Dental biofilms produce acids from carbohydrates that result in caries. According to the extended caries ecological hypothesis, the caries process consists of 3 reversible stages. The microflora on clinically sound enamel surfaces contains mainly non-mutans streptococci and Actinomyces, in which acidification is mild and infrequent. This is compatible with equilibrium of the demineralization/remineralization balance or shifts the mineral balance toward net mineral gain (dynamic stability stage). When sugar is supplied frequently, acidification becomes moderate and frequent. This may enhance the acidogenicity and acidurance of the non-mutans bacteria adaptively. In addition, more aciduric strains, such as 'low-pH' non-mutans streptococci, may increase selectively. These microbial acid-induced adaptation and selection processes may, over time, shift the demineralization/remineralization balance toward net mineral loss, leading to initiation/progression of dental caries (acidogenic stage). Under severe and prolonged acidic conditions, more aciduric bacteria become dominant through acid-induced selection by temporary acid-impairment and acid-inhibition of growth (aciduric stage). At this stage, mutans streptococci and lactobacilli as well as aciduric strains of non-mutans streptococci, Actinomyces, bifidobacteria, and yeasts may become dominant. Many acidogenic and aciduric bacteria are involved in caries. Environmental acidification is the main determinant of the phenotypic and genotypic changes that occur in the microflora during caries.
Organic acids in caries lesions play important roles in initiation and progress of dental caries. We investigated relationships between clinical types of dentin caries and acid profile or pH in the lesions. Caries lesions in dentin from 76 permanent teeth were classified into active, arrested, situated beneath a restoration, and unclassified types. The pH of carious dentin was distinctly lower than that of sound dentin (p < 0.001). Carious dentin with a high percentage of lactate had a lower pH than that with a high percentage of acetate and propionate (p < 0.001). Dentin from active lesions showed a mean pH of 4.9, and the dominant acid was lactate (mean percentage, 88.2). In contrast, carious dentin from arrested lesions showed a higher pH, 5.7, with acetate and propionate as the dominant acids (mean percentages of acetate and propionate, 64.0 and 18.2, respectively). The acid profile (mean percentages of acetate and propionate, 54.0 and 27.7, respectively) and pH (mean 5.8) of carious dentin sampled from lesions beneath a restoration were similar to those of dentin from arrested lesions. This study showed a clear relationship between clinical classification of dentin caries and acid profile and pH, suggesting that both factors are important in dentin caries etiology.
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