Periodontal bacterial invasion and infection: contribution to atherosclerotic pathology

Abstract

Objective The objective of this review was to perform a systematic evaluation of the literature reporting current scientific evidence for periodontal bacteria as contributors to atherosclerosis. Methods Literature from epidemiological, clinical and experimental studies concerning periodontal bacteria and atherosclerosis were reviewed. Gathered data were categorized into seven “proofs” of evidence that periodontal bacteria: 1) disseminate from the oral cavity and reach systemic vascular tissues; 2) can be found in the affected tissues; 3) live within the affected site; 4) invade affected cell types in vitro; 5) induce atherosclerosis in animal models of disease; 6) non‐invasive mutants of periodontal bacteria cause significantly reduced pathology in vitro and in vivo; and 7) periodontal isolates from human atheromas can cause disease in animal models of infection. Results Substantial evidence for proofs 1 to 6 was found. However, proof 7 has not yet been fulfilled. Conclusions Despite the lack of evidence that periodontal bacteria obtained from human atheromas can cause atherosclerosis in animal models of infection, attainment of proofs 1 to 6 provides support that periodontal pathogens can contribute to atherosclerosis.

Periodontal Disease and its Association with Angiographically Verified Coronary Artery Disease

“…Procjenjuje se da je u 2008. godini od kardiovaskularnih bolesti (CVD) umrlo 17,3 milijuna ljudi, što je 30 posto svih smrtnih slučajeva u svijetu, a od toga broja (17,3 mi-lijuna) oko 7,3 milijuna bolovalo je od koronarne bolesti srca (CHD) (7). Mogući utjecaj parodontitisa na koronarnu arterijsku bolest jest prodor bakterija i njihovih produkata iz usne šupljine u krvotok (8,9). Posljedica je aktivacija upalne reakcije domaćina koja pridonosi nastanku ateroma, njegova sazrijevanja i konačno oslobađanja, što rezultira nastankom krvnog ugruška (tromba) koji vodi prema CHD-u.…”

“…The impact of periodontitis on CAD is likely to occur with the entry of bacteria and its products from oral cavity into the bloodstream (8,9). The activation of host inflammatory response contributes to the atheroma formation, followed by maturation and finally exacerbation which results in formation of blood cloth (thrombus) leading to CHD.…”

Relationship between serine dipeptide lipids of commensal Bacteroidetes and atherosclerosis

“…Unfortunately, not much is known about the capacity of oral and intestinal organisms, such as Bacteroidetes, to promote atherosclerosis although inflammatory mechanisms acting in concert to increase systemic inflammation in periodontal disease and to promote or exacerbate atherogenesis have been reviewed [9], and ‘proofs’ for how periodontal bacteria can contribute to atherosclerosis have been listed [10]. An interesting study, assessing the relationship between serine dipeptide lipids of Bacteroidetes bacteria in human arteries and atherosclerosis, was recently published in the Journal of Lipid Research [11].…”

Periodontal Disease as a Possible Risk Factor for Alzheimer’s Disease

“…To date, periodontal disease has been reported as a risk factor for diabetes mellitus (DM), cardio-and cerebrovascular disease, aspiration pneumonia, premature and low birth weight infants, bacterial endocarditis, glomerulonephritis, arthritis, and palmoplantar pustulosis [1][2][3][4][5]. The following three pathways are assumed to be the mechanism of the systemic spread of periodontal disease: direct action of bacterial body and toxin of periodontal disease-related bacteria at the local periodontal site that spread to target organs through the hematogenous route or respiratory tract [4]; the action of inflammation-inducing substances such as cytokines, which are produced by the inflammatory response within periodontal tissue or immune response that spread hematogenously to the target organs [5]; and a pathway that results in intracerebral spread through the nervous system [6,7]. There are various data on intravascular infiltration of periodontal disease-related bacteria and its spread to target organs thus far, but its mechanism of affecting diseases is not fully understood.…”