We absolutely agree with Dr. Hujoel and his colleagues that there are no data available to our knowledge that show that the increased risk due to periodontal disease would reverse itself with subsequent removal of the source of inflammation ("Examining the Link Between Coronary Heart Disease and the Elimination of Chronic Dental Infections," July JADA).
However, we would like to point out several important concepts regarding the possible relationship between periodontal and cardiovascular disease, or CVD.
Research suggests that
- – coronary heart disease, or CHD, takes a decade or more to develop1;
- – the involvement of periodontal disease in the pathogenesis of CHD is related to endothelial injury that is postulated to be at a very early stage of this disease process2;
- – once endothelial damage is inflicted, subsequent removal of the same risk factor may not bring the endothelium to prior-to-injury state.3
Therefore, we suggest that primary prevention may be the only way to reduce the risk. We suggest some additional consideration be given to several statements presented by the authors.
First, while we agree that "the extraction of teeth is a definitive and long-term therapeutic option to eliminate chronic dental infections" may be true, the resulting edentulism may bring in another source of increase in risk: unhealthy eating habits. There are published data indicating that edentulous persons ingest less fruits, vegetables and fiber and more sugar and carbohydrates.4 These dietary factors may increase the risk of CVD.5
Also, the edentulous group might have experienced prior severe periodontal disease as well as dental caries, and either may have caused antecedent endothelial damage. Thus, hypothesizing that the edentulous state is totally risk-free may not be true, as the authors have suggested. On the other hand, this study has substantial merit in documenting that the relationship between periodontal disease and CHD is not reversible on a secondary prevention level.
Similar null effects of secondary prevention have been shown in the relationship of estrogen replacement therapy, which is postulated to be involved in early pathogenesis of CVD.6 Therefore, the authors’ conclusion that "periodontitis may occur coincidentally with, but does not cause, increased cardiovascular risk" may not be valid.
Another point relates to the authors’ assertion that "intervention studies of other chronic infectious diseases are based on the assumption that the effect of chronic infections on CHD risk is reversible."7 This point may not be applicable to periodontal disease. The Campbell study was based on Chlamydia infection, which is thought to have a slightly different mode of involvement in the pathogenesis of CHD. Chlamydia infection seems to be involved in the rupture of artherosclerotic plaque, which may happen at a much later stage than the endothelial damage.8
In conclusion, the authors’ study indicated that removal of risk factors (periodontal disease and caries as the primary indications for extraction) may not decrease the risk of CVD. However, this result should not be extrapolated to the periodontal-CVD relationship because of the bias caused by the study design; namely, the reference group may also have experienced similar increased risks.
We suggest that due consideration be given to the hypothesis that the only way to reduce the risk of CVD may be via primary prevention—avoiding periodontal disease altogether—which should start very early.
Finally, we thank Dr. Hujoel and his colleagues for their excellent and highly insightful work and look forward to further epidemiologic studies examining the hypothesized links between oral and systemic diseases.
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