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The prevalence of developmental defects of enamel was assessed in 243 children aged 12-14 yr using the FDI Index. The teeth were not cleaned or dried prior to examination for which fibre optic lighting was used. At least one tooth with defective enamel was seen in 63% of children with a demarcated white opacity present in 44% of children. The enamel was abnormal in 11.7% of teeth, diffuse patchy opacities and demarcated white opacities occurring in 4.4 and 4.2%, respectively. Although defects were found most frequently in the maxillary central incisors, the ranking order of prevalence and the distribution for demarcated and diffuse opacities was quite different. Sex, residence, and the common childhood illnesses did not alter the prevalence of defects which was, however, increased significantly in 22 children with a history of a serious illness or accident (0.01 greater than P greater than 0.001). The prevalence of the diffuse opacities was significantly increased with increased exposure to fluoride either in tablets or in the drinking water (0.01 greater than P greater than 0.001).

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Intensified plaque acidogenicity in caries–prone subjects was reported many years ago, but emerging evidence has suggested that the relationship may not be as strong as once thought. We have now determined a range of acidogenicity variables in subjects having both caries prevalence and incidence data, and have included plaque mineral data in the analysis. pH measurements were made in 20 randomly selected subjects from a high–caries group (mean DMFS = 8.95) and 20 from a caries–free group of Beijing children aged 12 years participating in a caries prediction study. Subgroups with a 12–month DMFS increment ≥2 or = 0 were also formed from the two groups, respectively. Measurements were made with an iridium oxide electrode inserted between teeth 13/14, 23/24, 34/35 and 44/45, before and every 5 min for 30 min after rinsing with 10% sucrose, and the 4 resulting ‘Stephan curves’ averaged using a plaque pH analysis program. Supragingival plaque was collected from buccal and lingual smooth surfaces of posterior and upper anterior teeth and its acid extract analysed for Ca, P and F. Caries–free subjects (based on past experience) had a significantly higher maximum plaque pH and pH value after 30 min (reflecting a faster return to resting pH), a lower minimum enamel dissolution capacity of plaque and recorded less time below pH 7.0 than did high–caries subjects. No other differences were significant, including those of the principal acidogenic parameters ‘minimum pH attained after a sugar rinse’, ‘curve area below the critical pH of 5.5’ and ‘time below the critical pH’. Selection of the caries groups on the basis of both experience and incidence did not reveal significant differences in more parameters. Upper arch plaque was significantly more acidogenic than lower arch plaque, and there was a consistently strong association between upper and lower arch values in individuals. Ca, P and F in the subjects’ plaque had little or no influence on the principal acidogenic parameters. Our failure to find a relationship between caries prevalence or activity and these principal acidogenicity parameters may be related to differences between fissure and smooth surface plaque, temporal variations in acidogenicity and/or to use of F toothpaste during the 1–year observation period. These results support the view that factors such as the frequency of acidogenic episodes may be more important in caries progression than the degree of acidogenicity during any one episode.

An acetate buffer system, supersaturated with fluorapatite but not with hydroxyapatite, produced lesions in abraded bovine enamel which resembled human enamel caries lesions, both morphologically and in their F distribution. A gelatin-lactate system gave similar results when unpurified gelatin was used. Systems containing deionized gelatin, diphosphonate, or Ca and phosphate but no F, failed to produce caries-like lesions.

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A urea-MFP mineralizing solution increased the average concentration of calcium in artificial plaque in 5 subjects from 7.6 to 219 μg/mg protein, but the concentration fell to 59.6 μg/mg protein during subsequent cariogenic glucose exposures. The concentration of phosphate rose from 5.4 to 107 μg/mg protein and then fell to 32.7 while fluoride rose from 0.008 to 7.62 and then fell to 4.27 μg mg protein. Following the cariogenic challenges, enamel beneath mineralized plaque showed an average increase in Knoop diamond indentation length of 4.3 μm (compared to 25.01 μm beneath unmineralized plaque) and no radiographic evidence of demineralization. Enamel softening was inversely related to the amount of mineral in the overlying plaque. When the maintenance was high, the development of experimental caries was virtually eliminated. Common ion suppression of enamel dissolution is the most likely explanation for the caries-protective effect.

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