Caries Management - Science and Clinical Practice. Группа авторов

Чтение книги онлайн.

СКАЧАТЬ “bacteria,” and “diet.” While the combination of two factors will produce a contribution (e.g., bacteria + tooth → plaque; bacteria + diet → acid), the interaction of all three is required for caries initiation. Lesions are initiated only at sites where plaque accumulates. In economically developed populations, primary caries lesions are initiated in children on the enamel surface: most commonly in occlusal pits and fissures, less often on approximal surfaces, and rarely on smooth surfaces. In young adulthood, approximal caries increases. In older people, root surfaces exposed by gingival recession are sites for new primary lesions, and the margins of restorations are sites for secondary or recurrent caries lesions.⁶

      Caries tends to progress relatively slowly (over months or years) and in the early stages demineralization produces subsurface lesions which can in principle be arrested or reversed. Between cariogenic challenges, plaque pH returns toward “resting” levels which are approximately neutral, and this allows the possibility that mineral ions in plaque can contribute to re-deposition of mineral within the caries lesion: a process known as remineralization. Thus, the caries process is not one-directional but involves a dynamic process of mineral loss and regain⁷ (Fig. 2.2). If the balance between these processes favors demineralization, caries lesions progress and ultimately the damage to the tissue, due to mechanical breakdown (enamel) or to bacterial action (dentin), becomes irreversible. Restoration or extraction then becomes the only treatment option.

      Fig. 2.1 Venn diagram summarizing the etiology of caries. The diagram demonstrates that caries requires both the presence of acidogenic bacteria and availability of a diet from which the bacteria can produce acid, in conjunction with acid-susceptible dental tissues.⁵

      Despite this apparently simple etiology, caries is regarded as a multifactorial disease, for two main reasons. First, despite much research, it has not been proven whether it is caused by one specific pathogen or by several bacteria. Second, the risk of caries occurrence, and the rate at which the disease progresses, are influenced by a large number of factors.^6,8 These form a hierarchy at individual, behavioral, and social levels:

      • Individual factors: the oral bacterial flora; the solubility of tooth mineral; hard tissue structure; salivary flow rate and composition

      • Behavioral factors: frequency with which foods containing fermentable carbohydrate are consumed; frequency and effectiveness of oral hygiene; pattern of dental check-ups

      • Social factors, such as level of education and socioeconomic status, influence aspects of individual behavior which impinge on caries. Caries incidence in children is strongly influenced by the level of care provided by those looking after them, especially with respect to diet, attention to oral hygiene, and attendance at the dentist. Care provision is in turn influenced by the care-giver's background.

      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 СКАЧАТЬ