Abstract 9952: Periodontal Inflammation, Periodontal Bacterial Load and Virulence Genes Expression Are Risk Factors for Myocardial Infarction

Abstract

Background: A causal relationship between periodontitis and Myocardial Infarction (MI) is stipulated but remains incompletely characterised. Methods: Prospectively recruited 160 acute MI patients underwent periodontal exam to quantify periodontal inflamed surface area (PISA), probing pocket depths (PPD) and clinical attachment loss (CAL). Porphyromonas gingivalis, Tannerella forsythia, Aggregatibacter actinomycetemcomitans and Prevotella intermedia loads were assessed in subgingival plaque, venous blood, aspirated intra-coronary thrombi and deployment balloons using quantitative polymerase chain reaction. Expression of periodontal bacterial virulence genes (n=13) was quantified with reverse transcription PCR. Myocardial injury was estimated by 12-hour troponin (TnI) and severity of coronary artery disease (CAD) burden by SYNTAX-I scores. CAD-symptom free controls (n=50) of similar age/gender distribution were used for comparison. Results: Compared to controls, MI patients had worse periodontitis and higher bacterial loads (all p <0.05). In MI cohort, after adjusting established risk factors, hierarchical linear regression showed that PISA (5%), mean PPD (3%), mean CAL (2%), P. gingivalis load (4%) and upregulated expression of bioF-3 , fimA , prtH , prtP , ltxA , cdtB virulence genes (4-9%) were associated with an increase in Tnl release, all p <0.05. Similarly, mean PPD (5%), mean CAL (4%), P. gingivalis load (5%) and upregulated expression of bioF-3 , fimA , prtP and ltxA virulence genes (4-9%) were associated with higher SYNTAX-I score, all p <0.05. Every 200 mm 2 PISA, 1mm mean PPD, 1mm mean CAL and 10 9 P. gingivalis copies/ng DNA was responsible for 19,000, 32,000, 38,000 and 10,000 ng/L increase in TnI release, respectively. The SYNTAX-I score increased by 3, 4 and 1 unit with every 1mm mean PPD, 1mm mean CAL and 10 9 P. gingivalis copies/ng DNA, respectively. Periodontal bacterial DNA was detected in coronary thrombi and subgingival plaque sampled from the same patients, with a strong correlation for P. gingivalis and T. forsythia bacterial loads (Spearman's rho=0.6 for both, p <0.05). Conclusions: These findings enable further recognition of periodontitis as a risk factor for MI; a new candidate for primary and secondary prevention.