Oral humoral immune response to oxidized LDL epitopes and periodontal pathogens in coronary artery disease and periodontitis.

Thesis event information

Date and time of the thesis defence

Place of the thesis defence

Leena Palotie hall (101A) Aapistie 5 A, 90220 Oulu. Remote access: https://oulu.zoom.us/j/67635321327

Topic of the dissertation

Oral humoral immune response to oxidized LDL epitopes and periodontal pathogens in coronary artery disease and periodontitis.

Doctoral candidate

Licentiate of Dentistry Ramin Akhi

Faculty and unit

University of Oulu Graduate School, Faculty of Medicine, Research Unit of Biomedicine

Subject of study

Medical Microbiology and Immunology

Opponent

Associate Professor Mataleena Parikka, Tampere University

Custos

Professor Sohvi Hörkkö, University of Oulu

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Oral humoral immune response to oxidized LDL epitopes and periodontal pathogens in coronary artery disease and periodontitis.

Atherosclerosis is a chronic inflammatory disease, characterized by retention of low-density lipoproteins (LDL) in the arterial wall, leading to atherosclerotic plaque formation. Subsequently, the retained LDL go through oxidative reactions forming immunogenic Oxidized-LDL (Ox-LDL). The humoral immune response to model oxidized epitopes, such as Malondialdehydeacetaldehyde adducts (MAA-LDL), and copper-oxidized LDL play a key role in atherogenesis.

Accumulating evidence has shown the link of atherosclerosis with oral health. Periodontitis is an inflammatory disease where the tooth-surrounding tissue is compromised. Periodontitis contributes to systemic inflammation and if left untreated, leads to tooth loss. The association of atherosclerosis with periodontitis has been extensively studied and several mechanisms have been suggested. Molecular mimicry of malondialdehyde epitopes with key periodontal pathogen virulence factor Porphyromonas gingivalis A hemagglutinin domain (Rgp44) epitope has been reported. On the other hand, an atherosclerotic mouse model immunized with Rgp44 showed increased levels of IgM to MAA-LDL. The above-mentioned findings raise the question whether atherosclerosis and periodontitis are associated through the cross-activation of mucosal humoral immune response by molecular mimicry.

The aim of the current thesis work was to characterize salivary antibodies to oxidized epitopes and examine their cross-reactivity with antibodies to periodontal pathogens. Finally, the aim was to explore whether salivary immunoglobulins are associated with coronary artery disease (CAD) or periodontal diseases. In the first study, the salivary immunoglobulins to oxidized epitopes were characterized. In study I and II, the cross-reactivities of salivary IgA to MAA epitopes with periodontal pathogens virulence factors Rgp44 and Aggregatibacter actinomycetemcomitans Heat Shock Protein 60 (Aa-HSP60) were shown. In the second study, an independent association of salivary IgA to MAALDL with CAD and acute coronary artery syndrome (ACS) was also reported. Finally, in the third study, salivary IgA to MAA-LDL was shown to associate independently with periodontal pocket depth (PPD) 4- 5 mm, which is a major symptom of periodontitis.

The findings of this thesis highlight the potential role of humoral mucosal immune response to oxidized epitopes in atherosclerosis and periodontal disease.
Last updated: 11.8.2021