Dental caries is the most common disease worldwide. The term dental caries can be used to describe both the disease process and the cavitated or noncavitated lesions that form as a result of the disease process.5 The caries disease process is biofilm-mediated, sugar-driven, multifactorial, and dynamic in the phasic demineralization and remineralization of dental hard tissues.6
The relationship between caries and carbohydrates is fairly well understood; dental hard tissues are demineralized by acidic by-products produced by bacteria in biofilm (dental plaque) via fermentation of dietary carbohydrates.6 More specifically, there is a rapid fall in pH (to 5.5 or below) in tooth biofilm after carbohydrates are ingested. This lower pH can also affect the balance of microbes in the biofilm such that there is a higher proportion of acidic biofilm species, compounding tooth demineralization.7 Carbohydrate consumption is therefore an important nutritional factor in the development of caries.
For more information on dental caries, visit the ADA Oral Health Topics page on caries risk assessment and management.
Types of Carbohydrates
The relationship between carbohydrates and dental caries depends on the type of carbohydrate (sugars or starches) consumed because the cariogenic potential (i.e., promoting the development of tooth decay) of a given carbohydrate is dependent on how efficiently it can be metabolized by the bacteria that ferment it.8 Sugars, specifically, are considered to be the most important drivers of caries development. The term free sugar includes all sugars added to food/beverages, as well as the naturally occurring sugars found in fruit juices and concentrates, honey, and natural syrups. Collectively, natural and free sugars (e.g., sucrose, glucose, fructose) are considered the primary necessary factors in the development of caries.8 Sucrose, a disaccharide of glucose and fructose, is the most cariogenic sugar.8 Sucrose acts as a substrate for the synthesis of intra- and extracellular polysaccharides in dental plaque.8-10 Additionally, dental plaque formed in the presence of sucrose has been shown to have lower concentrations of calcium, inorganic phosphate, and fluoride, which are the ions required to remineralize enamel and dentin.10, 11 Sucrose and its constituent monosaccharides, glucose and fructose, are also more cariogenic than starches because they enter the glycolytic pathway more rapidly and result in a more pronounced drop in pH.12 Although lactose is also a sugar, it is less cariogenic than sucrose, fructose, and glucose because its fermentation produces a smaller drop in pH.9, 13
Amount/Frequency of Sugar Intake
In addition to the type of sugar consumed, the amount consumed may affect caries development. A 2014 systematic review examining the effect of free sugar consumption on dental caries observed a consistent association between free sugar intake and caries development; higher incidence of caries was found in populations where free sugar intake was greater than 10% of total energy intake compared to those with free sugar intake of less than 10%.14 This systematic review informs the World Health Organization (WHO) guidelines for sugar intake, which recommends that free sugars be less than 10% of total energy intake, with a further reduction to less than 5% suggested.15
Frequency, or how often free sugars are consumed, may also play a role in caries development. Increased frequency of sugar consumption and additional snacking between meals have been hypothesized to be more important in predicting caries risk than total sugar consumption.16-18 A possible rationale for this concept is that it takes approximately 30 minutes for the pH to drop after an intake of sugar, so additional sugar intake within that 30-minute period is less harmful than additional intake after 30 minutes.16 It is, however, difficult to determine the relative contribution of amount of sugar and frequency of sugar consumption to dental caries risk, given that the two are highly interrelated.16, 19
The recent systematic reviews and guidelines mentioned above14, 15, 20 present data that support the association between sugar consumption and/or snacking with caries development. Although not evidence for causality, these reviews are consistent in their findings that increased free sugar consumption is associated with an increased risk of caries.
There is ongoing research to determine strategies to decrease the consumption of sugar-sweetened beverages (SSBs), as they are a significant contributor to free sugar consumption. A tax on SSBs is one strategy that has been attempted; studies suggest that taxation of SSBs may decrease SSB consumption, caries incidence, and caries-related costs. Although public acceptance and efficacy of this strategy are still unclear, a 2019 systematic review and meta-analysis21 found that the equivalent of a 10% tax on SSBs was associated with an average decline in SSB purchase and intake of 10.0%.21-23 In addition to interventions effective at the population level, there is a need for high-quality evaluations with long-term study designs examining efficacy.24
Early childhood caries (ECC) is the presence of one or more decayed, missing, or filled tooth surface in children under 6 years of age.25 ECC was formerly referred to as “baby bottle tooth decay” and is primarily due to prolonged exposure of the enamel to sweetened liquids causing caries in small children. To address ECC, both the Academy of Nutrition and Dietetics and American Academy of Pediatrics promulgate guidance limiting fruit juice consumption by babies and toddlers.25, 26
Limited income or access to food can have a negative impact on intake of fruits and vegetables, lean meat, whole grains, and dairy. This inadequate consumption of nutrient-dense foods combined with a lower health literacy and limited access to oral health care can put low-income populations at an increased risk for caries and other oral diseases.25
Foods such as milk and dairy products, apples, cranberries, tea, and high-fiber foods have been suggested to have cariostatic properties (i.e., inhibiting the development of caries), although more careful examination is needed.27 It has been postulated that the calcium in dairy products offsets some of the cariogenic properties of lactose by limiting enamel undersaturation during acidogenesis. As mentioned above, lactose fermentation also results in a smaller reduction in pH compared with other simple sugars. Data from studies examining the association between milk consumption and caries suggests milk consumption does not increase caries risk and may actually reduce it.28
Some studies indicate that sugar alcohols such as xylitol and sorbitol used in chewing gums and as artificial sweeteners may have cariostatic effects, but overall findings are equivocal. Postulated mechanisms by which xylitol may reduce caries risk include simple substituting for fermentable carbohydrates,29 reducing the acidogenic potential,30 inhibiting the growth of Streptococcus mutans (plaque bacteria that contribute to tooth demineralization),31 or just increasing salivary flow (especially in the case of sugar-free chewing gums).32, 33 Although non-sugar sweetened gum is eligible for application to the ADA Seal of Acceptance, the ADA does not have a policy on the use of xylitol for caries prevention. The Council on Scientific Affairs expert panel report on Nonfluoride Caries-Preventive Agents concluded that evidence of xylitol’s benefit as an adjunctive therapy in children and adults who are at a high risk for developing caries is of low quality.34 For more information on chewing gum, visit the ADA Oral Health Topics page.
Vitamin D
Vitamin D influences the regulation of calcium and phosphate metabolism.35 According to some observational studies, higher prenatal intakes of vitamin D and prenatal serum vitamin D levels may be associated with reduced caries risk in children and infants.36, 37 Historical reports38 as well as a 2016 cross-sectional study suggest an association between dental caries and lower serum levels of vitamin D in children.39
