Dental caries is “the most common chronic disease in the United States and among the most common diseases in the world” and one of the most frequently occurring preventable infectious diseases of the oral cavity, globally affecting up to 90% of individuals in some countries (5
). It is a major cause of tooth loss in children and adults in the United States. It occurs more often than asthma, the second most common chronic pediatric disease (5
). In 2000, the US Surgeon General reported that approximately 80% of the caries incidence in children and adolescents was present in approximately 25% of the population (5
). More current reports show the problems remain, with the greatest incidence being among those in lower socioeconomic groups and children in the United States and globally (34
). According to data from the National Health and Nutrition Examination Survey (NHANES 1999 to 2004), among 2- to 11-year-olds, the prevalence of dental caries in primary dentition is approximately 42% for the time period 1999 to 2004; in permanent teeth, the prevalence is approximately 21% for this age group (37
). Among adults, the incidence of caries is substantially higher, approximately 90% for coronal caries and 14% for root caries, according to NHANES 1999 to 2004 data (37
). The US Surgeon General has labeled children’s tooth decay as America’s silent epidemic and continues to be a major unmet health need in the United States (5
). Data on the percentage of US children and adolescents who are caries free by age and ethnicity from the 1988 to 1994 NHANES survey are shown in Figure 73.2
The extent of dental decay in a population may be measured by decayed-missing-filled surfaces (DMFS), representing the sum of the number of permanent tooth surfaces (out of a possible 128 surfaces on 32 teeth) that are decayed, missing, or filled (39
). According to NHANES data for 1999 to 2004 (the most recent for which data are available for this statistic) for children between the ages of 6 and 11, 42% had caries in their primary teeth (27
); and for 6- to 19-year-olds using NHANES data for 1999 to 2002, 41% had caries in their permanent teeth (37
). In contrast, NHANES III data for 1988 to 1994 show that, among US children aged 5 to 17 years old who were examined, more than one half (54.7%) had a cariesfree permanent dentition; however, the mean DMFS was 2.5 (36
). In comparison, in the 1979 to 1980 survey conducted by the National Institute of Dental Research (NIDR) survey, 37% of school children examined had no caries in their permanent teeth, and the mean DMFS was 4.77. However, dental decay increases with age, so by 15 years of age approximately two thirds of US teens had experienced caries in their permanent dentition (see Fig. 73.2
). Cavitation occurs most frequently on the occlusal or chewing surface of the tooth. The prevalence of decay and unfilled tooth surfaces tends to be greater among low-income children than those of higher income strata according to US and global data (27
Role of Carbohydrates in Dental Caries
Dental caries is a multifactorial oral infectious disease. Fermentable carbohydrates are only one component in the etiology, along with the oral environment and dental plaque (Fig. 73.3
). Fluoridated water and oral hygiene practices can have a dramatic impact on caries risk and development. Tooth erosion, which impairs tooth integrity, is not an infectious disease, but the resultant defects increase risk of caries. Presence and adequacy of saliva, immune status, and lifestyle behaviors affect caries risk.
Fig. 73.3. Major factors that interact in the dental caries process. (Adapted with permission from Navia JM. Carbohydrates and dental health. Am J Clin Nutr 1994;59[Suppl]:719S-27S.)
In addition to fluoride, primary factors influencing this balance are nutrition and diet (48
). Nutrition has a systemic effect, whereas diet has a local effect. For example, systemically, malnutrition has a negative impact on the volume, antibacterial properties, and physiochemical properties of saliva. In addition, nutrition during development can affect the integrity of the tooth and salivary glands and the ability of the tooth to withstand bacterial challenge. Systemic diseases, medications affecting the integrity of the oral cavity, and salivary flow also can have an impact on nutritional well-being as well as oral health and oral infectious disease (including caries) risk (48
Sugars and cooked starches are fermentable carbohydrates. Sugars are found in the diet either as intrinsic, which are those found naturally in foods such as fruits, honey, and dairy products, or extrinsic, which are sugars added to foods during processing (50
). Examples of added sugars include white or brown sugar, honey, molasses, maple, malt, corn syrup or high-fructose corn syrup, fructose, and dextrose (48
). Other disaccharides, in particular trehalose and isomaltose, have a lesser cariogenic risk than sucrose. Starches are subsequently digested by salivary amylase to oligosaccharides, which may be fermented by the oral microflora. According to Lingstrom et al, only the gelatinized starches are susceptible to breakdown by salivary amylase into maltose, maltotriose, and dextrins (53
). Examples of cooked starches would include cereals (even those advertised as having no added sugar), cakes, cookies, pies, and snack foods.
Locally, dietary sources of fermentable carbohydrates are metabolized to acids by plaque bacteria, thus causing a drop in pH. Fermentable carbohydrates are carbohydrates
(sugars and starch) that begin digestion in the oral cavity with salivary amylase. The low pH (<5.5) favors the growth of Streptococcus mutans
(primary bacteria in the development of caries). In contrast, a diet with plenty of calcium-rich cheese eaten around mealtime favors remineralization.
Epidemiologic surveys, animal experiments, and early controlled human studies have all linked sugars to the development of dental caries. Studies from the later part of the twentieth century and the 2001 Caries Consensus Conference reported that diet could only explain a relatively small percentage of caries risk because of the introduction and widespread use of fluoride toothpastes (48
). However in 2009, Anderson et al conducted an evidence analysis of sucrose intake (quantity and patterns) and dental caries and reported that there was a significant relationship between frequency of sucrose intake and dental caries but not overall quantity (57
). Konig and Navia (58
) provided four inherent limitations in quantifying the relationship between dietary sources of sugars and dental caries: (a) variability in sugar consumption patterns that alter duration of exposure of the teeth to the sugars; (b) lack of specificity provided by diet recalls or food diaries, which are limited to an approximation of self-reported intake of actual sugars and eating patterns; (c) the differences in data timing—in other words, that sugar intake patterns can be calculated annually, but caries formation can take several years; and (d) other factors including fluoride, calcium, and phosphorus in the diet, along with oral hygiene habits and education level, all of which influence caries risk (58
The results of the 2001 National Institutes of Health Consensus Development Conference on Caries at which 69 studies on diet and caries published between 1980 and 2000 were reviewed showed that only two found a strong diet-caries relationship, 16 showed a moderate relationship, and 18 demonstrated a weak relationship (56
). The authors did not differentiate between sugars consumed as sucrose and other monosaccharides and disaccharides; however, these authors concluded that diets that promote coronal caries also promote root caries. They emphasized that the reviewed studies differed from sugar-caries studies published in the decades before fluoride. Although the articles reviewed indicated a decline in caries risk in relation to sugar intake, they attributed the relative drop to fluoride use. The evidence for the diet-caries relationship is clear in their conclusion that “sugar consumption is likely to be a more powerful indicator for risk of caries infection in persons that don’t have regular exposure to fluoride” (49
). This relationship has been further supported by relevant articles (34
As the per capita consumption of sucrose increased in England and the United States in the last 100 years, the prevalence of caries rose (51
). Since the later part of the twentieth century, sugar intake by adults and children has increased considerably; per capita consumption of added sugars increased 23% from 1970 to 1999 (50
). Added sugars intake increased in the period from 1989 to 1991 to the period from 1994 to 1996, an increase from 13.2% to 15.8% of total energy intake (60
). Using the NHANES 2004 data, at that time Americans consumed an average of 22.4 teaspoons of sugar daily (55
). In 2005 to 2006, the most frequently reported source of added sugars in the US diet was nondiet sodas, energy drinks, and sport drinks, which accounted for approximately 35% of total intake of sugars (52
In humans, the presence of sucrose in the mouth increases the volume and rate of plaque formation. Sucrose has a unique role in permitting bacteria to colonize on the teeth. When high concentrations of sucrose are present, S. mutans is able to produce extracellular polysaccharides, glucans, which form an organic matrix on the tooth. These insoluble, sticky polymers permit bacterial colonies to adhere to the tooth. In addition to glucans, S. mutans produces intracellular polysaccharides, primarily fructans, from sucrose that are stored and used in glycolysis when dietary carbohydrates are unavailable.
The critical concentration of carbohydrate in a food that will cause human caries is unknown. The Hopewood House Study showed that children eating diets containing complex carbohydrates but few refined sugars had low caries increments (61
). In a longitudinal study of school children in England where the fluoride level in the drinking water was low, the relationship between sugar intake and caries increment was examined; the highest significant correlation was between grams of sugar eaten daily and caries experience (62
The other monosaccharides and disaccharides—glucose, fructose, maltose, and lactose—found in fruits, dairy products, and processed foods are also readily used by oral microorganisms. These sugars diffuse rapidly through dental plaque to become available for bacterial fermentation. Within a few minutes of ingestion, fructose and glucose cause a decline in plaque pH similar to sucrose; thus, they are considered as cariogenic as sucrose.
When eaten with meals, fruits pose a lower caries risk than when eaten alone as a snack. For citrus fruits and melons, this is attributed to the high water content and the presence of citric acid (citrus only), which stimulates saliva secretion; for others it’s because the combination of foods and increased salivary flow has the potential to modulate the salivary pH. Fresh fruits vary in sucrose content from 10% to 15% by weight in apples, bananas, and some grapes; 7% to 8% in citrus fruits; and to 2% in berries, cherries, and pears. Foods with a high acid content may prevent bacterial fermentation but cause enamel erosion.
Sugars in solution (e.g., beverages) have been considered less harmful to teeth than solid sweets because beverages clear the mouth quickly. In 1940, however, Stephan showed that a 10% glucose rinse lowered the plaque pH to less than 5.5 (63
). The total amount of sugars in carbonated beverages, fruit drinks, and fruit juices is approximately 10%; and sport drinks contain approximately 4.4% total
sugars. Based on sugar content, acidity, and changes in plaque pH after rinsing with these beverages, all of them appear to have similar cariogenic potential (64
). Use of sugar-sweetened soft drinks three or more times between meals on a daily basis increases odds of having a high decayed-missing-filled teeth (DMFT) score. However, over time, food manufacturers have replaced some of the sucrose in beverages with high-fructose corn syrup, saccharin, or aspartame. Whether beverages formulated with high-fructose corn syrup are less cariogenic is unknown. Sports and energy drinks have a low pH associated with increased risk of caries (<5.5) (65
). Drinking sugarsweetened tea or coffee over an extended period of time can lead to enamel dissolution.
Sugar alcohols notably seen in sugar-free gums and beverages can have a positive impact on caries risk (51
). Examples include sorbitol, xylitol, mannitol, erythritol, and isomalt. Sugar-free gums with these polyols serve to stimulate saliva, thereby speeding clearance of fermentable carbohydrates from the oral cavity and serving as an oral buffer (51
). Chewing sugar-free gum following meals and snacks when brushing is not possible is a reasonable caries risk-reduction measure.
Frequent use of chewing gum sweetened with xylitol or xylitol/sorbitol mixtures causes significant reductions in dental plaque as well as plaque and saliva levels of S. mutans
). Gum chewing stimulates salivary flow and pushes saliva into the interproximal area, where salivary buffers can neutralize bacterial acids. Chewing also removes food particles from plaque and the soft tissues. The net result is that the stimulation of salivary flow caused by the physical act of chewing, coupled with the helpful effects of a noncaloric and noncariogenic sweetener, can be beneficial to oral health by “neutralizing” the plaque bacteria’s acid response to fermentable carbohydrate-containing foods.
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