title: Treatment of periodontal disease results in improvements in endothelial dysfunction and reduction of the carotid intima-media thickness.
abstract: Several cohort studies reported a relation of cardiovascular events and periodontal disease. In particular, Porphyromonas gingivalis is associated with the development of atherosclerotic plaques. We verified in a longitudinal study whether inflammation biomarkers, endothelial adhesion molecules, leukocyte activation markers, and intima-media thickness could be beneficially modified by periodontal treatment alone. Thirty-five otherwise healthy individuals affected by mild to moderate parodontopathy were enrolled in the study. Echo-Doppler cardiography of the carotid artery, fluorescence-activated cell sorting analyses on lymphocytes and monocytes, and plasma inflammatory indices were evaluated at baseline and at multiple time points after the periodontal treatment. Results showed that inflammation biomarkers were abnormally increased at baseline. Periodontal treatment resulted in a significant reduction of the total oral bacterial load that was associated with a significant amelioration of inflammation biomarkers and of adhesion and activation proteins. Notably, intima-media thickness was significantly diminished after treatment. Inflammatory alterations associated with the genesis of atherosclerotic plaques are detected in otherwise healthy individuals affected by parodontopathy and are positively influenced by periodontal treatment. Reduction of oral bacterial load results in a modification of an anatomical parameter directly responsible for atherosclerosis. These results shed light on the pathogenesis of atherosclerosis and could have practical implications for public health.
authors.affiliation: Infectious Diseases Unit, Hospital Luigi Sacco, Milan, Italy.
authors.forename: Stefania
authors.initials: S
authors.lastname: Piconi
authors.forename: Daria
authors.initials: D
authors.lastname: Trabattoni
authors.forename: Cristina
authors.initials: C
authors.lastname: Luraghi
authors.forename: Edoardo
authors.initials: E
authors.lastname: Perilli
authors.forename: Manuela
authors.initials: M
authors.lastname: Borelli
authors.forename: Michela
authors.initials: M
authors.lastname: Pacei
authors.forename: Giuliano
authors.initials: G
authors.lastname: Rizzardini
authors.forename: Antonella
authors.initials: A
authors.lastname: Lattuada
authors.forename: Dorothy H
authors.initials: DH
authors.lastname: Bray
authors.forename: Mariella
authors.initials: M
authors.lastname: Catalano
authors.forename: Antonella
authors.initials: A
authors.lastname: Sparaco
authors.forename: Mario
authors.initials: M
authors.lastname: Clerici
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000097:blood; D002318:Cardiovascular Diseases / Q000209:etiology; D017536:Carotid Artery, Common / Q000033:anatomy & histology / Q000000981:diagnostic imaging / Q000473:pathology*; D015331:Cohort Studies; D004730:Endothelium, Vascular / Q000000981:diagnostic imaging / Q000473:pathology*; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D007249:Inflammation / Q000473:pathology; D008137:Longitudinal Studies; D008297:Male; D008875:Middle Aged; D010510:Periodontal Diseases / Q000000981:diagnostic imaging / Q000473:pathology* / Q000628:therapy; D012307:Risk Factors; D016896:Treatment Outcome; D017539:Tunica Intima / Q000000981:diagnostic imaging / Q000473:pathology*; D017540:Tunica Media / Q000000981:diagnostic imaging / Q000473:pathology*; D014463:Ultrasonography
chemical_list: D015415:Biomarkers