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This study evaluated if Carbon dioxide (CO2) (λ 10.6 μm) laser irradiation combined with acidulated phosphate fluoride gel application (APF gel) enhances "CaF2" uptake by demineralized enamel specimens (DES) and inhibits enamel lesion progression. Thus, two studies were conducted and DES were subjected to APF gel combined or not with CO2 laser irradiation (11.3 or 20.0 J/cm(2), 0.4 or 0.7 W) performed before, during, or after APF gel application. In study 1, 165 DES were allocated to 11 groups. Fluoride as "CaF2 like material" formed on enamel was determined in 100 DES (n = 10/group), and the surface morphologies of 50 specimens were evaluated by scanning electron microscopy (SEM) before and after "CaF2" extraction. In study 2, 165 DES (11 groups, n = 15), subjected to the same treatments as in study 1, were further subjected to a pH-cycling model to simulate a high cariogenic challenge. The progression of demineralization in DES was evaluated by cross-sectional microhardness and polarized light microscopy analyses. Laser at 11.3 J/cm(2) applied during APF gel application increased "CaF2" uptake on enamel surface. Laser irradiation and APF gel alone arrested the lesion progression compared with the control (p < 0.05). Areas of melting, fusion, and cracks were observed. CO2 laser irradiation, combined with a single APF application enhanced "CaF2" uptake on enamel surface and a synergistic effect was found. However, regarding the inhibition of caries lesion progression, no synergistic effect could be demonstrated. In conclusion, the results have shown that irradiation with specific laser parameters significantly enhanced CaF2 uptake by demineralized enamel and inhibited lesion progression.

Various authors have shown that the caries decline in the industrialized countries during recent decades is based on the use of fluorides, of which local fluoride application in the form of fluoridated toothpastes is of primary importance. The caries-protective potential of fluorapatite is quite low; in contrast, dissolved fluorides in the vicinity of enamel are effective both in promoting remineralization and inhibiting demineralization. Considering the fact that the caries decline occurred at the same time that local fluoridation measures became widely used, the conclusion seems justified that regular application of F⁻ can inhibit caries.

The benefits of using fluoride to prevent caries have been known for many years, but a complete understanding of this mechanism is still being researched. The fluoride concentration in the apatitic structure of enamel does not have as significant an effect on reducing caries as a continuous presence of fluoride in the plaque liquid. Concentrated, topical fluoride agents (such as in toothpaste, fluoride mouth rinses, gels, or varnishes) have a different mechanism of fluoride protection than low-concentration applications (such as fluoridated water). In initial caries lesions and plaque, concentrated agents form globules of a calcium fluoride-like material on the enamel surface. This material is fairly insoluble, possibly because it is coated with phosphates or proteins. This mechanism explains how the topical application of a fluoride varnish, two or three times a year, can result in caries reduction.

All currently used topical fluoride agents deposit soluble fluoride as calcium fluoride on enamel or in lesions. Calcium fluoride serves as a source of fluoride for the formation of fluorapatite. The latter phase is formed when pH drops in plaque, not during topical application. The potential for calcium fluoride formation should probably be increased in topical fluoride agents. In countries with low caries prevalence, the clinical recommendations for topical fluoride need to be reconsidered. Toothpaste is the basic fluoride regimen recommended for everybody. The need for additional fluoride supplementation depends on caries activity. There is no distinct difference in the caries-preventive effects of concentrated fluoride solutions, gels, or varnishes. Thus, the choice of method depends on costs, convenience, patient acceptance, and safety. The use of fluoride varnishes has proven to be a feasible and safe method of fluoride application. With fluoride varnishes, the amounts of fluoride exposure can be better controlled, and less chair-time is required compared with conventional solutions and gels. No dose-response effect to concentrated fluoride agents is apparent, and the benefit of frequent application is not clearly established. In individuals with the most severe cariogenic challenge, combinations of fluoride and antimicrobials may give better clinical effects than fluoride alone.

The formation of CaF2 was measured on sound enamel and in artificial, standardized (acidified gelatin, pH 4.5) caries-like enamel lesions after exposure to: (a) dentifrice/saliva slurries adjusted to relevant F-concentrations of approximately 100 or 8 ppm by appropriate addition of 1,000 ppm F NaF or Na monofluorophosphate (MFP) dentifrice, respectively, or (b) a mixture of saliva with a 0.2% NaF solution obtained by a usual 1-min rinse procedure or an aqueous solution of 0.2% NaF. CaF2 was determined after extraction with KOH and fluoride analysis by gas chromatography. Only negligible amounts of CaF2 were produced on sound enamel ranging from (mean +/- SEM) 0.76 +/- 0.14 micrograms F/cm2 with the 0.2% NaF solution to as little as 0.04 +/- 0.06 with the MFP dentifrice slurry. In caries-like enamel lesions, the CaF2 production with the 0.2% NaF solution/saliva mixture corresponded to 3.7 +/- 0.4 micrograms F/cm2 and corresponding amounts obtained with the dentifrice/saliva slurries were 1.5 +/- 0.19 micrograms F/cm2 with NaF, but only 0.19 +/- 0.04 with MFP. It was suggested that the deposition of CaF2 in the micropores of early lesions can be expected to be an important mechanism with F rinses, probably to some extent with NaF dentifrices, but barely with MFP dentifrices. The formation of CaF2 on sound enamel is unlikely to play a significant role in the caries-reducing effect of F rinses and F dentifrices.

The formation of calcium fluoride (CaF2) was measured on sound enamel (SE) and in caries-like enamel lesions (CL) after treatment in vitro with 2% neutral NaF or Duraphat. The caries-like lesions were created by exposure to acidified gel at pH 4.5 within a 0.07-cm2 window punched in water-repellant tape. The same window area was used in series (n = 10) of SE or CL during the application of NaF for 1 or 5 min or for 18 h or Duraphat for 6 or 18 h. CaF2 was extracted with 1 M KOH for 24 h, and fluoride was determined by gas chromatography. The short-term applications of NaF produced only negligible amounts of CaF2 on SE. The amounts of CaF2 in CL after 5 min application of NaF corresponded to (mean +/- SEM) 27 +/- 2.0 micrograms F/cm2. More than half of this amount was observed after only 1 min exposure to the NaF solution. The quantities of CaF2 in CL were similar after 6 and 18 h application of Duraphat, amounting to 26 +/- 2.2 and 31 +/- 2.2 micrograms F/cm2, respectively, suggesting that the reaction was essentially terminated after 6 h. These amounts were only about one fourth of the quantity obtained after 18 h exposure to the NaF solution. Thus, the conventional 5-min treatment with NaF produced the same amount of CaF2 in CL as 6 or 18 h exposure to Duraphat.

This paper discusses loosely bound fluoride and its role in dental caries and prevention. Loosely bound fluoride (abbr. by Fa) is fluoride adsorbed onto enamel mineral crystallites. Several recent studies indicate that a high total level of fluoride in enamel does not guarantee protection against caries. This leads to the conclusion that a major part of fluoride present in the solid enamel is not active in prevention. The adsorption of Fa to the mineral under acidic conditions is described. Most likely there is a dynamic equilibrium between fluoride in solution and adsorbed Fa at the crystal surface interface. When the crystallite is completely covered by adsorbed Fa, there is a maximum inhibition of dissolution. The rate of dissolution of mineral depends on pH, the actual concentrations of calcium and phosphate in the liquid in contact with the crystallites, and on the fraction of the surface covered by adsorbed fluoride. The fluoride, Fs, localized in the inner part of the crystallites is relatively unimportant. "CaF2-like" material can be formed on and in enamel depending on conditions. The in vivo-formed globular "CaF2-like" material is not pure CaF2 and releases F- ions when dissolving; these ions will also be partly adsorbed as Fa in and on enamel. Presently, the amount and importance of Fa originating from in vivo-formed "CaF2-like" material are not known. The level of fluoride, Fa, necessary for strong inhibition of enamel demineralization in vitro is estimated to correspond to a fluoride concentration, FL, in the liquid phase of 1 ppm or 50 mumol/L fluoride ions.(ABSTRACT TRUNCATED AT 250 WORDS)

The retention of alkali soluble (CaF2) and alkali insoluble (fluorapatite) fluoride in sound enamel and demineralized enamel 2 wk after application of Duraphat was investigated in a group of orthodontic patients from whom pairs of homolog premolars were to be extracted. Demineralization of the enamel was induced during a 4-wk period prior to application of fluoride by applying orthodontic bands to the premolars. The bands also remained attached to the teeth during and after application of fluoride (2 wk) to maintain a cariogenic environment. Three consecutive enamel layers (approximately 5 microns) were subsequently etched off. A significant uptake of fluoride in the first and second layer of sound enamel and in all the three enamel layers of demineralized enamel was found. More fluoride was found in demineralized enamel and a higher proportion of this fluoride was found to be in an alkali insoluble form compared with the fluoride in sound enamel. The SEM study showed a rough enamel surface after three consecutive acid etchings. The etching pattern differed within the etched area. It was suggested that the variation in etching pattern might be due to differences in orientation of the crystallites and the original surface morphology.

Clinical experiments were performed to investigate the effect of fluoride on carious lesion development and on lesions established during fixed orthodontic therapy. All presently available fluoride agents are developed from the concept of fluoridating the enamel in the form of fluorhydroxyapatite. Recent research has indicated, however, that calcium fluoride formation may be a major aspect of the mechanism of the cariostatic effect of topical fluoride. Therefore a fluoride solution with very low pH (1.9) that induced large amounts of calcium fluoride also was tested on lesion development underneath orthodontic bands. Daily fluoride mouth rinsing with a 0.2% solution sodium fluoride (NaF) retarded lesion development significantly, whereas the fluoride solution with low pH inhibited lesion formation completely. Fluoride applied as a mouth rinse to plaque-covered lesions underneath orthodontic bands retarded lesion progression. The remineralizing capacity of saliva was found to be rapid in the absence of any fluoride. Although white spot lesions may remineralize and even disappear, most of the emphasis should be directed against prevention of carious lesion development during treatment with fixed orthodontic appliances.

Demineralization of enamel was induced by applying orthodontic bands in 15 patients having two of their premolars extracted for orthodontic reasons. After a 4-wk caries induction period, eight patients were instructed to rinse their teeth once daily with a neutral 0.05% NaF solution, whereas seven patients received a single treatment with a neutral 2% NaF solution. The bands were reattached to the teeth during the fluoride treatment period and the teeth were extracted after two more weeks. Three consecutive enamel layers were etched off, and a significant uptake of fluoride in all three layers were found in both treatment groups. A larger part of the deposited fluoride was retained in an alkali insoluble form (i.e. fluorapatite) compared with previous studies of sound enamel. It is suggested that the chemical conditions in the cariogenic milieu were favorable for transformation of the fluoride into a stable apatite structure.

Acidulated phosphate fluoride (APF), Duraphat or Fluor Protector, was applied to the molar teeth of rats fed a cariogenic diet. The first maxillary molar teeth were subjected to a microbiopsy procedure for fluoride analysis and the mandibular molars scored for caries. All three topical fluoride agents produced a significant increase in the fluoride content of the outermost 5.0 micron of enamel. Only APF produced a significant reduction in caries incidence at all sites.