The ability of S. mutans to initiate smooth surface caries and form large amounts of adherent plaque depends on its ability to polymerise sucrose into high-molecular-weight, dextran-like, extracellular polysaccharides (glucans) (Box 3.2). The cariogenicity of S. mutans depends as much on its ability to form large amounts of insoluble extracellular glucans as on its ability to produce acid.

Glucans enable streptococci to adhere to one another and to the tooth surface, probably via specific receptors. In this way, S. mutans and its glucans may initiate their attachment to the teeth and enable critical masses of plaque to be built up. Production of sticky, insoluble, extracellular glucan produced by strains of S. mutans is strongly related to their cariogenicity.

The importance of sucrose in this activity depends on the high energy of its glucose–fructose bond which allows the synthesis of polysaccharides by glucosyltransferase without any other source of energy. Sucrose is thus the main substrate for such polysaccharides. Other sugars are, to a variable degree, less cariogenic (in the absence of preformed plaque), partly because they are less readily formed into cariogenic glucans.

Plaque polysaccharides, synthesised by bacteria, play an essential role in the pathogenesis of dental caries. The proportions of the different types of polysaccharide, and the overall amounts formed, depend both on the kinds of bacteria present and the different sugars in the diet.

On a sucrose-rich diet, the main extracellular polysaccharides are glucans. Fructans formed from fructose are produced in smaller amounts. They are more soluble than glucans and less important in caries. Acid-producing microorganisms that do not produce insoluble polysaccharides do not appear to be able to cause caries of smooth surfaces. Even mutant strains of S. mutans which produce more soluble polysaccharides seem not to be cariogenic. Polysaccharides thus contribute to the adhesiveness, bulk and resistance to solution of plaque.

In the past, lactobacilli were thought to be the main cause of dental caries because they are numerous in the saliva and can be isolated from carious cavities. They are also acidogenic. However, they are present only in relatively small numbers in dental plaque until after caries has developed.

In gnotobiotic animals, lactobacilli are weakly cariogenic but some can produce fissure caries where adherent plaque formation is less important. Overall, there is little evidence that lactobacilli are clinically important in initiating dental caries, but they may contribute to tooth destruction after the process has started.

Many other microorganisms can also be found in plaque. The role of the many filamentous forms is not known. Strains of actinomyces are also found, particularly when caries is rampant, but appear capable only of causing root surface lesions.

Though bacteria are responsible for acid production, bacterial plaque (Fig. 3.4) enables large concentrations of them to adhere to the teeth and, in stagnation areas, prevents effective buffering of bacterial acids by saliva. Important points about microbiological aspects of dental caries are summarised in Box 3.3.

The cariogenicity of S. mutans depends on properties summarised in Box 3.4.

If teeth are thoroughly cleaned by polishing with an abrasive, plaque quickly re-forms (Box 3.5).

Sucrose diffuses rapidly into plaque and acid production quickly follows. These changes have been measured directly in the human mouth using microelectrodes in direct contact with plaque. It has been shown by this means that, after rinsing the mouth with a 10% glucose solution, the pH falls within 2–5 minutes, often to a level sufficient to decalcify enamel. Even though no more sucrose may be taken and the surplus is washed away by the saliva, the pH level remains at a low level for about 15–20 minutes; it returns only gradually to the resting level after about an hour. These changes (the so-called Stephan curve) are shown diagramatically in Figure 3.7. The rapidity with which the pH falls is a reflection of the speed with which sucrose can diffuse into plaque and the activity of the concentration of enzymes produced by the great numbers of bacteria in the plaque. The slow rate of recovery to the resting pH – a critical factor in caries production – depends mainly on factors summarised in Box 3.6.

In addition to bacteria and their polysaccharides, salivary components also contribute to the plaque matrix. Calcium, phosphorus and, often, fluorides are present in significant amounts. There is some evidence of an inverse relationship between calcium and phosphate levels in plaque and caries activity or sucrose intake. The ability of plaque to concentrate calcium and phosphorus is used in mineralising mouthwashes. The level of fluoride in plaque may be high, ranging from 15 to 75 ppm or more, and is largely dependent on the fluoride level in the drinking water and diet. This fluoride is probably mostly bound to organic material in the plaque but, at low pH levels, may become available and active in ionic form.

As discussed earlier, the cariogenicity of plaque depends on its ability to adhere to the teeth, to resist dissolution by saliva and its protection of bacterial acids from salivary buffering. These properties depend on the formation of insoluble polysaccharides produced particularly by cariogenic strains of S. mutans.

Colonisation by cariogenic bacteria, especially S. mutans, is highly dependent on the sucrose content of the diet. In the absence of sucrose, S. mutans cannot usually be made to colonise the mouths of experimental animals. In humans, the plaque counts of S. mutans also appear to depend on the sucrose content of the diet. Severe reduction in dietary sucrose causes S. mutans to decline in numbers or disappear from plaque.

Experimental evidence for the essential contribution of sucrose to caries activity is summarised in Box 3.7.

The importance of sucrose in human caries depends mainly on epidemiological studies and a few interventional studies. The findings of epidemiological studies are summarised in Box 3.8.

In such studies, no association has been found between malnutrition and caries. Generally, the reverse is true and, when nutrition is poor, caries is infrequent. These diets also vary widely in content, from rice as the staple in China or coarsely ground cereals in Africa to a mainly meat and fish diet among Eskimos. The common feature of these diets, and one differentiating them sharply from westernised diets, is low or negligible consumption of refined sugar, particularly sucrose.

Britain is an example of a country where consumption of sucrose is exceptionally high and where the rest of the diet is more than adequate. A survey in England and Wales in 1973 showed, for example, that (in spite of the benefits of a National Health Service) 78% of 8-year-old children had active decay and many teeth which had been filled or lost from this cause. A survey in 1978 showed that dentate adults had on average only 13 sound and unfilled teeth. Though there has been dramatic improvement nationally, such consequences are still found in some populations.

In Britain and other countries, the incidence of caries has risen roughly parallel with rising consumption of sucrose. The incidence of caries has risen in spite of the much greater consumption of so-called ‘protective’ foods, namely dairy products, meat and fruit, in recent years. As a consequence of this more varied diet, carbohydrates overall have formed a smaller proportion of the diet. Nevertheless, sucrose forms a higher proportion of the carbohydrate component.

Where there has been a change from simple natural diets to a westernised diet, as in Alaska, caries has increased sharply and Inuit children now have a caries incidence at least as high as other American children. A similar state of affairs is developing in Africa as sweet eating and sweet between-meals ‘snacks’ have become popular. In Nigeria, many of the older adults are still totally caries-free, but the prevalence of dental caries among children and young people who have picked up sweet-eating habits is rising rapidly. This effect has also been strikingly well documented in the population of Tristan da Cunha who, up to the late 1930s, lived on a simple meat, fish and vegetable diet with a minimal sucrose content and had a very low caries prevalence. With the adoption of westernised diet, the caries prevalence had risen up to eightfold in some age groups by the mid-1960s. Even in Europe, in the 1930s and 1940s there were isolated communities, such as the Outer Hebrides or the Lötschental in Switzerland, where dental caries prevalence rose 20-fold or more when sucrose and sweets became widely consumed.

The effect of limiting sucrose consumption was shown on a vast scale during the Second World War. Those countries which suffered food shortages during the 1939–45 war had severe restrictions, mainly of meat, fats and sucrose. To maintain an adequate caloric intake, overall consumption of starchy carbohydrates rose considerably. In occupied Norway, where shortages were particularly severe, the pattern of dental caries during and after the war is shown diagrammatically in Figure 3.8. As sucrose became more plentiful at the end of the war, caries prevalence progressively rose.

Caries has become epidemic only in relatively recent years as sucrose became cheaper and widely available. In Britain, there was a sudden, widespread rise in sucrose consumption in the middle of the 19th century. This resulted both from the falling cost of production and, in 1861, the abolition of a tax on sugar. Evidence from exhumed skulls confirms the low prevalence of caries before sucrose became widely available and the steady rise in prevalence thereafter.

Patients unable to metabolise fructose as a result of an enzyme deficiency cannot tolerate fructose-containing foods including disaccharides such as sucrose where fructose forms part of the molecule. These children therefore learn to avoid all sucrose-containing foods and have an unusually low incidence of caries.

In the Vipeholm study, over 400 adult patients were studied in a closed institution. They received a basic low-carbohydrate diet to establish a baseline of caries activity for each group. They were then divided into seven groups which were each allocated different diets. A control group received the basic diet made up to an adequate calorie intake with margarine. Two groups received supplements of sucrose at mealtimes, either in solution or as sweetened bread. The four remaining groups received sweets (toffees, caramels, or chocolate) which were eaten between meals.

The effects of sucrose in different quantities and of different degrees of adhesiveness, and of eating sucrose at different times were thus tested over a period of 5 years. Caries activity was greatly enhanced by the eating, between meals, of sticky sweets (toffees and caramels) that were retained on the teeth. Sucrose at mealtimes only had little effe/>