JADA, Vol. 132, December 2001 1643 sign; namely, the reference group may also have experi- enced similar increased risks. We suggest that due consid- eration be given to the hypothe- sis that the only way to reduce the risk of CVD may be via pri- mary prevention—avoiding periodontal disease altogether— which should start very early. Finally, we thank Dr. Hujoel and his colleagues for their ex- cellent and highly insightful work and look forward to fur- ther epidemiologic studies ex- amining the hypothesized links between oral and systemic diseases. Sok-Ja K. Janket, D.M.D., M.S. Dental Service V.A. Medical Center Bedford, Mass. Alison Baird, M.D., Ph.D. National Institute of Neurological Disorders and Stroke National Institutes of Health Bethesda, Md. Sung-Kiang Chuang, D.M.D., M.D. Harvard School of Dental Medicine Boston Judith A. Jones, D.D.S., M.P.H. Boston University Goldman Schools of Dental Medicine and Public Health 1. Danesh J. Coronary heart disease, Helicobacter pylori, dental disease, Chlamydia pneumoniae, and cytomegalovirus: meta-analyses of prospective studies. Am Heart J 1999; 138:S434-S437. 2. Beck J, Garcia R, Heiss G, Vokonas PS, Offenbacher S. Periodontal disease and car- diovascular disease. J Periodontol 1996;67(10 Suppl):1123-37. 3. Hujoel P, Drangsholt M, Spiekerman C, DeRouen T. Examining the link between coro- nary heart disease and the elimination of chronic dental infections. JADA 2001;132(7):883-9. 4. Johansson I, Tidehag P, Lundberg V, Hallmans G. Dental status, diet and cardio- vascular risk factors in middle-aged people in northern Sweden. Community Dent Oral Epidemiol 1994;22(6):431-6. 5. Joshipura KJ, Hu FB, Manson JE, et al. The effect of fruit and vegetable intake on risk for coronary heart disease. Ann Intern Med 2001;134(12):1106-14. 6. Hulley S, Grady D, Bush T, et al. Randomized trial of estrogen plus progestin for secondary prevention of coronary heart disease in post-menopausal women. Heart and Estrogen/progestin Replacement Study (HERS) Research Group. JAMA 1998;280(7):605-13. 7. Campbell LA, Kuo C, Wang S, Jackson L, Grayston JT. Prescription for cardiovascular disease: are antibiotics effective. Washington Public Health 1999;16:5-7. 8. Higuchi ML, Sambiase N, Palomino S, et al. Detection of Mycoplasma pneumoniae and Chlamydia pneumoniae in ruptured atherosclerotic plaques. Braz J Med Biol Res 2000;33(9):1023-6. Authors’ response: Dr. Janket and colleagues agree that the complete and irre- versible elimination of all dental infections does not appear to im- pact CHD risk. Their letter ex- pands upon and provides vari- ous arguments for one possible interpretation of these findings: periodontitis may irreversibly increase CHD risk and, as a re- sult, the prevention of the onset of periodontitis (primary preven- tion) rather than the treatment of established periodontitis (sec- ondary prevention) should be- come the focus of interest. As we indicated in our discus- sion, such a scenario is possible but would require “a rethinking of the causal mechanisms, in- cluding the rationale for sug- gesting treatments for chronic infections.” Currently, all the focus is on the treatment, rather than pri- mary prevention, of chronic in- fections. For instance, the National Institute of Dental and Craniofacial Research has re- cently 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 indi- cates 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 promo- tion of an unhealthy diet. While this is undoubtedly true in com- parison with a normal healthy population, our data do not indi- cate that vitamin A and C in- take, as measured from a 24- hour food frequency questionnaire at baseline, differ between the edentulous and those with periodontitis. Indeed, adjustments for vita- min A and C intake do not ap- preciably affect our estimates of the risk for CHD. In fact, the es- timates shift slightly toward higher relative risks of eden- tulism as compared with peri- odontitis (relative risks of 1.04 compared with 1.02), a result that, if anything, contradicts the idea that dietary factors nega- tively affect the edentulous more than those with periodontitis. We purposely chose to com- pare people who had periodonti- tis with those who were edentu- lous, since these groups are similar with respect to many CHD risk factors, but are dif- ferent in that the edentulous are completely free of dental infections. LETTERS Copyright ©1998-2001 American Dental Association. All rights reserved.