Dental caries is an infectious, transmissible disease. As early as 1954, Orland et al demonstrated that, although germ-free animals do not develop caries, even with frequent sugar intake, all animals in the group rapidly develop carious lesions when human cariogenic bacteria (mutans streptococci) are introduced in the mouth of one animal. Specific bacteria (acidogenic and aciduric) that colonize the tooth surfaces are recognized as etiologic factors in dental caries. Frequent intake of fermentable carbohydrates, such as sugar, is regarded only as an external (environmental) modifying risk factor or prognostic risk factor. In the presence of these and other external risk factors, the outcome may be modified by internal host factors, such as the quality of the teeth and the amount and quality of saliva:
1. Microflora: acidogenic bacteria that colonize the tooth surface.
2. Host: quantity and quality of saliva, the quality of the tooth, etc.
3. Diet: intake of fermentable carbohydrates, especially sucrose, but also starch.
4. Time: total exposure time to inorganic acids produced by the bacteria of the dental plaque.
The development of a clinical carious lesion involves a complicated interplay among a number of factors in the oral environment and the dental hard tissues. A simplified explanatory model of the major events is illustrated in Fig 2. The carious process is initiated by bacterial fermentation of carbohydrates, leading to the formation of a variety of organic acids and a fall in pH. Initially, H+ will be taken up by buffers in plaque and saliva; when the pH continues to fall (H+ increases), however, the fluid medium will be depleted of OH- and PO3 4-, which react with H+ to form H2O and HPO2
4- On total depletion of these compounds, the pH can fall below the critical value of 5.5, at which point the aqueous phase becomes undersaturated with respect to hydroxyapatite. Therefore, whenever surface enamel is covered by a microbial deposit, the ongoing metabolic processes within this biomass cause fluctuations in pH, and occasional steep falls in pH, which may result in dissolution of the mineralized surface.
In their classic study of experimental caries in humans, von der Fehr et al (1970) showed that, in the absence of oral hygiene (ie, with free accumulation of plaque and rinsing nine times a day with a sucrose solution), clinical signs of enamel caries develop within 3 weeks. When the same research team repeated the study, but introduced chemical plaque control (rinsing twice a day with 0.2% chlorhexidine solution), the subjects did not develop caries, even though they rinsed with sucrose solution nine times a day for 3 weeks (Loe et al, 1972). In other words, when the
etiologic factor was suppressed or eliminated, the precondition for caries did not exist, and no lesions developed, despite the subjects' very frequent exposure to sucrose.
Like the inflammation induced in the gingival soft tissues adjacent to the gingival plaque, carious lesions of enamel, which develop on individual tooth surfaces beneath the undisturbed bacterial plaque, represent the net result of an extraordinarily complex interplay among "harmless" and "harmful" bacteria, antagonistic and synergistic bacterial species, their metabolic products, and their interaction with the many salivary and other host factors. This explains why combinations of different nonspecific plaque control programs have been so effective against caries, gingivitis,
and periodontitis (for review, see Axelsson, 1994, 1998). However, more recently, there has been intense interest in the role plaque (amount, formation rate, and ecology) and specific cariogenic microflora play in the etiology of dental caries.
