Chapter 4
Periodontal diagnosis
Risk factor assessment
Introduction
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First, it may be possible to identify patients who are at higher risk of future disease before this has become established, allowing the implementation of an appropriate preventative regime. Second, the assessment of a patient’s risk of future disease may affect treatment planning decisions because these may influence likely outcomes of treatment. Third, some, but not all, risk factors may be modifiable by intervention, resulting in a reduced risk of future disease. Finally, a better understanding of how different risk factors may act to cause increased susceptibility to disease in some patients may in the future result in the development of novel treatments aimed at controlling or removing these risk factors.
About risk factors
The terminology used to describe the factors that are associated with increased risk of disease is somewhat confusing and inconsistent. However, in general, the term “risk factor” is used to describe something that is causally related to increased risk of disease, whereas the term “risk marker” is a factor that, although associated with increased risk of disease, is not necessarily causally related. For example, age is a well-recognized marker of disease in that there is an increased prevalence of periodontitis in older people. However, this is not necessarily because getting older increases one’s susceptibility to disease but, rather, because periodontal attachment loss is cumulative, so more people in older age groups are likely to have the disease. Therefore, demonstrating an association between the presence of a factor and increased risk of disease is only the first stage in demonstrating a true causally related risk factor.
An association between two measurements does not necessarily demonstrate that one is causing the other. An association is merely a statistically significant relationship between the two measurements. Associations may be due to one factor causing the increased risk of disease—for example, the presence of plaque being associated with an increased likelihood of developing periodontitis in the future. Second, an association may be the result of the presence of a shared risk factor that results in an increase in both conditions. For example, an association between periodontal disease and risk of cardiovascular disease may be partly explained by the fact that smoking is a recognized causal risk factor for both conditions. Third, some associations may be spurious. Thus, the relationship between two factors may be mathematically associated but the factors may have no real or biological link to each other. There are many classic examples of spurious correlations, many of which are amusing and can be readily found by a quick Internet search.
To demonstrate the causal relationship between the presence of a risk factor and increased risk of disease, a number of other criteria can be applied to test the causal relationship, including the following:
• There should be a longitudinal relationship such that the presence of a risk factor in a prospective study results in the subsequent increased susceptibility to disease development.
• There should be a dose–response relationship; for example, the more someone smokes, the more likely he or she is to develop periodontitis.
• There should be a biologically plausible mechanism to explain the association.
• Removal of the risk factor results in lowering of risk of disease in the future.
The latter criterion is perhaps the most important and most convincing way of demonstrating a causal relationship between a risk factor and increased disease susceptibility.
Another important aspect of understanding risk factors is that their effects can be quantified. It is thus potentially possible to describe the fact that the presence of a risk factor increases the risk of disease by a certain magnitude. For example, current smokers are more than twice as likely to suffer a myocardial infarction than are people who have never smoked. In risk factor studies, the effect of the factor is quantified in terms of relative risk. Thus, a relative risk of 2 signifies a doubling of the overall risk of future disease. In cross-sectional and retrospective studies, this is calculated as an “odds ratio,” which is a statistical approximation to the relative risk of the factor. In epidemiological terms, the importance of a risk factor is determined by (1) the frequency of the presence of the risk factor, (2) the magnitude of the relative risk of the factor, and (3) the overall prevalence of disease.
For example, the importance of smoking as a risk factor in periodontal disease can be shown by the frequency of smoking in the population (e.g., ~25% of the population), the relative risk of smoking in developing periodontal disease (estimates up to approximately five times), and the overall prevalence of periodontitis in the population (e.g., ~15%).
In studies of the main risk factors for periodontal disease, it is not always possible to estimate the magnitude of the risk because of the fact that many risk factors are not simply “present” or “absent” but, rather, may vary in effects according to the size of the factor. For example, as discussed in
Risk factors for periodontal disease
The following are the main risk factors that have been shown to increase susceptibility to periodontitis:
Smoking
It is well established that smoking is one of the most important risk factors for periodontitis. The magnitude of the effects of smoking on periodontitis varies considerably among different studies. In patients who regularly smoke more than 10 cigarettes daily, it has been estimated that the relative risk of periodontitis may be as high as fivefold. The effect of smoking is both time and dose dependent, such that the longer a patient has smoked and the more the patient smokes, which can be estimated in terms of “pack-years,” the greater the risk of periodontitis. It appears that the effects of smoking are largely due to a systemic effect resulting in an impaired inflammatory response, with, for example, reduced neutrophil numbers and function at the inflammatory site. Studies of the direct local effects of smoking on the plaque microflora are equivocal, although some studies have suggested an increased number of pathogenic bacteria present in plaque of smokers. It is interesting to note that although the effects of smoking on periodontitis have been described for many years, until approximately two decades ago it was thought that the main effect of smoking on periodontitis risk was that smokers tended to have poorer oral hygiene. In fact, current studies are unequivocal in demonstrating that smoking is a major risk factor for periodontitis independent of any effects on dental plaque. In addition, as discussed in
The clinical appearance of periodontal disease in smokers is usually characterized by reduced gingival bleeding, and often the gingivae have a relatively pink and uninflamed appearance because of the supp/>
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