The effects of intra-oral mechanical forces on caries initiation, progression, and arrestment are evaluated by examination of different in vivo caries models. The models are grouped in four categories: (1) a population study, (2) short-term clinical trials, (3) clinical experiments, and (4) controlled clinical observations. Taken together, these in vivo studies convincingly demonstrate that partial or total elimination of the intra-oral mechanical forces operating during mastication or toothbrushing leads to evolution of cariogenic plaque, resulting in localized carious enamel dissolution. In addition, they show that re-exposure to the partly or totally eliminated mechanical forces not only arrests further lesion progression, but also results in partial lesion regression. The data from in vivo caries studies also show that the clinical and structural changes associated with lesion arrestment or partial regression are not related to any salivary repair mechanism, but are solely the result of mechanical removal of the cariogenic biomass which is physically interrelated with the eroded surface of the active, dull-whitish enamel lesion. No indications of superficial mineral deposition or "blocking" of the external intercrystalline spaces are seen in the surface layer of lesions arrested in vivo. For this reason, the conventional usage of the terminology 'remineralization' is considered absolutely misleading when used to describe the mechanisms responsible for the arrest of lesion progression in vivo.

The present study was designed to assess the effect of F compound and F concentration in dentifrices on fluoride in whole saliva after ordinary toothbrushing. The dentifrices tested had the same basic composition and contained NaF: 500, 1,000 or 1,500 ppm F or MFP: 1,000 or 1,500 ppm F. Whole saliva samples were collected at different times up to 120 min after brushing with controlled amounts of dentifrice. With all dentifrices tested, total F in whole saliva remained higher than controls for more than 60 min. Total F and F^–– levels showed a simple relationship to the F concentration in the dentifrices. The F^–– levels were initially significantly lower with the MFP than with comparable NaF preparations, but 10 min after brushing similar F^–– levels were observed with the two compounds. With the MFP dentifrices the proportion of F^–– to total F increased from 4% after 0.5 min to about 65% after 10 min indicating that MFP was subjected to rapid hydrolysis in the oral environment.

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 MKOH 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 μg 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 μg 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.

Fluoride concentrations in mixed saliva were measured at different intervals following topical treatments with various fluoride preparations and procedures such as dentifrice, tablets, mouthrinse and topical solution. The results were related to available caries reduction data from corresponding clinical trials previously published. Salivary fluoride levels varied widely reflecting the different dosages applied, whereas the caries reduction data irrespective of type of treatment appear very similar, with a magnitude of about 30%. When combining salivary fluoride data with recent understanding of enamel-fluoride kinetics it was possible to explain the clinical caries reductions.

In 1969, a caries preventive program was initiated in a part of Denmark where parents of infants were offered prescriptions for fluoride tablets for daily use. When requested new prescriptions were supplied free of charge by the County Dental Officer. In 1976, samples of children about 7 years of age who had received a total of 0, 1–800, 800–1,600 and more than 1,600 0.25 mg F tablets were examined. A positive association between number of tablets prescribed and dental fluorosis was found in erupted permanent teeth. The frequency of localized enamel opacities was similar in the four study groups. A significant inhibition of dental caries in the primary dentition was recorded only for those, who in total received more than 1,600 tablets and used them continuously through the years. No difference in caries was observed in the permanent dentition. The findings indicate in accordance with current theories that topical effects of fluoride rather than the systemic effects have prevented dental caries.