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

Abstract

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.