Sugars Under The Microscope
In the United Kingdom an attempt has been made to classify sugars according to their potential to cause tooth decay. In 1989 the Committee on Medical Aspects of Food Policy (COMA) produced a report entitled Dietary Sugars and Human Disease (1). The COMA panel decided to categorise milk sugars, essentially lactose, as non- cariogenic and to distinguish sugars naturally integrated into the cellular structure of a food (intrinsic) from those that were present in the free form or added to food (extrinsic, non-milk extrinsic [NME]). Intrinsic and extrinsic sugars are the same chemically and are principally glucose, fructose and sucrose all of which are, individually, cariogenic in animal models (as is lactose from milk). The extrinsic/intrinsic dichotomy was established in line with the prevailing view that sugars in the free form were more readily available for metabolism by dental plaque bacteria and were therefore cariogenic. Thus sugars in whole apples, for example, were considered to only have acidogenic potential in the mouth, when the cellular structure of the apple had been disrupted, by mashing or stewing, and the sugars externalised. At that point this was a simple hypothesis and had not been tested in humans.
When tested, this hypothesis was rejected. In 1996 Pollard et al (2) working in Leeds, investigated the effects of some intrinsic and non- milk extrinsic sugars on plaque pH. Three fruits, (apple, orange and banana), either whole, homogenised or juiced were tested in adult volunteers. The results showed that homogenisation of the fruits had little effect on acidogenicity, even though the intrinsic sugars had been converted to extrinsic sugars; it was concluded that there was no significant difference in the acidogenic potential between intrinsic sugars and extrinsic sugars derived from fruits.
Later we (3) tested the hypothesis that raw fruits, whether whole or pulped, would be cleared rapidly from the mouth and that the sugars in the whole and pulped fruits would be fermented with equal efficiency to acids by the oral microflora. Groups of 7-9 adult subjects chewed 10g of raw, whole or pulped fruit (apple, banana, orange, pear and pineapple) for 1 min and whole, unstimulated saliva samples were collected during the following 60-min interval. Each saliva sample was assayed for the concentrations of fruit-derived sugars (glucose, fructose and sucrose), fruit-derived acids (malic and citric) and acids which may be produced as a result of bacterial fermentation (acetic, lactic, formic and succinic).
We found the fruit-derived sugars and acids were rapidly cleared from the mouth (within 5 min). The major bacterially produced acids were lactic and succinic, which reached maximum concentrations in the 5-min sample, by which time the fruit-derived acids had been effectively cleared from the mouth (Fig 1). The results of this study supported those reported by Pollard et al. Within each fruit, there was no significant difference in the salivary levels of any of the sugars or acids between the raw whole or raw pulped forms. Clearly the teeth rapidly and efficiently disrupt the plant cells, releasing the intrinsic sugars, which the oral bacteria very rapidly covert to acids. The terms `intrinsic' and `extrinsic' do not appear to have relevance with respect to their availability and their potential to be metabolised by the oral microflora to acids.
Although the oral bacteria produce acids from the sugars in whole fruit, epidemiological evidence does not support a significant role for raw fruit in the caries process. It would be extremely unwise to suggest reducing fruit intake to protect the dentition, given the very significant benefits of fruit to general health. Although dried fruits, in which the sugars are concentrated, and which are sticky, may be a particular hazard to the dentition and their regular consumption should be limited.
The other sugar that the COMA panel considered was lactose. When consumed as a component in milk, lactose, although readily fermented by the majority of dental plaque bacteria, does not cause caries: the high calcium and phosphate levels of milk, and its high buffering capacity effectively neutralise the lactose-derived acid. Milk is usually swallowed quickly, but if it remains in the mouth, unswallowed for long periods, the lactose is fermented to acid. In extreme situations, this will cause tooth destruction, even in breast-fed infants.
The conclusion is quite simple: bacteria on the teeth are not concerned with the human classification of sugars. If a sugar can be fermented, the oral bacteria will produce acids and if a sugar- containing food is consumed frequently, that acid will contribute to the caries process.
References
1. Department of Health, 1989. Dietary Sugars and Human Disease.
Report of the Panel on Dietary Sugars. Report on Health and
Social
Subjects No 37 HMSO.
2. Hussein I, Pollard MA, Curzon ME. 1996. A comparison of the
effects of some extrinsic and intrinsic sugars on dental plaque pH. Int J Paediatr Dent. 6:81-6.
3. Beighton D, Brailsford SR, Gilbert SC, Clark DT, Rao S, Wilkins JC, Tarelli E, Homer KA. 2004. Intra-oral acid production associated with eating whole or pulped raw fruits. Caries Res. 38:341-9.
The article was first published in Dental Digest in February
2005
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