This study has shown that the exposure of human dental enamel to acid solutions in vitro produces three basic etching patterns. In the most common, called type 1 etching pattern, prism core material was preferentially removed leaving the prism peripheres relatively intact. In the second, type 2 etching pattern, the reverse pattern was observed. The peripheral regions of prisms were removed preferentially, leaving prism cores remaining relatively unaffected. In the type 3 etching pattern, there was a more random pattern, areas of which corresponded to types 1 and 2 damage together with regions in which the pattern of etching could not be related to prism morphology. These findings differ from previous studies in which the type 1 pattern was ascribed to acid action and type 2 etching pattern to attack by chelators. The results therefore suggest that there is no one specific etching pattern produced in human dental enamel by the action of acid solutions. Such differences produced by acids are difficult to explain on the basis of variation in chemical composition, and crystallite orientation. This further highlights the variation in structure that can occur in enamel not only from tooth to tooth, or surface to surface, but also from site to site on a single tooth surface.

Studies of the microbiota of dental plaque have been hampered by an inability to cultivate all or even a majority of microorganisms present in this site. Failure to recover the microorganisms could be attributed to at least 3 types of losses; inadequate dispersion, adhesion to glassware used in dilution and spreading, and an inability of any single cultural environment to recover all of the resident microorganisms. Clumps of microorganisms could be more effectively dispersed by sonic oscillation than tissue grinders. Anaerobic sonication proved to be significantly more effective in maintaining viability of plaque isolates than aerobic sonication while dispersion in dilute salt solutions permitted recovery of greater numbers of organisms than dispersion in broth. About 5% of the organisms were lost due to adsorption to glassware as determined by pouring molten agar media over the used apparatus and counting the resultant colonies. Optimum recovery of plaque organisms occurred in this study when samples were dispersed by anaerobic sonic oscillation in pre‐reduced anaerobically sterilized 1/4 strength Ringer's solution supplemented with 1% sodium metaphosphate, 0.05% L cysteine, and 0.0001% resazurin. When the resulting suspension was anaerobically serially diluted, and plated on trypticase soy 5% sheep blood agar plates which were incubated in Brewer jars containing 80% N2, 10% H2. and 10% CO2, 60% of the total microscopic cell count could be recovered. The use of additional primary isolation environments including blood agar plates incubated aerobically, as well as trypticase soy and reduced benzyl viologen roll tubes increased the recovery an additional 15%. Thus an average of 75% of the microscopic count could be cultivated. An additional 5% was lost due to adsorption to glassware and an average of 10% of the microbiota remained undispersed in clumps.

We examined the effects of phosphoric acid, the most common enamel etchant in composite resin therapy, on dentine collagen. Dentine collagen pretreated with 7M phosphoric acid was shown to be more susceptible to trypsin digestion than untreated collagen. This susceptibility increased with increasing duration of exposure to the acid. The results indicate that phosphoric acid induces a conformational change in dentine collagen (denaturation or perturbation) similar to that observed with 0.39 M HCl, which has a similar pH value (0.65). However, phosphoric acid-pretreated dentine collagen, when treated with tannic acid for 2 h, became as resistant to tryptic digestion as intact dentine collagen. The present results suggest that tannic acid may work as a dentine conditioner in composite resin therapy, in view of the fact that phosphoric acid etchant is applied, either deliberately or inadvertently, to dentine, and would thus induce denaturation or perturbation of collagen.