Caries Management - Science and Clinical Practice. Группа авторов

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СКАЧАТЬ which suggests that acidogenic, acid-tolerant bacteria besides S. mutans contribute to the caries process and, in the absence of S. mutans, could be the sole agents of caries initiation.^14,15

      A third hypothesis, the ecological plaque hypothesis, emphasizes the importance of the oral environment in determining the composition and properties of the plaque microflora.¹⁶ According to this hypothesis (Fig. 2.3), in the mouths of persons consuming a low-sugar diet the plaque bacteria would derive their energy predominantly from slow breakdown of complex salivary and dietary molecules, so would experience only small and infrequent drops in pH. An increased frequency of sugar intake disrupts the homoeostasis of such a plaque because it favors growth of acidogenic, aciduric bacteria and hence promotes low-pH conditions. Bacteria which are sensitive to low pH grow less well under these conditions and are selected against. Thus an increased availability of sugar causes an ecological shift in the plaque microflora which establishes caries-conducive conditions. Since bacteria are selected solely on the basis of their ability to produce acid and to withstand low pH, this process is nonspecific and the bacteria which increase in a high-sugar environment can include a range of species, as noted above. However, if S. mutans has colonized the mouth its growth will certainly be favored, especially under conditions of very high sugar intake, which will result in the creation of extremely acidic conditions which give this species a competitive advantage. Such a sugar-rich, low-pH environment would also favor colonization by lactobacilli and by the fungus Candida.

      The ecological plaque hypothesis is supported by considerable evidence. The microflora of plaque from the approximal region is complex and dominated by Gram-positive, rod-shaped bacteria (mainly Actinomyces) and streptococci, of which the most abundant is typically S. sanguinis, with smaller proportions of other bacteria, such as Bacteroides, Neisseria, Veillonella, Fusobacterium, Rothia, and Lactobacillus. However, the composition of the flora varies considerably between different sites on the tooth surface. An increased sugar intake results in a higher proportion of acidogenic/aciduric bacteria,¹⁷ and increases in S. mutans, Lactobacillus, and others have been observed, along with a decrease in the less acid-tolerant S. sanguinis¹⁸ (Fig. 2.4). Plaque from caries-active people has a higher proportion of acidogenic bacteria than that from caries-free people: these changes affect plaque in general, not just on surfaces on which lesions form.¹⁹ Changes in the plaque flora can be difficult to identify because of extensive intra- and inter-individual variation, but in caries-active people the proportion of S. sanguinis and of Actinomyces naeslundii typically fall. During the initial stages of caries, the abundance of S. mutans, S. oralis, acidogenic actinomyces, such as A. gerencseriae, and lactobacilli increase. In advanced (cavitated) lesions, there may be moderate increases in S. mutans, but the flora is dominated by lactobacilli, Bifidobacterium, and Prevotella.^20,21

      Fig. 2.3 Ecological plaque hypothesis: conversion of noncariogenic plaque (low-sugar diet) to cariogenic plaque (frequent sugar intake). Increased sugar intake causes plaque pH to fall to low levels more frequently or more deeply. If sugar intake is maintained, this leads to a positive feedback loop in which the more acidic plaque environment drives ecological selection of acidogenic, aciduric bacteria and this in turn increases the acidity of the plaque environment. Ultimately the ecological shift favors conditions acidic enough for caries to be initiated.

      Proponents of the specific plaque hypothesis recognize the powerful ecological effect of dietary sugar in determining the composition of plaque microflora, but would argue that only the increases in abundance of S. mutans are etiologically significant. However, while there is little doubt that S. mutans is a major agent of caries initiation,²² it is very likely that other acidogenic/aciduric bacteria play important roles in both initiation and progression of lesions.^14,15

      Fig. 2.4 Selected examples of population shifts in the microflora of plaque formed in situ, as a result of exposure to sucrose. “Sucrose” plaques were rinsed with 10% sucrose 6 times a day for 7 days while control plaques were exposed to equivalent numbers of saline rinses. Sucrose exposure results in reduced numbers of the nonacidogenic species, Streptococcus sanguinis, but increases in numbers of acidogenic species and of lactate-utilizing Veillonella. (Data from ref.¹⁸.)

       NOTE

      Caries is probably not a “classical” infectious disease, that is, one caused by a specific bacterium not normally found in the body. Instead, it is probably due to over-growth of acid-producing, acid-resistant members of the normal oral flora, driven by excessive consumption of sugars. However, some species, especially Streptococcus mutans, do have a prominent, well-documented role in caries etiology.

      Chemistry of Dental Minerals

      Solubility, Dissolution, and Crystal Growth

      The processes underlying the phenomena of demineralization and remineralization in caries are crystal dissolution and precipitation. In caries, the latter process is usually manifested as re-growth of partly-dissolved crystals, although precipitation of new crystals can occur. Dissolution and crystal growth are both surface-related processes. At the surface of a solid immersed in an aqueous solution (e.g., enamel crystals bathed in saliva), ions are constantly detaching from the surface and entering the solution and other ions are following the reverse path to become incorporated into the solid (A and B in Fig. 2.5). When the rates of these processes are equal, the solid is in equilibrium with the solution and no net dissolution or crystal growth will occur. In this situation, the solution is said to be “saturated” with respect to that particular solid. The concentration of dissolved solid in a saturated solution is a measure of the solid's solubility. When the solution contains less than the equilibrium concentration of dissolved solid it is said to be undersaturated and when the concentration of dissolved solid in solution is greater than at equilibrium, the solution is supersaturated. When in contact with an undersaturated solution, the rate of ions leaving the solid will tend to exceed that of ions leaving the solution. This means that the solid will tend to dissolve and that crystal growth is not possible. In a supersaturated solution, crystal growth will tend to occur, as more ions leave the solution and are added to the surface of the solid, but the opposite process of dissolution cannot take place. In this description, the use of “will tend to” rather than “will” is deliberate. The reason is that in the complex environment of the mouth, both dissolution and crystal growth can be heavily influenced by another surface-related process: adsorption to the crystal surface of ions or molecules that inhibit movement of ions between the solid and the solution (C in Fig. 2.5). Inhibitory substances, including macromolecules such as peptides and proteins (e.g., statherin) and low-molecular-weight substances such as the pyrophosphate ion, abound in biological fluids,²³ including saliva^1,2 and the interstitial fluid of plaque.

      Fig. 2.5 Crystal growth (A) and dissolution (B) as surface processes of exchange of ions/molecules СКАЧАТЬ