Myocardial infarction risk is increased by periodontal pathobionts: a cross-sectional study

Abstract

To establish the role of periodontal pathobionts as a risk factor for myocardial infarction, we examined the contribution of five periodontal pathobionts and their virulence genes' expressions to myocardial injury (Troponin-I) and coronary artery disease burden (SYNTAX-I scores) using hierarchical linear regression. Pathobiont loads in subgingival-plaques and intra-coronary-thrombi were compared. Troponin-I release increased with one 16S rRNA gene copy/ng DNA of Porphyromonas gingivalis (β = 6.8 × 10^-6, 95% CI = 1.1 × 10^-7-2.1 × 10^-5), one-fold increased expressions of fimA (β = 14.3, 95% CI = 1.5-27.1), bioF-3 (β = 7.8, 95% CI = 1.1-12.3), prtH (β = 1107.8, 95% CI = 235.6-2451.3), prtP (β = 6772.8, 95% CI = 2418.7-11,126.9), ltxA (β = 1811.8, 95% CI = 217.1-3840.8), cdtB (β = 568.3, 95% CI = 113.4-1250.1), all p < 0.05. SYNTAX-I score increased with one 16S rRNA gene copy/ng DNA of Porphyromonas gingivalis (β = 3.8 × 10^-9, 95% CI = 3.6 × 10^-10-1.8 × 10^-8), one-fold increased expressions of fimA (β = 1.2, 95% CI = 1.1-2.1), bioF-3 (β = 1.1, 95% CI = 1-5.2), prtP (β = 3, 95% CI = 1.3-4.6), ltxA (β = 1.5, 95% CI = 1.2-2.5), all p < 0.05. Within-subject Porphyromonas gingivalis and Tannerella forsythia from intra-coronary-thrombi and subgingival-plaques correlated (rho = 0.6, p < 0.05). Higher pathobiont load and/or upregulated virulence are risk factors for myocardial infarction.Trial registration: ClinicalTrials.gov Identifier: NCT04719026.

Figure 1

Change in the predicted (A) 12-h Troponin I, (B) SYNTAX-I scores, with worsening markers of periodontitis and P. gingivalis load. (A) the incremental effect of three clinical indicators of periodontitis (PISA, mean-PPD, mean-CAL) and subgingival P. gingivalis load on 12-h Troponin I levels, (B) incremental effect of mean-PPD, mean-CAL and subgingival P. gingivalis load on SYNTAX-I score. PISA periodontal inflamed surface area, PPD probing pocket depths, CAL clinical attachment loss.

Figure 2

Comparison of within-subject periodontal pathobiont loads in intra-coronary thrombi and subgingival plaques collected from the myocardial infarction patients (n = 10). Corresponding bacterial loads (16S rRNA gene copies/ng DNA) of four periodontal pathobionts: P. gingivalis (yellow), T. forsythia (green), P. intermedia (red) and A. actinomycetemcomitans (purple) in aspirated intra-coronary thrombi and subgingival plaque samples from ten ST-segment elevation myocardial infarction patients (dashed lines show paired samples for each patient). Rho-spearman’s correlation coefficient, * = p < 0.05.

Figure 3

Study flow-chart (STROBE-type diagram).