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Infection and Immunity, October 2003, p. 6012-6018, Vol. 71, No. 10
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.10.6012-6018.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Role for Periodontitis in the Progression of Lipid Deposition in an Animal Model

Ashish Jain,1 Eraldo L. Batista Jr.,1 Charles Serhan,2 Gregory L. Stahl,2 and Thomas E. Van Dyke1*

Department of Periodontology and Oral Biology, Goldman School of Dental Medicine, Boston University,1 Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Preoperative and Pain Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts2

Received 12 February 2003/ Returned for modification 29 April 2003/ Accepted 30 June 2003

Epidemiologic studies have implicated periodontitis as a risk factor for the development of cardiovascular disease. However, no prospective studies investigating this potential relationship have been carried out. Age- and sex-matched New Zealand White rabbits were maintained on a diet consisting of 0.5% fat for 13 weeks to induce the accumulation of lipid deposits in the aorta as a model for atherogenesis. One-half of the animals received silk ligatures around their mandibular premolars followed by an application of a periodontal pathogen, Porphyromonas gingivalis, to induce periodontitis. Animals were sacrificed after 14 weeks. Periodontal disease severity was quantified radiographically, histologically, and by direct visualization of bone loss on defleshed skulls. Lipid deposition was evaluated by computer-assisted morphometry in the aortas en face after lipid deposits were stained with Sudan IV. Animals with experimentally induced periodontitis had more extensive accumulations of lipids in the aorta than did nonperiodontitis animals (P < 0.05), and there was a positive correlation between the severity of periodontal disease and the extent of lipid deposition (r2 = 0.9501). The results provide direct evidence that periodontitis may be a risk factor and may contribute to the pathogenesis of atherosclerosis. The data support the concept that infections at remote locations can modulate atherosclerotic events distantly.

* Corresponding author. Mailing address: Goldman School of Dental Medicine, Department of Periodontology and Oral Biology, 100 East Newton St., Rm G-05, Boston, MA 02118. Phone: (617) 638-4758. Fax: (617) 638-4799. E-mail: tvandyke{at}bu.edu.

Editor: J. D. Clements

Infection and Immunity, October 2003, p. 6012-6018, Vol. 71, No. 10
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.10.6012-6018.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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