Gregory J. Seymour, BDS, MDSc, PhD, FRCPath, FFOP(RCPA), FRACDS(Perio)
Pauline J. Ford, BDentSt, BDSc
Erica Gemmell, BSc, PhD
Kazuhisa Yamazaki, DDS, PhD
ABSTRACT There is increasing evidence that chronic infections are associated with cardiovascular diseases. A number of hypotheses have been put forward to explain these associations, including common susceptibility, systemic inflammation, direct infection of the blood vessels, and cross-reactivity or molecular mimicry between bacterial and self-antigens. In terms of common susceptibility, a person who is susceptible to progressive periodontal disease is also susceptible to atherosclerosis, but the periodontal disease does not cause the atherosclerosis. In recent years much research has been focused on the role of systemic inflammation and the increase in circulating cytokines and inflammatory mediators. These cytokines and mediators can lead to direct endothelial damage and ultimately to atherosclerosis. A number of studies have shown that periodontal bacteria can directly invade the endothelium and thereby lead to inflammation in the blood vessel wall resulting in atherosclerosis. In terms of molecular mimicry, it is proposed that because of the homology between bacterial GroEL antigens and human heat shock protein (HSP), the local immune response to the periodontopathic bacteria cross-reacts with self-HSP expressed on the endothelium leading to vascular inflammation and hence atherosclerosis. There is increasing evidence in support of this hypothesis; however, none of these possible mechanisms are mutually exclusive, and it is likely that in different people different mechanisms may explain the link between periodontal infection and cardiovascular disease.
There is increasing evidence that chronic infections are associated with cardiovascular diseases (CVDs). These infections include Helicobacter pylori, Chlamydia pneumoniae, cytomegalovirus, and, more recently, periodontopathic bacteria such as Porphyromonas gingivalis. Although a large number of potential mechanisms have been postulated, the mechanism by which these infections associate with CVDs is still unclear. A number of hypotheses nevertheless exist, including common susceptibility, systemic inflammation with increased circulating cytokines and inflammatory mediators, direct infection of the blood vessels, and, finally, cross-reactivity or molecular mimicry between bacterial and self-antigens. This final hypothesis is gaining support and will be discussed in this review.