Nachweis parodontalpathogener Bakterien-DNA, von Lipopolysaccharid-Binding-Protein (LBP), LBP-Rezeptor (CD14), Makrophagen (CD68) sowie von Herzinsuffizienzmarkern (proBNP NT) im humanen Myokard Ergebnisse einer Pilotstudie
Detection of periodontal pathogenic bacteria DNA, lipopolysaccharide binding protein (LBP), LBP receptor (CD14), macrophages (CD68) and heart failure markers (proBNP NT) in the human myocardium
by Christoph Rost
Date of Examination:2016-12-07
Date of issue:2016-12-07
Advisor:Prof. Dr. Rainer Mausberg
Referee:PD Dr. Bernhard C. Danner
Referee:Prof. Dr. Margarete Schön
Files in this item
Name:Dissertation Christoph Rost.pdf
Size:1.74Mb
Format:PDF
Abstract
English
Aim of the study: The aim of this pilot study was the verification of a study model with appropriate clinical microbiological protein biochemical as well as immunohistochemical parameters for the clarification of possible clinical correlations between periodontitis and heart failure. Materials and methods: Ten patients were selected for the study. During an aortic valve replacement surgery heart tissue was taken. The blood collected during the operation as well as the removed tissue from the valve atrium and ventricle was secured for further analysis in the laboratory. In the participating patients both the periodontal and periodontal conditions were collected as well as samples taken from the periodontal sulcus and the cheek mucosa. These samples were examined with micro- and molecular biology methods for periodontopathogenic bacteria and IL-1 polymorphisms. The heart tissue described above was analyzed by the Western blot method. This was used to detect LBP and proBNP NT. In addition attempts were also made to detect LBP and proBNP NT by the ELISA method in patients' blood. Furthermore the tissue samples were histologically and immunohistochemically prepared and scored to HE inflammation LBP CD14 and CD68. Results: In all patients a highly increased number of bacteria (> 104) of the red complex was detected. The same bacteria were found in the atrium and ventricle. It seems that bacteria from the oral cavity find their way to the heart and can attach to the heart tissue. All patients had an IL-1 genotype associated with an increased genetic risk of periodontitis or a reduced genetic inflammation inhibition. In the studies on the heart tissue the highest concentrations of LBP on the valve tissue were found which is in contrast to the prevalence of the periodontopathogenic bacteria. ProBNP NT was measured at six (atrium) and four (ventricular) samples with an increased number. The investigation of the blood serum on LPS and BNP showed that no relationship to the LBP concentration at the heart or the degree of inflammation can be proven. However the results for BNP confirmed the prevalence of heart failure in all patients. The histological analysis showed an increased concentration of the inflammatory parameters CD14 and CD 68. All patients had a moderate to severe periodontal disease with increased genetic risk of periodontitis. The results show that both the periodontopathogenic bacteria from the oral cavity and their toxin the lipopolysaccharide can be detected not only on the valve but also in the heart muscle of the atrium and ventricle. Therefore PCR Western blot and immunohistochemistry used for this purpose seem to be usefull examination methods. The study showed the presence of oral bacterial DNA in human myocardium where the LBP was detected biochemically and immunohistochemically. In further immunohistochemical analyzes CD14 (LBP binding receptor) and CD 68 (macrophages) were also detected. However further studies are required. The presented study could serve as a model.
Keywords: periodontitis; heart failure; LBP; BNP; IL-1-polymorphysm; bacteremia
Schlagwörter: Parodontitis; Herzinsuffizienz; LBP; BNP; IL-1-Polymorphismus; Bakteriämie