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Clinical and Diagnostic Laboratory Immunology, March 2002, p. 425-432, Vol. 9, No. 2
1071-412X/02/$04.00+0     DOI: 10.1128/CDLI.9.2.425-432.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Systemic Inflammation in Cardiovascular and Periodontal Disease: Comparative Study

Ingrid Glurich,1 Sara Grossi,1 Boris Albini,2 Alex Ho,1 Rashesh Shah,3 Mohamed Zeid,3 Heinz Baumann,4 Robert J. Genco,1 and Ernesto De Nardin1,2*

Department of Oral Biology,1 Department of Microbiology, State University of New York at Buffalo,2 Departments of Cardiovascular Surgery and Pathology, Buffalo General Hospital,3 Department of Cell and Molecular Biology, Roswell Park Memorial Institute, Buffalo, New York 142144

Received 20 February 2001/ Returned for modification 18 April 2001/ Accepted 15 November 2001

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.

* Corresponding author. Mailing address: Department of Oral Biology, 210 Foster Hall, 3435 Main St., Buffalo, NY 14214. Phone: (716) 829-3998. Fax: (716) 829-3942. E-mail: ernesto_denardin{at}acsu.buffalo.edu.

Clinical and Diagnostic Laboratory Immunology, March 2002, p. 425-432, Vol. 9, No. 2
1071-412X/02/$04.00+0     DOI: 10.1128/CDLI.9.2.425-432.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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