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J Am Dent Assoc, Vol 132, No 7, 883-889. © 2001 American Dental Association

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	ABSTRACT

TOP ABSTRACT MATERIALS AND METHODS RESULTS DISCUSSION CONCLUSION REFERENCES

 
Background. While it has been suggested that periodontal disease may be associated with coronary heart disease, or CHD, there are no data to suggest that the elimination of chronic dental infections actually lowers the risk of developing chronic CHD. The goal of this study was to determine whether people with a definitive elimination of all potential dental infections—edentulous people, who are at the optimum endpoint of dental infection elimination from a CHD perspective—lower their CHD risk over time when compared with people who have a specific dental infection, periodontitis.

Methods. The authors examined data from a prospective cohort of 4,027 people who participated in the First National Health and Nutrition Examination Survey, or NHANES I, Epidemiologic Follow-up Study. The primary outcome measure was the first CHD event.

Results. During a mean follow-up of 17 years, there were 1,238 CHD events (538 fatal). The confirmed elimination of chronic dental infections did not lead to a decreased risk of experiencing a CHD event (relative risk, 1.02; 95 percent confidence interval, 0.86–1.21). The CHD risk among people with and without chronic dental infections remained constant over time with respect to each other (test for increasing or decreasing trend over time: not significant, ²₁ = 0.48; P = .93).

Conclusions. People who had a complete, definitive and long-term elimination of all potential dental infections through extraction of all teeth did not have lower CHD risk when compared with people with diagnosed periodontitis.

Clinical Implications. Until evidence is found to the contrary, the authors suggest that prevention of CHD should not be used as the basis for recommending treatment to eliminate chronic dental infections.

It has been suggested that periodontal treatments may lower the risk of coronary heart disease, or CHD.^1–4 This recommendation is based on three assumptions. The first assumption is that the small associations between CHD and periodontitis are not spurious.⁵ The second is that the CHD risk associated with periodontitis is reversible. The third is that the currently used treatments for periodontitis can reverse an increased risk of developing CHD. While a number of studies have investigated the plausibility of a causal association between periodontitis and cardiovascular disease,^6–11 there are no data available to suggest that the assumed increased risk of developing CHD associated with periodontitis is reversible, or that periodontal treatments can reverse an assumed increased risk of developing CHD.

The presence of periodontitis may occur coincidentally with, but does not cause, increased cardiovascular risk.

Conducting a prospective trial on the effectiveness of periodontal treatments is difficult owing to large sample sizes that would be required for reliable detection of an impact on CHD. Edentulous people, therefore, may provide a first insight into whether the assumed CHD risk associated with periodontitis is reversible. The extraction of all teeth obviously achieves a definitive, pharmacologically inactive and long-term elimination of all potential dental infections. If, indeed, dental infections have a reversible causal association with CHD, one would expect that people at an optimum therapeutic endpoint would lower their risk of developing CHD when compared with dentate people who have ongoing dental infections (specifically for our study, diagnosed periodontitis). The goal of our study was to evaluate this hypothesis.

	MATERIALS AND METHODS

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Study population. Researchers have reported the details of the design and sampling of the First National Health and Nutrition Examination Survey, or NHANES I, and the NHANES I Epidemiological Follow-up Study , or NHEFS, as it relates to dental studies.^12,13 Briefly, a U.S. population–based probability sample of noninstitutionalized civilians was obtained (excluding Alaska, Hawaii and reservation lands of American Indians). Of 31,973 people contacted, 11,348 completed both the medical examination and the dental examination and were followed up longitudinally in the NHEFS. Four follow-up examinations were completed: one from 1982 through 1984; one in 1986 (only those people who were 55–74 years of age at baseline; n = 3,980); one in 1987; and one in 1992.

Edentulous people, as compared with people who had periodontitis, were more likely to be older, female, less educated and white.

Outcome and exposure definition. We defined a CHD event as one of the following outcomes:

– death with underlying cause of death, coded according to the International Classification of Disease, ninth revision, or ICD-9, as anything from 410 through 414;

– a nonfatal myocardial infarction, as suggested by a hospital stay with a discharge diagnosis code of 410 through 414 according to the ICD-9 Clinical Modification Codes;

– either of two coronary revascularization procedures, ICD-9 Clinical Modification Codes 36.1 (coronary revascularization) or 36.0 (removal of coronary obstruction).

We used the first occurrence of any of these three events (fatality, hospitalization because of CHD or hospitalization because of revascularization) as the event defining CHD.

Based on the Russell Periodontal Index,¹⁴ the NHEFS researchers defined two dental conditions: periodontitis (the presence of Grade 4+ pockets on any of the teeth present, n = 1,857) and edentulism (all teeth missing, n = 2,170). People with periodontitis had a periodontal pocket with attachment loss—that is, not merely a deepened gingival crevice due to swelling in the free gingiva.

Potential confounding variables measured at baseline. Demographic variables included age at baseline, sex, race (classified as white, African-American and other), years of education, poverty index and married state (categorized as ever married vs. never-married) of the examined person. Cardiovascular risk factors evaluated included systolic and diastolic blood pressure, serum cholesterol, diabetes, physical activity, height, weight, daily alcohol consumption, smoking status and history of nervous breakdown. A history of a stroke, heart failure or heart attack was taken as evidence of prior cardiovascular disease. For smoking, both the duration (number of years) and intensity (average number of cigarettes per day) at the baseline examination were derived from interview data collected from 1982 through 1984. Validation studies have indicated that surrogate- and self-response data on cigarette smoking obtained at the 1982–1984 follow-up interview are not remarkably different from those obtained at the baseline interview (1971–1975).^15,16

Statistical methodology. To assess whether people who were edentulous at the baseline interview in the 1970s have since been at lower risk of developing CHD people with periodontitis during the follow-up, we fitted a Cox proportional hazards model with hazard specified by

where x₁ indicates a confirmed elimination of all chronic dental infections, and z₁ through z_n are the confounding variables. The variable t is the time from study entry, and the time t_o is the mean follow-up time. The number of years at risk was censored if the person was alive at last contact, traced alive with or without direct subject contact, or died from a cause other than CHD. The coefficient, ß₁, can be interpreted as the relative risk of developing CHD for edentulous people, when compared with people who had chronic periodontitis at the mean follow-up time. (The terms "relative risk" and "hazard ratio" are used interchangeably.)

Three different approaches for taking into account the sampling design were possible: a model-based analysis assuming the sample was a simple random sample¹⁷; a design-based analysis taking into account the stratification and clustering, but ignoring the sampling weights¹⁸; and a design-based analysis incorporating the clustering, the stratification and the sampling weights.¹⁹ Which analysis is appropriate is a subtle question¹⁸ that depends on a trade-off between efficiency and lack of bias. Since the associations between periodontitis and CHD were small and sensitive to the analytic approach we selected, we presented all three approaches for the hazard ratios so that we could evaluate the robustness of the conclusions. Our analyses included adjustments for the sampling design and weights using statistical software (SUDAAN, Research Triangle Institute).^20,21 We excluded from the primary analyses people who had evidence of prior cardiovascular disease (a report of a prior myocardial infarction, stroke or heart failure or of use of medication for a weak heart). We assessed baseline differences using analysis of variance models for continuous variables and logistic regression models for binary variables.

Dental procedures should not be recommended for the purpose of lowering risk of coronary heart disease.

	RESULTS

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At the baseline examination, people with periodontitis had, on average, 20 teeth with high debris and calculus indexes. Edentulous people, as compared with people who had periodontitis, were more likely to be older, female, less educated and white (Table 1). Furthermore, edentulous people were more likely to be less active and to have diabetes, a higher serum cholesterol level, a higher systolic blood pressure, a lower diastolic blood pressure and a lower alcohol consumption level.

View this table: [in this window] [in a new window]   TABLE 1 BASELINE DEMOGRAPHICS AND CARDIOVASCULAR RISK FACTORS ACCORDING TO DENTAL STATUS.*

 
Dental infection elimination and CHD risk. During the 17 years of follow-up, there were 1,238 CHD events (538 fatal). Unadjusted for sampling design and confounding variables, the data showed that people without dental infections (edentulous people) had 27.1 CHD events per 1,000 person-years, and people with diagnosed periodontitis had 18.3 CHD events per 1,000 person-years. A preliminary comparison of these unadjusted rates indicated that the elimination of dental infection sources was associated with a 50 percent increased risk of experiencing CHD events (relative risk, or RR, = 1.49; 95 percent confidence interval, or CI, 1.33–1.66) (Table 2, page 887). However, since there were substantial differences at baseline between the edentulous cohort and the cohort with periodontitis, it is important to adjust for these confounding variables in any comparison.

View this table: [in this window] [in a new window]   TABLE 2 SUMMARY STATISTICS REGARDING CORONARY HEART DISEASE, OR CHD, INCIDENCE AMONG PEOPLE WITH AND WITHOUT CHRONIC DENTAL INFECTIONS.

 
After results were adjusted for confounders and sampling design, they revealed that people with an absence of dental infections had a risk of experiencing CHD events that was similar to that of people with dental infections (RR,1.02; 95 percent CI, 0.86–1.21). When we adjusted data for the sampling weights, we found that the magnitude of the hazard ratio was 0.89 (95 percent CI, 0.70–1.13). The inclusion of a time-dependent covariate to assess whether the CHD risk among people with an absence of dental infections decreased over time indicated no evidence of such a relationship (test for increasing or decreasing trend over time: NS; ²₁ = 0.48; P = .93). The results regarding fatal CHD events were similar (Table 3, page 887).

View this table: [in this window] [in a new window]   TABLE 3 HAZARD RATIOS FOR CORONARY HEART DISEASE, OR CHD, EVENTS AND FATALITIES ASSOCIATED WITH ELIMINATION OF DENTAL INFECTIONS.

 

	DISCUSSION

TOP ABSTRACT MATERIALS AND METHODS RESULTS DISCUSSION CONCLUSION REFERENCES

 
The findings of this study indicate that people with a complete, definitive and long-term elimination of dental infections—edentulous people—do not have a lower risk of developing CHD than do people who have periodontitis. Other studies have suggested that dental procedures may be associated not only with cardiovascular risks such as bacterial endocarditis²² and perioperative myocardial ischemia owing to anxiety and use of local anesthetics,^23–25 but also with as an increased chance of inducing sepsis when the procedure precedes open-heart surgery.²⁶ Therefore, unless evidence becomes available that the hypothesized CHD-preventive benefits of eliminating dental infections outweigh the known cardiovascular risks of dental treatments, dental procedures should not be recommended for the purpose of lowering CHD risk.

The extraction of teeth is a definitive and long-term therapeutic option to eliminate chronic dental infections; this procedure eliminates all tooth-associated infections and re-establishes the oral cavity’s primary site of bodily defense mechanisms, an intact epithelial barrier.^27,28 Between 1920 and 1940, full-mouth extractions were commonly used to treat the assumed systemic consequences of chronic dental infections. In the absence of controlled evidence that people treated with focal infection elimination did better than untreated people, the focal infection theory was widely adopted by the dental profession,²⁹ but it fell out of favor in the 1950s. Today, in the absence of controlled evidence that people treated for chronic dental infections have better CHD outcomes than people who are not treated, both extractions and other dental treatments are suggested.^1,2,4,30,31

The study of dental extractions as a method of eliminating infection has several advantages. First, by using dental extractions rather than a pharmacological agent to eliminate dental infections, the possibility of nonantibiotic therapeutic effects on CHD risk is eliminated.³² Second, extraction is a permanent cure for chronic dental infections, thereby eliminating the possibility of reinfection^33,34 and the therapeutic challenges of using short-term antibiotic treatments for long-term chronic infections.³⁵ Third, the large sample size of the NHEFS study provided the opportunity to detect moderate-to-small treatment effects that may not be immediately apparent in most other studies.

The low attrition of and detailed information on most potentially confounding variables minimized the potential for bias in our study. Nevertheless, differences in cumulative infection history among the compared groups may have led to biases. Edentulous people may have had a larger past infection exposure that irreversibly elevated the CHD risk. While possible, such scenarios would require a rethinking of the causal mechanisms, including the rationale for suggesting treatments for chronic infections and lowering CHD risk. Intervention studies of other chronic infectious diseases are based on the assumption that the effect of chronic infections on CHD risk is reversible.³³ In our study, we expected to find that the risk of developing CHD among people with no dental infections would decrease over time, while it would increase over time among people with periodontitis. Since we observed neither of these trends, the hypothesized causality of the association between chronic dental infections and fatal CHD needs to be re-examined.

	CONCLUSION

TOP ABSTRACT MATERIALS AND METHODS RESULTS DISCUSSION CONCLUSION REFERENCES

 
Our findings in this study are consistent with the hypothesis that the presence of periodontitis may occur coincidentally with, but does not cause, increased cardiovascular risk. Dental infections such as periodontitis are known to be strongly associated with factors that also elevate cardiovascular risk, such as smoking. Since elimination of dental infections does not necessarily affect these underlying risk factors, the elimination of dental infections may not reduce cardiovascular risk. We found no evidence in this study that the elimination of chronic dental infections decreases a person’s risk of developing CHD. Until controlled evidence is found that treated people have a lower incidence of CHD than nontreated people, we suggest that prevention of CHD should not be used as a basis for recommending dental treatments.

	FOOTNOTES

Dr. Drangsholt is an instructor, Department of Dental Public Health Sciences, School of Dentistry, University of Washington, Seattle, and Department of Oral Medicine, School of Dentistry, University of Washington, Seattle.

Dr. Spiekerman is a research scientist, Department of Dental Public Health Sciences, School of Dentistry, University of Washington, Seattle, and Department of Biostatistics, Cardiovascular Health Research Unit, School of Public Health, University of Washington, Seattle.

Dr. DeRouen is a professor and the associate dean for research, Department of Dental Public Health Sciences, School of Dentistry, University of Washington, Seattle; and a professor, Department of Biostatistics, School of Public Health, University of Washington, Seattle.

This study was supported by National Institutes of Health/Agency for Healthcare Research and Quality grants R29-DE12190 and P30-DE09743.

The NHANES I Epidemiologic Follow-up Study was developed and funded by the National Center for Health Statistics; National Institute on Aging; National Cancer Institute; National Institute of Child Health and Human Development; National Heart, Lung, and Blood Institute; National Institute of Mental Health; National Institute of Diabetes and Digestive and Kidney Diseases; National Institute of Arthritis and Musculoskeletal and Skin Diseases; National Institute of Allergy and Infectious Diseases; National Institute of Neurological and Communicative Disorders and Stroke; Centers for Disease Control and Prevention; and U.S. Department of Agriculture. The field work was conducted by Westat Inc. (contract numbers 233-80-2049 and 282-84-2111).

	REFERENCES

TOP ABSTRACT MATERIALS AND METHODS RESULTS DISCUSSION CONCLUSION REFERENCES

 

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This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by HUJOEL, P.P. Articles by DEROUEN, T.A. Search for Related Content PubMed PubMed Citation Articles by HUJOEL, P.P. Articles by DEROUEN, T.A. Related Collections Infection Control