Periodontal pathogens are present in atherosclerotic plaques where, like other infectious microorganisms such as C. pneumoniae, they may play a role in the development and progression of atherosclerosis leading to coronary vascular disease and other clinical sequelae.

Epidemiological studies have implicated periodontal disease (PD) as a risk factor for the development of cardiovascular disease (CVD). These studies addressed the premise that local infection may perturb the levels of systemic inflammatory mediators, thereby promoting mechanisms of atherosclerosis. Levels of inflammatory mediators in the sera of subjects with only PD, only CVD, both diseases, or neither condition were compared. Subjects were assessed for levels of C-reactive protein (CRP), serum amyloid A (SAA), ceruloplasmin, ␣ 1 -acid-glycoprotein (AAG), ␣ 1 -antichymotrypsin (ACT), and the soluble cellular adhesion molecules sICAM-1 and sVCAM by enzyme-linked immunoabsorbent and/or radial immunodiffusion assays. CRP levels in subjects with either condition alone were elevated twofold above subjects with neither disease, whereas a threefold increase was noted in subjects with both diseases (P ‫؍‬ 0.0389). Statistically significant increases in SAA and ACT were noted in subjects with both conditions compared to those with one or neither condition (P ‫؍‬ 0.0162 and 0.0408, respectively). Ceruloplasmin levels were increased in subjects with only CVD (P ‫؍‬ 0.0001). Increases in sVCAM levels were noted in all subjects with CVD (P ‫؍‬ 0.0054). No differences in sICAM levels were noted among subject groups. A trend toward higher levels of AAG was noted in subjects with both conditions and for ACT in subjects with only PD. Immunohistochemical examination of endarterectomy specimens of carotid arteries from subjects with atherosclerosis documented SAA and CRP deposition in association with atheromatous lesions. The data support the hypothesis that localized persistent infection may influence systemic levels of inflammatory mediators. Changes in inflammatory mediator levels potentially impact inflammation-associated atherosclerotic processes.Hypercholesterolemia, lipid metabolism imbalances, hypertension, age, gender, body mass index, diabetes mellitus, homocysteine, stress, and smoking are widely accepted as "classic" risk factors for development of cardiovascular disease (CVD). However, it has also become clear that the contribution of these factors cannot be supported in 25 to 50% of subjects who develop CVD and cerebrovascular disease (39, 53). These observations have intensified initiatives to identify additional risk factors for the development of atherosclerosis and vascular ischemic diseases. Recent evidence indicates that the development of CVD correlates with elevated levels of C-reactive protein (CRP) (25,30,35,45,54,55) and soluble cellular adhesion molecules (CAM) (27,48,56,76) which are produced in response to cellular damage. These observations have led to a reexamination of one of the earliest theories regarding the etiology of atherosclerosis and coronary heart disease (CHD): inflammatory processes which may arise in association with infection (39, 42).In the mid-1800s, Virchow drew attention to the presence of two distinct lesions along arterial vessel walls: the classical "fatty streak" and a second ...

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Approximately half of biopsies of oral conditions that clinically resembled typically DIF-positive vesiculobullous diseases did not yield positive findings on DIF testing. Instead, a wide range of oral diseases can mimic these lesions clinically. With the exception of pemphigus vulgaris, DIF is essential for establishing a definitive diagnosis for known DIF-positive diseases.

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