and one predemineralized specimen in each subject was treated once with sodium fluoride (NaF) varnish or solution (Treatment A); TiF(4) varnish or solution (Treatment B); or placebo varnish or no treatment (Treatment C). The initially sound enamel specimens were exposed to severe cariogenic challenge (20% sucrose, eight times daily for 5 min each time), whereas the predemineralized specimens were not. Eleven subjects were able to finish all experimental phases. The enamel alterations were quantified by surface hardness and transversal microradiography. Demineralization of previously sound enamel was reduced by all test formulations except for the NaF solution, while both TiF(4) formulations were as effective as NaF varnish. For the predemineralized specimens, enamel surface hardness was increased only by TiF(4) formulations, while subsurface mineral remineralization could not be seen in any group. Within the experimental protocol, TiF(4) was able to decrease enamel demineralization to a similar degree as NaF varnish under severe cariogenic challenges, while only TiF(4) formulations remineralized the enamel surface

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BMD and histomorphometric parameters in trabecular region of tibiae from A/J and 129P3/J mice treated with 0, 10 or 50 ppm F in drinking water for 8 weeks.

<p>Values are mean ± SD, n = 8/group. A =  Bone mineral density (BMD); B =  Specific bone surface (BS/BV); C =  Bone volume fraction (BV/TV); D =  Bone surface density (BS/TV); E =  Trabecular separation (Tb.Sp); F =  Trabecular thickness (Tb.Th); G =  Trabecular number (Tb.N); H =  Trabecular bone pattern factor (Tb.Pf). *<i>p</i><0.05, **<i>p</i><0.01 and *** <i>p</i><0.001 represents significant differences between strains, for each group. No statisticallly significant differences were found for each strain after receiving F.</p

BMD and histomorphometric parameters in cortical region of femur from A/J and 129P3/J mice treated with 0, 10 or 50 ppm F.

<p>Values are mean ± SD, n = 8/group. A =  Bone mineral density (BMD); B =  Mean total cross-sectional tissue area (T.Ar); C =  Mean total cross-sectional bone area (B.Ar); D =  Mean total cross-sectional tissue perimeter T.Pm); E =  Mean total cross-sectional bone perimeter (B.Pm); F =  Mean polar moment of inertia (MMI). *<i>p</i><0.05, **<i>p</i><0.01 and *** <i>p</i><0.001 represents significant differences between strains, for each group. No statisticallly significant differences were found for each strain after receiving F.</p

Quantification of ALP activity in plasma from A/J and 129P3/J mice treated with 0, 10 or 50 ppm F in the drinking water for 8 weeks.

<p>Results are shown as mean ± SD of enzymatic activity (nmol of p-NP per min per mg of total protein). ^*Represents significant differences between strains for each group (<i>p</i><0.05). No statistical differences were found for each strain after receiving F.</p