title: Intraplaque hemorrhage, a potential consequence of periodontal bacteria gathering in human carotid atherothrombosis.
abstract: Periodontal diseases are multifactorial inflammatory diseases, caused by a bacterial biofilm involving both innate and adaptative immunity, characterized by the destruction of tooth-supporting tissues. In the context of periodontitis, the spread of weak pathogenic bacteria into the bloodstream has been described. These bacteria will preferentially localize to existing clot within the circulation. Atherothrombosis of the carotid arteries is a local pathology and a common cause of cerebral infarction. Intraplaque hemorrhages render the lesion more prone to clinical complications such as stroke. The main objective of this study is to explore the biological relationship between carotid intraplaque hemorrhage and periodontal diseases. This study included consecutive patients with symptomatic or asymptomatic carotid stenosis, admitted for endarterectomy surgical procedure (n=41). In conditioned media of the carotid samples collected, markers of neutrophil activation (myeloperoxidase or MPO, DNA-MPO complexes) and hemoglobin were quantified. To investigate the presence of DNA from periodontal bacteria in atherosclerotic plaque, PCR analysis using specific primers was performed. Our preliminary results indicate an association between neutrophil activation and intraplaque hemorrhages, reflected by the release of MPO (p&lt;0,01) and MPO-DNA complexes (p&lt;0,05). Presence of DNA from periodontitis-associated bacteria was found in 32/41 (78%) atheromatous plaque samples. More specifically, DNA from Pg, Tf, Pi, Aa was found in 46%, 24%, 34% and 68% of the samples, respectively. Hemoglobin levels were higher in conditioned media in carotid samples where the bacteria were found, but this was not statistically significant. Our data confirm the relationship between intraplaque hemorrhage and neutrophil activation. In addition, the presence of periodontal bacteria DNA in carotid atheromatous plaque, may contribute to this activation. Further analysis is needed to fully explore the raw data and specimens.
authors.affiliation: Laboratory for Vascular Translational Science, Inserm UMR_S1148; Paris Descartes University - Sorbonne Paris Cité University; Department of Periodontology, Service of Odontology, Bretonneau Hospital, APHP;. adrian.brun@parisdescartes.fr.
authors.forename: Adrian
authors.initials: A
authors.lastname: Brun
authors.forename: Hélène
authors.initials: H
authors.lastname: Rangé
authors.forename: Bastien
authors.initials: B
authors.lastname: Prouvost
authors.forename: Olivier
authors.initials: O
authors.lastname: Meilhac
authors.forename: Mikael
authors.initials: M
authors.lastname: Mazighi
authors.forename: Pierre
authors.initials: P
authors.lastname: Amarenco
authors.forename: Guy
authors.initials: G
authors.lastname: Lesèche
authors.forename: Philippe
authors.initials: P
authors.lastname: Bouchard
authors.forename: Jean-Baptiste
authors.initials: JB
authors.lastname: Michel
mesh_terms: D001419:Bacteria / Q000302:isolation & purification*; D002340:Carotid Artery Diseases / Q000150:complications / Q000382:microbiology*; D055113:Chronic Periodontitis / Q000150:complications / Q000382:microbiology*; D006470:Hemorrhage / Q000150:complications / Q000382:microbiology*; D006801:Humans; D058226:Plaque, Atherosclerotic / Q000150:complications / Q000382:microbiology*