University of Oulu

Akhi, R., Wang, C., Nissinen, A. E., Kankaanpää, J., Bloigu, R., Paju, S., … Hörkkö, S. (2019). Salivary IgA to MAA-LDL and Oral Pathogens Are Linked to Coronary Disease. Journal of Dental Research, 98(3), 296–303.

Salivary IgA to MAA-LDL and oral pathogens are linked to coronary disease

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Author: Akhi, R.1,2,3; Wang, C.1,2,3; Nissinen, A. E.1,2,3;
Organizations: 1Medical Microbiology and Immunology, Research Unit of Biomedicine, University of Oulu, Oulu, Finland
2Medical Research Center, Oulu University Hospital and University of Oulu, Oulu, Finland
3Nordlab, Oulu University Hospital, Oulu, Finland
4Medical Informatics and Statistics Research Group Oulu, University of Oulu, Oulu, Finland
5Oral and Maxillofacial Diseases, University of Helsinki and Helsinki University Hospital, Helsinki, Finland
6nstitute of Dentistry, University of Eastern Finland, Kuopio, Finland
7Kuopio University Hospital, Oral and Maxillofacial Diseases, Kuopio, Finland
8Division of Periodontology, Department of Dental Medicine, Karolinska Institutet, Huddinge, Sweden
9HUCH Heart and Lung Center, Helsinki University Hospital, Helsinki, Finland
Format: article
Version: accepted version
Access: open
Online Access: PDF Full Text (PDF, 0.9 MB)
Persistent link:
Language: English
Published: SAGE Publications, 2019
Publish Date: 2019-08-27


A large body of literature has established the link between periodontal disease and cardiovascular disease. Oxidized low-density lipoproteins (OxLDLs) have a crucial role in atherosclerosis progression through initiation of immunological response. Monoclonal IgM antibodies to malondialdehyde-modified low-density lipoprotein (MDA-LDL) and to malondialdehyde acetaldehyde–modified low-density lipoprotein (MAA-LDL) have been shown to cross-react with the key virulence factors of periodontal pathogens Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans. We have previously shown that salivary IgA antibodies to MAA-LDL cross-react with P. gingivalis in healthy humans. In this study, we aim to assess whether oral mucosal immune response represented by salivary IgA to MAA-LDL and oral pathogens is associated with coronary artery disease (CAD). Also, the molecular mimicry through antibody cross-reaction between salivary IgA to MAA-LDL and oral pathogens was evaluated. The study subjects consisted of 451 patients who underwent a coronary angiography with no CAD (n = 133), stable CAD (n = 169), and acute coronary syndrome (ACS, n = 149). Elevated salivary IgA antibody levels to MAA-LDL, Rgp44 (gingipain A hemagglutinin domain of P. gingivalis), and Aa-HSP60 (heat shock protein 60 of A. actinomycetemcomitans) were discovered in stable-CAD and ACS patients when compared to no-CAD patients. In a multinomial regression model adjusted for known cardiovascular risk factors, stable CAD and ACS were associated with IgA to MAA-LDL (P = 0.016, P = 0.043), Rgp44 (P = 0.012, P = 0.004), Aa-HSP60 (P = 0.032, P = 0.030), Tannerella forsythia (P = 0.002, P = 0.004), Porphyromonas endodontalis (P = 0.016, P = 0.020), Prevotella intermedia (P = 0.038, P = 0.005), and with total IgA antibody concentration (P = 0.002, P = 0.016). Salivary IgA to MAA-LDL showed cross-reactivity with the oral pathogens tested in the study patients. The study highlights an association between salivary IgA to MAA-LDL and atherosclerosis. However, whether salivary IgA to MAA-LDL and the related oral humoral responses play a causal role in the development in the CAD should be elucidated in the future.

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Series: Journal of dental research
ISSN: 0022-0345
ISSN-E: 1544-0591
ISSN-L: 0022-0345
Volume: 98
Issue: 3
Pages: 296 - 303
DOI: 10.1177/0022034518818445
Type of Publication: A1 Journal article – refereed
Field of Science: 313 Dentistry
3121 General medicine, internal medicine and other clinical medicine
Funding: We are grateful to Sirpa Rannikko for excellent technical assistance. This work was supported by the University of Oulu Graduate School (R.A.), Finnish Dental Society Apollonia (R.A. and P.J.P.), University of Oulu Scholarship Foundation (R.A.), Academy of Finland (P.J.P., 1266953), Sigrid Juselius Foundation (P.J.P.), Päivikki and Sakari Sohlberg Foundation (P.J.P.), and Paulo Foundation (P.J.P.). The authors declare no potential conflicts of interest with respect to the authorship and/or publication of this article.
Copyright information: © International & American Associations for Dental Research 2019. Reprinted by permission of SAGE Publications. Version of Record can be found at