Caries Management - Science and Clinical Practice. Группа авторов

      Fig. 2.2 The demineralization–remineralization balance in caries etiology. During the course of a day, intakes of sugar lead to episodes of reduced plaque pH. Not all present a threat to the tooth tissues (asterisks): only those in which pH falls below the critical pH can induce demineralization (shaded areas). Where sugar intake is infrequent and limited (top), the proportion of time spent below the critical pH is small and the resulting demineralization is compensated by remineralization during periods when plaque pH is approximately neutral. However, the demineralization–remineralization balance is tipped in favor of demineralization if increased amounts of sugar are ingested leading to deeper, more prolonged pH falls (middle), or if sugar is ingested more frequently (bottom). In both cases, the proportion of time when plaque conditions favor demineralization is increased at the expense of time when remineralization could replace the lost mineral.

      Caries is profoundly influenced by exposure to fluoride, which reduces demineralization and enhances remineralization.^7,9 As fluoride is most often delivered in the form of toothpaste, social and behavioral influences on oral hygiene habits take on a special significance (see Chapter 13).

      The aims of this chapter are to outline the relevant biological and chemical factors, and to describe their interactions in caries initiation and progression. In particular this chapter will cover:

      • Microbiology: changes in plaque flora associated with caries

      • Chemistry of dental minerals: concepts of solubility, dissolution and crystal growth; properties of tooth minerals; the effects of fluoride

      • The cariogenic challenge: properties of dental plaque; acid production from sugar and its effect on pH; factors influencing severity of the cariogenic challenge

      • Chemistry of caries: physicochemical processes controlling lesion formation and arrest

      Caries is not the only demineralization-related oral disease. Dental erosion, caused by direct action of acids on tooth surfaces without bacterial action, results in increased wear.¹⁰ A brief discussion of dental erosion concludes the chapter.

      Microbiology of Caries

      In his chemo-parasitic theory (1890), Miller postulated that caries was caused by acids produced in the mouth by bacteria metabolizing dietary carbohydrate in food particles retained between the teeth.⁶⁸ Until the 1960s lactobacilli were favored as the likely pathogens because they are highly acidogenic (capable of rapidly converting sugar to acid) and aciduric (capable of withstanding low-pH conditions). Then, from a series of classic experiments with rodents, it was concluded that caries was an infectious, transmissible disease¹¹ and attention shifted to streptococci, especially Streptococcus mutans, first isolated in 1928. Besides being acidogenic and aciduric, S. mutans synthesizes an insoluble, sticky extracellular polysaccharide from sucrose which promotes adhesion of the organism. Since the 1960s, an enormous body of research on the microbiology of caries has accumulated and many observational, longitudinal, and intervention studies have provided strong evidence for an association of S. mutans with caries.¹² Indeed, many workers have concluded that S. mutans is the sole pathogen involved in caries. Usually, this is extended to include other members of the taxonomic group to which S. mutans belongs—the mutans streptococci (see Chapter 1)—particularly S. sobrinus, which is also isolated from cariogenic plaque of humans, although less frequently and in smaller numbers than S. mutans. The hypothesis that caries is caused by infection with S. mutans or the mutans streptococci, is known as the specific plaque hypothesis.¹³

      However, S. mutans usually makes up only a very small proportion of the plaque flora, is not always detectable in plaque associated with caries, and can occur in plaque without caries developing.¹⁴ Further, while S. mutans is particularly acidogenic and aciduric, these properties are also exhibited to some extent by a variety of plaque bacteria. These include not only S. sobrinus but several “low-pH” members of the Streptococcaceae, such as strains of S. oralis. Other acidogenic/aciduric plaque bacteria include strains of Actinomyces, such as A. israelii and A. gerencseriae, bifidobacteria, and lactobacilli. Recognition of this fact underlies the nonspecific plaque hypothesis, 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