Brian A. Burt, B.D.S., Ph.D., M.P.H.:
Risk is the possibility that an event will occur. The word, of course, is used in everyday language with more or less that meaning, but it has more specific meanings in the worlds of insurance and epidemiology. In epidemiology it is related to probability and to causality, and it is most often used to express the degree of probability that a particular outcome will occur following a human being�s exposure to a particular action or event. There are very few circumstances that constitute a sufficient cause in chronic or infectious disease (a sufficient cause being one where exposure to a specific action or event will probably result in a particular outcome). If there were, it would not be necessary to deal with risk, which essentially deals with varying degrees of necessary cause (a necessary cause being human exposure to an action or event that must always precede a particular outcome). The concept of risk in epidemiological study has also spread to include broader issues, such as risk assessment and risk-benefit analysis. This paper suggests definitions of risk and risk-related terms that can be used by the consensus panel for this conference.
There is general agreement that the term "risk factor" means an action or event that is statistically related in some way to an outcome�smoking, for example, is a risk factor for periodontitis. But beyond that broad generality there is little agreement. There is uncertainty in the literature on whether a risk factor should be truly causal�that is, a necessary link in the etiological chain�or whether it can be only occasionally associated with an outcome.
There is also uncertainty about what strength of association is needed for an action or event to be called a risk factor for a disease, and just how directly it needs to be associated with the outcome. There is also disagreement over whether a risk factor must be immutable, like race or gender, or whether it is something that can be modified�for example, a smoking habit. In the current studies to determine if periodontitis is a risk factor for cardiovascular disease, it is already clear that there is a measure of association between the two factors. However, it is also evident that periodontitis is neither a necessary nor sufficient cause of cardiovascular disease, and it remains to be demonstrated whether periodontitis interacts with other factors in leading to cardiovascular disease, or whether it is causal only in particular circumstances, or whether it is not causal at all but is a marker for other conditions that may be causal�that is, people with periodontitis are likely to exhibit other factors which may be more directly linked with heart disease.
Any branch of science demands specific terminology, where words have precisely the same meaning among researchers who come from a variety of backgrounds, live and work in different parts of the world, and speak different languages. If we think about an enterprise like constructing the orbiting space station, for example, which involves multidisciplinary teams of scientists from different countries, it is clear that the project would quickly degenerate into chaos if there was not total uniformity in the meaning of many complex terms. Even in less demanding scientific projects, a failure to use precise terminology can result in frustration, inefficiency, and ultimately an inability to move our knowledge base forward.
Epidemiology is a relatively new science, and perhaps it is not surprising that there is uncertainty in our use of terms. The literature on measures of risk is replete with terms of uncertain definition, and supposedly standard terms are used in variable ways by different authors. Even the use of a supposedly standard term like "risk factor" is far from uniform. Rarely does an author define how the term is being used, and the evidence that leads to identification of a risk factor is often unclear. The term comes with a cluster of related terms like risk indicator, modifiable risk factor, risk marker, determinant, and demographic risk factor, which are often used more or less interchangeably in the literature. This sort of uncertainty means that the reader has to decide what the author has in mind.
If we turn to the standard dictionaries on epidemiology, we find they are not particularly helpful. In Last�s Dictionary of Epidemiology (Last,1995), a risk factor (a term only in use since the 1960s) is defined as an aspect of personal behavior or lifestyle, exposure to an environmental event, or an inborn or inherited characteristic which on the basis of epidemiological evidence is known to be associated with health-related condition(s) whose prevention is considered important. That is a broad and rather loose definition that leaves unanswered questions about causal role, strength of association, and modifiability. The definition then goes on to list several different meanings that have been ascribed to the term "risk factor":
Last agrees that the term "risk factor" is rather loosely used, and I think we would agree that these definitions still leave important issues unanswered. In an effort to clarify the matter, Beck (1998) offered a definition that was adopted for the World Workshop on Periodontics in 1996:
Risk factor: an environmental, behavioral, or biologic factor confirmed by temporal sequence, usually in longitudinal studies, which if present directly increases the probability of a disease occurring, and if absent or removed reduces the probability. Risk factors are part of the causal chain, or expose the host to the causal chain. Once disease occurs, removal of a risk factor may not result in a cure.This definition is longer than the one offered by Last, but in my view it is much clearer. The key contributions of this definition are (a) the emphasis on a temporal sequence of events preceding the outcome; (b) the unequivocal acceptance that a risk factor is part of a causal chain; and (c) the acceptance that risk factors are involved in the onset of disease but not necessarily in its progression or resolution.
Beck argues convincingly that it must be clearly established that the action or event occurred before the outcome, or before conditions exist that make the outcome likely. This in turn means that longitudinal studies are necessary to demonstrate risk factors. However, there are many situations in biomedicine, and certainly in dentistry, where this has not been done, and indeed where it is unlikely that it will ever be done. In these circumstances, exposure to an event that is associated with an outcome only in cross-sectional data is called a "risk indicator." A risk indicator may be a probable, or putative, risk factor, but the cross-sectional evidence upon which it is based is weaker than longitudinal data. This is because a temporal association usually cannot be specified from cross-sectional data.
If these definitions of the terms "risk factor" and "risk indicator" were used consistently, knowledge would most likely progress more quickly.
References
Beck JD. Risk revisited. Community Dent Oral Epidemiol 1998;26:220�5.Burt BA. Risk factors, risk markers, and risk indicators... [editorial]. Community Dent Oral Epidemiol 1998;26:219.
Last JM, ed. A dictionary of epidemiology. 3rd edition. New York: Oxford University Press, 1995.
Brian A.Burt, B.D.S., Ph.D., M.P.H., and Satishchandra Pai, B.D.S., M.D.S., M.P.H.:
The recognition that sugars have an etiological role in dental caries has been with us for a long time. This relationship, however, may be changing. Per capita consumption of all sugars in the United States has risen over the last 25 years or so, while the incidence of caries in permanent teeth has declined. This changed relationship may be the result of widespread exposure to fluoride. The specific question to be examined in this review is: In the modern age of extensive fluoride exposure, do individuals with a high level of sugar intake, measured either as total amount or high frequency, experience greater caries severity relative to those with a lower level of intake?
Materials and Methods
Our review began with a search of the MEDLINE and EMBASE databases for papers on sugar and dental caries published between January, 1980, and July, 2000. The year 1980 was chosen as a reasonable starting point for the era of populationwide fluoride exposure in the United States. Only reports in English were considered for inclusion in the review. Other specific inclusion and exclusion criteria were applied, and an extensive search expression was developed with the assistance of an experienced librarian.
The initial search produced 809 reports. This set was divided into two halves alphabetically, and a different reader examined each half. The first assessment was based on each paper�s title and abstract, and clearly irrelevant articles were discarded. This reduced the original 809 reports to 134. After those were read, another 65 papers were eliminated because they did not satisfy all inclusion/exclusion criteria. This left 69 papers, including 26 cohort studies, 4 case-control studies, and 39 cross-sectional studies.
Categories for scoring the individual papers were then established. The maximum score was 100, and the scores of the papers ranged from 12 to 79. In order to base the final results on papers of good quality, we included only those that scored 55 or higher, a total of 36. We then rated the risk of sugar-associated caries among the subjects of the papers according to the risk ratio correlation coefficient or beta coefficient given by the authors.
The Results
The two readers were acceptably uniform in their judgments of the papers. The correlations of readers� scores on five randomly-chosen papers was high (Pearson�s r = 0.87), and there was no significant difference in mean scores (p = 0.56).
Table 1 shows the distribution of the reports that found a strong, a moderate, or a weak relation between sugars intake (any measure) and caries experience, and displays these relations by type of study design. By our criteria, only one report showed a strong relation. Nineteen papers found a moderate relationship between sugars intake and caries development, while the remaining 16 found the relationship to be weak-to-none.
Table 1. Distribution of 36 studies showing strong, moderate, and weak relation between sugars intake and dental caries by type of study design.
|
Strong |
Moderate |
Weak |
Total |
|
|
Cohort studies |
1 |
6 |
5 |
12 |
|
Case-control studies |
0 |
1 |
0 |
1 |
|
Cross-sectional studies |
1 |
9 |
13 |
23 |
|
Total |
2 |
16 |
18 |
36 |
Discussion
The predominant design used in the papers was cross-sectional (23 of the 36), even though that was probably the weakest design with which to address the question. A cohort design would be strongest for this question, but such studies are expensive and include a number of inherent problems (e.g., nature of dietary records, definitions of meals and snacks). Of the remaining studies, 12 were cohort studies and only 1 was a case-control study.
Of the 23 cross-sectional studies, 16 studied the permanent dentition, as did 7 of the 12 cohort studies. Eight of those 12 were conducted for periods of 2 years or less, which may hardly be long enough to permit the true relationship to be discerned. Only 2 small-scale studies among the 36 dealt with root caries, and both concluded that a diet which promotes coronal caries also promotes root caries. With an aging population and greater retention of teeth, root caries is likely to grow as a public health issue.
Nearly all of the studies dealt with the relationship between the means of caries status and sugars exposure, rather than distributions. It seems likely that while the reduced risk of sugar consumption in the fluoride age has an overall population benefit, there are still some identifiable subgroups who do not benefit. Further research could focus on these differences.
The findings of our review are relevant to questions 2, 3, and 5 of the six conference questions:
2. What are the best indicators for an increased risk of dental caries?
Persons with high sugar consumption, whether measured in frequency or amount, usually have higher counts of cariogenic bacteria than people who have low consumption. This relationship is not always linear, however, and what constitutes "high" and "low" consumption is unclear; high bacterial counts do not by themselves always relate to a clinical caries outcome. Sugar consumption, however, is likely to be a more powerful indicator of risk of caries infection in persons who do not have regular exposure to fluoride.
3. What are the best methods available for primary prevention of dental caries initiation throughout life?
Where there is good exposure to fluoride, sugar consumption is a moderate-to-mild risk factor for caries in most people. Hence, avoiding consumption of excess sugar is a justifiable part of caries prevention, if not the most crucial aspect.
5. How should clinical decisions regarding prevention and/or treatment be affected by detection methods and risk assessment?
A patient assessed to be at high risk for caries needs to be aware that sugar consumption increases the risk. The clinician can therefore conduct a dietary assessment to identify how sugar consumption can reasonably be curtailed. For a patient assessed to be at low risk of caries, this procedure is probably unnecessary.
In conclusion, our findings are consistent with the view that restriction of sugar consumption still has a role to play in the prevention of caries, but this role is not as strong as it was in the prefluoride era.
Further Research Needs
References
Burt BA, Eklund SA, Morgan KJ, Larkin FE, Quire KE, Brown LO, et al. The effects of sugars intake and frequency of ingestion on dental caries increment in a three-year longitudinal study. J Dent Res 1988;67:1422�9.
Gibson S, Williams S. Dental caries in pre-school children: associations with social class, toothbrushing habit and consumption of sugars and sugar-containing foods. Further analysis of data from the National Diet and Nutrition Survey of children aged 1.5-4.5 years. Caries Res 1999;33:101�13.
Kleemola-Kujala E, Rasanen L. Relationship of oral hygiene and sugar consumption to risk of caries in children. Community Dentistry Oral Epidemiol 1982;10:224�33.
Rugg-Gunn AJ, Hackett AF, Appleton DR, Jenkins GN, Eastoe JE. Relationship between dietary habits and caries increment assessed over two years in 405 English adolescent school children. Arch Oral Biol 1984;29:983�92.
Brian A. Burt, B.D.S., Ph.D., M.P.H., and Satishchandra Pai, B.D.S., M.D.S., M.P.H.:
Low birthweight is a public health issue because it is closely related to infant mortality and a host of infant morbidity conditions. In 1997, 7.5 percent of all live births in the United States were babies of low birthweight (<2500 grams), and 1.4 percent were of very low birthweight (<1500 grams). Risk factors for low birthweight include maternal age (both <17 and >34 years), low socioeconomic status, the mother�s being unmarried, and poor obstetric care during pregnancy. One especially depressing fact is that the proportion of low birthweight babies has remained fairly constant over the last 30 years.
The relationship between low birthweight and dental condition has not received much attention, and most of what has been done looks at enamel defects, such as hypoplasia, in low birthweight children. Little is known about whether low birthweight children are more prone to develop caries in later life, so this review addresses the following question: Do low birthweight children (birthweight <2500 grams) subsequently develop more caries than children with normal-to-high birthweight?
Material and Methods
Our study began with a search of the MEDLINE and EMBASE databases for English-language papers published between January, 1966, and July, 2000. Search terms included low birthweight, normal birthweight, premature birth, maternal nutrition, nutrition in pregnancy, enamel hypoplasia, hypomineralization, and hypomineralized enamel. The search terms were drawn up by an experienced librarian, and the full search expression is available from the authors on request.
The initial search produced a total of 198 reports. The first assessment was made by title and abstract, and clearly irrelevant articles were discarded. This reduced the original 198 reports to 37. These 37 were read in full by two readers. Another 33 papers were then eliminated because they did not satisfy all of our inclusion/exclusion criteria; the few differences between the readers at this point were settled by consensus.
Categories for scoring the quality of individual papers were established by the two readers, with a maximum score of 100 for each category. Table 1 shows the categories.
Table 1. Scoring categories for studies of low birthweight relation to caries
|
Clearly-stated research aims |
12 |
||||||
|
Number of controls |
10 |
||||||
|
Nature of controls |
10 |
||||||
|
Stated inclusion/exclusion criteria for participants |
7 |
||||||
|
Individual birthweights certified |
8 |
||||||
|
Level of caries diagnosed (cavitated, noncavitated) |
6 |
||||||
|
Nature of caries diagnosis (clinical, x-ray, FOTi, etc.) |
7 |
||||||
|
Examiner reliability quantified |
8 |
||||||
|
Confounders accounted for |
12 |
||||||
|
Measure of risk stated |
8 |
||||||
|
Internally valid conclusions |
12 |
||||||
|
Total: |
100 |
||||||
The Results
Only four papers qualified under the criteria applied. These were read by both readers, and the few minor differences were settled by consensus. The scores for the four papers were 61, 60, 49, and 31. None of these papers reported any relationship between low birthweight and caries development.
Discussion
One of the reports involved children who were examined soon after eruption of their primary teeth, while the others involved children between 3 and 5 years of age. All four studies assessed the condition of the primary dentition only. (That is, no study was found that related caries in the permanent dentition to low birthweight.) It should be noted, however, that many of the 37 studies found a relationship between developmental defects of enamel and low birthweight, though that issue was not specifically studied. The literature also seems to assume that developmental enamel defects are more prone to become carious than normal enamel. Low birthweight is clearly a health problem to be prevented as far as possible, and seems to be related to conference questions 2 and 5:
2. What are the best indicators for an increased risk of dental caries?
If low birthweight does turn out to be associated with caries development, the link could either be a directly biological one through hypoplasia and other enamel defects, or it could be because low birthweight is so often a marker for deprived circumstances and all the caries risks that come with it. This review, however, found no evidence that low birthweight in itself is a risk factor for caries.
5. How should clinical decisions regarding prevention and/or treatment be affected by detection methods and risk assessment?
When clinicians are treating a low birthweight child for caries treatment or prevention, the child should be considered at high risk of caries. Even though a direct link has not been established, low birthweight is a marker of social deprivation that often leaves a child at high risk.
Further research could include documenting any link between developmental enamel defects and subsequent caries development, and the role of birth complications, frequently with the use of ventilators and intubation, in the later development of caries. Studies should also be conducted with older children to assess the effect of low birthweight on the permanent dentition.
References
Fearne JM, Bryan EM, Elliman AM, Brook AH, Williams DM. Enamel defects in the primary dentition of children born weighing less than 2000 g. Br Dent J 1990;168:433�7.
Lai PY, Seow WK, Tudehope DI, Rogers Y. Enamel hypoplasia and dental caries in very-low birthweight children: a case-controlled, longitudinal study. Pediatr Dent 1997;19:42�9.
Li Y, Navia JM, Bian JY. Caries experience in deciduous dentition of rural Chinese children 3-5 years old in relation to the presence or absence of enamel hypoplasia. Caries Res 1996;30:8�15.
Peretz B, Kafka I. Baby bottle tooth decay and complications during pregnancy and delivery. Pediatr Dent 1997;19:34�6.