Caries risk prediction--the way of the future.

D ental caries almost never kills anyone but it certainly causes pain and treatment is expensive. Loesche1 has pointed out that in the USA, the annual cost of treat­ ing dental caries was about 10 billion dollars in 1977, an amount that had increased to 22 billion dollars by 1984 and 29 billion dollars by 1988.2 Incredibly, this cost was only for the approximately 50% of people who consulted a dentist. In England, Miller et al? estimated that 5 million days were dis­ turbed by toothache and 1 million nights of sleep were lost, associated with the loss of some 12 million working days each year.4 Prevention of dental caries was promoted by Miller,5 the father of modem cariology. In 1890 he linked oral bacteria to the disease and demonstrated that organic acids fermented from foods by oral bacteria initiated the disease. This concept is still accepted today.2 Miller explained that prevention would require oral hygiene, limiting the consumption of fermentable substances and the intelligent use of antiseptics to control or destroy oral bacteria. Earlier this century Mellanby6,7 postulated that it was the quality of tooth substance that made one less or more suscepti­ ble to caries. This concept fitted well with her research into vitamin deficiency, rickets and quality of diet. She postulated a classification of enamel hypoplasia with varying risks for the development of caries. Mellanby’s belief was on the right track. During the late 1930s and early 1940s, a United States Public Dental Service Officer, Trendley Dean, and colleagues8 used epidemiology to confirm that as the water concentration of fluoride increased so dental caries decreased. Fluoride in the drinking water had been known to be associated with stained and pitted teeth since the work of Black0 and McMay,10 among others. The description of an inverse relationship between caries and fluoride was a significant advance in dental science. Multifocal discoveries are common in science and around the same time, Ockerse,11 a school dentist in South Africa, showed a low prevalence of caries in the north-western Cape, where the fluoride concentration in the water was high. Dean et al.* suggested restoring fluoride to drinking water at a level of 1 ppm F. to reduce caries. At this level the caries rate is low and fluorotic staining of teeth is limited to about 10% of indi­ viduals. In 1947 water fluoridation studies were begun in several American and Canadian cities;12 these continue to this day and have confirmed benefit to the community at low cost. In South Africa, a Commission of Inquiry13 recommended in 1967 that water fluoridation be introduced in this country. Sadly, this has not yet happened. As well as water fluoridation, other preventive measures have been adopted.14 Fluoride has been placed in toothpastes, rinses, gels and tablets. Methods to improve oral hygiene have been introduced as has the sealing, with adhesives, of the fis­ sures of posterior teeth, where most caries usually begins. Microbiological research has progressed since Miller’s time and mutans streptococci have been designated the prime bac­ terial aetiological factor.2 These organisms produce dextrans which help them to cling to teeth and ferment carbohydrate there, just as Miller5 had suggested. An enzyme, dextranase, which broke down dextrans,1516 enjoyed a brief vogue, but has not been widely used because administration is inefficient given the short contact between enzyme and substrate. Diet has been implicated in caries development since the time of Hippocrates who associated the eating of figs with the disease.17 White sugar was labelled as ‘pure white and deadly’18 or as the ‘arch criminal’ of dental caries19 and pressure to reduce sugar intake increased. Walker and Cleaton-Jones20 22