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Secondary caries is one of the main reasons to replace restorations. Due to the pressure to eliminate or reduce the number of amalgam restorations in many countries, fluoride-releasing composites have gained in importance. This review limits itself to information relevant to secondary caries near fluoride-releasing anterior or posterior composites. Although many parameters are very important in composite functioning, a weak spot near a filling is always the interface and the locally present interfacial gap between the composite and the hard tissues, where secondary caries takes place due to plaque action. Relevant parameters such as the amount of fluoride released in vitro in μg.cm-2, the rate of fluoride release, and the period of fluoride release are compared for several composites. In vitro F release has been measured for some fluoridating composites for more than five years. Unfortunately, F release in vivo or in situ cannot be measured adequately. The fluoride released by the composites considered is partly taken up by the surrounding tissues, partly released to the saliva, and partly efficacious in possible marginal gaps and defects. A major part of this paper pertains to in vitro, in situ, and in vivo secondary caries reduction experiments. In vitro caries reductions in the order of 40% from F-releasing composites vs. controls have been found. In in situ model investigations under plaque and saliva conditions, secondary caries reduction percentages of between 40 and 50% have been experimentally measured in gaps in enamel near F composites.

Seventeen subjects with more than 3 x 10(5) mutans streptococci per millilitre of saliva completed this randomised, cross-over study. Four different chewing-gums, containing: (1) 70% xylitol, (2) 35% xylitol + 35% sorbitol, (3) 17.5% xylitol + 52.5% sorbitol, and (4) 70% sorbitol, were tested. The participants used 12 pieces of each gum per day for 25 days. During the four experimental periods, they wore a removable palatinal plate containing two demineralised enamel samples, and brushed their teeth with a non-fluoridated toothpaste. The results showed that an increased concentration of xylitol in the gum resulted in a lower number of mutans streptococci in both saliva and dental plaque, although the decreases were only significant in the saliva samples (p

In this paper, data are presented on the in situ demineralization of human enamel as a function of the demineralization period. To quantify the mineral loss parameters versus time, it is important to obtain information on the kinetics, and thus on the mechanism of dental caries. The results show that for in situ enamel demineralization, the lesion depth as well as the mineral loss parameter both vary linearly with the demineralization time. This is in contrast to in vitro lesion formation where the third power, or the square power of the lesion depth is linearly related to the demineralization time. In in situ demineralization, the rate-determining step of the demineralization process is the inhibitor-controlled dissolution process at the enamel crystallite surfaces, while the inhibitor content (F-, proteins etc.) in the lesion originating from the plaque, saliva and enamel is high. Furthermore, the study indicates that in in situ demineralization, interprismatic mineral loss is very important.

The in situ remineralization of 100-microns-deep enamel lesions positioned in a full prosthesis just under the first molar was determined in 13 participants after 3 months. The outer surface of the samples was always flush with the acrylic surface: there was no measurable plaque accumulation on the samples. The effect of not brushing of the samples (A) is compared with the effect of brushing with a nonfluoridated dentifrice (B) or with a fluoridated paste (C) containing 1,250 ppm F. The results show that lesion depth (and mineral loss) data increase by about 50% (case A), do not change statistically in case B and decrease by about 40% in case C. The increase of lesion depth in case A is most likely due to acidic food and/or beverage intake by the participants. With respect to nonbrushing, the remineralization effect of brushing with an F-free paste is about 50% and with the fluoridated paste about 90% in 3 months. It is suggested that the remineralization efficacy of fluoridated pastes is due to the cleaning effect of the brushing by the dentifrice (presumably on the pellicle) as well as due to the fluoride effect on mineral nucleation and growth.

In this in vivo study the amount of fluoride present on and in human enamel was followed longitudinally for a period of 3 months. The fluoridating agents were an APF gel and the fluoridating lacquers

Shallow initial enamel lesions approximately 50 μm in depth were experimentally induced by plaque in sound intact human enamel. The lesions were subsequently remineralized in vivo without any fluoride

Three patients with a partial natural dentition in one jaw and a full denture in the other participated in this study. Enamel treated with APF gel, Duraphat or Fluor Protector and untreated controls were positioned in a full denture for periods up to 3 months. Plaque accumulation on the enamel blocks was evaluated by scanning electron microscopy. The results show that in all 3 patients studied the formation of CaF2 inhibited dental plaque accumulation.