How Fluoride Protects from Caries

The first and primary protective effect of fluoride is due to its strong, spontaneous reaction with metal ions. Biologically, the most important of these ions is the calcium ion, large amounts of which interact with phosphate to form bones and teeth. Studies show that fluoride reduces apatite solubility in acids by an isomorphic replacement of hydroxide ions with fluoride ions to form fluoro-hydroxyapatite and difluoro-apatite (Fig. 16.6a). 

Apatites must undergo a solid-state transition to amorphous calcium phosphate before they can dissolve and the spontaneous replacement of hydroxide with fluoride ions slows the rate at which this transition occurs (Fig. 16.6b). Conversely, as an acid environment becomes more alkaline, fluoride ions promote the precipitation and crystallization of amorphous calcium monohydrogen phosphate/calcium fluoride into fluoro- and difluoro-apatites faster than amorphous calcium phosphate would crystallize into hydroxyapatite. Thus, fluoride ions have two effects on enamel that protect from caries they slow enamel dissolution in lactic acid and promote its re-precipitation and crystallization when the lactic acid is neutralized. 

A second mechanism of protection from caries is the incorporation of fluoride into bacterial biofilms where it inhibits enolase. Enolase catalyzes the production of phospho-enolpyruvate, the precursor of lactate in glycolysis, from 2-phosphoglycerate during glycolysis (Fig. 16.7 - see also Fig. 1.7). In addition, oral bacterial uptake of mono- and disaccharides mostly utilizes the phosphoenolpyruvate transport system to transfer them into the cytosol (Sect. 15.2.2). Fluoride therefore inhibits not only lactic acid production, but also the phosphoenolpyruvate transport system-mediated uptake of saccharide substrates. In short, fluoride inhibits saccharolytic fermentation by many oral bacteria. 

Although high levels of fluoride ( 3,000 ppm) kill most bacteria, there is little evidence that common levels of fluoride (1-10 ppm) alter the types of bacterial species or their relative concentrations in biofilms. Mutans and other streptococci in the biofilm may switch to asaccharolytic fermentation (Sect. 1.3.2). A fluoride-mediated reduction in bacterial acid production, ensues without a detectable change in bacterial biofilm composition. Correspondingly, fluoride has no effect on the development of gingivitis or its progression to periodontitis. 

NOTE Studies in the 1980s determined that large doses of fluoride do not protect from osteoporosis (Sect. 10.2.3), or decrease the incidence of bone fractures. It appears that increased fluoride in the diet inhibits osteoblast activity more than osteoclast activity women on fluoride supplements suffer from more bone fractures, not less. Fluoride therapy for osteoporosis was popular in the 1980s, but the reports published after 1990 reduced enthusiasm for this treatment and it is not now recommended for post-menopausal bone loss. 

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In the USA, water fluoridation became widely available after 1955 and fluoridated toothpastes after 1975 and caries in adolescent children has decreased by 66%. The effects of fluoride on caries are topical from the surface to the interior. Water fluoridation ensures small amounts of fluoride throughout a tooth and fluoridated toothpaste enhances the fluoride concentration at the tooth surface. Protection from caries by artificial fluoridation of water supplies and fluoridated toothpaste is cumulative. Investigations as to how fluoridation protects from caries has identified three mechanisms of caries protection (1) inhibition of demineralization, (2) enhancement of remineralization, and (3) inhibition of bacterial enolase activity reducing lactate production from ingested carbohydrates. Fluoride has little effect on bacterial growth, and gives no direct protection from gingivitis, periodontitis, or osteoporosis... 

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