Chapter 32 Microbiology of dental caries
Dental caries is a chronic endogenous infection caused by the normal oral commensal flora. The carious lesion is the result of demineralization of enamel – and later of dentine – by acids produced by plaque microorganisms as they metabolize dietary carbohydrates. However, the initial process of enamel demineralization is usually followed by remineralization, and cavitation occurs when the former process overtakes the latter. Once the surface layer of enamel has been lost, the infection invariably progresses to dentine, with the pulp becoming firstly inflamed and then necrotic.
Dental caries (with periodontal disease) is one of the most common human diseases and affects the vast majority of individuals. Although caries was not uncommon in the developing world, the recent affluence in these regions has resulted in a remarkable upsurge in caries due to the ready and cheap availability of fermentable carbohydrates. In contrast, caries prevalence is falling overall in the developed world due to the increasing awareness of cariogenic food sources and the general improvement in oral hygiene and the dental care delivery systems. Caries of enamel surfaces is particularly common up to the age of 20 years, after which it tends to stabilize. However, in later life, root surface caries becomes increasingly prevalent, due to gingival recession, exposing the vulnerable cementum to cariogenic bacteria.
The primary lesion of caries is a well-demarcated, chalky-white lesion (Fig. 32.2) in which the surface continuity of enamel has not been breached. This ‘white-spot’ lesion can heal or remineralize, and this stage of the disease is therefore reversible. However, as the lesion develops, the surface becomes roughened and cavitation occurs. If the lesion is not treated, the cavitation spreads into dentine and eventually may destroy the dental pulp, finally leading to the development of a periapical abscess and purulent infection (see Chapter 34).
The structure of enamel, and of dentine in root caries, is important: some areas of the same tooth are much more susceptible to carious attack than others, possibly because of differences in mineral content (especially fluoride).
The mechanical washing action of saliva is a very effective mechanism in the removal of food debris and unattached oral microorganisms. It has a high buffering capacity, which tends to neutralize acids produced by plaque bacteria on tooth surfaces, and it is supersaturated with calcium and phosphorus ions, which are important in the remineralization of white-spot lesions. Saliva also acts as a delivery vehicle for fluoride.
There is a direct relationship between dental caries and the intake of carbohydrates. The most cariogenic sugar is sucrose, and the evidence for its central role in the initiation of dental caries includes:
Sucrose is highly soluble and diffuses easily into dental plaque, acting as a substrate for the production of extracellular polysaccharides and acids. Cariogenic streptococci produce water-insoluble glucan from sucrose, which, in addition to facilitating initial adhesion of the organisms to the tooth surface, serve as a nutritional source and a matrix for further plaque development. The relationship between sucrose and dental caries is complex and cannot be simply explained by the total amount of sugar consumed. The frequency of sugar intake rather than the total amount of sugar consumed appears to be of decisive importance. Also relevant are the stickiness and concentration of the sucrose consumed, both factors influencing the period for which sugar is retained in close contact with the enamel surface.
Carbohydrates other than sucrose, e.g. glucose and fructose, are also cariogenic, but less so than sucrose. Polyol carbohydrates, ‘sugar alcohols’ (e.g. xylitol), with low cariogenicity have been produced and are sought after as sugar substitutes in products such as chewing gum and baby foods.
Microorganisms in the form of dental plaque are a prerequisite for the development of dental caries. The different types of plaque and the factors involved in their development are described in Chapter 31.
Although mutans streptococci have been recognized as the major group of organisms involved in caries, there is some controversy as to whether one or more specific groups of bacteria are principally involved in caries – the specific plaque hypothesis – or whether the disease is caused by a heterogeneous mixture of non-specific bacteria – the non-specific plaque hypothesis.
Given the extreme variation in the composition of supragingival plaque from the same site in the same mouth at different times, it is unlikely that the initiation and progression of all carious lesions are associated with specific organisms such as Streptococcus mutans. Further, other plaque bacteria also possess some of the biochemical characteristics thought to be important in cariogenicity. Therefore, it seems likely that combinations of bacteria other than mutans streptococci and lactobacilli may be able to initiate carious lesions, and the plaque flora may be non-specific in nature. The current evidence implies that some bacteria (mutans streptococci, Lactobacillus spp. and Actinomyces spp.) may be more important than others in the initial as well as subsequent events leading to both enamel and root surface caries.
There is a vast literature on the role of the mutans streptococci in caries. ‘Streptococcus mutans’ is a loosely applied group name for a collection of seven different species (S. mutans, S. sobrinus, S. criceti, S. ferus, S. ratti, S. macacae and S. downei) and eight serotypes (a–h). S. mutans serotypes c, e, f and S. sobrinus serotypes d, g are the species most commonly found in humans, with serotype c strains being the most prevalent, followed by d and e. The others are rarely encountered. The evidence for the aetiological role of mutans streptococci in dental caries includes the following:
Note: not all strains of mutans streptococci possess all of the above properties; thus, some strains are more cariogenic than others. Caries may therefore be an infectious disease in a minority, with a highly pathogenic strain being transmitted from one individual to another. Despite this apparently strong relationship between S. mutans and caries, a number of longitudinal studies in children have failed to find such a strong correlation.