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After de- and subsequent remineralization at 0.03 and 1.0 ppm fluoride and either 0, 1, 10, 20 or 25 mM carbonate, artificial lesions in bovine enamel were demineralized again. The amount of secondary demineralization was determined after 15, 30 and 70 h of demineralization by means of quantitative microradiography. The results showed that fluoride incorporated during the remineralization period retards lesion formation during secondary demineralization. Carbonate incorporated during the remineralization period enhances secondary demineralization. An interaction between both ions was observed.

Some newly designed surface-active phosphates were investigated with respect to their capacity to inhibit caries lesion formation in vitro. On the labial or buccal surfaces of sound human third molars, windows were prepared for investigation. One half of each window was treated with the test compound at pH values of 7.5, 5.5, or 3.5. The other half served as a control. Both halves were demineralized and the generated caries lesions in both parts were compared by means of quantitative microradiography. Mono-, bis- and trisphosphates differed only marginally in their effect on the demineralization. The compounds diminished the demineralization down to 30% of that of untreated enamel. Per molecule at least one long alkyl chain (more than 12 C atoms) was required for achieving decreased demineralization, indicating the importance of a low surface tension. The results suggest that some of the tested compounds have promising properties for their use as anticaries agents, especially when applied in combination with fluoride.

To estimate permeability properties of bovine dental enamel, complex impedance measurements and radioisotope diffusion experiments were carried out before and after X-ray irradiation (single dose, 72 Gy) of enamel specimens. Neither impedance measurements nor diffusion experiments showed significant changes in permeability.

Third molars just erupting and premolars (before eruption or half a year or 3.5 years after eruption) were extracted and sawn vertically through the buccolingual plane. Tracings of the Ca, P, Na and Mg contents of the outer 100-µm layer of the enamel were made with an electron microprobe. Care was taken to limit the diameter of the excited volume to about 1 µm and to suppress the evaporation of Na. On the unerupted and freshly erupted surfaces the Na and Mg content varied from 50 to 80% of the content at 100 µm depth. However, half a year or 3.5 years after eruption the Na and Mg contents were negligibly small at the tooth surface and they remained smaller than in unerupted or freshly erupted teeth up to a depth of 10–30 µm. These data suggest that posteruptive maturation occurs in the mineral of the outer layer of tooth enamel whereby it builds up a higher resistance to carious breakdown. This interpretation is corroborated by clinical findings reported in the literature. The consequences of wear and abrasion on these phenomena are not known yet. The above-mentioned depth of 10–30 µm agrees with the penetration depth of pH changes estimated to result from the consumption of foods and drinks with varying pH.

Point count analyses were made with the electron microprobe for Ca, Na and Mg in a vertical cross-section through the enamel of a freshly erupted human pre-molar in the approximal area. A low excitation energy was chosen to limit the size of the excited volume and to suppress the evaporation of Na. The Na content showed variations with a wavelength of 6 ± 1 µm, which equals the distance of cross-striations. The Mg content showed variations with a wavelength of 25 ± 4 µm which equals the distance of striae of Retzius, whereby these striae probably contain a higher Mg content. On the assumption that higher Na and/or Mg contents represent mineral with a higher solubility, the observed variations in mineral composition help to explain the fine structure of carious lesions as observed frequently by microscopy and microradiography.

The adherence of 4 strains of oral bacteria to hydroxyapatite and to chemically modified hydroxyapatite was investigated in vitro. It was found that successive treatment of hydroxyapatite beads with potassium phytate and hexadecylamine lead to complete inhibition of the adherence of three Gram-positive strains, Streptococcus mutans, Streptococcus sanguis and Actinomyces viscosus, but not of the Gram-negative Fusobacterium strain. Coating of the hydroxyapatite surface with saliva prior to treatment with phytate and amine did not significantly change bacterial adherence. When phytate and amine-treated hydroxyapatite was post-treated with saliva, the adherence of S. mutans and A. viscosus, but not of S. sanguis, was still completely blocked.

Artificial laminated carious lesions were made on the buccal surface of human premolars. The volume percentage of mineral was determined as a function of depth by microradiography. Using the electron microprobe, the signals for Ca, Na, Mg, P and Cl were recorded as a function of depth both through the lesions and through the adjacent sound enamel. In the demineralized parts of the lesions there was a preferential loss of Na and a preferential retention of Cl. In the surface layers and the laminations the Na/Ca and Cl/Ca ratios were practically the same as in the adjacent sound enamel. This indicates that these surface layers and laminations were not formed by gross dissolution of the original mineral followed by gross precipitation of another, less soluble calcium phosphate, but that they remained there during the continuous demineralization due to the fact that the microcrystals became resistant to dissolution, perhaps due to protection by a thin layer of precipitated fluorapatite or fluoridated hydroxyapatite. In a previous study the same was found for surface layers and laminations in natural laminated carious lesions. This indicates that during continuous in vitro demineralization tooth enamel mineral behaves similarly as during intermittent in vivo demineralization.

Slices of bovine enamel and intact human enamel were treated with (a) a two-step treatment consisting of phytate followed by hexadecyl amine, or (b) 2-O-stearoylglycerol-1,3-diphosphate (Glydip), or (c) phosphatidic acid. The effect of these agents on the rate of caries lesion formation and on the permeability of dental enamel was quantitatively determined. Glydip had the most pronounced effect on lesion formation and showed a strong inhibiting effect on the rate of demineralization, combined with a reduction of the permeability. The results indicate that at least a part of the effect of Glydip on the demineralization was caused by a reduction of the rate of dissolution of the enamel mineral. The reduction in permeability may have had an additional effect.

The rate of dissolution of whole human enamel was studied by carrying out artificial caries experiments in buffers of known pH and known degree of undersaturation with respect to hydroxyapatite and by