Salivary IgA antibody to malondialdehyde–acetaldehyde associates with mild periodontal pocket depth

Objective Oxidized epitopes such as malondialdehyde–acetaldehyde (MAA) play a crucial role in the progression of atherosclerosis through activation of the humoral immune response. The exact mechanism of the association between atherosclerosis and periodontal diseases is not fully understood. The aim of the current study is to evaluate the association of oral humoral immune response to oxidized epitopes with parameters of periodontal disease. Materials and methods The Parogene cohort consist of patients who have undergone coronary angiography due to cardiac symptoms. In this study, 423 patients were randomly selected for an extensive oral examination. Salivary Immunoglobulin A to oxidized epitopes and bacterial antigens was determined by chemiluminescence immunoassay. Results In a binary logistic regression model adjusted with periodontal disease confounders, periodontal pocket depth (PPD) 4–5 mm associated with salivary IgA antibodies to MAA‐LDL (p = 0.034), heat shock protein 60 of Aggregatibacter actinomycetemcomitans (p = 0.045), Porphyromonas gingivalis (p = 0.045), A. actinomycetemcomitans (p = 0.005), P. intermedia (p = 0.020), and total IgA (p = 0.003). Conclusions The current study shows the association of salivary IgA to MAA‐LDL with PPD 4–5 mm in a cohort of patients with chronic coronary artery disease. Humoral immune cross‐reactivation to oxidized epitopes such MAA‐LDL could partly explain the link of periodontitis with systemic diseases.