A. Richards

It is now well-established that a linear relationship exists between fluoride dose and enamel fluorosis in human populations. With increasing severity, the subsurface enamel all along the tooth becomes increasingly porous (hypomineralized), and the lesion extends toward the inner enamel. In dentin, hypomineralization results in an enhancement of the incremental lines. After eruption, the more severe forms are subject to extensive mechanical breakdown of the surface. The continuum of fluoride-induced changes can best be classified by the TF index, which reflects, on an ordinal scale, the histopathological features and increases in enamel fluoride concentrations. Human and animal studies have shown that it is possible to develop dental fluorosis by exposure during enamel maturation alone. It is less apparent whether an effect of fluoride on the stage of enamel matrix secretion, alone, is able to produce changes in enamel similar to those described as dental fluorosis in man. The clinical concept of post-eruptive maturation of erupting sound human enamel, resulting in fluoride uptake, most likely reflects subclinical caries. Incorporation of fluoride into enamel is principally possible only as a result of concomitant enamel dissolution (caries lesion development). At higher fluoride concentrations, calcium-fluoride-like material may form, although the formation, identification, and dissolution of this compound are far from resolved. It is concluded that dental fluorosis is a sensitive way of recording past fluoride exposure because, so far, no other agent or condition in man is known to create changes within the dentition similar to those induced by fluoride. Since the predominant cariostatic effect of fluoride is not due to its uptake by the enamel during tooth development, it is possible to obtain extensive caries reductions without a concomitant risk of dental fluorosis.

The main aim of the present study was to compare the erosive capabilities of some fruit-flavoured drinks, fresh or saturated with CaF2, with their content of acids and with previous results from some carbonated soft drinks. The other aim was to measure and compare the rates of dissolution of CaF2 in some carbonated and non-carbonated drinks and water. Seven commercially available fruit-flavoured drinks were diluted for drinking. Two human molars, each with two approximately 4 x 4 mm windows, were exposed continuously to 500 ml of each drink with or without prior equilibration with CaF2 under gentle agitation for 48 h. The depths of the erosions were then measured on microradiographs made from sections. Dissolution rate of CaF2 was measured by suspending 0.5 g of the salt in 0.5 litre of the drinks for 2, 10 and 60 min followed by solution analysis. The pH of the drinks was 2.83-3.51. The amount of NaOH required to bring pH to 5.5 ranged from 12-42 mmol/l, which is more than the amount necessary for most carbonated soft drinks. Equilibration with CaF2 gave total fluoride concentrations of 3-8 ppm. The depths of the lesions induced by the drinks without added fluoride were 450-625 microm whilst those developed by the drinks equilibrated with CaF2 were 350-625 microm. The dissolution of CaF2 was faster in the carbonated drinks and in distilled water than in the non-carbonated drinks. In conclusion, non-carbonated fruit-flavoured drinks contain considerable amounts of acids which, in vitro, induce erosions in teeth similar to those induced by carbonated soft drinks. Saturation with CaF2 reduced the in vitro development of erosions by 28% induced by drinks with pH above 3; in drinks with pH below 3, erosions were not affected by pH, despite total fluoride concentrations of up to 20 ppm.

The aim of this study was to test whether dental fluorosis can be produced by administration of chronic doses of fluoride during only the post-secretory stage of enamel mineralization. Eight control and eight experimental pigs matched by weight and litter were fed a low-fluoride diet (less than 0.05 mg F-/kg b.w. daily) from weaning to slaughter at 14 months. The test group received an oral dose of 2 mg F-/kg b.w. per day from 8 months of age. Lower fourth pre-molars were at the post-secretory stage at the start of fluoride administration (confirmed by tetracycline marker) and were just erupting at slaughter. All of the fourth pre-molar teeth from the test group developed diffuse enamel hypomineralization indistinguishable from human fluorosis. No such lesions were seen in any of the teeth from the control animals. It was concluded that enamel fluorosis may be caused by fluoride exposure in the maturation phase only. The pathogenic mechanism may be an effect either on the selective loss of protein or on the influx of mineral, both of which occur during the post-secretory or maturation stage of enamel formation.