Does Periodontal Inflammation Produce CAD?
Abstract & Commentary
Comment by Harold L. Karpman, MD, FACC, FACP, Clinical Professor of Medicine, UCLA School of Medicine, and Associate Editor, Internal Medicine Alert.
Synopsis: This study provides evidence of a direct relationship between periodontal microbiology and subclinical atherosclerosis. This relationship exists independent of C-reactive protein.
Source: Desvarieux, M et al. Circulation. 2005;576-582.
Cardiologists had previously thought that high-grade stenoses or complete obstruction were the cause of most acute coronary events but we now know that the majority of acute coronary syndrome (ACS) events occur in coronary arteries whose lumens have usually been narrowed by no more than 50% by atherosclerotic plaquing. Over the past several years it has been clearly demonstrated that inflammation is a critical factor in all aspects of the atherosclerotic coronary artery disease (CAD) process. When present in the coronary arterial wall, inflammation generates the formation of foam cells followed by plaque formation that, over time, may develop into a vulnerable plaque with subsequent fissuring, rupture and thrombosis resulting in any or all manifestations of the ACS. Recently published studies have suggested that patients with ACS often exhibit a significant degree of systemic inflammation and in fact, an emerging body of evidence supports a critical role for the leukocyte in the development of the vulnerable plaque, as well as in the adverse outcomes which often occur following acute myocardial infarctions. It has been suggested that activation of a leukocyte enzyme appears to be an important factor in the initiation and propagation of the inflammatory process in the vulnerable plaque.1-6
Desvarieux and associates in the INVEST study investigated whether or not periodontal infections may predispose patients to the development of subclinical atherosclerosis and/or symptomatic CAD. They collected 4561 sub gingival plaque samples from 657 subjects and quantitatively assessed the samples for 11 known periodontal bacteria and then evaluated each patient for cardiovascular risk factor measurements, a white blood cell count, a C-reactive protein determination and finally they assessed the carotid intima-media thickness (IMT).
They found that the overall periodontal bacterial burden was related to the degree of carotid arterial thickness and that this relationship was specific to the causative bacterial burden and the dominance of etiologic bacteria in the observed microbiological niche. C-reactive protein values were unrelated to the periodontal microbiological status. They concluded that there was evidence of a direct relationship between periodontal microbiology and subclinical atherosclerosis independent of the observed C-reactive protein values.
Comment
Myeloperoxidase (MPO) is an abundant leukocyte enzyme that may serve as a central participant in the initiation and propagation of the inflammatory process in vulnerable coronary arterial plaques thereby promoting instability of the fibrous cap and rendering the plaque more susceptible to rupture.1-6 An elevated MPO level has been demonstrated to be of prognostic value in patients presenting with chest pain and also has been found to be an independent predictor of adverse cardiac outcomes in patients with ACS.1,2 These adverse events are probably due to leukocyte activation, which produces an increased propensity for thrombus formation in the setting of plaque instability. Multiple studies all point toward the emerging role of MPO as a central participant in the inflammatory cascade which leads to acute myocardial infarctions.
Increased carotid IMT measurements have been found to be associated with a 2.3-increased relative risk for nonfatal MI or coronary death.7 Patients with a dominance of oral pathogens causally related to periodontal disease in the INVEST study demonstrated thicker carotid IMT measurements then did noninfected patients even after adjustment for conventional risk factors. The study provided the first direct evidence of a possible role of periodontal bacteria in the development of coronary atherosclerosis and the relationship appears to be independent of the C-reactive protein level. One must recognize that the results of the study may have been confounded by the effects of the hundreds of bacterial species that ordinarily colonize the oral cavity and that were not studied and therefore, additional carefully controlled population studies will have to be performed. If the findings of the INVEST study are confirmed in these subsequent studies, the relationship of periodontal disease to CHD could prove to be of great public health importance because of the possibility that premature coronary atherosclerotic damage could be reduced or perhaps even reversed through selective control of the appropriate pathogenic periodontal bacteria by antibacterial or immunologic means.
References
1. Brennan ML, et al. N Engl J Med. 2003;349: 1595-1604.
2. Baldus S, et al. Circulation. 2003;108:1440-1445.
3. Sugiyama S, et al. Arterioscler Thromb Vasc Biol. 2004;24:1309-1314.
4. Hazen SL. Arterioscler Thromb Vasc Biol. 2004;24: 1143-1146.
5. Vita JA, et al. Circulation. 2004;110:1134-1139.
6. Askari AT, et al. J Exp Med. 2003;197:615-624.
7. Hodis HN, et al. Ann Intern Med. 1998;128:262-269.
This study provides evidence of a direct relationship between periodontal microbiology and subclinical atherosclerosis. This relationship exists independent of C-reactive protein.
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