Sucrose dental caries

The Sugars Task Force s Select Committee on Nutrition and Human Needs recommended a daily consumption of sugars at 10% of total calories, which approximates current (11%) daily intake levels in the United States. At this level, sucrose does contribute to the development of dental caries however, no firm evidence exists that it causes dietary imbalances or deficiencies of vitamins (qv), minerals, or trace nutrients (62). 

Alditols are sweet. Xyhtol has essentially the same sweetness as sucrose sorbitol is about half as sweet as sucrose. In chewing gum, polyols provide texture, sweetness, and mouthfeel and reduce the iacidence of dental caries. 

Mutans streptococci are the major pathogenic organisms of dental caries in humans. The pathogenicity is closely related to production of extracellular, water-insoluble glucans from sucrose by glucosyltransferase and acid release from various fermentable sugars. Poly(catechin) obtained by HRP catalyst in a phosphate buffer (pH 6) markedly inhibited glucosyltransferase from Streptococcus sorbrinus 6715, whereas the inhibitory effect of catechin for this enzyme was very low. 

A wider problem exists with the possible role of liquid medications in dental caries formation [63], The extent of acid production in the oral cavity is closely related to caries formation. In a study of liquid medication, investigators have observed that medications with sucrose concentrations higher than 15% were able to significantly lower pH there was an inverse relation between sucrose content and a decrease in oral cavity pH [64], In a comparison of sorbitol and sucrose-sweetened liquid iron preparations, only sucrose-containing products produced a significant decrease in oral cavity pH [65],... 

Sucrose and Dental Caries The most prevalent infection in humans worldwide is dental caries, which stems from the colonization and destruction of tooth enamel by a variety of acidifying microorganisms. These organisms synthesize and live within a water-insoluble network of dextrans, called dental plaque, composed of (al 6)-linked polymers of glucose with many (a 1 >3) branch points. Polymerization of dextran requires dietary sucrose, and the reaction is catalyzed by a bacterial enzyme, dextran-sucrose glucosyltransferase. 

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. 

Sweetness is one of the most important taste sensations for humans. Sucrose has been widely used for its sweetness as well as for functional properties such as texture, mouthfeel, bulking agent, and preservative. However, the specialized dietary requirements of diabetics and health concerns about obesity and dental caries have prompted a considerable research effort into the development of alternative sweeteners (1-6). 

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. 

Low sweetness sweeteners are of interest because they are generally metabolized in the body yet do not contribute to dental caries, and tend to have a lower effect on blood glucose in diabetics. Four examples are discussed here. Where sweetness equal to sucrose is desired, a high intensity sweetener can be mixed with it in most countries. However low sweetness caloric sweeteners are of particular interest for persons with kidney disease, where it is often difficult to get them to take enough calories. Use of glucose syrups to "stuff calories" with little water is often unacceptable to the patient because of the excessively sweet taste. Perhaps someone will develop a low sweetness metabolizable sweetener for these people. 

Many excipients used by the pharmaceutical industry in the last 15 years in sugar-free medical preparations probably come under the category of essentially new excipients. Pressure for their introduction has been encouraged by the definite relationship between the dietary consumption of sucrose and the incidence of dental caries. " "" These materials include intense sweeteners such as saccharin and cyclamate plus bulk sweeteners such as the polyols sorbitol, xylitol, and lactitol. These materials are all either approved for food use or have pharmacopoeia monographs in existence or in draft. Fiterature reviews show number of... 

The consumption of sucrose as a sweetener has been associated with several nutritional and medical problems, with dental caries being the most well-documented [1]. Sucrose intake may also be a factor in cardiovascular disease, diabetes mellitus, obesity, and micronutrient deficiency [2]. Therefore, there has been a continual demand for novel... 

Excessive oral fructose consumption (>75g daily) in the absence of dietary dextrose in any form (e.g., sucrose, starch, dextrin, etc.) may cause malabsorption in susceptible individuals, which may result in flatulence, abdominal pain, and diarrhea. Except in patients with hereditary fructose intolerance, there is no evidence to indicate that oral fructose intake at current levels is a risk factor in any particular disease, other than dental caries. ... 

Lactitol has a sweetening power about one-third that of sucrose. It does not promote dental caries and has a caloric value of 9.9J/g (2.4cal/g). 

Starch and sucrose, key substrates for the development of dental caries, are exclusively synthesized by plants. They are made in plant leaves by a process called photosynthesis, which utilizes sunlight as the energy source. This chapter outlines the light and dark reactions of photosynthesis and compares the light reaction with mitochondrial electron transport (Sect. 1). The key dark reaction, the production of phosphoglycerate by the enzyme ribulose bisphosphate carboxylase (rubisco), is described along with the production of fructose, sucrose, and starch (Sect. 2). The chapter concludes with a detailed discussion of the roles of starch and sucrose in plant metabolism (Sect. 3). 

This chapter describes dental caries (tooth decay) and its causes. Sucrose and other mono- and disaccharides are metabolized to acid (lactate) by bacteria that remain in stagnation areas of the teeth. Rats and hamsters fed a 50% sucrose diet developed a caries-sensitive, predominantly gram-positive microbiota that became caries resistant when the rodents were fed penicillin (Sect. 1). Further studies identified Streptococcus mutans (S. mutans) as the etiological agent. This organism synthesizes an insoluble polysaccharide capsule that is stable and retains lactate at the enamel surface (Sect. 2). The key enzyme, glucosyl transferase, is related to salivary amylase which adheres to oral bacteria and enhances bacterial acid production. The chapter concludes with a discussion of salivary and other factors responsible for the marked variation observed in individual caries experience (Sect. 3). 

In 1945, the Vipeholm study was set up to determine whether increasing sucrose intake actually increased human caries experience. The marked variation in caries severity between individuals (Sect. 15.2.1) had led to doubts that increased sucrose consumption was really responsible. The study was conducted at the Vipeholm Hospital for individuals with mental handicaps outside the University City of Lund, Sweden. The study examined the effects of different diets on dental caries in the inmates and it ended in 1951. The results indicated that sticky sugar candies (toffees) between meals and popular with the inmates increased their DMFT by an average of one cavity per year. The use of mentally handicapped subjects was criticized in the Swedish press and all studies on mentally handicapped individuals were stopped in 1954. 

How Sucrose Connects 5. mutans to the Oral Microbiota and Dental Caries... 

Fig. 15.11 Factors affecting pH after a 10% glucose or sucrose mouth rinse. Dashed line indicates pH 7. Vectors 1 and 4 increase the pH vectors 2 and 3 decrease the pH. The short-chain carboxylic acids (SCCA) may be produced from amino acids along with ammonia, or from the catabolism of lactic acid (see text and also Fig. 1.8). (From Fig. 9 in Kleinberg I, 2002. A mixed-bacterial ecological approach to understanding the role of the oral bacteria in dental caries causation an alternative to Streptococcus mutans and the specific-plaque hypothesis. Crit Rev Oral Biol Med 13 108-125)...

---