Periodontal diseases are chronic infections affecting the supporting structures of teeth. Several cross-sectional, case-control, and longitudinal studies have reported an increased risk for vascular disease and related clinical events in individuals with periodontal disease. In these studies the risk was independent of other known risk factors, including smoking, diabetes, and the blood lipid profile .
Multiple pathogenic mechanisms likely underlie these observations, including, at least in part, direct infection of the vasculature by oral pathogenic bacteria, and/or generalized inflammation secondary to lipopolysaccharide or other bacterial products that engage host defense mechanisms. Indeed, more recent evidence has indicated that patients with severe periodontal disease have increased serum levels of CRP, IL-1, and IL-6, hyperfibrinogenemia, and moderate leukocytosis compared to unaffected controls .
The findings above have been extended, as a relationship between periodontal disease, tooth loss, and subclinical vascular disease (carotid intima-media thickening or carotid plaque presence) has also been recently reported [3, 4]. In the Oral Infections and Vascular Disease Epidemiology Study (INVEST), the investigators identified that tooth loss, a measure of cumulative periodontal disease, was associated with the prevalence of carotid artery plaque. Among subjects with no to nine missing teeth, 46 percent displayed carotid artery plaque, whereas individuals with 10 or more missing teeth displayed a prevalence of carotid plaque of
60 percent. These statistically significant findings suggested that measures of subclinical atherosclerosis paralleled the severity of periodontal disease in these subjects.
Although periodontal infection is not a cause of atherosclerosis, it may act as a potent modifier of disease, syner-gizing with classical risk factors such as hyperlipidemia, diabetes, or elevated blood pressure. However, some published evidence is not supportive and data from a randomized controlled clinical trial evaluating the effect of periodontal therapy on the risk for vascular disease are not available to date.
The state of microvascular function has been suggested to correlate with frank macrovascular disease. Thus, assessment of flow-mediated dilation may provide a window into vascular inflammation and atherosclerosis. These correlations have been found in subjects with periodontal disease as well; subjects with advanced periodontal disease displayed significantly lower flow-mediated dilation of the brachial artery on ultrasonography compared with age-matched control subjects. These considerations have led to the suggested use of flow-mediated dilation as a surrogate marker for the presence/extent of atherosclerosis. However, the link between such surrogates and definitive clinical events such as myocardial infarctions/death and the response to therapeutic intervention is not yet fully clarified, and conflicting evidence exists.
The development of suitable animal models provides a way to assess these concepts experimentally and dissect the pathways by which periodontal infections are linked to vascular inflammation and atherosclerosis.
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