Steven Borzak, MD
Chen Z-Y, Chiang C-H, Huang C-C, et al. The association of tooth scaling and decreased cardiovascular
disease: A nationwide population-based study. Am J Med. 2012;125:568-575.
The association between vascular inflammation and vascular events is strong. Inflamed vascular plaque has unstable characteristics and increases the likelihood of an event mediated by a culprit lesion.1 Numerous circulating mediators or markers of inflammation, particularly high-sensitivity C-reactive protein (hs-CRP), have proven valuable for identifying increased risk for vascular events. However, the precise mechanisms by which inflammation and atherosclerotic events are mediated, especially
in the long term, remain controversial and incompletely understood.2
The search for a microorganism responsible for vascular events is still under way. A variety of lines of evidence have linked oral inflammation and/or organisms, which may reside in inflamed oral tissue, with vascular events. One hypothesis suggests that inflammatory mediators of chronic oral infection may themselves cause vascular inflammation.
Another hypothesis suggests organisms that may be present in inflamed periodontal tissue, such as Chlamydia pneumoniae, may trigger vascular inflammation
or infection, and thus be an etiologic agent in the pathogenesis of vascular plaque instability.3 Perhaps the most definitive test of the hypothesis that oral infections can lead to vascular events would be to direct antibiotics specifically toward potentially culpable agents in a large, randomized trial. A series of such trials has found no benefit for azithromycin, gatifloxacin, or roxithromycin for secondary prevention of vascular events in tens of thousands of patients in 8 large trials.3 Although some concerns about study design always remain, the hope that antimicrobial treatment can prevent vascular events remains dim.
However, mechanical treatment of periodontal disease would be expected to reduce the burden of oral pathogens and diminish local inflammation. A recent small study conducted in India showed that in a consecutive series of patients, oral treatment that decreased gingivitis was associated with a lower level of hs-CRP at follow-up.4 A larger, randomized study in North America of 308 subjects randomized to periodontal care or routine care did not show significant reductions in hs-CRP, but nearly half of the routine-care group received oral care off-protocol. When reanalyzed to compare subjects who did or did not receive care irrespective of randomization, hs-CRP was found to be lower in the group receiving treatment.5 Thus, oral care may have a potential role in mediating systemic inflammation, and possibly influence vascular inflammation.
Chen et al’s6 well-conducted cohort study further investigates the intriguing idea that treatment of periodontal disease may be related to vascular events. Using a national claims registry in Taiwan, the authors enrolled approximately 10,900 matched pairs of adults who had and who had not undergone dental scaling (total sample size, 21,876 subjects). These subjects were then observed for 7 years to determine if a myocardial infarction (MI), stroke, or cardiovascular event had occurred. Subjects were identified in a national claims database that was universal for both medical and dental coverage nationwide. Although administrative diagnoses were confirmed in work cited by the authors previously, such databases inherently have limited insight into clinical events when compared with clinical databases.7
Their subjects were propensitymatched, which led to as comparable a set of patients as can reasonably be achieved in a cohort study. The average age of the subjects was 61 years, with about a third having hypertension; onesixth having diabetes, hypercholesterolemia, or prior coronary artery disease (but not prior MI); and just over 1 in
20 having chronic kidney disease or arrhythmia.
The group that underwent scaling had a lower incidence of MI, stroke, and cardiovascular events (Table). In a Cox proportional hazards model that accounted for baseline variables, the adjusted hazard ratio (HR) for MI was 0.69 (95% confidence interval [CI], 0.57-0.85), 0.85 for stroke (95% CI, 0.78-0.93), and 0.84 for any vascular event (95% CI, 0.77- 0.91). The association between dental hygiene and vascular events was further strengthened when a dose-response relationship was demonstrated. Subjects with infrequent scaling had fewer events than those who had no dental care, but had more events than subjects who had scaling at least once every 2 years. These findings would seem to suggest that poor oral hygiene, with the likelihood of higher prevalence or severity of periodontal disease in the unscaled cohort, is associated with vascular events.
1. Libby P, Ridker PM, Hansson GK; for the Leducq Transatlantic Network on Atherothrombosis. Inflammation in atherosclerosis: from pathology to practice. J Am Coll Cardiol. 2009;54:2129-2138.
2. Libby P, Ridker PM, Hansson GK. Progress and challenges in translating the biology of atherosclerosis. Nature. 2011;473:317-325. 3. Anderson JL. Infection, antibiotics, and atherothrombosis—end of the road or new beginnings? N Engl J Med. 2005;352:1706-1709.
4. Rastogi P, Singhal R, Sethi A, Agarwal A, Singh VK, Sethi R. Assessment of the effect of periodontal treatment in patients with coronary artery disease: A pilot survey. J Cardiovasc Dis Res. 2012;3:124-127.
5. Offenbacher S, Beck JD, Moss K, et al. Results from the Periodontitis And Vascular Events (PAVE) Study: A pilot, multicentered, randomized, controlled trial to study effects of periodontal therapy in a secondary prevention model of cardiovascular disease. J Periodontol. 2009;80:190-201.
6. Chen Z-Y, Chiang C-H, Huang C-C, et al. The association of tooth scaling and decreased cardiovascular disease: a nationwide population-based study. Am J Med. 2012;125:568-575.
7. Grams ME, Plantinga LC, Hedgeman E, et al. Validation of CKD and related conditions in existing data sets: a systematic review. Am J Kidney Dis. 2011;57:44-54.
Oral Care and Cardiovascular Health
Interpretation of associations derived from cohort studies, even when using propensity matching, always neglects important and relevant variables that are unmeasured.
A key characteristic in the present study is the likelihood that subjects who did get dental care were more attentive to their health issues and needs than those who did not
go to the dentist. These dentist-visiting subjects may have been more likely to exercise, take preventive aspirin, pursue a healthier lifestyle and diet, or be less disease-prone. Socioeconomic status including household income is likely different and potentially higher in the scaled group, even though universal dental care is offered to the entire population of Taiwan through national coverage. Further, clinical variables that were measured in the study, such as hypertension and diabetes, were considered dichotomous and could not discriminate between long-standing or severe comorbid disease or milder chronic and coexistent conditions. Thus, while provocative and suggestive of an association between dental hygiene, the limitations of a cohort study such as the present one means that the association cannot be construed as causation, and it would be inappropriate to recommend dental scaling as a means to prevent vascular events. Of course, routine dental care has value to prevent tooth decay, gum disease, and tooth loss.
What has the present study accomplished? For one, the relationship between the mouth and the coronary arteries does remain alive, albeit still opaque. Further, the authors’ findings do strengthen the hypothesis that mechanical oral care may be a preventive target that is more attractive than antibiotics, and deserves consideration in a large randomized trial. Although the present study did not consider untoward effects, the safety and wisdom of routine oral care for the maintenance of the teeth and gums is established as safe and effective with no concern for risk. Regular dental care is prudent, even though uncertainty remains as to its contribution to vascular protection.
About the Author
Steven Borzak, MD, is in private practice at the Florida Cardiology Group in Lake Worth, FL. He is Adjunct Associate Professor at the University of Miami Miller School of Medicine and Affiliate Associate Professor of Clinical Biomedical Science at the Charles E. Schmidt College of Medicine of the Florida Atlantic University. Dr Borzak received his MD from the University of Illinois College of Medicine in Chicago and was Resident and Chief Resident at the Michael Reese Hospital in Chicago. His Research/Clinical Fellowship in Cardiology was at the Brigham & Women’s Hospital and Harvard Medical School in Boston, MA.