Archs oral Bd. Vol. 35, Suppl., pp. IS-7% 1990 Printed in Great Britain. All rights reserved
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OO03-9969/90 $3.00 + 0.00 1990 Pergamon Press plc
1. Epidemiology of caries and periodontal disease
EPIDEMIOLOGY
OF DENTAL G.
CARIES
B. WINTER
Department of Children’s Dentistry, Institute of Dental Surgery, Eastman Dental Hospital, 256 Gray’s Inn Road, London WCIX SLD, England Summary-The most recent epidemiological data on the prevalence of dental caries in children indicate a halting of the increasing levels in many developing countries and a continuing decrease in many highly industrialized countries of the world. However, a further fall in caries levels predicted for 5-yr-old children in the U.K. has not occurred and the decline in caries may have begun to level out. ‘Polarization’ of caries to a minority of high-risk individuals is occurring in the developed world, with 20-29~ of children accounting for more than 50% of the disease. Socio-economic factors are important in determining the proportion of high-risk children in these countries. The multifactorial aetiology of caries allows a number of different interpretations to account for changes in the prevalence of the disease with time, in both the developing and developed countries. These changes are variously ascribed to alterations in dietary habits, especially the consumption of sugar; variations in the patterns of oral hygiene; increased contact with trace elements, especially fluoride, in the environment; changes in the ecology and/or virulence of oral and dental plaque microflora and alterations in the oral protective mechanisms including the immune status. The epidemiological evidence available on the relationship of all these social, environmental and other factors to changes in the prevalence levels of caries does not, however, fully explain all the changes that have
been observed. The claim that caries is no longer a public health problem is premature, as it ignores the still high proportion of individuals with tooth decay throughout the world. Key words: dental caries, epidemiology, aetiological factors.
IZyr-old Sydney children were found in only 12% of subjects (Burton et al., 1984). Evidence from the Child Dental Health Survey in the U.K. in 1983 showed that 60% of all DMFT were found in 25% of this age group (Picton, 1986). Similarly, the National Preventive Demonstration Programme in the U.S.A. showed that 20% of a control group of IO-1 I-yr-old children resident in fluoridated communities accounted for 55% of all new decay in that group (Klein et al., 1985). A considerable shift in the pattern of dental caries is also evident from recent surveys. The National Survey of Oral Health in U.S. schoolchildren in 1986-87 showed that the prevalence of approximal caries had fallen by 54% between 1980 and 1987 and that occlusal caries accounted for almost twothirds of the disease present in 1987 (Johnson, 1988). The proportion of caries experience attributable to occlusal lesions in permanent molars and premolars of Irish schoolchildren in both fluoridated and nonfluoridated communities has recently been shown to vary from 41 to 50% in the three age groups examined (Holland, Welton and O’Mullane, 1986). Socio-economic factors are important in determining the proportion of high caries-risk children in industrialized societies (Winter et al., 1971a; Bedi, 1989). Pre-school children resident in the inner London borough of Camden have been subjected to repeated cross-sectional surveys over over the past 20 yr. The most recent survey in 1986/87 showed an apparent increase in caries in 3-yr-old children
INTRODUCTION
Epidemiological surveys of population groups assessing the prevalence of dental caries are extremely useful tools in determining trends in disease patterns on a nationwide or worldwide basis. For global information, the data bank held by WHO is an invaluable source, available for study. The most recent data on dental caries levels in lZyr-old children in May 1989 (WHO, 1989) clearly indicate the halting of increasing prevalence levels in many developing countries and its reversal in Singapore, Hong Kong and Malaysia. These three are not now typical developing countries, but were in that category at the time their caries levels increased and preventive measures, particularly fluoridation of water, were introduced to combat the trend (Barmes, personal communication). WHO data (Table 1) and those more recently obtained by national surveys in the U.S.A. (Johnson, 1988) (Fig. 1) also show a continuing decrease in caries prevalence levels in many of the highly industrialized countries of the world. At the same time it is evident from epidemiological surveys in these developed countries that there has been ‘polarization’ (Marthaler, 1975) of caries to a minority of the population who retain relatively high levels of the disease (Winter, 1988). In the early years of this decade approximately half the DMFT of Abbreviation:
DMFT, decayed, missing and filled (permanent) teeth. 1s
G. B. WINTER
2s
Table 1. Dental caries levels in 12-yr-old children for countries with available data Number of countries with available data Baseline (1980) 1989 Dental caries levels at 12 yr
Developing (No.) (X)
3 DMF teeth or less More than 3 DMF teeth
53 27
Developed (No.) (%)
66.3 33.7
4 25
13.8 86.2
Developing (No.) (%) 75 41
64.7 35.3
Developed (No.) (%) 15 21
41.7 58.3
Modified from WHO (1989).
compared with those examined in 1980. Seventy-two per cent were observed to be caries free compared to 78% in the earlier study and the children affected by rampant caries had risen from 4 to 10%. These changes in disease patterns in the borough appeared to be related to shifts in socio-economic conditions. The most recent social class data showed a greater proportion of children had come from families with single parents or where the fathers were unemployed. Alterations in socio-economic circumstances were also accompanied by changes in parental behaviour in that the proportion of sweetened comforters given to children increased from 19 to 51% in the 6 yr between the studies (Holt et al., 1988). The important relationship between sweetened comforters and rampant caries in young children is well documented (Winter, Hamilton and James, 1966; Winter, 1980). Despite the considerable improvement of dental health amongst children in the developed world over the past 25 yr there remain a significant minority with relatively high levels of disease. Indeed a further fall in the caries levels in 5-yr-old children in the U.K., predicted from the 1973 and 1983 national surveys, has not occurred and the decline in caries in the youngest age groups may have begun to level out (Downer, 1989; Rugg-Gunn et nl., 1989). Apart from the problem of coronal caries in children, which has attracted most of the attention to date, there is evidence of an increasing prevalence of root surface caries in the adult population. Although related to the increased life span of individuals, root caries seems to be age-associated and not directly due to the ageing processes. It appears to be caused by increasing root surface exposure with age, especially
20 .......1971.1973 (NCHS) 15 I
---
-
1979.1980 (NIDR) 1986.1987 (NIDR)
Age
,..’ ,:’ ,.,’
(Years)
Fig. 1. Age-specific prevalence of dental caries (DMFS) in 3 national surveys in the U.S.A.-NCHS (National Child Health Survey); NIDR (National Institute of Dental Research) (after Johnson, 1988).
that associated with untreated periodontal disease. Altered salivary function associated with chronic illness, drug addiction and irradiation may also contribute to the problem (Walls, 1989). The multifactorial aetiology of caries allows of a number of different interpretations to account for changes in the prevalence of the disease with time, in both the developed and developing countries. These changes are variously ascribed to alterations in dietary habits, especially the consumption of sugar, variations in the patterns of dental hygiene, and increased contact with trace elements, especially fluoride in the environment, whether this be by ingestion or by local action within the mouth. Other factors are changes in the ecology and/or virulence of the oral and dental plaque microflora and alterations in the oral protective mechanisms including the immune status. Epidemiological methods have been used to assess caries prevalence levels, at the same time as assessing the other aspects of the problem in population groups. From these data, statistical comparisons have been drawn and assumptions made on the aetiological importance of each factor. However, it is timely to point out that associated phenomena are not necessarily causally related and that in discussions on the aetiology of dental caries this fact has frequently been forgotten. DIETARY PATTERNS
Without any doubt the most important dietary component contributing to caries risk is fermentable carbohydrate, especially sugar. The presence of sugar around plaque-covered tooth surfaces is essential for more than very limited caries development (RuggGunn and Edgar, 1984). Of all the sugars, sucrose appears to be the most cariogenic (Newbrun, 1967; Winter, 1968). In a mixed diet the part played by one factor is complex and the cariogenicity of one food cannot be predicted with any degree of accuracy. Whilst the increase in caries prevalence in the developing world still appears to be related to the increasing consumption of dietary sugar (Rugg-Gunn, 1989), the observed fall in prevalence levels in a number of industrialized countries has occurred without a concomitant reduction in sugar consumption. A 50% decline of caries in 5-8-yr-old Massachusetts children has been noted over the past 30 yr in areas with and without water fluoridation, despite the fact that there has been an actual increase in the total consumption of caloric sweeteners during this period (De Paola et al., 1982). Similarly, in Ireland, while the consumption of sugar rose from 26 kg/person/yr in 1948 to 44 kg/person/yr in 1984/85 (the highest in any EC member state), the caries levels in 5-yr-old
Epidemiology of dental caries children fell from a DMFT of 5.6 in 1962 prior to water fluoridation, to 1.8 in fluoridated and 3.0 in non-fluoridated areas in 1984, and in 12-yr-olds from DMFT of 4.7 in 1962 to 2.6 (fluoridated) and 3.3 (non-fluoridated) in 1984 (Hobdell and O’Hickey, 1989; O’Mullane, 1989). DENTAL HYGIENE It has been difficult in many studies of children to obtain a significant correlation between the indices for plaque and those for caries (Newman, 1986). There is also a lack of evidence that mechanical cleaning of teeth, particularly by tooth brushing is carried out sufficiently well to prevent caries in susceptible individuals (Addy, 1986). A recent Swedish study involving 4-, 8- and 13-yr-old children analysed a number of variables thought to be associated with caries and showed that the child’s age when its organized dental care had started and its tooth brushing frequency were more significantly correlated to the disease than dietary factors (Stecksen-Blicks, Arvidsson and Holm, 1985). Studies in young children appear to show more consistent correlations between tooth-brushing habits (as determined by parental interview), plaque scores and caries of anterior teeth (Winter et al., 1971b; Sutcliffe, 1977). In a South African study involving 5 groups of pre-school children, 2-yr-old rural black children with consistently high plaque scores had the highest prevalence of caries despite their having consumed a low quantity and frequency of sucrose-containing food (Cleaton-Jones et al., 1984a). A further study of 5-yr-old Indian children resident around Johannesburg, which compared amount and frequency of sucrose consumption and oral hygiene in relation to caries prevalence, found oral hygiene was the dominant variable (Cleaton-Jones et a/., 1984b). TRACE ELEMENTS
Fluoride is the only trace element shown conclusively from long-term epidemiological studies to be associated with reduced caries prevalence. Extensive studies have been undertaken on the relationship of caries to fluoride in the drinking water in areas where the water is naturally or artificially fluoridated. All these studies have confirmed the reduced prevalence of caries at levels above 0.7 parts/lo’ F in drinking water and that this effect persists throughout the life of the individual (Jackson, Murray and Fairpo, 1973; Naylor and Murray, 1989). The precise mode of action of the fluoride ion in achieving this effect is still debatable but epidemiological evidence suggests that the topical effect of the ion in the mouth is of considerable importance (Fejerskov, Thylstrup and Joost, 1981; Hardwick Teasdale and Bloodworth, 1982). This has been confirmed by laboratory studies that have shown the significant effect of the fluoride ion in promoting remineralization of the early carious lesion and concomitant inhibition of plaque acid demineralization of enamel (White, 1988). Although prolonged exposure to dietary fluoride during childhood may promote a generally lower prevalence of caries, this does not imply that susceptible individuals may not have relatively high
3s
levels of disease. Two studies in Northumberland are of interest in this respect. The first showed that despite a reduction of caries prevalence of 58% in 5-yr-olds in Newcastle compared to the control area, there were still 12% of children with toothache and 7% who requried a general anaesthetic for tooth extraction in the fluoridated area (French et al., 1984) The more recent study of 5-yr-old children in the same areas showed that fluoridation reduces but does not eliminate social inequalities in relation to caries, leaving social disadvantage, social background and social class as major factors in determining the caries prevalence for this age group (Carmichael, RuggGunn and Ferrell, 1989). A number of epidemiological studies (Glass, 1981; Kalsbeek, 1982; Thylstrup, Bille and Bruun, 1982; Truin et al., 1981) have highlighted the fact that caries prevalence has fallen substantially, independently of water fluoridation, and in populations which do not receive fluoride in a controlled way. The use of fluoride supplements and toothpastes in these population groups has been suggested as the most likely factor contributing to the reduced caries prevalence (K&rig, 1982). Fluoridated toothpastes have been shown to reduce caries prevalence and incidence in many doubleblind controlled clinical trials. Indeed their almost universal use in industrialized societies has promoted the view that they are a major factor in the reduction of caries prevalence in recent years (Hargreaves et al., 1983; Glass, 1986; Hargreaves, Cleaton-Jones and Burchell, 1989; Downer, 1989; Renson, 1989). The apparent crucial role that fluoride toothpaste is playing in the decreasing prevalence of dental caries needs, however, to be considered with care as there are a number of factors that are inconsistent with this view. These are as follows: (i) The prevalence of caries in young children in the U.K. started to decline in the early 1960s a full decade before fluoride toothpaste became established on the market. (ii) Epidemiological studies of caries in young children in the U.K. have shown similar levels of decay whether or not the children’s teeth are regularly brushed (Holt, Joels and Winter, 1982). (iii) The level of caries in lZyr-old children in West Germany remains high and showed no reduction in the IO-yr period between 1973 and 1983 (WHO, 1989) despite that country’s considerable production of fluoride toothpaste, which is the highest in Europe. West Germany produced 1.37 g/head of population/day of fluoridated toothpaste in 1984 compared to 1.13 g/head/day in the U.K. (Valentine, 1989) (Table 2); indeed the U.K. has shown a considerable reduction of caries prevalence in the period between 1973 and 1983. (iv) From Japan, a highly industrialized country that experienced an increase in caries prevalence later than most developed countries, there is evidence showing that the trend peaked in the latter part of the 1970s and has now started to decrease (Barmes, personal communication). Fluoride toothpaste is estimated to hold only 15% of the Japanese market and a strong environmental lobby inhibits the use of other forms of fluoride except topical applications by dentists (FDI Technical Report No. 24, 1985). The prevalence of caries in 3-yr-old Japanese children
G. B. WINTER
4s Table 2. Toothpaste production in a number of European countries in 1984 Country
Production (g) per head of population/day
W. Germany U.K. Italy France Scandmavia Spain Holland Switzerland Portugal Austria Belgium Yugoslavia Greece Turkey
1.37 1.13 0.72 0.62 0.84 0.40 0.66 1.14 0.43 0.58 0.55 0.26 0.39 0.10
Valentine (1989).
declined from 84.2% in 1975 to 66.7% in 1987 (Ministry of Health and Welfare, Japan, 1989) and in 12-yr-old children from DMFT of 5.9 in 1975 to 4.9 in 1987 (WHO, 1989). ORAL AND PLAQUE
MICROFLORA
There were relatively few epidemiological studies assessing the interrelationship of oral and plaque microflora to caries in the three decades following the identification of Streptococcus mutans in human caries by Clarke in 1924. Those studies that were made suggested the possibility that acid-producing, acid-tolerant streptococci and lactobacilli were both intimately associated with the disease. During this period Lactobacillus acidophilus was the microorganism thought principally responsible for caries (Bunting, 1930) and this led to the lactobacillus count as a measure of caries activity (Hadley, 1933; Diamond, 1950). The demonstration of the essential role of streptococci and lactobacilli in the initiation and progression of dental caries and the concept of the infectious and transmissible nature of the disease derive from a series of elegantly controlled laboratory studies involving experimental animals (Orland et al., 1955; Keyes, 1960; Fitzgerald and Keyes, 1960; Zinner et al., 1965; Fitzgerald, Jordan and Archard, 1966; Gibbons et al., 1966; Krasse, 1966; and Krasse and Carlsson, 1970). These were rapidly supplemented by epidemiological studies in human population groups, which confirmed the cariogenic role of streptococci (Gibbons and Loesche, 1967; Loesche and Henry, 1967; Krasse et al., 1968; Jordan, Englander and Lim, 1969; Schamschula and Barmes, 1970; Schamschula and Charlton, 1971). Several longitudinal studies have since shown that Strep. mutans and lactobacilli are related to the development of caries on the smooth surfaces of enamel (Edwardsson, 1986) and that these microorganisms are the most numerically stable as far as the development of coronal fissure caries is concerned (Burt, Loesche and Eklund, 1985). Epidemiological studies have also considered the interrelationship of streptococci and lactobacilli to other oral and plaque microflora such as actinomyces, veillonella and yeasts, and the effects on the development of caries (Walls, 1989).
The presence of yeasts in saliva has been associated with an increased risk of a high caries increment (Pienihlkkinen, 1987) but actinomyces spp. have been found equally prevalent on carious and sound root surfaces (Bryan, Reynolds and Zambon, 1985 and Ellen, Banting and Fillery, 1985). During the past decade, considerable efforts have been given to developing accurate methods for predicting high caries-risk groups in the population. These have included the development of new and simplified methods for the bacteriological assessment of cariogenie microorganisms, such as the dip-slide tests for the identification of lactobacilli (Dentocult, Orion Diagnostica, Helsinki) and of Strep. mutans (Dentocult S. M., Orion Diagnostica, Helsinki) (Alaluusua et al., 1984). These tests have increased the sensitivity, specificity and predictive values in the assessment of high caries-risk groups (Krasse, 1988). A similar dip-slide method has been developed to identify salivary yeasts (Oricult N ‘, Orion Diagnostica, Helsinki). These screening procedures have indicated that over the past 10 yr the numbers of Strep. mutans per millilitre of saliva indicative of high caries-risk individuals have fallen from 10’ or lo6 per ml to IO5 per ml, a level considered low for the same degree of risk in earlier studies (Krasse, 1988). Such observations suggest changes in one important aspect of oral and plaque ecology that could influence caries levels in population groups. Changes in the virulence of cariogenic microorganisms have also been offered as a reason for differences in caries prevalence levels. The virulence of cariogenic bacteria may be judged by measurement of adherence to tooth surfaces, transportation of sugars and the excretion of acidic fermentation products (Marsh, Keevil and Ellwood, 1984). With respect to cariogenic bacteria there is no evidence presently available to support the view that these values have changed in population groups. ORAL PROTECTIVE
MECHANISMS
The initiation and progression of dental caries are subject to a number of controlling mechanisms in the mouth, which may be subdivided into non-specific salivary factors and immune status. Non-speciJic saiivary factors
The non-specific salivary factors that have been investigated by epidemiological means in relation to caries prevalence are salivary pH, buffer capacity, concentration of urea and ammonia, levels of calcium and phosphate and enzymes such as amylase, lysozyme and lactoperoxidase (Courtis, 1985). While xerostomia associated with congenital absence, disease or irradiation of salivary glands is known to be associated with increased caries risk (Silverstone et al., 1981), the other non-specific salivary factors have shown conflicting results when assessed against caries prevalence. The introduction of a simple calorimetric method (Dentobuff, Orion Diagnostica, Helsinki) for screening the buffer capacity of saliva (Frostell, 1980) has awakened interest in this particular factor for predicting high caries risk. As a sole test for caries activity the correlation proved weak, but taken with other microbiological tests it has been shown to increase the
Epidemiology of dental caries predictive capability (Pienihlkkinen, 1987). Salivary enzymes have not demonstrated specific activity against cariogenic bacteria, but may influence the ecological balance of oral flora by discriminating against transient organisms in the mouth (Newbrun, 1983) and by enhancing the antimicrobial effect of secretory IgA (Tenovuo et al., 1982). Immune
status
Several epidemiological studies have investigated the relationship between immunoglobulins and antibodies to Strep. mutans in serum and saliva and related these factors to caries experience (Edgar, 1989). Other studies have also assessed the caries levels in patients with immunodeficiencies and compared these with normal matched controls (Kilian and Bratthall, 1989). While significant correlations have been observed between serum and salivary antibodies to Strep. mutans, there is no conclusive evidence that these antibodies can influence dental caries activity in man (Krasse, Emilson and Gahnberg, 1987). This statement is even more relevant when consideration is given to other cariogenic microorganisms such as lactobacilli. Despite all the research undertaken into oral protective mechanisms over the past 30 years there is little evidence to suggest that the rise or fall in the prevalence of caries can be accounted for by changes in oral protective mechanisms directed against cariogenie microflora. CONCLUSIONS
The claim that dental caries is no longer a public health problem is premature; Newbrun (1989) is correct in suggesting that it ignores the still high proportion of children with the disease. It also ignores the increasing prevalence of root surface caries in the adult population. There remain numerous high-risk population groups in the world, both in the developed and developing countries (Konig, 1982). Fallacious suggestions about the imminent eradication of an infectious bacterial disease have been made in the past. Such claims were made for gonorrhoea after the introduction of penicillin therapy (King, 1958). While the increased prevalence of caries in the developing countries appears to follow the pattern of increased sugar consumption with reasonable reliability, the cause of the decreased caries prevalence in many industrialized countries is more obscure. A widely held view is that fluoride in toothpastes, rinses and community water supplies provides the best possible single association with caries reduction (Glass, 1982). This concept is increasingly difficult to sustain and is not supported by all the presently available evidence. Further research is required into the precise mechanism controlling caries prevalence levels in population groups. The outcome of these investigations should determine more effective methods of prevention in the future. REFERENCES
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Krasse B., Jordan H. V., Edwardsson S., Svensson I. and Trell L. (1968) The occurrence of certain “caries inducing” streptococci in human dental plaque material. Archs oral Biol. 13, 911-918. Krasse B., Emilson C-G. and Gahnberg L. (1987) An anticaries vaccine: report on the status of research. Curies Res. 21, 255-276. Loesche W. J. and Henry C. A. (1967) Intracellular microbial polysaccharide production and dental caries in a Guatemalan indian village. Archs oral Biol. 12, 189-194. Marsh P. D., Keevil C. W. and Ellwood D. C. (1984) Relationship of bioenergetic processes to the pathogenic properties of oral bacteria. J. dent. Res. 63 (3) 40-406. Marthaler T. (1975) Selective intensivprophylaxe zur weitgehenden verhiintung von zahnkaries, gingivitis und parodontitis beim schulkind. Schweiz. Mschr. Zuhnheilk. 85, 1227-1243.
Ministry of Health and Welfare, Japan (1989) Caries prevalence rate in Japanese children. In Report on Survey of Denral Disease. Medical Affairs Bureau, Tokyo. Naylor M. N. and Murray J. J. (1989) Fluorides and dental caries. In The Prevention of Dental Disease (Edited by Murray J. J.) 2nd edn, pp. 115-199. Oxford University Press, Oxford. Newbrun E. (1967) Sucrose, the arch criminal of dental caries. Odont. Rev. 18, 373-386. Newbrun E. (1983) Current concepts in caries etiology. In Curiology, 2nd edn, p. 29. Williams & Wilkins, Baltimore. Newbrun E. (1989) Guest editorial: Uses and abuses of the news release/press conference. J. denf. Res. 67, 1442-1443.
Newman H. N. (1986) The relation between plaque and dental caries. JI R. Sot. Med. 79 (Suppl. 14), I-5. O’Mullane D. (1989) Fluoride-its role in caries prevention. Good Dietary Practice News 1, 2. Orland F. J., Blayney J. R., Harrison R. W., Reyniers J. A., Trexler P. C., Ervin R. F., Gordon H. A. and Wagner M. (1955) Experimental caries in germ free rats innoculated with enterococci. J. Am. dent. Ass. 50. 2599272. Picton D. C. A. (1986) Basis for the nse of topical and systemic fluorides in caries prevention. JI R. Sot. Med. 79 (Suppl. 14) 18-21. Pienihiikkinen K. (1987) Caries prediction through combined use of incipient caries lesions, salivary buffering capacity, lactobacilli and yeasts. Communify Dept. oral Epidemiol. 15, 325-328.
Renson C. E. (1989) Global changes in caries prevalence and dental manpower requirements: 2. The reasons underlying the changes in prevalence. Dent. Update 16, 345-351. Rugg-Gunn A. J. (1989) Diet and dental caries. In Prevention of Dental Disease (Edited by Murray J. J.) 2nd edn, pp. 9-11. Oxford University Press, Oxford. Rugg-Gunn A. J. and Edgar W. M. (1984) Sugar and dental caries: A review of the evidence. Community dent. Hlth 1, 85-92.
Rugg-Gunn A. J., Carmichael C. L., Ferrell R. S. and Furness J. A. (1989) Caries levels in five year olds in Newcastle, U.K., in 1976, 1981 and 1987 after 18 years’ fluoridation. Curies Res. 23, 101 (Abstr.). Schamschula R. G. and Barmes D. E. (1970) A study of the streptococcal flora of plaque in caries free and caries active primitive peoples. Aust. dent. J. 15, 377-382.
of dental caries Schamschula R. G. and Charlton G. (1971) A study of caries aetiology in New South Wales schoolchildren. Aust. dent. J. 16, 77-82. Silverstone L. M., Johnson N. W., Hardie J. M. and Williams R. A. D. (1981) The Microbiology of dental caries. In Denial Caries Aetiology, Pathology and Prevenfion, p. 61-62. Macmillan, London. Stecksen-Blicks C., Arvidsson S. and Holm A.-K. (1985) Dental health, dental care, and dietary habits in children in different parts of Sweden. Acta odont. stand. 43,59-67. Sutcliffe P. (1977) Caries experience and oral cleanliness of 3 and 4 year old children from deprived and non-deprived areas in Edinburgh, Scotland. Communify Dem. oral Epidemiol. 5, 2 13-2 19.
Tenovuo J., Moldoveanu Z., Mestecky J., Pruitt K. M. and Mansson-Rahemtulla B. (1982) Interaction of specific and innate factors of immunity: IgA enhances the antimicrobial effect of the lactoperoxidase system against Streptococcus mutans. J. Immun. 128, 726-73 1. Thylstrup A., Bille J. and Bruun C. (1982) Caries prevalence in Danish children living in areas with low and optimal levels of natural water fluoride. Caries Res. 413-420. Truin C. J., Plasschaert A. .I. M., Konig K. G. and Vogels A. L. M. (1981) Dental caries in five, seven, nine and 11 year old school-children during a nine year dental health campaign in The Hague. Community Dent. oral Epidemiol. 9, 55-60.
Valentine W. E. (1989) Toothpaste market in Europemajor trends. Grace toothpaste seminar 1989(W. R. Grace Ltd), Camogli, Italy.
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Walls A. W. G. (1989) Prevention in the ageing dentition. In The Prevention of Dental Disease (Edited by Murray J. J.) 2nd edn, pp. 303-312. Oxford University Press, Oxford. White D. J. (1988) Reactivity of fluoride dentifrices with artificial caries. Caries Res. 22, 27-36. WHO (1989) Dental caries levels at 12 years, pp. l-19. World Health Organisation, Geneva. Winter G. B. (1968) Sucrose and cariogenesis-A review. Br. dent. J. 124, 407-411. Winter G. B. (1988) Prediction of high caries risk-diet, hygiene and medication. Ini. dent. i 38, 227-230. Winter G. B. (1980) Problems involved with the use of comforters. Ik. d&t. J. 30, 28-38. Winter G. B., Hamilton M. C. and James P. M. C. (1966) Role of the comforter as an aetiological factor in rampant caries of the deciduous dentition. Archs Dis. Child. 41. 207-212.
Winter G. B., Rule D. C., Mailer G. P., James P. M. C. and Gordon P. H. (197la) The prevalence of dental caries in me-school children aged 1 to 4 years. Br. dent. J. 130, 271-277. Winter G. B., Rule D. C., Mailer G. P., James P. M. C. and Gordon P. H. (1971b) The prevalence of dental caries in pre-school children aged I to 4 years. Br. dent. J. 130, 434-436. Zinner D. D., Jablon J. M., Aran A. P. and Saslaw M. S. (1965) Experimental caries induced in animals by Streptococci of human origin. Proc. Sot. exp. Biol. Med. 118, 766-770.
Copyright 0
OO03-9969/90 $3.00 + 0.00 1990 Pergamon Press plc
1. Epidemiology of caries and periodontal disease
EPIDEMIOLOGY
OF DENTAL G.
CARIES
B. WINTER
Department of Children’s Dentistry, Institute of Dental Surgery, Eastman Dental Hospital, 256 Gray’s Inn Road, London WCIX SLD, England Summary-The most recent epidemiological data on the prevalence of dental caries in children indicate a halting of the increasing levels in many developing countries and a continuing decrease in many highly industrialized countries of the world. However, a further fall in caries levels predicted for 5-yr-old children in the U.K. has not occurred and the decline in caries may have begun to level out. ‘Polarization’ of caries to a minority of high-risk individuals is occurring in the developed world, with 20-29~ of children accounting for more than 50% of the disease. Socio-economic factors are important in determining the proportion of high-risk children in these countries. The multifactorial aetiology of caries allows a number of different interpretations to account for changes in the prevalence of the disease with time, in both the developing and developed countries. These changes are variously ascribed to alterations in dietary habits, especially the consumption of sugar; variations in the patterns of oral hygiene; increased contact with trace elements, especially fluoride, in the environment; changes in the ecology and/or virulence of oral and dental plaque microflora and alterations in the oral protective mechanisms including the immune status. The epidemiological evidence available on the relationship of all these social, environmental and other factors to changes in the prevalence levels of caries does not, however, fully explain all the changes that have
been observed. The claim that caries is no longer a public health problem is premature, as it ignores the still high proportion of individuals with tooth decay throughout the world. Key words: dental caries, epidemiology, aetiological factors.
IZyr-old Sydney children were found in only 12% of subjects (Burton et al., 1984). Evidence from the Child Dental Health Survey in the U.K. in 1983 showed that 60% of all DMFT were found in 25% of this age group (Picton, 1986). Similarly, the National Preventive Demonstration Programme in the U.S.A. showed that 20% of a control group of IO-1 I-yr-old children resident in fluoridated communities accounted for 55% of all new decay in that group (Klein et al., 1985). A considerable shift in the pattern of dental caries is also evident from recent surveys. The National Survey of Oral Health in U.S. schoolchildren in 1986-87 showed that the prevalence of approximal caries had fallen by 54% between 1980 and 1987 and that occlusal caries accounted for almost twothirds of the disease present in 1987 (Johnson, 1988). The proportion of caries experience attributable to occlusal lesions in permanent molars and premolars of Irish schoolchildren in both fluoridated and nonfluoridated communities has recently been shown to vary from 41 to 50% in the three age groups examined (Holland, Welton and O’Mullane, 1986). Socio-economic factors are important in determining the proportion of high caries-risk children in industrialized societies (Winter et al., 1971a; Bedi, 1989). Pre-school children resident in the inner London borough of Camden have been subjected to repeated cross-sectional surveys over over the past 20 yr. The most recent survey in 1986/87 showed an apparent increase in caries in 3-yr-old children
INTRODUCTION
Epidemiological surveys of population groups assessing the prevalence of dental caries are extremely useful tools in determining trends in disease patterns on a nationwide or worldwide basis. For global information, the data bank held by WHO is an invaluable source, available for study. The most recent data on dental caries levels in lZyr-old children in May 1989 (WHO, 1989) clearly indicate the halting of increasing prevalence levels in many developing countries and its reversal in Singapore, Hong Kong and Malaysia. These three are not now typical developing countries, but were in that category at the time their caries levels increased and preventive measures, particularly fluoridation of water, were introduced to combat the trend (Barmes, personal communication). WHO data (Table 1) and those more recently obtained by national surveys in the U.S.A. (Johnson, 1988) (Fig. 1) also show a continuing decrease in caries prevalence levels in many of the highly industrialized countries of the world. At the same time it is evident from epidemiological surveys in these developed countries that there has been ‘polarization’ (Marthaler, 1975) of caries to a minority of the population who retain relatively high levels of the disease (Winter, 1988). In the early years of this decade approximately half the DMFT of Abbreviation:
DMFT, decayed, missing and filled (permanent) teeth. 1s
G. B. WINTER
2s
Table 1. Dental caries levels in 12-yr-old children for countries with available data Number of countries with available data Baseline (1980) 1989 Dental caries levels at 12 yr
Developing (No.) (X)
3 DMF teeth or less More than 3 DMF teeth
53 27
Developed (No.) (%)
66.3 33.7
4 25
13.8 86.2
Developing (No.) (%) 75 41
64.7 35.3
Developed (No.) (%) 15 21
41.7 58.3
Modified from WHO (1989).
compared with those examined in 1980. Seventy-two per cent were observed to be caries free compared to 78% in the earlier study and the children affected by rampant caries had risen from 4 to 10%. These changes in disease patterns in the borough appeared to be related to shifts in socio-economic conditions. The most recent social class data showed a greater proportion of children had come from families with single parents or where the fathers were unemployed. Alterations in socio-economic circumstances were also accompanied by changes in parental behaviour in that the proportion of sweetened comforters given to children increased from 19 to 51% in the 6 yr between the studies (Holt et al., 1988). The important relationship between sweetened comforters and rampant caries in young children is well documented (Winter, Hamilton and James, 1966; Winter, 1980). Despite the considerable improvement of dental health amongst children in the developed world over the past 25 yr there remain a significant minority with relatively high levels of disease. Indeed a further fall in the caries levels in 5-yr-old children in the U.K., predicted from the 1973 and 1983 national surveys, has not occurred and the decline in caries in the youngest age groups may have begun to level out (Downer, 1989; Rugg-Gunn et nl., 1989). Apart from the problem of coronal caries in children, which has attracted most of the attention to date, there is evidence of an increasing prevalence of root surface caries in the adult population. Although related to the increased life span of individuals, root caries seems to be age-associated and not directly due to the ageing processes. It appears to be caused by increasing root surface exposure with age, especially
20 .......1971.1973 (NCHS) 15 I
---
-
1979.1980 (NIDR) 1986.1987 (NIDR)
Age
,..’ ,:’ ,.,’
(Years)
Fig. 1. Age-specific prevalence of dental caries (DMFS) in 3 national surveys in the U.S.A.-NCHS (National Child Health Survey); NIDR (National Institute of Dental Research) (after Johnson, 1988).
that associated with untreated periodontal disease. Altered salivary function associated with chronic illness, drug addiction and irradiation may also contribute to the problem (Walls, 1989). The multifactorial aetiology of caries allows of a number of different interpretations to account for changes in the prevalence of the disease with time, in both the developed and developing countries. These changes are variously ascribed to alterations in dietary habits, especially the consumption of sugar, variations in the patterns of dental hygiene, and increased contact with trace elements, especially fluoride in the environment, whether this be by ingestion or by local action within the mouth. Other factors are changes in the ecology and/or virulence of the oral and dental plaque microflora and alterations in the oral protective mechanisms including the immune status. Epidemiological methods have been used to assess caries prevalence levels, at the same time as assessing the other aspects of the problem in population groups. From these data, statistical comparisons have been drawn and assumptions made on the aetiological importance of each factor. However, it is timely to point out that associated phenomena are not necessarily causally related and that in discussions on the aetiology of dental caries this fact has frequently been forgotten. DIETARY PATTERNS
Without any doubt the most important dietary component contributing to caries risk is fermentable carbohydrate, especially sugar. The presence of sugar around plaque-covered tooth surfaces is essential for more than very limited caries development (RuggGunn and Edgar, 1984). Of all the sugars, sucrose appears to be the most cariogenic (Newbrun, 1967; Winter, 1968). In a mixed diet the part played by one factor is complex and the cariogenicity of one food cannot be predicted with any degree of accuracy. Whilst the increase in caries prevalence in the developing world still appears to be related to the increasing consumption of dietary sugar (Rugg-Gunn, 1989), the observed fall in prevalence levels in a number of industrialized countries has occurred without a concomitant reduction in sugar consumption. A 50% decline of caries in 5-8-yr-old Massachusetts children has been noted over the past 30 yr in areas with and without water fluoridation, despite the fact that there has been an actual increase in the total consumption of caloric sweeteners during this period (De Paola et al., 1982). Similarly, in Ireland, while the consumption of sugar rose from 26 kg/person/yr in 1948 to 44 kg/person/yr in 1984/85 (the highest in any EC member state), the caries levels in 5-yr-old
Epidemiology of dental caries children fell from a DMFT of 5.6 in 1962 prior to water fluoridation, to 1.8 in fluoridated and 3.0 in non-fluoridated areas in 1984, and in 12-yr-olds from DMFT of 4.7 in 1962 to 2.6 (fluoridated) and 3.3 (non-fluoridated) in 1984 (Hobdell and O’Hickey, 1989; O’Mullane, 1989). DENTAL HYGIENE It has been difficult in many studies of children to obtain a significant correlation between the indices for plaque and those for caries (Newman, 1986). There is also a lack of evidence that mechanical cleaning of teeth, particularly by tooth brushing is carried out sufficiently well to prevent caries in susceptible individuals (Addy, 1986). A recent Swedish study involving 4-, 8- and 13-yr-old children analysed a number of variables thought to be associated with caries and showed that the child’s age when its organized dental care had started and its tooth brushing frequency were more significantly correlated to the disease than dietary factors (Stecksen-Blicks, Arvidsson and Holm, 1985). Studies in young children appear to show more consistent correlations between tooth-brushing habits (as determined by parental interview), plaque scores and caries of anterior teeth (Winter et al., 1971b; Sutcliffe, 1977). In a South African study involving 5 groups of pre-school children, 2-yr-old rural black children with consistently high plaque scores had the highest prevalence of caries despite their having consumed a low quantity and frequency of sucrose-containing food (Cleaton-Jones et al., 1984a). A further study of 5-yr-old Indian children resident around Johannesburg, which compared amount and frequency of sucrose consumption and oral hygiene in relation to caries prevalence, found oral hygiene was the dominant variable (Cleaton-Jones et a/., 1984b). TRACE ELEMENTS
Fluoride is the only trace element shown conclusively from long-term epidemiological studies to be associated with reduced caries prevalence. Extensive studies have been undertaken on the relationship of caries to fluoride in the drinking water in areas where the water is naturally or artificially fluoridated. All these studies have confirmed the reduced prevalence of caries at levels above 0.7 parts/lo’ F in drinking water and that this effect persists throughout the life of the individual (Jackson, Murray and Fairpo, 1973; Naylor and Murray, 1989). The precise mode of action of the fluoride ion in achieving this effect is still debatable but epidemiological evidence suggests that the topical effect of the ion in the mouth is of considerable importance (Fejerskov, Thylstrup and Joost, 1981; Hardwick Teasdale and Bloodworth, 1982). This has been confirmed by laboratory studies that have shown the significant effect of the fluoride ion in promoting remineralization of the early carious lesion and concomitant inhibition of plaque acid demineralization of enamel (White, 1988). Although prolonged exposure to dietary fluoride during childhood may promote a generally lower prevalence of caries, this does not imply that susceptible individuals may not have relatively high
3s
levels of disease. Two studies in Northumberland are of interest in this respect. The first showed that despite a reduction of caries prevalence of 58% in 5-yr-olds in Newcastle compared to the control area, there were still 12% of children with toothache and 7% who requried a general anaesthetic for tooth extraction in the fluoridated area (French et al., 1984) The more recent study of 5-yr-old children in the same areas showed that fluoridation reduces but does not eliminate social inequalities in relation to caries, leaving social disadvantage, social background and social class as major factors in determining the caries prevalence for this age group (Carmichael, RuggGunn and Ferrell, 1989). A number of epidemiological studies (Glass, 1981; Kalsbeek, 1982; Thylstrup, Bille and Bruun, 1982; Truin et al., 1981) have highlighted the fact that caries prevalence has fallen substantially, independently of water fluoridation, and in populations which do not receive fluoride in a controlled way. The use of fluoride supplements and toothpastes in these population groups has been suggested as the most likely factor contributing to the reduced caries prevalence (K&rig, 1982). Fluoridated toothpastes have been shown to reduce caries prevalence and incidence in many doubleblind controlled clinical trials. Indeed their almost universal use in industrialized societies has promoted the view that they are a major factor in the reduction of caries prevalence in recent years (Hargreaves et al., 1983; Glass, 1986; Hargreaves, Cleaton-Jones and Burchell, 1989; Downer, 1989; Renson, 1989). The apparent crucial role that fluoride toothpaste is playing in the decreasing prevalence of dental caries needs, however, to be considered with care as there are a number of factors that are inconsistent with this view. These are as follows: (i) The prevalence of caries in young children in the U.K. started to decline in the early 1960s a full decade before fluoride toothpaste became established on the market. (ii) Epidemiological studies of caries in young children in the U.K. have shown similar levels of decay whether or not the children’s teeth are regularly brushed (Holt, Joels and Winter, 1982). (iii) The level of caries in lZyr-old children in West Germany remains high and showed no reduction in the IO-yr period between 1973 and 1983 (WHO, 1989) despite that country’s considerable production of fluoride toothpaste, which is the highest in Europe. West Germany produced 1.37 g/head of population/day of fluoridated toothpaste in 1984 compared to 1.13 g/head/day in the U.K. (Valentine, 1989) (Table 2); indeed the U.K. has shown a considerable reduction of caries prevalence in the period between 1973 and 1983. (iv) From Japan, a highly industrialized country that experienced an increase in caries prevalence later than most developed countries, there is evidence showing that the trend peaked in the latter part of the 1970s and has now started to decrease (Barmes, personal communication). Fluoride toothpaste is estimated to hold only 15% of the Japanese market and a strong environmental lobby inhibits the use of other forms of fluoride except topical applications by dentists (FDI Technical Report No. 24, 1985). The prevalence of caries in 3-yr-old Japanese children
G. B. WINTER
4s Table 2. Toothpaste production in a number of European countries in 1984 Country
Production (g) per head of population/day
W. Germany U.K. Italy France Scandmavia Spain Holland Switzerland Portugal Austria Belgium Yugoslavia Greece Turkey
1.37 1.13 0.72 0.62 0.84 0.40 0.66 1.14 0.43 0.58 0.55 0.26 0.39 0.10
Valentine (1989).
declined from 84.2% in 1975 to 66.7% in 1987 (Ministry of Health and Welfare, Japan, 1989) and in 12-yr-old children from DMFT of 5.9 in 1975 to 4.9 in 1987 (WHO, 1989). ORAL AND PLAQUE
MICROFLORA
There were relatively few epidemiological studies assessing the interrelationship of oral and plaque microflora to caries in the three decades following the identification of Streptococcus mutans in human caries by Clarke in 1924. Those studies that were made suggested the possibility that acid-producing, acid-tolerant streptococci and lactobacilli were both intimately associated with the disease. During this period Lactobacillus acidophilus was the microorganism thought principally responsible for caries (Bunting, 1930) and this led to the lactobacillus count as a measure of caries activity (Hadley, 1933; Diamond, 1950). The demonstration of the essential role of streptococci and lactobacilli in the initiation and progression of dental caries and the concept of the infectious and transmissible nature of the disease derive from a series of elegantly controlled laboratory studies involving experimental animals (Orland et al., 1955; Keyes, 1960; Fitzgerald and Keyes, 1960; Zinner et al., 1965; Fitzgerald, Jordan and Archard, 1966; Gibbons et al., 1966; Krasse, 1966; and Krasse and Carlsson, 1970). These were rapidly supplemented by epidemiological studies in human population groups, which confirmed the cariogenic role of streptococci (Gibbons and Loesche, 1967; Loesche and Henry, 1967; Krasse et al., 1968; Jordan, Englander and Lim, 1969; Schamschula and Barmes, 1970; Schamschula and Charlton, 1971). Several longitudinal studies have since shown that Strep. mutans and lactobacilli are related to the development of caries on the smooth surfaces of enamel (Edwardsson, 1986) and that these microorganisms are the most numerically stable as far as the development of coronal fissure caries is concerned (Burt, Loesche and Eklund, 1985). Epidemiological studies have also considered the interrelationship of streptococci and lactobacilli to other oral and plaque microflora such as actinomyces, veillonella and yeasts, and the effects on the development of caries (Walls, 1989).
The presence of yeasts in saliva has been associated with an increased risk of a high caries increment (Pienihlkkinen, 1987) but actinomyces spp. have been found equally prevalent on carious and sound root surfaces (Bryan, Reynolds and Zambon, 1985 and Ellen, Banting and Fillery, 1985). During the past decade, considerable efforts have been given to developing accurate methods for predicting high caries-risk groups in the population. These have included the development of new and simplified methods for the bacteriological assessment of cariogenie microorganisms, such as the dip-slide tests for the identification of lactobacilli (Dentocult, Orion Diagnostica, Helsinki) and of Strep. mutans (Dentocult S. M., Orion Diagnostica, Helsinki) (Alaluusua et al., 1984). These tests have increased the sensitivity, specificity and predictive values in the assessment of high caries-risk groups (Krasse, 1988). A similar dip-slide method has been developed to identify salivary yeasts (Oricult N ‘, Orion Diagnostica, Helsinki). These screening procedures have indicated that over the past 10 yr the numbers of Strep. mutans per millilitre of saliva indicative of high caries-risk individuals have fallen from 10’ or lo6 per ml to IO5 per ml, a level considered low for the same degree of risk in earlier studies (Krasse, 1988). Such observations suggest changes in one important aspect of oral and plaque ecology that could influence caries levels in population groups. Changes in the virulence of cariogenic microorganisms have also been offered as a reason for differences in caries prevalence levels. The virulence of cariogenic bacteria may be judged by measurement of adherence to tooth surfaces, transportation of sugars and the excretion of acidic fermentation products (Marsh, Keevil and Ellwood, 1984). With respect to cariogenic bacteria there is no evidence presently available to support the view that these values have changed in population groups. ORAL PROTECTIVE
MECHANISMS
The initiation and progression of dental caries are subject to a number of controlling mechanisms in the mouth, which may be subdivided into non-specific salivary factors and immune status. Non-speciJic saiivary factors
The non-specific salivary factors that have been investigated by epidemiological means in relation to caries prevalence are salivary pH, buffer capacity, concentration of urea and ammonia, levels of calcium and phosphate and enzymes such as amylase, lysozyme and lactoperoxidase (Courtis, 1985). While xerostomia associated with congenital absence, disease or irradiation of salivary glands is known to be associated with increased caries risk (Silverstone et al., 1981), the other non-specific salivary factors have shown conflicting results when assessed against caries prevalence. The introduction of a simple calorimetric method (Dentobuff, Orion Diagnostica, Helsinki) for screening the buffer capacity of saliva (Frostell, 1980) has awakened interest in this particular factor for predicting high caries risk. As a sole test for caries activity the correlation proved weak, but taken with other microbiological tests it has been shown to increase the
Epidemiology of dental caries predictive capability (Pienihlkkinen, 1987). Salivary enzymes have not demonstrated specific activity against cariogenic bacteria, but may influence the ecological balance of oral flora by discriminating against transient organisms in the mouth (Newbrun, 1983) and by enhancing the antimicrobial effect of secretory IgA (Tenovuo et al., 1982). Immune
status
Several epidemiological studies have investigated the relationship between immunoglobulins and antibodies to Strep. mutans in serum and saliva and related these factors to caries experience (Edgar, 1989). Other studies have also assessed the caries levels in patients with immunodeficiencies and compared these with normal matched controls (Kilian and Bratthall, 1989). While significant correlations have been observed between serum and salivary antibodies to Strep. mutans, there is no conclusive evidence that these antibodies can influence dental caries activity in man (Krasse, Emilson and Gahnberg, 1987). This statement is even more relevant when consideration is given to other cariogenic microorganisms such as lactobacilli. Despite all the research undertaken into oral protective mechanisms over the past 30 years there is little evidence to suggest that the rise or fall in the prevalence of caries can be accounted for by changes in oral protective mechanisms directed against cariogenie microflora. CONCLUSIONS
The claim that dental caries is no longer a public health problem is premature; Newbrun (1989) is correct in suggesting that it ignores the still high proportion of children with the disease. It also ignores the increasing prevalence of root surface caries in the adult population. There remain numerous high-risk population groups in the world, both in the developed and developing countries (Konig, 1982). Fallacious suggestions about the imminent eradication of an infectious bacterial disease have been made in the past. Such claims were made for gonorrhoea after the introduction of penicillin therapy (King, 1958). While the increased prevalence of caries in the developing countries appears to follow the pattern of increased sugar consumption with reasonable reliability, the cause of the decreased caries prevalence in many industrialized countries is more obscure. A widely held view is that fluoride in toothpastes, rinses and community water supplies provides the best possible single association with caries reduction (Glass, 1982). This concept is increasingly difficult to sustain and is not supported by all the presently available evidence. Further research is required into the precise mechanism controlling caries prevalence levels in population groups. The outcome of these investigations should determine more effective methods of prevention in the future. REFERENCES
Addy M. (1986) Plaque control as a scientific basis for the prevention of dental caries. Jl R. SW. Med. 79 (Suppl. 14). 610. A”B35supp -B
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Alaluusua S., Savolainen J., Tuompo H. and Griinroos L. (1984) Slide scoring method for estimation of Streptococcus mutans levels in saliva. Stand. J. dent. Res. 92, 127-133.
Bedi R. (1989) Ethnic indicators of dental health for young Asian school children resident in areas of multiple deprivation. Br. dent. J. 166, 331-334. Bryan A. R., Reynolds H. S. and Zambon J. J. (1985) Prevalence of Actinomyces species in human root surface caries. J. dent. Rex 64 (Spec. B.S.), 192 (Abstr. 162). Bunting R. W. (1930) Certain considerations in the problem of dental caries. Dent. Cosmos 72, 399-407. Burt B, A.,, Loesche W. J. and Eklund S. A. (1985) Stability of selected plaque species and their relationship to caries in a child population over 2 years. Caries Res. 19, 193-200.
Burton J. B., Rob M. I. Craig G. G. and Lawson J. S. (1984) Changes in the caries experience of I2 year old Sydney school children between 1963 and 1982. Med. J. Aust. 140, 4055407. Carmichael C. L., Rugg-Gunn A. J. and Ferrell R. S. (1989) The relationship between fluoridation. social class and caries experience in 5 year old children in Newcastle and Northumberland in 1987. Er. dent. J. 167, 57-61. Clarke J. K. (1924) On the bacterial factor in the aetiology of dental caries. Br. J. exp. Path. 5, 141-147. Cleaton-Jones P. E., Richardson B. D., Winter G. B., Sinwell R. E., Rantsho J. M. and Jodaikin A. (1984a) Dental caries and sucrose intake in five South African pre-school groups. Community Dent. oral Epidemiol. 12, 381-385.
Cleaton-Jones P. E., Richardson B. D., Sinwel R., Rantsho J. and Granath L. (1984b) Dental caries, sucrose intake and oral hygiene in 5 year old South African Indian children. Caries Res. 18, 472-477. Courtis C. (1985) Salivary lactobacillus counts. Dentocult and Dentobuff tests in a group of children. MSc Report, University of London. De Paola P. F., Soparkar P. M., Tavares M.. Allukian M. Jr and PeFerson H. (1982) A dental survey of Massachusetts school children. J. dent. Res. 61, 1356-1360.
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