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

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 ApoE^null mice.

Methods: ApoE^null 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 ApoE^null mice.