Commentary
Much of the current periodontal literature seems to be focused on the importance of oral health by demonstrating its impact on systemic health. Although we know that the health of the oral cavity is not a separate component of general health, proving an association is difficult. The challenge is that the mechanism underlying chronic diseases such as cardiovascular disease and PD are not completely understood. Thus, we must rely on observational studies in order to draw inferences about the potential effect of a suspected causative factor on the development or progression of a disease. In designing studies to examine the strength of the relationship between oral and systemic diseases, a number of conditions must be met. These include biological plausibility, temporality, specificity and a dose–response gradient.
Scientists are beginning to piece together some of the pieces of this puzzle. Periodontal pathogens have been found in atherosclerotic plaques. Atherothrombogenic mediators such as C-reactive protein are elevated in periodontal disease. Periodontal disease and CAD share many common risk factors including age, smoking, socio-economic status and glycaemic control. Thus the specificity of the association between the two is not clear cut. There is some evidence of a dose–response gradient. For example, the findings of this meta-analysis suggest the risk of CAD may be related to the number of remaining teeth (tooth loss being the ultimate outcome of untreated PD).
Bahekar and colleagues have produced a high-quality systematic review. It is both methodologically and statistically sound. Only studies that had adjusted for confounding variables known to contribute to CAD were included in the meta-analysis. The more robust statistic of RR (versus OR) was used where appropriate. Unlike previous systematic reviews and meta-analyses, they also analysed cohort, case–control and cross-sectional studies separately. This provides an excellent example of how evidence from lower quality trials can overestimate effect. Nonetheless, the findings reflect those of earlier systematic reviews: that PD may contribute to the risk of CAD. The mechanism underlying the association between periodontal infection and CAD remains unclear.
The authors point out several weaknesses in the current literature. The most glaring is the lack of a standardised protocol to determine PD and CAD. Some studies used self-report, which probably under-reports levels of disease, whereas others included gingivitis and periodontitis, which would overestimate disease prevalence. In reality, these studies are not comparing similar predictor variables. The research community needs to address this issue and develop consensus so that results from future meta-analyses have some weight.
Practice point
This review adds strength to the hypothesis that PD is a risk factor for CAD. Given the high mortality rate of cardiovascular diseases, and the relatively minor morbidity of periodontal therapy, maintenance of periodontal health should be among the recommendations for prevention of heart disease.
