Noninvasive Therapy: 11 Caries Management by Modifying Diet


Noninvasive Therapy: 11 Caries Management by Modifying Diet

Bennett T. Amaechi

As described in the previous chapters, caries occurs when the equilibrium between the teeth and the biofilm is in imbalance. Imbalance means that the pH in the biofilm frequently drops from neutral to below a critical range for dental hard tissues, resulting in net demineralization of the tooth′s surface. The main factor that fosters this imbalance is the composition and mode of intake of the diet. In a consensus statement on diet, the FDI Second World Conference on Oral Health Promotion recognized food as being a complex mixture of macro- and micro- components. Following prolonged contact with the oral cavity, the diet can influence the oral microflora and can constitute a caries risk.1 The major components of diet—carbohydrates, proteins, fats, fruits, vegetables, and various additives to foods—all modulate the caries process, playing either a promotional or inhibitory role. Fermentable carbohydrates play a promotional role in the development of dental caries. In particular, sucrose has been named as the “arch criminal” in the caries process.2 Indeed, sucrose is the most cariogenic dietary carbohydrate, and diet with a high proportion of sucrose is known to increase the caries risk of an individual. Nonetheless, bacteria have the ability to ferment a wide variety of dietary carbohydrates to produce organic acids. Some proteins, fats, fruits, vegetables, and other food components may play a protective role in caries development. This chapter will describe the scientific basis of the influence of these food components on the caries process and caries risk of individuals. In particular this chapter will cover:

  • The mechanisms of carbohydrate fermentation in the biofilm

  • The role of sugar alcohols and intense sweeteners

  • The mode of action of some protective food constituents

  • Certain groups being at risk due to dietary patterns

  • Guidelines for “tooth friendly” nutrition

Carbohydrates (Sugars) in the Caries Process

The evidence implicating carbohydrate as being essential in the etiology of dental caries is overwhelming. Several studies of adults between 30 and 50 years old, both longitudinal3,4 and interventional,5 showed a clear relationship between consumption of refined carbohydrate and the development of dental caries. The description of sugar (i.e., sucrose) as the “arch criminal” of dental caries2 was based on these findings and also its unusual biochemical properties and the form in which it is consumed by humans. However, not all sugars are involved in the caries process. There are three types of sugars ( Table 11.1 ): The conventional sugars consist of sucrose, lactose, glucose, fructose, and corn syrups, while the most widely used sugar alcohols (polyols) are xylitol, sorbitols, mannitol, lactitol, maltitol, and the products Lycasin and Palatinit. Among the intense sweeteners (synthetic or artificial sweeteners) are acesulfame-K, aspartame, neotame, saccharin, sucralose, and steviol glycosides. It is the conventional sugars and polyols, also referred to as nutritive sugars due to their calorific value, that play significant roles in the caries process, either promoting (conventional sugars) or inhibiting (sugar alcohols) the process.

Conventional Sugars

Monosaccharides (glucose and fructose) and disaccharides (sucrose, lactose, and maltose) constitute the readily fermentable carbohydrates, and are substantially more cariogenic than starch.6,7 Starch is typically noncariogenic, because its molecules are too large to diffuse into the dental biofilm, but may be cariogenic in populations with high caries activity in that it can be hydrolyzed by salivary and plaque amylase into maltose, some glucose and dextrins. In rats a starch/sucrose mixture was shown to be more cariogenic than sucrose alone.6 Although sucrose is regarded as the most cariogenic dietary carbohydrate,8 probably because it is the most frequently ingested sugar, there is little difference in the cariogenicity of sucrose, glucose, and fructose.9,10 Although cariogenic bacteria such as Streptococcus mutans can become established in the absence of sugar, the ingestion of sugar enhances the ability of these microorganisms to colonize tooth surfaces. Whereas in the absence of sucrose there is reversible adsorption of these bacteria to the tooth surface, in the presence of readily fermentable carbohydrate there is a stabilized attachment of the microorganisms to the tooth surface.11

Types of sugars

Type of sugar





Conventional sugars





Corn syrups












Sugar alcohols (Polyols)













Intense (artificial) sweetners







Steviol glycosides














Although sucrose is regarded as the most cariogenic dietary carbohydrate, probably because it is the most frequently ingested sugar, there is little difference in the cariogenicity of sucrose, glucose, and fructose.

Sugar Metabolism and Acid Production by Cariogenic Microorganisms

A diet rich in readily fermentable carbohydrates promotes the development of dental caries due to the efficient metabolism of these sugars by cariogenic microorganisms, such as S. mutans. When a sucrose-rich diet is ingested, these bacteria do not only use the sugar as a primary energy source, but they also utilize it to initiate additional biochemical events which are responsible for the caries process. These biochemical activities occur through two major pathways: extracellular and intracellular ( Fig. 11.1 ).12 Because S. mutans is the best investigated cariogenic microorganism, sugar metabolism will be explained taking this bacterium as an example, although other caries-related microorganisms are thought to show similar metabolic patterns.

Intracellular Pathway

In the intracellular pathway, sucrose taken into the bacterial cell can be distributed within the cell in the following ways.

Direct phosphorylation. This proceeds via the glycolytic pathway into organic acid production ( Fig. 11.2 ): Many oral microorganisms in plaque biofilm produce organic acids in the presence of sucrose.13 All S. mutans strains are homolactic fermenters converting over 90% of hexose to lactic acid by the glycolytic pathway, since S. mutans does not possess the enzymes of the Krebs cycle or cytochromes. The ability of S. mutans to produce acid rapidly from sugar is the property most associated with the development of dental caries.14,15 Each episode of fermentable sugar ingestion is followed by a rapid production of acid by microorganisms, which depresses the pH of the plaque, and values as low as 4 have been recorded.16

Glycogen production. Many cariogenic microorganisms have the capacity to produce and store intracellular polysaccharides (IPS) which are branched glycogens of the amylopectin type,17 and are readily catabolized. A positive correlation has been reported between the numbers of IPS-containing microorganisms and the caries experience (DMFS).18 Intracellular glycogen in the form of the extra-cellular polysaccharides (fructans and glucans, see below) serve as substrate reservoirs which the microorganisms may utilize for energy production as the exogenous supplies of readily metabolized carbohydrate are depleted. In this manner both types of polysaccharide may play a role in the survival of the microorganisms and in their potential to prolong acid production via glycolysis well beyond meal time.

Illustration of the efficient metabolism of sucrose by Streptococcus mutans. EPS: extracellular polysaccharides; IPS: intracellular polysaccharides.
Fig. 11.2 Schematic Illustration of the anaerobic glycolytic pathway of bacterial metabolism. Streptococcus mutans can alter the acid profile in plaque according to the amount of sugar in the environment using a self-regulatory mechanism, which is facilitated by its dual metabolic systems, proton motive force (PMF) system, and phosphotransferase (PTS) system. The PMF is a low affinity sugar uptake system activated by a proton gradient, and operates at low pH. Streptococcus mutans uses this system to transport and metabolize sugars under high extracellular glucose concentrations such as during mealtimes. With excess intracellular glucose, the breakdown products of glucose in the glycolytic pathway—which include glucose-6-phosphate, fructose-1, 6-diphosphate, glyceraldehyde-3-phosphate, and phosphoenol pyruvate (PEP)—will all be in excess. In the presence of excess glucose-6-phosphate, pyruvate kinase (which catalyses the conversion of PEP to pyruvate) is activated so that excess pyruvate is produced, limiting the amount of PEP available at any one time. In the presence of fructose-1, 6-diphosphate, lactate dehydrogenase (LDH), which catalyses the conversion of pyruvate to lactate, is activated, so more lactate (lactic acid) is produced. At the same time, with excess glyceraldehyde-3-phosphate, pyruvate formate lyase (PFL) (which catalyses the conversion of pyruvate to formate, acetate, or ethanol) is inhibited, so little or none of these by-products is produced. The overall effect is that in the presence of high amounts of extracellular glucose, such as during and a few minutes after a meal of fermentable carbohydrates, more lactic acid is produced and less of other acids. The PTS, on the other hand, is a high affinity sugar uptake mechanism driven by PEP and operates at neutral pH. Under low extracellular sucrose concentrations such as between meals, S.mutans utilizes this system to transport the scarcely available sugar intracellularly. With limited sugar, the activating action of glucose-6-phosphate on pyruvate kinase will be withdrawn due to this metabolite′s low concentration. This in effect will limit the conversion of PEP to pyruvate, resulting in accumulation of PEP. The increased PEP will trigger the PEP/PTS system to transport more glucose into the cell. At the same time, the inhibitory action of glyceraldehyde-3-phosphate on PFL will be withdrawn, favoring the production of formic acid, acetic acid, and ethanol. Thus the overall effect at low extracellular glucose concentration is production of formic acid, acetic acid, and ethanol within the plaque as a by-product of bacterial metabolism.

Invertase activity. Sucrose-adapted microorganisms possess significant levels of invertase, an enzyme which hydrolyzes sucrose intracellularly to free glucose and fructose. The glucose and fructose can either be directly phosphorylated to lactic acid or converted to intracellular polysaccharide (glycogen), as described above.

Extracellular Pathway

In the extracellular pathway, S. mutans, through its cell surface-associated enzymes, glucosyltransferases (Gtf) and fructosyltransferases (Ftf), polymerizes the glucose and the fructose moieties of sucrose to synthesize two types of extracellular polysaccharides (EPS): glucans and fructans, respectively.19 These enzymes act by transferring glucosyl or fructosyl moieties from sucrose to primer molecules. No phosphorylated intermediates are involved, but the energy required for this activity is derived from the energy-rich disaccharide bond of sucrose, and this explains why this sugar is the essential substrate. The glucans provide binding sites for colonization by bacteria, promote the accumulation of microorganisms on the tooth surface (plaque formation), and contribute to the bulk and further development of the plaque biofilm.20,21 The fructans synthesized by the S. mutans are also highly soluble and can be degraded by plaque bacteria, and therefore do not persist in plaque. The EPS serve as a reservoir of fermentable sugars for oral bacteria when extraneous sources are lacking (between meals),22,23 with a consequent extended period of acid production and prolonged tooth tissue demineralization. EPS can also protect the microorganisms from the inimical influences of antimicrobials and other environmental assaults.24,25


A high sucrose diet places an individual at a high risk of developing dental caries. Through their fast and efficient metabolism of sucrose, cariogenic bacteria produce substantial amounts of organic acids. Moreover, they store extracellular and intracellular polysaccharides that serve as reservoirs of fermentable sugar for extended periods of acid production and prolonged tooth tissue demineralization.

Factors Modifying the Role of Sugars in Caries Development

As discussed above, each time cariogenic microorganisms come into contact with food or drink that contains readily fermentable sugars (monosaccharides or disaccharides) these are metabolized for energy and organic acids are produced as metabolic by-products. These acids are localized within the biofilm adjacent to the tooth tissue (enamel or dentin). The drop of pH leads to a demineralization of dental hard tissues (see Chapter 2) and demineralization proceeds as long as sufficient acid is available. In thick gel-plaque the pH drops within seconds of contact with dietary sugars, and it can stay low for up to 2 hours.

Frequency of Sugar Intake

The effect of frequency of sugar intake on the initiation and progression of caries can be better understood if we realize that caries does not develop by continuous cumulative loss of mineral, but its formation is a highly dynamic process characterized by alternating periods of demineralization and remineralization. Under neutral conditions, there is a well-balanced equilibrium between the two. However, this balance is lost when both dental plaque and sugar are frequently present in the oral cavity. As discussed above, ingestion of sugar in the oral cavity harboring cariogenic bacteria is followed by acid production and depression of plaque pH below the critical pH for tooth tissue dissolution. Time is needed for saliva to neutralize this acid through its buffering action to establish a neutral pH required for remineralization of the demineralized tissue. It is pertinent to mention that the time required to achieve this neutral environment varies from individual to individual, and can be as long as two hours in individuals with thick plaque due to poor oral hygiene. If sugar is ingested again before this required time lapse, the circle of acid production resumes again, thus the pH of the plaque remains below the neutral level, so preventing remineralization, or at worst, below the critical pH with continued demineralization. In this situation, demineralization will outweigh remineralization and caries begins and progresses. Caries therefore depends on the balance between demineralization and remineralization, that is, on the frequency of sugar intake. A frequent and prolonged eating pattern therefore increases the caries risk of an individual. Studies have shown that both prevalence and incidence of dental caries are related to the frequency of ingestion of readily fermentable sugars.2629 The result of a Swedish study showed that a group of subjects who consumed only 85 kg of sugar per year, 15 kg of which were ingested between meals, developed substantially more caries than their counterparts who consumed 94 kg with meals.5 Similarly, infants who suck for prolonged periods on bottles filled with syrup or other sugary solutions develop rampant caries.3032 It has also been demonstrated that the frequency of consumption of a carbohydrate solution needed to exceed seven times a day before significant demineralization was observed in situ in volunteers using fluoride toothpaste.33


A frequent and prolonged eating pattern increases the caries risk of an individual. In a frequent-eating condition, such as snacking with sugary food between meals, the pH is seldom allowed to return to neutrality. So demineralization continues and remineralization cannot keep pace with mineral loss, which leads to induction and progression of dental caries.

Consistency of the Sugary Food

The physical nature of the sugary food determines the rate of its clearance from the oral cavity, and influences its cariogenicity.34 Sugar clearance, determined by the consistency of the food as well as salivary flow rate, may be important in determining cariogenicity of foodstuffs and the caries risk of individuals. The level of dental caries is directly related to the duration for which sugar is present in the mouth.5 Sugar solutions are significantly less cariogenic than sugar ingested in solid form.35 The influence of the consistency of the sugary food in the caries process is similar to the effect of the frequency of sugar intake. It was easily understandable when subjects who chewed sticky toffees developed more caries than those who ingested a comparable amount of sugar in a nonsticky form ( Fig. 11.3 ).5 The toffee sticks on and between the teeth for a long time, leading to a steady supply of fermentable sugar to the microorganisms, with consequent continued acid production similar to frequent sugar consumption. Thus, it is not necessarily the frequency of ingestion of sugars per se that is related to development of caries, but the duration that sugars are available to microorganisms in the mouth, and in particular those in the plaque.36

Fig. 11.3 Results of the Vipeholm-Study. Caries increased significantly when sucrose-containing foods were ingested between meals. Sticky or adhesive forms of sucrose-containing foods, which can maintain high sugar levels in the mouth, were more cariogenic than those forms that were rapidly cleared (the Vipeholm study5).


The intake of a sticky, sugary food is much like frequent eating. The food sticks on and between the teeth for a long time, leading to a steady supply of fermentable sugar to the microorganisms, with consequent continued acid production over a prolonged period.

Amount of Sugar Intake

The relative importance of the amount as opposed to the frequency of consumption of carbohydrates for the development of dental caries remains controversial within the scientific community. Examination of published data and systematic reviews has also failed to convincingly show a positive correlation between the total amount of consumption and caries incidence.37,38 Weak correlation was observed between the amount of sugar consumed and caries occurrence.37 In a further analysis of data from the National Diet and Nutrition Survey of Children aged 1.5–4.5 years in the UK,39 the association between the amount of sugar consumed and caries was only evident in children whose teeth were brushed less than twice a day, so it was suggested that tooth brushing frequency has a stronger impact on dental caries development than the amount of sugar intake.

Investigation of cariogenic potential of foods by measurement of plaque pH has shown that a relationship exists between acidogenic/cariogenic potential of food and the presence of sugars, but much less their amount or concentration.30,32,33,40 Logically, the amount of carbohydrate may not have a significant effect in caries development provided adequate time is given for saliva to neutralize the acid produced in one episode of sugar ingestion before the next one. Consumption of sugar even at high levels was not importantly positively with caries increment when the sugar was taken up to four times a day with meals.5 The burden of cariogenic food depends more on frequency of intake than on total amount, although both may be directly related.41


The frequency of sugar consumption is more important than the amount of sugar, since the frequency of intake determines the duration that sugars are available to microorganisms in the mouth, and hence the duration of acid production and the consequent demineralization.

Thickness and Age of the Plaque

The ingestion of fermentable sugar enhances the proliferation of cariogenic microorganisms, such as S. mutans, and the development of dental plaque through the bacterial synthesis of EPS. Elevated amounts of EPS increase the stability, thickness, and the chemical nature of the plaque′s matrix from a liquid to a sticky, gel-like matrix. Thick gel-plaque allows the development of an acid environment against the tooth surface, while limiting the movement of charged ions needed for acid buffering, remineralization, and antimicrobial effects from saliva and other exogenous agents.42 Thus a thick and older plaque pre-disposes the teeth to longer periods of demineralization (and hence more demineralization) by prolonging the time it takes the saliva to penetrate the entire depth of the plaque to neutralize the acid produced by the large number of bacteria enmeshed within the thick plaque. Poor oral hygiene, therefore, predisposes an individual to the risk of dental caries, as a small quantity of sugar intake will tend to produce significant demineralization. Similarly, an oral cavity with thick plaque harbors a higher proportion of bacteria capable of synthesizing and storing EPS and IPS, which as stated previously serve as carbohydrate storage compounds for extended periods of acid production and demineralization, even when the ingestion of carbohydrate has stopped. It is also known that these bacteria utilize more environmental substrate (carbohydrates) and produce acid at higher rates than mutants defective in IPS synthesis. Thick plaque harbors a higher proportion of S. mutans in persons with poor oral hygiene.


Thick gel-plaque allows the development of an acid environment against the tooth surface, while limiting movement of charged ions needed for acid buffering, remineralization, and antimicrobial effects from saliva and other exogenous agents. Thus poor oral hygiene predisposes an individual to the risk of dental caries, as a small quantity of sugar intake can result in a significant demineralization.

Sugar Alcohols

The sugar alcohols (polyols) that are most frequently used as substitutes for sucrose are xylitol, sorbitol, and maltitol.


The most studied of the polyols is xylitol, which occurs naturally in many fruits, berries, and vegetables,43 and has been used as a sugar substitute for many years in confectionery.44 Xylitol has long been known to be noncariogenic in humans and animals,45 as demonstrated in clinical studies by its use in chewing gum,4649 oral syrup,50 and in candies such as gummy bears.51 The noncariogenicity of xylitol is based on the inability of the oral microorganisms to metabolize this sucrose substitute. The reduction of the prevalence and incidence of dental caries by xylitol is believed to be due its ability to decrease the number of mutans streptococci in saliva and inhibit formation of dental plaque.52,53 Reductions in S. mutans and S. sobrinus levels were observed after 6 weeks of gummy bear snack consumption containing xylitol at 11.7 or 15.6 g/day divided among three exposures.51 This effect of xylitol is strongly dependent on daily dose and frequency of consumption. Xylitol inhibits the growth and acid production of S. mutans in the presence of glucose by the mechanisms depicted in Fig. 11.4 .5457

The habitual consumption of xylitol by mothers can prevent dental caries in their children propably by suppression of mother–child transmission of S. mutans.58,59 This may be associated with the report that habitual consumption of xylitol can initiate an ecological shift in the plaque in favor of xylitol-resistant strains of S. mutans with impaired adhesion properties, that is, they shed easily into the saliva from plaque.60,61 Frequent use of xylitol by mothers, caregivers, and potential playmates of an unborn infant may endow this group of people with mutans streptococci that are incapable of adhering to the tooth surface, so when transmitted into the oral cavity of the infant following birth, the flora can hardly establish itself.

Xylitol has been reported by some scientists to facilitate remineralization of early caries,47,6264 and to arrest the progress of caries.64,65 These two functions were attributed to two factors: a) salivation stimulation 66 causing increased salivary flow with consequent acid neutralization providing a suitable environment and providing the necessary ions for remineralization; b) xylitol, in high concentration, has been shown to possess the ability to form complexes with calcium and phosphate ions,67 and to penetrate into demineralized enamel, where it can interfere with the transport of dissolved ions from the lesions to the demineralizing solution. Based on this fact, it is speculated that xylitol could participate in caries prevention by acting as calcium ion carrier and an agent that can concentrate calcium, but still there is no clinical evidence for this.

Two main reasons limit the use of xylitol as a substitute for simple sugars. First, xylitol is relatively expensive as a bulk sweetener. Second, it is poorly hydrolyzed in and/or absorbed from the small intestine and thus may cause osmotic diarrhea and flatulence when consumed in high amounts.68,69


The noncariogenicity of xylitol is based on the inability of cariogenic bacteria to metabolize this sugar substitute. Xylitol in gums and candies has been shown to have a caries-preventive effect which is probably based on stimulation of salivary flow, although an antimicrobial effect cannot be excluded. Its use, however, is limited due to adverse events such as diarrhea and its relatively high costs.

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May 23, 2020 | Posted by in General Dentistry | Comments Off on Noninvasive Therapy: 11 Caries Management by Modifying Diet
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