Floss or Die? This was an expression first coined in 1997 by Dr. Raul Garcia during a conference on periodontal diseases and human health at the University of North Carolina.1 Perhaps we should now extend this to Brush and Floss or Die? based on the interesting findings reported recently in the British Medical Journal,2 and subsequently commented on in Nature Reviews in Cardiology.3 It appears that poor oral hygiene is associated with a significant increased risk of an adverse cardiovascular event (HR 1.7 CI 1.3-2.3).
This study was based on an assessment of the self-reported oral hygiene practices of 11,869 individuals and their cardiovascular events over an average of 8.1 years. In addition, C-reactive protein (CRP) and fibrinogen serum concentrations were measured and found to be elevated in those individuals who rarely or never brushed their teeth. While self-reporting of behaviors and conditions is not always considered reliable, the authors point out that self-reported oral hygiene practices have been associated with clinically confirmed periodontal disease.4 With a study cohort who admits to poor oral hygiene, one cannot help but wonder about the general health beliefs of these individuals and their compliance with general medical advice regarding smoking, hypertension, obesity, and diabetes, all of which are known risk factors for adverse cardiovascular events. Interestingly, even after adjusting for these confounders, poor oral hygiene remained an increased risk factor for a cardiovascular event.
There are two possibilities as to how poor oral hygiene could lead to increased risk of adverse cardiovascular events. On the one hand, it may be as simple as increased bacterial load leading to increased bacteremia, which could explain the presence of periodontal bacteria being identified in atheromas. The presence of periodontal bacteria in the blood stream has been proposed to provide the necessary inflammatory stimulus for atheroma formation. Interestingly, it has been calculated that if poor oral hygiene is present in a one-month period, the relative exposure of bacteremia is 5,376 minutes.5 Within this model, the contributions from random bacteremia, chewing, and brushing are 88%, 9%, and 2%, respectively. Hence, in the presence of poor oral hygiene, tooth brushing contributes very little to the exposure of bacteremia, while random bacteremia and chewing account for 98% of the exposure. Thus, it is not surprising that poor oral hygiene (as measured by a lack of tooth brushing) accounts for a significantly increased risk of cardiovascular disease.
On the other hand, the interaction of poor oral hygiene and adverse cardiovascular events could be related to the well-documented relationship between inflammation and cardiovascular disease. In this concept, inflamed gingival tissues (either gingivitis or periodontitis) associated with poor oral hygiene can act as a reservoir for the cytokines and inflammatory mediators which can enter the bloodstream, add to the systemic inflammatory burden, and may participate in the development of atherosclerotic lesions. In this context, the findings of the de Oliveira et al. study,2 which show that individuals who had poor oral hygiene (as reported by rarely or never brushing their teeth) had elevated serum levels of CRP and fibrinogen, are interesting. These findings lend credence to the concept that there is a significantly increased inflammatory burden in individuals with periodontal disease (gingivitis or periodontitis).
Of course, it may be that the relationship between poor oral hygiene and adverse cardiovascular outcomes exists because of a combination of both bacteremia and local periodontal inflammation. To determine this further, molecular epidemiological and intervention studies are required. Whatever mechanisms are behind these emerging data, which demonstrate a strong (causal?) relationship between periodontal infection, inflammation, and cardiovascular disease, we can be certain that prevention (i.e., before periodontitis develops) is the best form of management. Utilizing such an approach, we will do no harm to our patients by extolling the virtues of efficient oral hygiene practices which will significantly minimize the bacterial load and inflammatory burden arising from the periodontal tissues. Of course, it must be said that should deep pockets be present (i.e., established periodontitis), then no amount of oral hygiene is likely to significantly reduce the infective and inflammatory burden, and interceptive periodontal treatment with on-going supportive periodontal therapy will be required.OC
1. Bader HI. Floss or die: implications for dental professionals. Dent Today 1998;17(7):76-82.
2. de Oliveira C, Watt R, Hamer M. Toothbrushing, inflammation, and risk of cardiovascular disease: results from Scottish Health Survey. BMJ 2010;340:c2451.
3. Genco RJ, Van Dyke TE. Reducing the risk of CVD in patients with periodontitis. Nat Rev Cardiol 2010;7(Sept):1-2.
4. Miller K, Eke PI, Schoua-Glusberg A. Cognitive evaluation of self-report questions for surveillance of periodontitis. J Periodontol 2007;78(7 Suppl):1455-1462.
5. Guntheroth WG. How important are dental procedures as a cause of infective endocarditis? Am J Cardiol 1984;54(7):797-801.