Progressive bacterial damage to teeth exposed to the saliva is referred to as caries. It is one of the most common of all diseases and a major cause of loss of teeth. The ultimate effect of caries is to break down enamel and dentine and thus open a path for bacteria to reach the pulp. The consequences are inflammation of the pulp and, later, of the periapical tissues. Acute pulpitis and apical periodontitis caused in this way are the most common causes of toothache. Infection can spread from the periapical region to the jaw and beyond. People occasionally die from this cause.
Extensive caries of decidous incisors and canines. This pattern of caries is particularly associated with the use of sweetened dummies and sweetened infant drinks.
Aetiology
In 1890, W. D. Miller showed that lesions similar to dental caries could be produced by incubating teeth in saliva when carbohydrates were added. Miller concluded that caries could result from decalcification caused by bacterial acid production followed by invasion and destruction of any remaining tissue. Though he took a laudably cautious view as to how these findings should be interpreted, Miller’s basic hypothesis has been upheld, even though the infective nature of the disease was not confirmed until 1954 when Orland and his associates in the USA showed that caries did not develop in germ-free animals. However, dental caries develops only in the presence of several interacting variables.
Microbiology
Substantial evidence indicates that streptococci are essential for development of caries, particularly of smooth (interstitial) surfaces. These are viridans streptococci which are a heterogeneous group including Streptococcus mutans, S. sobrinus, S. salivarius, S. mitior and S. sanguis.
Essential requirements for development of dental caries
1. Cariogenic (acidogenic) bacteria
2. Bacterial plaque
3. Stagnation areas
4. Fermentable bacterial substrate (sugar)
5. Susceptible tooth surfaces
The stagnation area in an occlusal pit. A ground section of a molar showing the size of the stagnation area in comparison with a toothbrush bristle placed above it. The complete inaccessibility of the stagnation area to cleaning is obvious.
Viridans streptococci vary in their ability to attach to different types of tissues, their ability to ferment sugars (particularly sucrose), and the concentrations of acid thus produced. They also differ in the types of polysaccharides that they form.
Certain strains of S. mutans are strongly acidogenic and, at low pH, with freely available sucrose, also store an intracellular, glycogen-like, reserve polysaccharide. When the supply of substrate dries up, this reserve is metabolized to continue acid production for a time. Drastic reduction in dietary sucrose intake is followed by virtual elimination of S. mutans from plaque and reduces or abolishes caries activity. When sucrose is made freely available again S. mutans rapidly recolonizes the plaque. Germ-free animals do not develop dental caries when fed a sucrose-rich diet which causes caries in animals with a normal oral flora. Experiments using gnotobiotes have shown that the most potent causes of dental caries are a limited number of strains of the S. mutans group which are able to form cariogenic plaque. S. mutans strains are a major component of plaque in human mouths, particularly in persons with a high dietary sucrose intake and high caries activity. S. mutans isolated from such mouths are virulently cariogenic when introduced into the mouths of animals.
However, simple clinical observation of the sites (interstitially and in pits and fissures) where dental caries is active, shows that the bacteria responsible are not those floating free in the saliva. Dental caries develops only at the interface between tooth surface and dental plaque in stagnation areas.
We will continue the article in second part.
