Dr. Janket and colleagues agree that the complete and irreversible elimination of all dental infections does not appear to impact CHD risk. Their letter expands upon and provides various arguments for one possible interpretation of these findings: periodontitis may irreversibly increase CHD risk and, as a result, the prevention of the onset of periodontitis (primary prevention) rather than the treatment of established periodontitis (secondary prevention) should become the focus of interest.
As we indicated in our discussion, such a scenario is possible but would require "a rethinking of the causal mechanisms, including the rationale for suggesting treatments for chronic infections."
Currently, all the focus is on the treatment, rather than primary prevention, of chronic infections. For instance, the National Institute of Dental and Craniofacial Research has recently funded a multicenter pilot trial of periodontal treatment for the secondary prevention of CHD events in patients with cardiovascular disease (NIDCR, grant 1UO1DE013940).
The epidemiological evidence from our study suggests that the findings of this trial might end up being negative, which would indicate either the absence of a causal relationship, or, if Dr. Janket is right, the need for a primary prevention trial, not a secondary prevention trial.
The letter from Dr. Janket also appears to imply that we have hypothesized edentulism to be "totally risk free." This does not represent the content of our article. Instead, our study indicates that the cardiovascular risk for edentulous patients does not appear to be any higher than that for those with periodontal disease.
Their letter also suggests that edentulism may increase the risk of CHD due to the promotion of an unhealthy diet. While this is undoubtedly true in comparison with a normal healthy population, our data do not indicate that vitamin A and C intake, as measured from a 24-hour food frequency questionnaire at baseline, differ between the edentulous and those with periodontitis.
Indeed, adjustments for vitamin A and C intake do not appreciably affect our estimates of the risk for CHD. In fact, the estimates shift slightly toward higher relative risks of edentulism as compared with periodontitis (relative risks of 1.04 compared with 1.02), a result that, if anything, contradicts the idea that dietary factors negatively affect the edentulous more than those with periodontitis.
We purposely chose to compare people who had periodontitis with those who were edentulous, since these groups are similar with respect to many CHD risk factors, but are different in that the edentulous are completely free of dental infections.
This makes these two groups an excellent choice for investigating the hypothesis that current chronic dental infections put one at higher risk of cardiovascular disease. We found no difference in risk between these two groups; this finding provides further evidence that chronic dental infections are not a cause of cardiovascular disease.
Although the hypotheses and interpretations of Dr. Janket and colleagues are interesting and provocative, we do not believe that they alter our main conclusion: based on a well-conducted, nationwide study of thousands of people, the complete, definitive and irreversible elimination of existing dental infections does not prevent coronary heart disease events
