Research Paper Volume 12, Issue 16 pp 16609—16620
Autoantibodies against M5-muscarinic and beta1-adrenergic receptors in periodontitis patients
- 1 Central Institute for Clinical Chemistry and Laboratory Diagnostics, Heinrich Heine University Düsseldorf, Medical Faculty, Düsseldorf, Germany
- 2 Cell Trend GmbH, Luckenwalde, Germany
- 3 Department of Periodontics, Preventive and Restorative Dentistry, University Medical Center Hamburg-Eppendorf, Hamburg, Germany
Received: May 27, 2020 Accepted: July 21, 2020 Published: August 28, 2020https://doi.org/10.18632/aging.103864
How to Cite
Copyright © 2020 Scherbaum et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Autoantibodies against muscarinic and beta1-adrenergic receptors are considered a potential cause and/or risk factor for chronic heart failure. Association of periodontitis with such autoantibodies and with impaired heart function has been observed in patients exposed to endemic Chagas' disease, which triggers by itself cardiomyopathy and receptor immunization.
Here we studied the association between periodontitis, markers of cardiac injury and receptor autoimmunization in periodontitis patients (n = 147) not exposed to Chagas' disease. The autoantibodies were determined by IgG binding to native intact muscarinic and beta1-adrenergic receptors or to a cyclic peptide mimicking the disease-relevant conformational autoepitope presented by the active beta1-adrenergic receptor. Possible cardiac injury and inflammatory status were judged by serum levels of proBNP/Troponin I and CRP/IL-6, respectively. These parameters were analysed in healthy and periodontally diseased individuals as well as before and after periodontal therapy.
Patients with periodontitis had significantly (p < 0.001) higher levels of autoantibodies against M5-muscarinic and beta1-adrenergic receptors, which further increased following periodontal therapy. Receptor autoantibodies were associated with increased inflammatory status but not with increased markers of cardiac injury. Thus, our data indicate that periodontitis triggers systemic inflammation, which is associated with receptor autoimmunization, and, independently thereof, with cardiac injury.