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 de-mineralized 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.

Intact human enamel was demineralized in vitro to obtain artificial caries lesions. Part of the lesions was then treated with different surface-active compounds and remineralized with a remineralizing solution. The other part of the lesions was de- and remineralized in the same way, but was not treated with a surface-active compound. The results indicate that none of the surface-active compounds do affect the remineralization of the caries lesions. Possible applications of the tested compounds in combination with fluoride, for the prevention of dental caries, are discussed.

The effect of 2-O-stearoyl glycerol-1,3-bisphosphate (Glydip) on caries lesion formation in root surfaces of sound human third molars was investigated in vitro. For this purpose parts of the root surfaces were treated with Glydip. Adjacent parts of the surfaces were not treated and served as control. Lesions were obtained by demineralization with an acetate buffer of pH 5.0. It was found that Glydip had no inhibiting effect on the rate of lesion formation. Additionally, pretreatments were performed with lauryl sulphate, a chloroform-methanol mixture, an aqueous solution of sodium hypochlorite, and coUagenase prior to the treatment with Glydip to enhance the accessibility of the tissue for Glydip. None of these pretreatments or combinations of them revealed an inhibiting effect of Glydip on the rate of caries lesion formation. This result is in contrast to the effect of Glydip on the demineralization of enamel.