An in vitro study of the effect of fluoridated milk on oral bacterial biofilms. (49/1729)

Microcosmic dental plaques were grown in artificial saliva and supplemented with either milk or fluoridated milk. The presence of fluoride in the milk increased the pH of the biofilms and reduced the proportions of streptococci, demonstrating that in this model, fluoridation of milk produces biofilms with reduced cariogenic potential.  (+info)

Disturbed enamel formation in wild boars (Sus scrofa L.) from fluoride polluted areas in Central Europe. (50/1729)

The pathological alterations of enamel structure in the teeth of wild boars from fluoride polluted areas in N-Bohemia (Czech Republic) and S-Saxony (Germany) were studied on a macroscopic and a microscopic level. Mandibular bone fluoride concentration (mg F(-)/kg, dry wt; mean +/-SD, individuals <24 months of age) in the specimens from N-Bohemia (754.3+/-149.6) and S-Saxony (490.8+/-135.1) was significantly higher than that of controls (free of dental fluorosis), originating from the western part of Germany (304.7+/-91.0). Fluoride content in bulk enamel (mg F(-)/kg, ash wt) of fluorotic permanent teeth from N-Bohemia (382.1+/-165.2) and S-Saxony (125.0+/-38.3) was likewise significantly increased over that of non-fluorotic control teeth from W-Germany (33.6+/-26.7). Macroscopically, fluorosed wild boar enamel exhibited opacity and discoloration of varying extent, accentuated perikymata as well as hypoplastic and posteruptive surface defects. Microradiographic and scanning electron microscopic analyses revealed enamel subsurface hypomineralization, accentuated Retzius lines and occurrence of broad, hypomineralized incremental bands of abnormal structure underlying hypoplastic enamel surface defects. The presence of zones of aprismatic enamel was associated with these bands. Incremental bands with altered enamel structure and enamel surface hypoplasias, both denoting a severe disturbance during the secretory stage of amelogenesis, have previously been observed in rodents following acute parenteral fluoride dosing. It is concluded that in the chronically fluoride exposed wild boars periods of especially elevated plasma fluoride levels exerted an acute toxic effect on the secretory ameloblasts. A feature not previously reported from fluorosed enamel was the occurrence of canal-like structures that originated at the broad incremental bands and extended into the external enamel. The presence of these canals presumably results from a delay in the resumption of secretory activity by groups of ameloblasts following a fluoride insult. Based on experimental evidence in domestic pigs and in sheep, the overall subsurface hypomineralization of fluorosed wild boar enamel is attributed to a disturbance of enamel maturation. The distribution of fluorotic enamel changes within the dentition of the wild boars could be related to the developmental sequence of tooth formation in the species. Teeth whose crown formation took place prenatally (deciduous teeth) or largely pre-weaning (permanent first molars) exhibited no or only moderate fluorotic enamel alterations. Based on the extension of enamel surface hypoplasias along the coronoapical axes of the tooth crowns, the timing of excess fluoride exposure that caused a marked disruption of enamel matrix secretion was estimated in specimens with a known date of death. The results indicate that the wild boars had been exposed to a particularly severe fluoride impact during autumn and winter of their first year of life.  (+info)

Modulation of glucan-binding protein activity in streptococci by fluoride. (51/1729)

Glucan-binding lectin (GBL) activity of Streptococcus sobrinus was significantly reduced by fluoride in the growth medium. Approximately 1.5 mM fluoride was required for a 50% reduction in GBL activity. In addition to the GBL, several other glucan-binding proteins were reduced when the bacteria were grown in subinhibitory fluoride. Fluoride had no effect on glucosyltransferases (GTFs), enzymes capable of converting sucrose into alpha-1,6-glucans. All the proteins were detected by use of enhanced chemiluminescence (ECL of fluorescein-labeled dextran) and Western blotting of renatured SDS-PAGE gels. The effects of fluoride on the bacteria were abrogated when the manganous ion was included in the growth medium. It thus appears that one mechanism of action of fluoridated water is its effects on glucan-binding proteins. The fluoride may be reducing metabolism of the mangano aquo ion, essential for expression of the glucan-binding proteins.  (+info)

Cytotoxicity of a trial resin composite liner containing TiK2F6 on rat dental pulp cells. (52/1729)

The aim of this study was to assess the toxicological responses of a resin composite containing TiK2F6 and NaF in rat dental pulp cells. Trial resin composite liners were made, containing 3 wt% fluorides (TiK2F6 or NaF). These specimens were immersed in 5 ml of cell culture medium supplemented at 37 degrees C for 24 hours. The eluates were used for the experiments. We judged the cytotoxicity of the samples by the cell viability. The original elute solution was serially diluted and then the medium was exchanged for the dilute medium. The cell viability at 1, 2 or 5 days after commencement of re-culturing was calculated. The viability of cells in the eluate from the resin composite liners containing TiK2F6 and NaF decreased with time. The cytotoxicity of TiK2F6 was weaker than that of NaF at all times.  (+info)

Inhibition of carious lesions in vitro around gallium alloy restorations by fluoride releasing resin-ionomer cement. (53/1729)

A new fluoride releasing resin-ionomer cement was used for bonding of gallium alloy restorations in vitro. Etching, priming, and fluoride releasing resin-ionomer cement were used in the experimental group (ARG), prior to placement of the gallium alloy restorations. Three different controls were used: gallium alloy only (G), no etching, fluoride releasing resin-ionomer cement, gallium alloy (RG), etching, priming, non-fluoride cement and gallium alloy (ACG). The mean shear bond strengths of ARG group to enamel and dentin were higher than those of the three control groups. Artificial secondary caries lesions around the restorations in the experimental group and the control groups were produced, using a strep. mutans culture. The microradiographs were examined for presence of a caries inhibition zone near the restoration. Caries inhibition zones were clearly detected around RG and ARG, but not around G and ACG. The results indicate that the fluoride releasing resin-ionomer cement provided good adhesion and caries inhibition in enamel and dentin.  (+info)

Release and recharge of fluoride by restorative materials. (54/1729)

This study investigated the release and recharge of fluoride by restorative materials. Resin-modified glass ionomers (RGIs), polyacid-modified composite resins (PMCRs) and resin composite containing fluoride were used for comparison of fluoride release. Non-fluoride-releasing resin composite was used as a control. The amounts of fluoride release from RGIs and PMCRs remarkably increased in the citrate-phosphate acid buffer compared with distilled water. The amounts of fluoride recharged in RGIs increased with the concentration of NaF solution, but those of PMCRs exposed to all concentrations of NaF solutions were less than 1.5 ppm. Neither resin composite containing fluoride and non-fluoride-releasing resin composite gave any evidence of recharge. RGIs and PMCRs affected by acid buffer solution could not recharge much fluoride even if they were immersed in the 1000 ppmF NaF solution. The results suggested that the matrix of RGIs and PMCRs functioned as a reservoir of fluoride, but the functions were lost by acid attack.  (+info)

Identification of fluoropyrogallols as new intermediates in biotransformation of monofluorophenols in Rhodococcus opacus 1cp. (55/1729)

The transformation of monofluorophenols by whole cells of Rhodococcus opacus 1cp was investigated, with special emphasis on the nature of hydroxylated intermediates formed. Thin-layer chromatography, mass spectrum analysis, and (19)F nuclear magnetic resonance demonstrated the formation of fluorocatechol and trihydroxyfluorobenzene derivatives from each of three monofluorophenols. The (19)F chemical shifts and proton-coupled splitting patterns of the fluorine resonances of the trihydroxyfluorobenzene products established that the trihydroxylated aromatic metabolites contained hydroxyl substituents on three adjacent carbon atoms. Thus, formation of 1,2, 3-trihydroxy-4-fluorobenzene (4-fluoropyrogallol) from 2-fluorophenol and formation of 1,2,3-trihydroxy-5-fluorobenzene (5-fluoropyrogallol) from 3-fluorophenol and 4-fluorophenol were observed. These results indicate the involvement of fluoropyrogallols as previously unidentified metabolites in the biotransformation of monofluorophenols in R. opacus 1cp.  (+info)

Pediococcus cerevisiae mutant with altered transport of folates. (56/1729)

A Pediococcus cerevisiae mutant that actively accumulated folate (PteGlu), in contrast to the wild-type, was also found to exhibit changes in the pattern of uptake of 5-methyl-tetrahydrofolate (5-CH3-H4PteGlu) and amethopterin. Most of the 5-CH3-H4PteGlue accumulated through a glucose- and temperature-dependent process, and a concentrative uptake was also found in gluocse-starved cells and in cells incubated at OC. About 75% of the accumulated 5-CH3-H4PteGlu exchanged with amethopterin. In contrast to the wild type, the mutant accumulated both diastereoisomers of 5-CH3-H4PteGlue by glucose-dependent and glucose-independent processes. Amethopterin and PteGlue competitively inhibited the uptake in both processes, with an apparent lower affinity of the carrier for PteGlu than for the analogue. p-Chloromercuribenzoate strongly inhibited the uptake (75%). The p-chloromercuribenzoate-nonsusceptible and temperature-independent uptake was also competed by amethopterin. Metabolic poisons like sodium azide, potassium fluoride, iodoacetate, and 2,4-dimitrophenol inhibited the glucose-dependent process. Uptake, in the absence of glucose, was enhanced by sodium azide and potassium fluoride.  (+info)