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Page 4 of 18 Kozarov et al. Vessel Plus 2020;4:10 I http://dx.doi.org/10.20517/2574-1209.2019.31

Furthermore, multivariate analysis of coronary heart disease (CHD) individuals demonstrated a higher
prevalence of oral diseases and lower compliance to oral disease prevention compared to healthy controls.
The analysis showed a positive association between edentulousness (OR = 1.37, 95%CI: 1.02 to 1.85), the
number of endodontic lesions (OR = 4.37, 95%CI: 1.69 to 11.28), chronic periodontitis (OR = 5.87, 95%CI: 1.17
[38]
to 29.4), and CHD .

Similarly, a 9-year follow-up study examined a possible correlation between the duration of periodontal
disease state and cardiometabolic risk factors. The odds ratio for the presence of ≥ 1 cardiometabolic risk
factor (hypertension, hyperglycemia, dyslipidemia or obesity) in individuals with a longitudinal presence
of periodontal pockets for ≥ 6 years was significantly higher compared to individuals without periodontal
[39]
pockets .

Finally, the recent Malmö Offspring Study is a population-based study using multivariable regression
models to analyze the presence of carotid plaque and asymptomatic carotid plaque as related to measures
of periodontal disease. This study demonstrated that the risk of developing a carotid plaque in study
subjects with periodontitis was significantly higher compared to periodontitis-free subjects, with odds
[40]
ratioof 1.75 (95%CI: 1.11 to 2.78) .
Not surprisingly, endodontic infections were also associated with vascular inflammations. For example,
endodontic infection was associated with higher prevalence of CHD and initial endothelial damage [41,42] .
In a cross-sectional study of the association between apical periodontitis (AP) and CVD using noninvasive
methods, flow-mediated dilatation (FMD) was found to be significantly impaired in AP patients (mean
= 4.9% ± 2.05%) in comparison with healthy individuals (mean = 9.74% ± 2.59%, P = 0.000). There was a
statistically significant difference observed between carotid IMT of the AP group (mean = 0.64 ± 0.12 mm)
and control group (mean = 0.54 ± 0.08 mm) (P = 0.000). Furthermore, there was a significant inverse
correlation observed between c-IMT and FMD (rs = -0.381, P < 0.001). This indicated an impaired FMD
and greater carotid IMT in AP patients, supporting an association between endodontic infection and
[43]
cardiovascular inflammatio .

Seroepidemiology
Serological animal and cell culture studies provided evidence that bacterial infection, often by the red
complex pathogen Porphyromonas gingivalis, a major etiologic agent of PD, emerges as a new, important
[44]
factor for atherosclerosis . Based on the accumulated epidemiological data, the infection hypothesis
for initiation/exacerbation of atherosclerosis has already been established [45,46] . Specifically, periodontal
inflammatory mediators were recognized as contributors to or triggers for systemic inflammatory
responses. Subgingival periodontal infection demonstrated an increased risk of developing atherosclerosis
[47]
in periodontal patients by 168% .

The ARIC study also presented an association between systemic antibody response to periodontal
pathogens and coronary heart disease in ever and never smokers . The latest ARIC data presented
[48]
significant association between high gingival inflammation, tooth loss, severe tooth loss, and severe
periodontitis with diabetes, coronary heart disease, hsCRP, and IL-6, while only severe disease was
[49]
associated with stroke .

Furthermore, coronary disease was more common among seropositive for P. gingivalis subjects, relative to
the seronegative (14.0% and 9.7%, respectively; P = 0.029). Hence, CHD was more prevalent in individuals
with a high combined antibody response against Aggregatibacter actinomycetemcomitans and P. gingivalis
than in those with a low response (17.4% and 11.1%, P = 0.026). When adjusted for age and several CHD
risk factors, the subjects with a high combined antibody response had an OR of 1.5 (95%CI: 0.95 to