391 Porphyromonas gingivalis Infection-induced Oral and Systemic Changes in ApoEnull Mice

Thursday, March 22, 2012: 2 p.m. - 3:15 p.m.
Presentation Type: Poster Session
I.M. VELSKO1, M.F. RIVERA2, S.S. CHUKKAPALLI2, J. LEE3, H. CHEN4, I. BHATTACHARYYA5, A.R. LUCAS4, and L. KESAVALU6, 1Periodontology, University of Florida, Gainesville, 2Periodontology, University of Florida, Gainesville, FL, 3College of Dentistry, Pusan National University, Pusan, Republic Of Korea, 4Medicine, College of Medicine, University of Florida, Gainesville, FL, 5Oral Diagnostic Sciences, College of Dentistry, University of Florida, Gainesville, FL, 6Dept. of Periodontology and Oral Biology, University of Florida, Gainesville, FL
Objectives: Periodontal diseases are complex, multifactorial diseases caused by polymicrobial subgingival infections and aggressive immune/inflammatory responses. A distinct pathogenic consortium is found in subgingival plaque in human periodontitis and includes Porphyromonas gingivalis (Pg), Treponema denticola (Td), and Tannerella forsythia (Tf). This study was designed to evaluate P. gingivalis 24 weeks chronic oral infection-induced periodontal disease and atherogenesis in hyperlipidemic ApoEnull mice.

Methods: ApoEnull mice (N=24) were orally infected (8 infections, 4 days/week consecutively) with Pg FDC 381, at 109 cells mixed with 4% carboxymethylcellulose. P. gingivalis infected mice were euthanized at 12 and 24 weeks. Oral plaque samples (PCR), serum antibody response (ELISA), gingival inflammation (Histology, histometry), horizontal alveolar bone resorption (morphometry), and intrabony defects were evaluated (Periodontal disease parameters). Heart, aorta, spleen, liver, lungs, and kidney were evaluated for systemic infection by PCR and aorta was examined for atherosclerotic lesion. 

Results: P. gingivalis genomic DNA was detected in oral plaque samples by PCR indicating their colonization in oral cavity. Infection elicited significantly higher levels of IgG antibodies and greater intrabony defects compared to sham-infected mice. P. gingivalis genomic DNA was detected in aorta and heart at 83 and 25%, respectively in infected mice. P. gingivalis specific genomic DNA, aortic plaque, histology and detection of bacteria by fluorescence in situ hybridization (FISH) are in progress.

Conclusions: This study examined the effect of P. gingivalis induced bacteremia, systemic infection, localization of bacteria, and atherosclerosis in vivo in ApoEnull mice.

This abstract is based on research that was funded entirely or partially by an outside source: NIH/NIDCR R01 DE020820

Keywords: ApoE-/- mice, Cardiovascular disease, Host-microbial interactions, Periodontal disease and Periodontal organisms