Hélène Rangé1, Julien Labreuche2, Liliane Louedec2, Philippe Rondeau3, Cynthia Planesse3, Uriel Sebbag4, Emmanuel Bourdon3, Jean-Baptiste Michel2, Philippe Bouchard5, Olivier Meilhac6. 1. Inserm U1148, CHU X. Bichat, APHP, 46 Rue Henri Huchard, 75018 Paris, France; Département de Parodontologie, Hôpital Rothschild, APHP, 5 Rue Santerre, 75012 Paris, France; Université Paris Diderot, UFR d'Odontologie, 5 Rue Garancière, 75006 Paris, France. 2. Inserm U1148, CHU X. Bichat, APHP, 46 Rue Henri Huchard, 75018 Paris, France. 3. Université de La Réunion, 15, Avenue René Cassin, 97744 Saint-Denis, Ile de La Réunion, France. 4. Centre Cardiologique du Nord, 36 Rue des Moulins Gémeaux, 93200 Saint-Denis, France. 5. Département de Parodontologie, Hôpital Rothschild, APHP, 5 Rue Santerre, 75012 Paris, France; Université Paris Diderot, UFR d'Odontologie, 5 Rue Garancière, 75006 Paris, France. 6. Inserm U1148, CHU X. Bichat, APHP, 46 Rue Henri Huchard, 75018 Paris, France; CHU de La Réunion, Saint Denis, Ile de La Réunion, France. Electronic address: olivier.meilhac@inserm.fr.
Abstract
OBJECTIVE: Epidemiological, biological and clinical links between periodontal and cardiovascular diseases are now well established. Several human studies have detected bacterial DNA corresponding to periodontal pathogens in cardiovascular samples. Intraplaque hemorrhage has been associated with a higher risk of atherosclerotic plaque rupture, potentially mediated by neutrophil activation. In this study, we hypothesized that plaque composition may be related to periodontal pathogens. METHODS: Carotid culprit plaque samples were collected from 157 patients. Macroscopic characterization was performed at the time of collection: presence of blood, lipid core, calcification and fibrosis. Markers of neutrophil activation released by carotid samples were quantified (myeloperoxidase or MPO, cell-free DNA and DNA-MPO complexes). PCR analysis using specific primers for Porphyromonas gingivalis, Aggregatibacter actinomycetemcommitans, Treponema denticola, Prevotella intermedia and Tannerella forsythia was used to detect DNA from periodontal pathogens in carotid tissues. In addition, bacterial lipopolysaccharide (LPS) and Immunoglobulins G against T. forsythia were quantified in atherosclerotic carotid conditioned medium. RESULTS: Intraplaque hemorrhage was present in 73/157 carotid samples and was associated with neutrophil activation, reflected by the release of MPO, cell-free DNA and MPO-DNA complexes. LPS levels were also linked to intraplaque hemorrhage but not with the neutrophil activation markers. Seventy-three percent of the carotid samples were positive for periodontal bacterial DNA. Furthermore, hemoglobin levels were associated with the detection of T. forsythia and neutrophil activation/inflammation markers. CONCLUSION: This study suggests a potential role of periodontal microorganisms, especially T. forsythia, in neutrophil activation within hemorrhagic atherosclerotic carotid plaques.
OBJECTIVE: Epidemiological, biological and clinical links between periodontal and cardiovascular diseases are now well established. Several human studies have detected bacterial DNA corresponding to periodontal pathogens in cardiovascular samples. Intraplaque hemorrhage has been associated with a higher risk of atherosclerotic plaque rupture, potentially mediated by neutrophil activation. In this study, we hypothesized that plaque composition may be related to periodontal pathogens. METHODS: Carotid culprit plaque samples were collected from 157 patients. Macroscopic characterization was performed at the time of collection: presence of blood, lipid core, calcification and fibrosis. Markers of neutrophil activation released by carotid samples were quantified (myeloperoxidase or MPO, cell-free DNA and DNA-MPO complexes). PCR analysis using specific primers for Porphyromonas gingivalis, Aggregatibacter actinomycetemcommitans, Treponema denticola, Prevotella intermedia and Tannerella forsythia was used to detect DNA from periodontal pathogens in carotid tissues. In addition, bacterial lipopolysaccharide (LPS) and Immunoglobulins G against T. forsythia were quantified in atherosclerotic carotid conditioned medium. RESULTS: Intraplaque hemorrhage was present in 73/157 carotid samples and was associated with neutrophil activation, reflected by the release of MPO, cell-free DNA and MPO-DNA complexes. LPS levels were also linked to intraplaque hemorrhage but not with the neutrophil activation markers. Seventy-three percent of the carotid samples were positive for periodontal bacterial DNA. Furthermore, hemoglobin levels were associated with the detection of T. forsythia and neutrophil activation/inflammation markers. CONCLUSION: This study suggests a potential role of periodontal microorganisms, especially T. forsythia, in neutrophil activation within hemorrhagic atherosclerotic carotid plaques.
Authors: Mariano Sanz; Alvaro Marco Del Castillo; Søren Jepsen; Jose R Gonzalez-Juanatey; Francesco D'Aiuto; Philippe Bouchard; Iain Chapple; Thomas Dietrich; Israel Gotsman; Filippo Graziani; David Herrera; Bruno Loos; Phoebus Madianos; Jean-Baptiste Michel; Pablo Perel; Burkert Pieske; Lior Shapira; Michael Shechter; Maurizio Tonetti; Charalambos Vlachopoulos; Gernot Wimmer Journal: J Clin Periodontol Date: 2020-02-03 Impact factor: 8.728
Authors: Luca Zanoli; Marie Briet; Jean P Empana; Pedro G Cunha; Kaisa M Mäki-Petäjä; Athanase D Protogerou; Alain Tedgui; Rhian M Touyz; Ernesto L Schiffrin; Bart Spronck; Philippe Bouchard; Charalambos Vlachopoulos; Rosa M Bruno; Pierre Boutouyrie Journal: J Hypertens Date: 2020-09 Impact factor: 4.776