Lipopolysaccharide, a possible molecular mediator between periodontitis and coronary artery disease
2017
Aim We aimed to study how lipopolysaccharide (LPS) in saliva and serum associates with each other,
periodontalmicrobial burden,
periodontitisand coronary artery disease (CAD). Materials and methods The used Parogene cohort comprised N = 505 Finnish adults. Coronary diagnosis was acquired by coronary angiography, and the main outcomes were as follows: no significant CAD (n = 123), stable CAD (n = 184) and acute coronary syndrome (n = 169).
Periodontitiswas defined according to clinical and radiographic examinations. Levels for 75 strains of subgingival bacteria were determined by
checkerboard
DNA–DNA hybridization. Saliva and serum LPS activity was analysed by
Limulus amebocyte lysateassay. Results The level of 11 bacterial strains, which were mainly oral and respiratory Gram-negative species, associated with salivary LPS levels in an age- and gender-adjusted linear regression. A total of 4.9% of the serum LPS, that is endotoxemia, variation was explainable by saliva LPS among patients with
periodontitis(n = 247, R2 = .049, Pearson's r = .222, p < .001). Endotoxemia associated with stable CAD in a confounder adjusted
multinomial logistic regressionmodel (OR 1.99, 95% CI 1.04–3.81, p = .039, 3rd tertile). Conclusions In particular in
periodontitispatients, subgingival microbial burden contributes to endotoxemia. LPS is a possible molecular mediator between
periodontitisand CAD.
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