Carbohydrates dental caries

Pathology. Tooth plaque produces acids during the fermentation of dietary carbohydrates, causing the underlying tooth mineral to solubilize (demineralization). Upon restoration of a neutral plaque pH, mineral can reprecipitate (remineralization). When this equilibrium is lost, net demineralization occurs, causing dental caries. 

The presence of S. mutans and other cariogenic bacteria contributes towards the formation of a biofilm known as dental plaque, and their metabolism of fermentable carbohydrates in the diet leads to the formation of acids [12]. Dental caries has been described as a complex imbalance in physiologic equilibrium between tooth mineral and biofilm [13]. Biofilms imply the involvement of microbiological species [14], but the key concept included within this definition is that the bacteria involved are native to the body, not a group of specific invasive bacteria causing infection [14]. 

There is no direct evidence that the consumption of simple sugars is harmful. Contrary to folklore, diets high in sucrose do not lead to diabetes or hypoglycemia. Also contrary to popular belief, carbohydrates are not inherently fattening. They yield 4 kcal/g (the same as protein and less than half that of fat, see Figure 27.5), and result in fat synthesis only when consumed in excess of the body s energy needs. However, there is an association between sucrose consumption and dental caries, particularly in the absence of fluoride treatment. 

There is overwhelming scientific evidence that dietary carbohydrates, and sugars in particular, contribute to dental caries (Newbrun,... 

Conversely, deposition of a chelating agent on the surface of teeth may sometimes be advantageous. Thus, dental caries and corrosion are claimed to be prevented by exposing teeth to calcium sugar phosphate166. The resulting deposit apparently inhibits subsequent chelation and dissolution of calcium that normally occurs in teeth as a result of the oxidation of carbohydrate particles to polyhydroxylic acids. 

The pathogenesis of dental caries may involve three distinct processes (1) adherence of the bacteria to the tooth, (2) formation of glycocalyx due to synthesis of a sticky glucan by the action of the bacterial enzyme glucosyl transferase on sucrose, and (3) accumulation of biobUm (plaque), within which there is continuing acid production by constituent bacteria (including streptococci and lactobacflli) able to metabolize carbohydrates at low pH values. This acid demineralizes an enamel. 

Polyols are unique among simple carbohydrates in their low ability to be fermented. This characteristic enables them to impart sweetness to foods while exhibiting lower caloric values than other carbohydrates and reducing the formation of dental caries. Polyols are used in a variety of applications in foods, confections, pharmaceuticals and industrial uses. Rising demand for low- and reduced-calorie foods and confections that contribute to a reduction in dental caries has contributed to the growth of these starch-derived products. 

In contrast to calculus, dental enamel contains over 96% w/w inorganic mineral [50]. The main constituent is a single calcium phosphate phase, HAP, the structure of which contains minor impurities such as magnesium, sodium, carbonate and chloride [50]. Dental caries is a disease of bacterial origin. Certain plaque bacteria can ferment sugars and other carbohydrates from the diet to produce lactic acid and other short chain organic acids [51], If the concentration of acid depresses the pH adjacent to the tooth surface below about pH 5.5, then the enamel dissolves. 

Carbonic anhydrase and sodium bicarbonate together neutralize the acids produced by bacterial metabolism of dietary carbohydrate (Fig. 12.2). When salivary carbonic anhydrase is swallowed, it adheres to the mucosal surface of the stomach where it remains active and forms carbonic acid from sodium bicarbonate in the gastric mucosa. A lack of salivary carbonic anhydrase causes acid to remain longer in the stomach, contributing to peptic disease in addition to dental caries (Sect. 15.3.3). 

The average American consumes 54 gal of soft drinks each year. This is more than the amount of water that he or she drinks. For comparison, the average American drank 20.4 gal of coffee in 1996 352 and also consumed 152 lb of sugars each year. About one-third of this comes from soft drinks, which use sucrose or high-fructose corn syrup or both. Both promote dental caries.353 A typical soft drink contains 10-14% sugar, 0.37% flavoring, and 0.185-0.74% citric acid in water saturated with carbon dioxide.354 It may also contain color, caffeine, and preservatives, such as sodium benzoate. Phosphoric acid and other acids may be used instead of citric acid. The pH before carbonation is 2.35-2.66. It contains no vitamins, minerals, protein (usually), fiber, or complex carbohydrates. Its consumption at such levels raises serious nutritional questions. If other beverages were substituted for it, container waste would drop. 

Another member of the viridans streptococci, S. mutans, plays an important role in the formation of dental caries and binds tightly to tooth surfaces. The bacterium is capable of binding salivary components such as salivary agglutinin. It has been shown that S. mutans can bind to Lewis antigen carbohydrate epitopes containing fucose residues that are present on salivary agglutinin [48],... 

It is possible that we are not yet perfectly adapted to such a high carbohydrate diet. Some students of tooth decay point out that dental caries is rare among primitive Eskimos and the meat eaters of the Great Rift Valley in Africa. Many seem to feel that the human race made a mistake in giving up its primitive, carnivorous diets and that dental ailments are the price we have paid for adoption of carbohydrate foods (49). However this may be, all indications are that carbohydrates are here to stay. Indeed, unless science can provide some alternative that is not yet in sight, the growth of even United States population may be expected eventually to force us by stages up toward the 85% carbohydrate level of the orientals. 

It would seem that the role of plaque in the etiology of dental caries is direefold to provide (a) a stable matrix and (b) a source of fermentable carbohydrate for addogenic bacteria, " and (c) a diffusion-... 

Tooth decay (dental caries) is one of the most common diseases in humans [8]. It has been defined as a chronic, dietomiaobial, site-specific disease caused by a shift from protective factors favouring tooth remineralization to destructive factors leading to demineralization [9]. The specific factors leading to destruction of the mineral phase of the tooth are the presence of oral bacteria, mainly Streptococcus mutans [10], and the availability of fermentable carbohydrates from the diet. This combination leads to the production of organic acids as a result of the metabolic process of the bacteria, of which the main one is lactic acid, though other weak acids, such as ethanoic and propanoic can also occur [11]. These acids dissolve the mineral component of the tooth, leading to loss of structure. 

Dietary non-cariogenic carbohydrate sweeteners Dental caries... 

Because this and much other evidence put forward for a relationship between sugar intake and dental caries in Man is circumstantial and the applicability of the results of animal experiments to humans was open to question, there was a need for a prolonged and well-controlled experiment on humans. Such an experiment was carried out in Sweden shortly after World War II over a period of 6 years on patients in a mental hospital at Vipeholm, where careful dietary supervision was possible. More than 400 subjects were fed on a nutritionally adequate basic diet which was rich in vitamins and other protective foods, contained 130 g carbohydrate and provided 7-5 MJ (1800 kcal). Groups of patients were then fed various supplements which raised their total calorie intake to 1T3 MJ (2700 kcal). The form of the supplements and the times at which they were provided were varied. Some groups were given extra bread or a sugar solution at meal times while others were provided with chocolate or toffees between meals. A summary of the... 

High incidence of dental caries is associated with dietary carbohydrates, primarily the monosaccharides (glucose and fructose) and the disaccharides (sucrose and lactose). But more important than their intake is the frequency and their form therefore, for good dental health the following should be practiced ... 

EUNCTIONS OE MOLYBDENUM. Molybdenum is a component of three different enzyme systems which are involved in the metabolism of carbohydrates, fats, proteins, sulfur-containing amino acids, nucleic acids (DNA and RNA), and iron. Also, it is found in the enamel of teeth, where it appears to prevent or reduce the incidence of dental caries, although this function has not yet been proven conclusively. 

Bones and teeth dissolve in acid. The insoluble calcium monophosphate salt, from which hydroxyapatite is made, is converted to the more soluble calcium dihydrogen phosphate salt in an environment whose pH is less than 6.2 (Sect. 9.1.1). The severity of caries was related to the pH produced in dental biofilms (plaques) after ingesting sucrose and other sugars by Richard M Stephan. The pH response he identified is referred to as Stephan Curve. He found that the starting pH, the extent of its drop, and the time for recovery to the starting pH were all related to caries severity. The pH drop was later associated with lactic acid production due to bacterial carbohydrate fermentation (saccharolytic fermentation, Sect. 1.3.2). The subsequent rise in pH was due to the production of ammonia by bacterial... 

As in rodents and other animals, there is much individual variation in human caries experience. In the Vipeholm study, 25% of subjects taking the sticky candies did not develop any cavities over 6 years, whereas a few cavities appeared in control subjects who received a diet that contained little carbohydrate and no refined carbohydrate. A few cavities also appeared in children of the Hopewood House study who received a similar diet. Within 74 junior and senior dental students attending the College of Dentistry at the University of Oklahoma in 1985 (mean age 26 years), the mean DMFT was 8.4 with a variability of 40% about the mean (Fig. 15.10). Two had only one tooth affected and two others had, respectively 15 and 16 teeth affected. The variation is due to differences in microbiota, dietary carbohydrate intake, sahva flow, fluoride exposure, and acquired immunity (Table 15.1). 

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