43 research outputs found

    Mechanisms of action of fluoride for caries control

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    Fluoride was introduced into dentistry over 70 years ago, and it is now recognized as the main factor responsible for the dramatic decline in caries prevalence that has been observed worldwide. However, excessive fluoride intake during the period of tooth development can cause dental fluorosis. In order that the maximum benefits of fluoride for caries control can be achieved with the minimum risk of side effects, it is necessary to have a profound understanding of the mechanisms by which fluoride promotes caries control. In the 1980s, it was established that fluoride controls caries mainly through its topical effect. Fluoride present in low, sustained concentrations (sub-ppm range) in the oral fluids during an acidic challenge is able to absorb to the surface of the apatite crystals, inhibiting demineralization. When the pH is re-established, traces of fluoride in solution will make it highly supersaturated with respect to fluorhydroxyapatite, which will speed up the process of remineralization. The mineral formed under the nucleating action of the partially dissolved minerals will then preferentially include fluoride and exclude carbonate, rendering the enamel more resistant to future acidic challenges. Topical fluoride can also provide antimicrobial action. Fluoride concentrations as found in dental plaque have biological activity on critical virulence factors of S. mutans in vitro, such as acid production and glucan synthesis, but the in vivo implications of this are still not clear. Evidence also supports fluoride’s systemic mechanism of caries inhibition in pit and fissure surfaces of permanent first molars when it is incorporated into these teeth pre-eruptively

    Fluoride mode of action: Once there was an observant dentist...

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    The discovery and implementation of fluoride in the prevention of dental caries is often praised as one of the most important achievements in health care. In the early 20th century, it took 30 y to identify fluoride as the cause of enamel mottling but also of reduced caries prevalence in a population drinking water containing fluoride. Similarly, from 1960 to 1990, it took major efforts to unravel the working mode of fluoride in such detail that a rational scheme of caries prevention could be formulated. This article describes the scientific struggle leading to a consensus on the topic. For a historic purpose, the field, the actors, and their main research achievements are described. Ultimately it was generally agreed that the effect of fluoride is primarily topical by fluorides in the oral fluids rather than systemic by incorporation of fluoride in the enamel mineral crystals. Fluoride concentrations, even <1 mg/L, enhance the deposition of calcium phosphates during remineralization of enamel (and dentin). Similarly, such low levels of fluoride are effective in reducing the dissolution of the calcified tissues. This understanding has led to the development of fluoride-containing caries-preventive products that had an undisputed beneficial effect on the levels of dental caries

    Influence of Genetic Background on Fluoride Metabolism in Mice

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    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

    Diverse outcomes of photodynamic antimicrobial chemotherapy on five Enterococcus faecalis strains

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    Objectives In the present study, the effectiveness of Photodynamic Antimicrobial Chemotherapy (PACT) was evaluated on planktonic cells and biofilms of five Enterococcus faecalis clinical isolates. Methods Planktonic cells and biofilms of E. faecalis E2, E3, ER3/2s, OS16 and AA-OR34 were grown in SDMY medium plus 0.4% glucose. Approximately 5.0 × 107 CFU planktonic cells and 24 h biofilms were subjected to PACT using the combination of Light Emitting Diodes (LEDs, Biotable®) and Photogem®. The metabolic activity of bacterial cells was evaluated by a resazurin assay. Biomass values of the biofilms were determined by a crystal violet assay. Results Compared to the water-treated control group, gradual increases of light energy led to greater reduction of metabolic activity of planktonic cells and biofilms of E. faecalis when the combination of LEDs and Photogem® was applied. Photogem® alone significantly reduced the metabolic activity of planktonic cells, whereas LEDs or Photogem® alone did not result in biofilm viability changes. PACT yielded similar antimicrobial outcomes on planktonic cells of all tested E. faecalis strains, whereas biofilms of E. faecalis E3, ER3/2s and OS16 were more resistant to PACT than biofilms of E. faecalis E2 and AA-OR34. Conclusions The efficacy of PACT on E. faecalis biofilms was strain dependent. PACT demonstrated its potential as an adjuvant antimicrobial treatment by killing of E. faecalis planktonic and biofilm cells
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