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Introduction

Nutrition and Tooth Structure

Nutrition, Diet and Dental Caries

Diet and Dental Erosion

Diet and Oral Cancer

Nutrition and Noma

Discussions and Conclusion

References

Teeth are valued, not least for their contribution to appearance and social acceptability. The cost of treating oral disease, though, is high - about £2.2 billion in the UK in 1999-2000. Nutrition and diet are major determinants of oral health or disease and the purpose of this lecture was to review their impact on the more important oral diseases: defects in the structure and appearance of teeth, dental caries, dental erosion, periodontal disease, noma, and oral cancer. There is growing realisation of the detrimental impact of dental impairment on food choice, nutrient intake and nutritional status. A common feature of many of these diseases is that the causes are well known. However, they are not yet preventable because their aetiology (and prevention) is intimately involved with lifestyle. Nevertheless, there are some hopeful signs of progress being made in several areas.

When King James IV extracted teeth from his subjects, dental decay was considered to be due to worms in teeth. The extent to which diet influenced the activity of these worms is unknown, for it was believed that the worms drank on the blood of the teeth and fed on the roots of the jaws. What is clear is that teeth were needed for chewing much more than now, and loss of teeth was a threat to survival.

Although King James would have been aware of the extent of oral disease, it is unlikely that this was ever quantified. We now live in an information era and we have a very good idea of the prevalence, cost and the causes of oral disease; armed with all this information, one would have thought we could have achieved oral health for all. We have failed to do so, for a variety of reasons. Nutrition and diet are important determinants of oral health or disease and today’s lecture is to review the evidence and to suggest ways of progressing the prevention of oral disease. Also, poor oral health or lack of teeth determines food choice, jeopardising general health, and this will be considered as well.

Oral disease is expensive. The total cost of NHS dental care in the UK is estimated to have been £2.2 billion in 1999-2000: this is 4.4% of total NHS expenditure. The cost of NHS dental care in Scotland was about £200 million. The vast majority of the cost - around 90% - is in primary dental care; the cost of hospital dental services being about £17 million in 1999-2000 (British Dental Association - personal communication). In the past, dental services have provided relief from toothache and operative treatment to prevent toothache; but the emphasis is now on preservation of sound teeth and in enhancing oral function and facial appearance. Facial appearance is tremendously important in determining an individual’s integration into society.

The UK is fortunate that comprehensive national surveys of oral health have been undertaken since 1968. These give a very clear picture of our much-improved oral health. In 1968, 37% of adults in the UK had no natural teeth at all - they were edentulous. These figures have fallen to 25% in 1978, 20% in 1988 and 14% in 1998.¹ From this we can predict the virtual eradication of edentulousness, in the working life of our present undergraduates. For children too, there has been much improvement. This is best quantified by adding the number of teeth, which are decayed, missing, and filled, and express this as mean per child - this is the DMFT index. The number of bad teeth per 14 year-old child was 7.4 in the first survey in 1973, 4.7 in 1983 and 1.5 in 1993.² For young children; the decline in caries in primary teeth also can be demonstrated, although there has been some levelling off in recent years. Thus, there has been considerable success in reducing dental morbidity but much disease still remains and it is increasingly unequally distributed within the population. Scotland’s oral health is amongst the worst in the UK - in the proportion of adults edentulous and in the mean number of bad teeth per child. As with most diseases, the socially deprived fare worse and marked differences between Health Boards are apparent also, with children in Greater Glasgow having two and a half times the number of bad teeth as children in the Borders.³

Most of the above statistics relate to dental decay (or dental caries) since this remains the most important oral disease. It causes infection and pain and is, thus, of medical, social and economic importance. It is very much a nutritionally related disease as will be discussed later. Other oral diseases are also affected by diet. The structure and subsequent appearance of teeth are affected by nutrition while teeth are forming, and diet can erode teeth after they erupt. Teeth are supported in the jaws by the periodontal ligament - periodontal disease causes infection and loss of teeth. Lastly, the oral mucosa -the most serious nutritionally related oral disease being cancer. It shouldn’t be forgotten, though, that the mouth has been termed ‘the mirror of the body’, with many nutrition deficiency diseases - e.g. iron and vitamin B complex, giving oral signs and symptoms.^4,5

Enamel formation of all primary teeth begins in-utero and is completed after birth; primary teeth erupt between about 6 and 30 months. Enamel of permanent teeth forms almost entirely post-natally. Insults during the period of enamel formation can affect the structure and appearance of teeth adversely, and nutrition is one of the more important influences.

Vitamin D is intimately involved with calcium metabolism and calcification, and it is not surprising that there has been considerable interest in its role in tooth formation. The story goes back nearly 90 years, to 1918, when Lady May Mellanby reported that dogs reared on a diet deficient in a ‘fat-soluble A accessory food factor’ (which she subsequently recognised as vitamin D) had delayed development of teeth, which had very deficient, poorly-calcified enamel.⁶ She carefully examined children’s teeth, both in the mouth and under the microscope, and concluded that many teeth were hypoplastic and that this was caused by vitamin D deficiency. She noticed that the appearance of children’s teeth improved between 1929 and 1943 and attributed this to improved diet, notably the introduction of cheap milk in 1934, the provision of cod liver oil to pregnant and lactating mothers, infants and young children, and the addition of vitamins A and D to margarine, and calcium carbonate to bread.⁷ Fewer hypoplastic teeth were observed in children attending private schools in London, compared with state-run schools, which strengthened Mellanby’s view that nutrition influenced the occurrence of hypoplastic teeth.

An explanation for the way in which nutrition may cause enamel hypoplasia was presented by Nikiforuk and Fraser in 1981. Their study involved the thorough examination of 56 patients in Toronto, Canada, over a period of 25 years.⁸ Ten patients had hereditary vitamin D dependency rickets, 25 patients had X-linked hypophosphataemia, and 21 patients had hypoparathyroid/pseudohypoparathyroid conditions. Enamel hypoplasia only occurred in children with hypocalcaemia and no relation was found between enamel hypoplasia and plasma phosphorus levels.

The importance of the role of vitamin D and plasma calcium levels in the aetiology and prevention of enamel hypoplasia was illustrated by the results of a randomised clinical trial carried out in Edinburgh some 20 years ago by Cockburn et al (1990). Five hundred and six pregnant women received vitamin D supplements from the twelfth week of pregnancy, and were compared with 633 control pregnant women who did not receive a supplement. Mothers who received the supplement, and their infants, had higher plasma concentrations of calcium than did the control mothers and infants. When the teeth of the infants were examined in their third year, the occurrence of hypoplasia was very much lower in the supplemented group than in the control group.

The appropriate use of fluorides has been the most important method of controlling caries and is likely to be of great benefit for some time to come: these benefits will be discussed later. The disadvantage of fluoride is that excessive ingestion causes developmental defects of enamel. Links between excessive fluoride ingestion and unsightly teeth go back a hundred years, when a series of classical epidemiological studies unravelled the relationship between dental opacities, fluoride ingestion and dental caries. While excessive fluoride ingestion is undoubtedly an important cause of enamel opacities, it is not always possible to be certain that excessive fluoride ingestion is the cause purely from appearance.

The importance of interactions between various causes of defects of enamel formation is now being recognised and I will illustrate this from two of our studies. Surveys carried out during our British Council link with Sri Lanka indicated that dental opacities were more common in Sri Lankan children than in children in north-east England for any given concentration of fluoride in water.¹⁰ Of course, Sri Lanka has a hotter climate than Newcastle, so that more water is drunk in Sri Lanka. Even allowing for this, the prevalence of opacities was higher in Sri Lankan children. Upsets to a child’s metabolism while teeth are forming can interrupt tooth formation and it is known that malnutrition can do just that. We had a chance to examine this issue further in a survey of oral health of Saudi Arabian children.¹¹ The number of teeth affected by opacities was, as expected, strongly related to the concentration of fluoride in drinking water. But, within each of these groups, children classed as malnourished fared worse; they had more opacities than well-nourished children. Research in America 50 years ago established a formula for calculating the optimum concentration of fluoride in drinking water, depending only on climatic temperature. However, these recommendations were based on information obtained from a well-nourished American population and the formula proposed for determining optimum water fluoride concentration may not be directly applicable to the many countries of the world where malnutrition in childhood is all too prevalent. Each country has to decide for itself an optimum fluoride policy based on more information than just climatic temperature and this caution is now included in World Health Organisation (WHO) publications.

Thus, there are many causes of developmental defects of enamel, some of which are related to nutrition. The most important cause of these nutritionally related defects is fluoride and the concentration of fluoride in water is very clearly positively related to the prevalence and severity of enamel defects. Adjusting fluoride concentration in water to the optimum for health, is a clear priority. Nutritional deficiencies also clearly cause defects in enamel formation, probably through a variety of mechanisms. It would seem that calcium plasma level is important, with hypocalcaemia a clear risk factor. Plasma acid-base balance would also appear to be important, since the occurrence of hypoplastic teeth is positively linked to premature birth, asthma and living at a high altitude, but the exact mechanism and its possible link with plasma calcium levels has yet to be established.

Figure 1: Caries experience of 5 year old children (mean DMFT) and 12 year old children (mean DMFT), and the annual per capita consumption of sugar in the UK, between 1948 and 1996. Redrawn from Downer12, with permission of the Editor of the British Dental Journal.

In the UK, dental caries prevalence was low until the 1850s. It then rose in parallel with the increasing importation and consumption of sugar. Recruitment of soldiers for the Boer War was a defining moment. Poor teeth were the most important cause of rejection of volunteers for service at that time; half of all recruits from Scotland were rejected. Surveys of school children between 1906 and 1908 revealed that 90% of 12- year-olds had experienced decay, with an average of four bad teeth per child. The prevalence of dental caries rose to its highest point in the late 1950s and 60s, although in children it fell by 40% and 30% during World War I and II, respectively.

Since the early 1970s, dental caries has declined sharply, and this has been largely due to the widespread use of fluoride. The influences of both sugar and fluoride were illustrated in a recent article by Downer, showing changes in caries experience in children between 1948 and 1996 (Figure 1).¹² This demonstrated a significant fall in caries experience and a positive correlation between sugar and caries over this time period; for 5-year-olds this was 0.6 and for 12-year-olds 0.8.

The dominant influence of sugars and fluoride on the devel-opment of caries was only established in the 1950s. The first half of the 20th century was the age of the discovery of vitamins and it was believed that dental caries was a deficiency disease. Because teeth are highly calcified tissue, much research focused on vitamin D. However; research showing the paramount importance of dietary sugars eclipsed interest in vitamins. Nevertheless, the issue of vitamin D is still relevant as, in our longitudinal study of diet and dental caries in adolescent Northumbrians, we found an inverse relation between dietary vitamin D and caries development.¹³ This was highly statistically significant - but only in boys.

A clinical trial conducted in the late 1940s and early 1950s changed our view of diet and caries. This was a study (unethical by current standards) of dietary supplementation conducted in a mental hospital in Vipeholm, Sweden.¹⁴ Patients were fed high sugar diets and the subsequent development of caries recorded. Although, the study included a vitamin and mineral supplementation phase, the results showed the paramount importance of sugar and, over the next 30 years, a wealth of other studies confirmed this view. Dietary sugar is metabolised by bacteria in the plaque layer on teeth to form acids and these acids dissolve the mineral in our teeth. When enough mineral has been dissolved, a hole develops. The process of dental caries, thus, is very simple.

As the amount of evidence grew, the need to reduce sugar intake became clear. From a public health perspective, targets for consumption had to be set and these would, in turn, determine policy. The crucial report for setting targets for sugar consumption was the report on Dietary Reference Values for the UK, published by the Department of Health in 1991.¹⁵ This set out recommendations for 40 nutrients, including sugar. Importantly, it divided carbohydrates into the desirable and undesirable. It grouped sugars found in milk, fruits and vegetables along with starch in the desirable component, leaving the remaining sugars - the added sugars - as the undesirable component. These sugars - added by the manufacturer, cook or consumer - are better called non-milk extrinsic (NME) sugars. The World Health Organisation calls these sugars ‘free sugars’ and both the Department of Health in London and WHO recommend that there is no nutritional need for these NME or free sugars and that their consumption should provide less than 10% of total food energy. ^15,16

Table 1: Sources of non-milk extrinsic sugars in the diets of Northumbrian adolescents.¹⁸

Importing, refining and selling sugar has been big business in the UK for over 150 years. Sales of sugar amount to about 2.2 million tons per year in the UK. Twenty-five per cent of sugar goes to the confectionery industry and their sales were just under £1 billion in 1999. Another 25% of sugar goes to the soft drinks industry, where sales totalled £7.4 billion in the same year. Not surprisingly, these powerful industrial companies have not taken kindly to the suggestion that we should cut down on eating sugars.

A reduction in sugar consumption in the UK has been Department of Health policy for over 30 years, but pressure from the sugar industry was one reason why the Committee on Medical Aspects of Food Policy created an expert panel to examine the relation between dietary sugars and human disease. The report, published in 1989, stated quite clearly that ‘non-milk extrinsic sugars should be reduced and replaced by staple starchy foods, fresh fruit and vegetables’.¹⁷ This would benefit general and dental health. It was left to the 1991 report, to set the ceiling of 10% of food energy coming from NME sugars.¹⁵ A large number of Department of Health reports since then, have all confirmed that policy. Importantly, the ‘Health of the Nation’, ‘The Scottish Diet’ and ‘Our Healthier Nation’ endorsed the COMA recommendations. They have been endorsed by the British Dental Association, British Medical Association and the British Dietetic Association. Thus, the UK has had clear and consistent broad guidelines of nutritional policy for many years.

What information is there on sugar consumption at the present time in the UK? From our own studies of young adolescent Northumbrians, 76% of total sugars were NME sugars.18 These 90 grams of NME sugars provided 17% of energy - much higher than the 10% recommended ceiling. The sources of these sugars are given in Table 1 - 72% coming from just three sources - confectionery, soft drinks and table sugar. Confectionery was also the second most important source of dietary fat in these children, more important than chips, butter or margarine. Using published data on the diets of American children, we compared the types of foods, which contributed to sugar consumption in American and English adolescents.⁴ Milk and fruit were much more important sources of dietary sugars in American children, while the reverse was true for confectionery and table sugar (Figure 2). Thus, American children got their sugar from desirable sources, in contrast to British children.

The beneficial effect of dietary fluoride has been mentioned already; this is a success story for dentistry. Unlike most other trace elements, which reach us via the soil and plants, the main dietary source of fluoride is water. The inverse relation between water fluoride concentration and caries was established in the 1940s. In this survey the concentration of fluoride in drinking water and the severity of dental caries in adolescents, living in 21 cities in America was documented .19 Children living in some of these cities were deficient in fluoride and, on 25th January 1945, fluoride was added to the water supply of Grand Rapid City, Michigan State, to bring the fluoride concentration in water up to the optimum of 1mgF/litre of water or 1ppm. Caries incidence in children in Grand Rapids fell, as predicted, and water fluoridation became a public health priority for large communities dependent on public water supplies. The proportion of the US population who drink fluoridated water has increased steadily and is presently about 62% - a high proportion of homes that are dependent on a public water supply.

Figure 2: Comparison of the mean daily intake of desirable sources of dietary sugars (milk and fruit) and undesirable sources of dietary sugars (confectionery and table sugar) by American and English adolescent school children.^4,5

About 300 million people worldwide drink fluoridated water. Unfortunately, we have a singularly unimpressive record of implementing water fluoridation in the UK. Only 5.5 million people (about 10% of the population) receive optimally fluoridated water; the major conurbations being the West Midlands and Newcastle areas. There are no schemes operating currently in Scotland.

Salt is an alternative dietary vehicle for fluoride - reaching approximately 100 million people in 12 countries. Fluoridated salt is not presently sold in the UK. The main dietary alternatives in the UK are fluoride dietary supplements (drops or tablets); although effective, their use remains low.

Since the carious process involves the removal of calcium and phosphorus from teeth, attempts have been made to reverse this by adding calcium and/or phosphorus to foods -the results of trials have been disappointing. But there are foods where calcium and phosphorus does seem to confer a caries-inhibitory property. One example is milk. Cow’s milk contains 5% lactose but is considered safe for teeth because it contains much calcium and phosphorus.⁴ Human milk contains more sugar but less protective factors and there are several reports of dental caries in infants who have been breast-fed on demand for many years.

One of the best protective roles of food is saliva stimulation. There have been several studies of dental caries in workers in sugar cane plantations. The results are equally divided between a positive and no relationship. It has been suggested that the high salivary flow induced by chewing the fibrous cane may reduce the harmful effect of the sugar.⁴

There is no better example of the favourable effect of saliva stimulation than chewing gum. At present, over three-quarters of chewing gum sold in the UK is sugar-free. Results of the many trials of the dental effects of chewing gum suggest that (a) sugared gum causes caries compared with no gum, (b) sugar-free gum is much better than sugared gum, and (c) sugar-free gum is better than no gum. This latter finding is interesting as it indicates that chewing sugarless gum positively benefits dental health and prevents dental caries. This positive action is due to the stimulation of salivary flow with its high pH and high concentration of calcium and phosphate.⁴ Our work in Newcastle shows that cheese has a similar caries preventive effect due to its good stimulation of saliva and its high calcium and phosphate content.²⁰

The number of non-sugar sweeteners allowed for use in foods in the UK has grown. The intense sweeteners are noncariogenic, xylitol is also non-cariogenic and the remaining bulk (or caloric) non-sugar sweeteners are virtually non-cariogenic. Not surprisingly, they are valued in preventing dental caries and have been used principally in confectionery, soft drinks and liquid oral medicines. Confectionery sweetened exclusively with non-sugar sweeteners is likely to pass the Swiss-based Toothfriendly test and can then be marketed as ‘safe for teeth’. Such sweets can be found in the UK but the scheme has been most effective in Switzerland where nearly all parents and children know the meaning of the symbol and where a quarter of confectionery is now ‘toothfriendly’.

Progress is slow at substituting non-sugar sweeteners for sugar in liquid oral medicines. At present, about 50% are sugar-free but the percentage could be higher if there was a will from the manufacturers, prescribers, consumers and their parents.²¹ It is inexcusable that some of the most vulnerable children on long-term medication should be at unnecessary risk of a second disease.

Thus, it can be seen that dental caries is preventable, but not yet prevented. Its rise to catastrophic proportions was due to sugar. Its decline over the past 30 years has been due mainly to the use of fluoride; in the UK, very largely in toothpaste. Sugar consumption remains too high and goals set in COMA documents and in The Scottish Diet would benefit general and oral health.

There is another acid-related disease of teeth - dental erosion. This differs from dental caries in several ways. Dental caries occur in areas where dental plaque accumulates. Erosion, though, occurs on the more exposed plaque-free tooth surfaces. It is a surface loss, while dental caries begins as a sub-surface lesion. Tooth surface loss may be due to attrition caused by chewing fibrous gritty foods and abrasion commonly caused by over zealous toothbrushing. While attrition and abrasion may be decreasing in prevalence due to our softer and cleaner diet, and better toothbrushes and toothpastes, there is a strong perception that the occurrence of dental erosion is increasing.

Erosion was included in our national dental surveys for the first time in 1993.² About half of young children had erosion in their primary teeth and, in half of these, the erosion involved the dentine or pulp. For permanent teeth, about one third of children had some erosion. Prevalence was higher in children in Scotland than in any of the other home countries.

The two major causes of dental erosion are dietary and regurgitation of gastric juices (with their very low pH). Perception is that the increase in the occurrence of erosion has paralleled the increase in soft drink consumption in the UK; an eight-fold increase has occurred since the 1950s. Erosion has been of particular concern in children and adolescents, who are the greatest consumers of soft drinks. Restoring appearance is expensive - prevention is a much better option.

The prevalence of frequent regurgitation is unknown, although it has been stated that 2% of people reflux at least once a month. There have been suggestions that the prevalence of anorexia nervosa and bulimia are increasing and now affect about 5% of young women.⁵

As far as dietary habits are concerned, five factors are likely to be relevant. The first two are: the time the drink or food is in contact with the teeth, and the frequency of consumption. Sipping an acid drink slowly over a long period is likely to be more harmful than drinking it quickly. Three drinks a day would be more harmful than one intake a day. The third variable is whether the drink or food was taken as part of a meal or separately as a snack. If taken as part of a meal, it would seem likely that the acids would be removed or neutralised fairly quickly. The fourth variable is related to the third, as it would seem likely that acid drinks taken last thing at night would be more damaging because they are not cleared from the mouth so quickly, as salivary flow is very slow during sleep.

Experimental clinical studies, animal and in vitro studies have investigated the erosiveness of various fruit juices and acids. The results appear to confirm that grapefruit juice is amongst the most erosive of fruit juices. Interpretation of the results of many of these studies is difficult as some authors emphasise the importance of the pH of the drink, while others have emphasised the type of acid (which have different pK) and the titratable acidity. Probably, all are important. Animal experiments have shown that phosphoric acid is very erosive at pH 2.5, but much less so at a pH of 3.3. Citric and malic acids are thought to be especially erosive because of their acidic nature and, at a high pH, their ability to chelate calcium. Carbonic acid is thought be the least erosive acid and carbonated water is not seen as an erosive threat. Historically, iron tonics had a very bad reputation as causing dental erosion as their pH was sometimes as low as pH 1.5. Some liquid oral medicines still have a low pH and their erosive potential should be suspected.

Manufacturers of soft drinks have not been insensitive to the criticism that their products erode teeth. Since teeth consist of calcium and phosphate, it is logical for manufacturers to consider adding these salts to drinks. Many calcium compounds are rather insoluble and calcium affects the taste of the drink. There are, though, calcium compounds, which seem to be acceptable additives and are presently marketed in the UK. The two present front-runners are calcium carbonate (added to Ribena Toothkind) and calcium-citrate-malate, which is more soluble and has less effect on taste.²²

Ribena has always had a bad reputation with dentists and, helped considerably by the media, sufficient pressure was put on the manufacturers to develop a dentally safe version some eight years ago. After about five years development and testing, Ribena Toothkind was launched in April 1998. There was sufficient evidence that it constituted a minimal risk to teeth - caries and erosion - for it to be accredited by the British Dental Association. Since its launch, Ribena Toothkind has substituted for original Ribena, and this must be good for dental health. Other manufacturers are following their lead, and I hope that in 10 or 15 years’ time, the majority of soft drinks will be safe for teeth.

Lord Anson was Commander-in-Chief of a fleet of ships sent, between 1741 and 1744, on an expedition to the south seas. He sailed from Portsmouth with almost 2000 men in six fighting ships and two supply ships. Having circled the globe, they returned to port after four years at sea; of the 2000 men who left Portsmouth, only 200 returned home, most of the rest having died of scurvy.²³ This voyage was only one of many such voyages with disastrous consequences and it was partly instrumental in stimulating Lind’s investigations of scurvy. Lind, who was a native and graduate of Edinburgh, conducted his classical and crucial trial just three years after Anson’s return. Loose teeth and bleeding gums characterise scurvy - a vitamin C deficiency disease - which is not surprising since the periodontal membrane consists of collagen bundles. Tissues surrounding the teeth also consist of epithelium, connective tissue, blood vessels and bone, all of which are known to be affected by deficiencies of various nutrients.

Observations by dental scientist’s fifty years ago recorded more severe periodontal disease in under-developed countries and suggested that nutritional deficiencies were to blame. Norwegian researchers were impressed by the severity of periodontal disease in Sinhalese and Tamils in Sri Lanka and, on return to Norway, examined 200 Norwegian male service recruits, to compare with the data of male Sri Lankan students of the same age.24 Periodontal disease was indeed more severe in the Sri Lankan sample, compared with the Norwegian group, but this could be explained wholly by the higher plaque levels in the Sri Lankan sample. So, from the epidemiological viewpoint, plaque quantity and age were of overriding importance as determinants of periodontal disease.

In spite of the dominant importance of plaque in the aetiology of periodontal disease, much research has been published on the effect of various nutrients on periodontal disease. It would be surprising if nutritional deficiencies did not adversely effect periodontal tissues. There is strong evidence of adverse effects from experiments on rats, guinea pigs and dogs, but much less evidence in humans. Only in the case of scurvy are the periodontal tissues primarily affected.

Scurvy is uncommon and usually confined to elderly people living alone and, occasionally, in infants fed heat-treated cow’s milk. Overall, periodontal tissues will benefit when diet is adequate but dietary supplementation of nutrients above what is commonly accepted as appropriate does not improve periodontal health further. Inadequate levels of folate appear to exist in the gingivae in defined groups of people and delivery of folate to these tissues locally in the mouth (for example in a mouthrinse) can be beneficial.²⁵ Fibrous foods and apples, in particular, have often been viewed as nature’s toothbrush - cleaning away plaque, which is so important in periodontal disease. While several studies have shown that animals eating soft diets develop more plaque and gingivitis than animals fed on a fibrous diet, this has not been demonstrated in humans, except under extreme circumstances. By far the most important way of maintaining periodontal health in humans is regular thorough physical removal of dental plaque with a satisfactory toothbrush.

The World Health Organisation estimated that in 1996 there were over 10 million new cases of cancer and over 7 million people died from cancer. Cancers of the mouth and pharynx are the fifth most common cancer in men and the sixth most common in women. For both genders combined, cancer of the mouth and pharynx ranks fifth, with an estimated 575,000 new cases, accounting for 5.6% of all new cases, in 1996. Survival rates are better for oral cancer than for some other cancers, so that cancer of the mouth and pharynx ranks sixth as a cause of cancer deaths in men and women.²⁶ The age standardised incidence rates in Scotland are almost twice as high as in England and Wales; in the ten years up to 1995, incidence of cancer of the oral cavity rose in Scotland by 43% in males and by 40% in females.²⁷ The rise is particularly evident in younger age-groups and, since incidence is cohort-based, a further rise can be expected in the future.

There have been various estimates of the relative importance that diet plays in the pathogenesis of cancer. In 1981, Doll and Peto (1981) estimated that at least one third of human cancers could be related directly to some dietary component .²⁸ This would mean that some half a million of new cases of cancer each year, in the European community, would have a major dietary basis.

By far the most important dietary influence on the occurrence of oral cancer is alcohol. The evidence is extensive and consistent.26 For example, reports of six retrospective and five prospective cohort studies yielded relative risks of between 1.3 and 8.6. Nineteen case-control studies gave odds ratios of between 1.3 and 7.2. For any given level of alcohol intake there is no clear difference in risk associated with specific types of alcoholic drinks. Although an early study in the USA found the highest relative risk in whisky drinkers, subsequent studies have reported similar risks of cancer of the mouth and pharynx amongst drinkers of different types of drinks - wines, beers, whisky and mixed drinks. There is a synergistic interaction between alcohol consumption and tobacco use. Individuals with high exposure to both alcohol and tobacco have a relative risk of 15.6, compared with those who neither smoke nor drink alcohol. The rise in incidence in Scotland is thought to be due to increased alcohol and tobacco consumption.²⁷

Betel quid chewing has long been linked to oral cancer -studies as long ago as 1933 suggested this. Although there are several and varied ingredients in the betel quid, only tobacco had been clearly related to oral cancer.

Of all the other dietary constituents, vegetables and fruit have consistently been associated with decreased risk of cancer of the mouth and pharynx.²⁶ Thirteen out of fifteen case-control studies reported statistically significant protective associations, for at least one vegetable and/or fruit category, with odds ratios varying between 0.2 and 0.6. Protective associations for vegetable and fruit consumption have remained significant after adjustment for smoking and other forms of tobacco consumption, and high alcohol consumption. Typically, the risk of cancer of the mouth and pharynx is halved in those who eat fruit and vegetables daily, versus less than daily consumption. Evidence is most consistent for carrots, citrus fruits and green vegetables. There is no protective association with consumption of pulses, grains, minerals and vitamins, other than vitamin C, where five case control studies have reported odds ratios of 0.3 to 0.6. While the UK Committee on Medical Aspects of Food and Nutrition Policy recommended increased consumption of fruit and vegetables to decrease the risk of cancer, it recommended the avoidance of betacarotene supplements and cautioned the use of high doses of purified supplements of other micro-nutrients, as they cannot be assumed to be without risk.²⁹

Data available provide no evidence that coffee or tea consumption increases risk of oral cancer. However, maté is commonly drunk as tea in some parts of South America and would appear to be a risk factor for oral cancer; regular drinkers of maté have approximately a two-fold increase in risk.²⁶ This is thought to be a consequence of the high temperature at which this beverage is usually consumed. There is no other convincing evidence that hot drinks increase risk of oral and pharyngeal carcinoma.

Oral cancer is a largely preventable disease. It has been estimated that almost 87% of the incidence of cancer of the mouth and pharynx can potentially be reduced by not smoking, decreasing alcohol intake and increasing consumption of vegetables and fruits. Excluding the non-dietary risk factors of smoking, a diet with a variety of vegetables and fruits and avoidance of alcohol may prevent between 30% and 50% of cases of cancer of the mouth and pharynx.

I have mentioned previously that nutritional deficiencies frequently have oral signs and symptoms. However, there is one disease, which is strongly linked to malnutrition and, where the mouth is the specific target. This is noma (or cancrum oris).30 Noma is most commonly found in Africa where its prevalence is estimated to be 1 to 7 per thousand population. It tends to occur in children aged 3-16 years and, if untreated, mortality is very high. The cause of noma has yet to be determined but it is very strongly linked to malnutrition, with deficiencies of zinc and vitamins A and C being suggested. Acute ulcerative gingivitis may be a precursor and may be linked to foot rot in animals, as close proximity of domestic animals appears to be a risk factor.

Over the millennia, our teeth have become much less important for ensuring adequate nutrition and survival. This does not mean that teeth are no longer of any importance. There are presently two concerns. Firstly, that lack of teeth or painful teeth in young children may cause under-nutrition and poor growth. Young children who have had teeth extracted are lighter in body weight, compared with the rest of the population. Appropriate advice, about the possibility that dental impairment causes under-nutrition in children should be given to parents of such children.

Secondly, older people who have few teeth left find eating difficult. There is ample evidence that loss of teeth and provision of complete dentures reduces the ability to break down foods by chewing. There are three levels at which evidence of the effects of dental impairment on nutrition can be considered.⁴ First, is food choice affected? Second, is nutritional intake affected? And third, is health impaired? There is most information on the first level. Vegetables, fresh fruit, nuts and meat are avoided. As far as nutritional intake is concerned, there have been far too few studies and all these have been of a cross-sectional design, which does not allow conclusions regarding cause and effect. Because of the recognised avoidance of fibrous foods by the dentally impaired, it is surprising that the first study of non-starch polysaccharide (NSP) intake in relation to dentition, was undertaken as late as 1994.³¹ The result of these studies in Newcastle, showed clearly that edentulous adults had a lower NSP intake than dentate adults.

The 1995 National Diet and Nutrition Survey was the first major study of the relation between dental impairment and nutrition.32 After statistical correction for the effects of age, gender, social class and region, the mean daily intakes of NSP, protein, calcium, non-haem iron, niacin, vitamin C, and intrinsic and milk sugars, were all significantly lower in edentulous adults. The same trends were also observed when dental status was expressed as 21 or more, versus 20 or fewer teeth. Intake of NSP was particularly sensitive to the number of occluding pairs of teeth present. Plasma iron concentration was lower in those with poor oral status and edentate subjects had lower plasma levels of retinol, ascorbate and alpha-tocopherol (the anti-oxidents), compared with dentate subjects.

There is little direct evidence that an impaired dentition causes ill health, but much indirect evidence that it is likely to do so. The indirect evidence that impaired dentition affects health is strong.

Choking on food is no joke. About 3000 people die in the USA per year from choking on food; it is the sixth most common cause of accidental death.⁴ In Canada, there are over 300 such deaths per year and, in the UK, over 300 deaths per year are recorded for foreign bodies in the pharynx and larynx -half of these in people over 65 years of age. There is likely to be considerable under-reporting of death by choking on food. There are at least nine publications which emphasise the role of poor dental health on food asphyxiation; a higher proportion of those choking to death on food were edentulous compared with the general population. The sizes of pieces of food responsible for death are frequently very large and usually show little evidence of mastication. Lack of intra-oral sensation in those who wear full dentures has been mentioned by several authors as one reason for people attempting to swallow large, unmasticated pieces of food.

Having reviewed the effects of diet and nutrition on teeth and other oral tissues, the importance of poor nutrition on food choice, adequate nutrition and health, what can be done to improve the situation? Fluorosis is still a global problem, although not in the UK. Caries may be decreasing in many countries but prevalence is increasing in others. In the UK, especially Scotland, it is far from prevented and sections of our society suffer greatly. Erosion seems to be increasing in some countries, including the UK, and the incidence of oral cancer is also increasing. Life expectancy is increasing and it is important to maintain a good dentition into old age to ensure adequate nutrition.

I believe that action needs to be taken at three levels. First, governments must take responsibility for ensuring that policies are directed towards health; failure to ensure optimum water fluoride concentration is an obvious example. In many countries, including the UK, production of sugar is subsidised, while production of staple starchy foods, vegetables and fresh fruit is not. Advertising of high sugar, high fat snack foods and high sugar erosive drinks goes unchecked. Research funding bodies have been slow to support interventional studies aimed at improving health through dietary changes, although they have been more willing to do so in recent years. Interventions need to be positive; for far too long the messages have been negative (‘don’t eat that’ or ‘cut down this’). Recommendations to change diet to improve oral health must be consistent with those to improve general health.

The second level of activity is in the community. Health policies are often organised on a local basis and it is very important that such policies are directed towards improving oral health. A good example is schools, where practices are not always seen as helping to improve oral health. There are, though, some excellent examples of what can be achieved.

The third level of activity is the individual patient. Health care personnel, including dental surgeons, see patients on a one-to-one basis. Too much of this care is for repair and not for prevention, oral care personnel must have an obligation to prevent the disease in the first place, and they can only do this if they understand the principles of preventing the major oral diseases. The purpose of this lecture has been to provide an outline of these principles.

Preventing oral disease is a challenge, but there are several reasons why this challenge can be met. First, we have a much clearer idea of disease processes and the actions needed to prevent oral diseases. Second, we have good information on disease prevalence or incidence in different sectors of our society, and on changes in prevalence and incidence. Third, there is a recognition that inequalities exist and there is a commitment to reduce these inequalities. Fourth, there is a better under-standing of the processes of health education and health promotion, and a strong commitment to bodies, such as HEBS. Fifth, there is a greater willingness to fund dietary intervention studies, which will increase the evidence base for promotional activities. And lastly, there has never been a time where there has been such unanimity between and within health professions on the way forward. These now need to be taken forward so as to prevent so many unnecessary oral diseases.

This article is the text of the King James IV Professorship Lecture given at the College of the Royal College of Surgeons of Edinburgh on 8th June 2001.

Part of the lecture, dealing with nutrition, diet and dental caries, has been published in the British Dental Journal and has been reproduced in the manuscript by kind permission of the Editor of the British Dental Journal.

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Correspondence: A.J. Rugg-Gunn, Dental School, Framlington Place, Newcastle upon Tyne NE2 4BW, U.K.
E-mail: A.J.Rugg-Gunn@ncl.ac.uk

	g	%
Confectionery	30	33
Soft drinks	24	27
Table sugar	11	12
Biscuits and cakes	10	11
Sweet puddings	5	6
Breakfast cereals	5	5
Sugars and preserves	2	2
Other	3	4
TOTAL	90	100