Evaluation of dietary factorsThe human longitudinal studies described earlier showed that, in individuals with little or no plaque control and no use of fluoride, frequent intake of sugar-containing products is a significant risk factor or prognostic risk factor for dental caries. In addition, in vivo plaque pH measurements have shown that the drop in pH and sugar clearance time in undisturbed plaque (more than 2 days old) is related to the sugar concentration and consistency of the food item being evaluated (see Figs 63, 64, 65, 66, 67, 68, and 69).

Influence of hydrogen ion concentration (pH) of plaque  It is generally accepted that enamel caries is the result of a disturbance in the equilibrium between enamel hydroxyapatite and the calcium and phosphate ion concentrations of the dental plaque covering the enamel surface. At neutral pH, plaque seems to be supersaturated with these ions. A fall in pH, however, caused by intraplaque bacterial fermentation of carbohydrates, leads to a shift in the equilibrium of concentrations and to dissolution of enamel.

Evidence from human longitudinal, interventional, and experimental studies There are many reasons why there are so few planned interventional human studies of diet and dental caries¾for example, the problem of persuading groups of people to maintain rigid dietary regimens for long periods of time. Although most of such studies involved providing daily sugar supplements to subjects¾a practice that would be considered unethical today¾these studies made an important contribution to dental knowledge.

Evidence from cross-sectional studiesNumerous cross-sectional observational studies in children have used dietary  interview and questionnaire methods to study the relationship between caries prevalence and consumption of sugar and sweets. The results are somewhat conflicting (Rugg-Gunn, 1989): A significant, but not very strong, correlation between caries and the total quantity of sugar consumed has been found in some studies but not in others. A closer relationship has been demonstrated between caries and the quantities of sweets and confectionery consumed, probably because these products are consumed in ways that enhance cariogenicity¾between meals and over long periods¾whereas consumption of even large quantities of sugar at meals seems to do little harm.

Evidence from epidemiologic studiesNumerous worldwide epidemiologic studies during the 20th century have shown thatcaries prevalence is low in developing countries or populations living on a local,carbohydrate-rich diet, based on starch instead of sucrose. Figure 51 shows sugarconsumption in 1977 in a number of countries worldwide. Consumption is extremelylow in China, and caries prevalence among 12 year olds is very low. On the otherhand, sugar consumption in Japan is only about half that of other industrializedcountries, but caries prevalence is moderate to high.

Role of fermentable carbohydrates (sugar and starch)A diet rich in fermentable carbohydrates (frequent sugar intake) is indisputably a verypowerful external RF and PRF for dental caries in populations with poor oral hygienehabits and an associated lack of regular topical fluoride exposure from toothpaste.However, in populations with good oral hygiene and daily use of fluoride toothpaste,sugar is a very weak RF and PRF, because clean teeth never decay, and fluoride is aunique preventive factor. The biochemical role of fermentable carbohydrates such assucrose in the development of an enamel caries lesion on a plaque-covered toothsurface is illustrated in Fig 2 (see chapter 1).

External Modifying Factors Involved in Dental CariesIntroductionAwareness of the multifactorial nature of dental caries is of fundamental importance.Figure 48 illustrates the interdependence of most of the determinate variablesassociated with dental caries. Besides etiologic, preventive, and control factors, manyother factors may modify the prevalence, onset, and progression of dental caries. Suchfactors may be divided into external (environmental) and internal (endogenous)factors (to be discussed in chapter 3).

Prediction and prevention of cariesThe younger the population and the lower the caries prevalence in the population, thehigher the percentage of caries-free subjects. In these populations, it is necessary tofocus on “high-risk strategy” and primary prevention, rather than secondaryprevention.For practicing primary prevention according to the high-risk strategy, the etiologicfactors used for caries prediction must be as sensitive as possible, that is, optimizingthe percentage of true high-risk individuals for cost effectiveness.

Rationale for combining salivary MS tests and PFRI for prediction of caries risk Like the inflammation induced in gingival soft tissues adjacent to dental plaque, carious lesions that develop on the individual enamel surface beneath bacterial plaque should be regarded as the net result of an extraordinarily complex interplay between harmless and harmful bacteria, antagonistic and synergistic bacterial species, their metabolic products, and their interaction with the many other external (fermentable carbohydrates etc) and internal (saliva and other host factors) modifying factors,which are discussed in more detail in chapters 2 and 3.

Selection of caries-risk patientsInability of a sole salivary MS test to predict caries riskAs already mentioned in this chapter, numerous cross-sectional as well as longitudinalstudies have shown significant correlations between salivary MS levels and cariesprevalence and caries incidence (for review, see Bratthall, 1991; Bratthall andEricsson, 1994; Beighton et al, 1989). At the surface level, even more significantcorrelations between MS colonization and caries incidence have been found(Axelsson et al, 1987b; Kristoffersson et al, 1985).

Accuracy ofrisk assessments in practiceA perfectrisk marker would have a sensitivity of 100% and a specificity of 100%, implying noerrors in risk assessment. Consequently, the false-positive and falsenegative rates wouldbe 0%, and positive and negative predictive values would be 100%.Having perfect accuracy means that the predicted high-risk group would consist ofonly true high-risk individuals and that only true low-risk individuals would be includedin the predicted low-risk group.

Prediction of Caries RiskPrinciples of risk predictionSome basic principles have to be followed for successful and cost-effective cariesprediction, caries prevention, and caries control:1. The higher the risk of developing caries for most of the population, the moresignificant the effects of one single preventive measure and the stronger thecorrelations between one single etiologic or modifying risk factor and the risk forcaries development.2. In populations in which only a minority of the people will develop new cariouslesions, it is necessary to use accurate risk predictive measures to select at-riskindividuals and introduce needs-related combinations of caries-preventive measures,in other words, a “high-risk strategy.

Cariogenicity of other bacteriaThere are overwhelming data from experimental and clinical studies in humans showing that S mutans and S sobrinus and lactobacilli are strongly correlated to caries etiology. However, the use of selective substrates in most of these studies may have introduced some bias. For example, Sansone et al (1993) found that plaque samples with and without MS and lactobacilli were equally acidogenic when cultured at low pH and in the presence of excess glucose.

EvidenceLactobacillus counts have been used to predict the incidence of new carious lesions. Crossner (1981) studied a group of children, who had been given dental treatment at baseline so that no open lesions were present at the bacterial sampling. Two subgroups in this material are of special interest: those with very low or very high lactobacillus counts. Very few individuals in the low lactobacillus group developed new carious lesions over a 64-week period. In the high lactobacillus group, many, but not all, developed new lesions.

Cariogenicity of lactobacilliAccording to the specific plaque hypothesis, some strains of lactobacilli are considered to be major caries pathogens along with S mutans and S sobrinus. Lactobacilli are acidogenic and even more aciduric than MS. Mutans streptococci are strongly correlated to the etiology of initial enamel and root surface lesions, because they can adhere to and colonize the tooth surfaces. Lactobacilli are more dependent on retentive sites for heavy colonization: Mutans streptococci are regarded as the pioneers, followed by lactobacilli in the succession toward more cariogenic plaque.

Methods of samplingAs mentioned earlier, the correlation between salivary MS counts and the number of MS-colonized tooth surfaces is relatively good (Lindquist et al, 1989), and simple salivary sampling methods are a more convenient and realistic means of assessing the severity of MS infection than sampling from individual tooth surfaces. Laboratory methods. Saliva is collected, mixed with a proper transport medium, and forwarded to a microbiologic laboratory. After incubation using a selective medium, mutans colonies are counted and the results are expressed as the number of colonyforming units per milliliter of saliva.

Cariogenicity of mutans streptococciMutans streptococci are acidogenic as well as aciduric and can adhere to tooth surfaces (Gibbons et al, 1986). Mutans streptococci can produce extracellular and intracellular polysaccharides from sucrose. Intracellular polysaccharides in particular can be degraded during periods of low nutrient supply, indicating that these polysaccharides increase the virulence of some MS species (S mutans and S sobrinus).  Because the microbial ecology of the mouth is highly complex, strains of the same species could vary considerably in virulence (Bowden and Edwardsson, 1994).

Role of Specific Cariogenic MicrofloraIntroductionMicroorganisms implicated in the etiology of dental caries must be acidogenic as well as aciduric. To initiate carious lesions in enamel, the microorganisms must also be able to colonize the tooth surface and survive in competition with less harmful species, forming biofilms¾the so-called dental plaque. As early as 1960, Fitzgerald and Keyes showed that certain microorganisms isolated from human dental plaque, when inoculated in germ-free rodents on a high-sucrose diet, resulted in the spread of rampant caries.

Strategies for prevention and control of caries based on plaque ecology hypothesis According to the plaque ecology hypothesis, low pH (less than 5) will promote overgrowth of aciduric microorganisms, such as the cariogenic mutans streptococci and lactobacilli, at the expense of less acid-tolerant plaque microorganisms, such as S oralis, which are associated with healthy tooth surfaces.  Therefore the treatment strategy would be to increase plaque pH and thereby promote reestablishment of the harmless normal microflora of the tooth surfaces.