title: Systemic inflammation in cardiovascular and periodontal disease: comparative study.
abstract: Epidemiological studies have implicated periodontal disease (PD) as a risk factor for the development of cardiovascular disease (CVD). These studies addressed the premise that local infection may perturb the levels of systemic inflammatory mediators, thereby promoting mechanisms of atherosclerosis. Levels of inflammatory mediators in the sera of subjects with only PD, only CVD, both diseases, or neither condition were compared. Subjects were assessed for levels of C-reactive protein (CRP), serum amyloid A (SAA), ceruloplasmin, alpha(1)-acid-glycoprotein (AAG), alpha(1)-antichymotrypsin (ACT), and the soluble cellular adhesion molecules sICAM-1 and sVCAM by enzyme-linked immunoabsorbent and/or radial immunodiffusion assays. CRP levels in subjects with either condition alone were elevated twofold above subjects with neither disease, whereas a threefold increase was noted in subjects with both diseases (P = 0.0389). Statistically significant increases in SAA and ACT were noted in subjects with both conditions compared to those with one or neither condition (P = 0.0162 and 0.0408, respectively). Ceruloplasmin levels were increased in subjects with only CVD (P = 0.0001). Increases in sVCAM levels were noted in all subjects with CVD (P = 0.0054). No differences in sICAM levels were noted among subject groups. A trend toward higher levels of AAG was noted in subjects with both conditions and for ACT in subjects with only PD. Immunohistochemical examination of endarterectomy specimens of carotid arteries from subjects with atherosclerosis documented SAA and CRP deposition in association with atheromatous lesions. The data support the hypothesis that localized persistent infection may influence systemic levels of inflammatory mediators. Changes in inflammatory mediator levels potentially impact inflammation-associated atherosclerotic processes.
authors.affiliation: Department of Oral Biology, State University of New York at Buffalo, 14214, USA.
authors.forename: Ingrid
authors.initials: I
authors.lastname: Glurich
authors.forename: Sara
authors.initials: S
authors.lastname: Grossi
authors.forename: Boris
authors.initials: B
authors.lastname: Albini
authors.forename: Alex
authors.initials: A
authors.lastname: Ho
authors.forename: Rashesh
authors.initials: R
authors.lastname: Shah
authors.forename: Mohamed
authors.initials: M
authors.lastname: Zeid
authors.forename: Heinz
authors.initials: H
authors.lastname: Baumann
authors.forename: Robert J
authors.initials: RJ
authors.lastname: Genco
authors.forename: Ernesto
authors.initials: E
authors.lastname: De Nardin
mesh_terms: D000210:Acute-Phase Reaction / Q000097:blood; D000328:Adult; D001053:Apolipoproteins / Q000032:analysis / Q000097:blood; D001161:Arteriosclerosis / Q000453:epidemiology* / Q000276:immunology* / Q000473:pathology; D002097:C-Reactive Protein / Q000032:analysis / Q000378:metabolism; D002339:Carotid Arteries / Q000737:chemistry / Q000473:pathology; D002570:Ceruloplasmin / Q000378:metabolism; D005260:Female; D005455:Fluorescent Antibody Technique; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D008297:Male; D009961:Orosomucoid / Q000378:metabolism; D010510:Periodontal Diseases / Q000453:epidemiology* / Q000276:immunology*; D012307:Risk Factors; D000685:Serum Amyloid A Protein / Q000032:analysis; D012995:Solubility; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood; D000514:alpha 1-Antichymotrypsin / Q000097:blood
chemical_list: D001053:Apolipoproteins; D009961:Orosomucoid; D000685:Serum Amyloid A Protein; D019010:Vascular Cell Adhesion Molecule-1; D000514:alpha 1-Antichymotrypsin; D018799:Intercellular Adhesion Molecule-1; D002097:C-Reactive Protein; D002570:Ceruloplasmin