Background: Chronic infection and persistent systemic inflammation are important risk factors for poor stroke outcomes. Chronic periodontitis (PD) are among the most common chronic immunoinflammatory infections of humans. Interestingly, in 2012, the American Heart Association reported that observational studies support an association between PD and atherosclerotic vascular disease. The association between PD and the occurrence of stroke has been explored clinically in retrospective studies. However, role of PD bacteria in hemorrhagic and ischemic stroke outcomes has not been investigated in preclinical animal models. Here we tested the hypothesis whether PD bacteria augments stroke outcomes. Methods: Ten-week-old male C57BL/6NHsd mice were randomly assigned to the infected (PD) and the sham-infected groups. Mice were infected by oral lavage with 4 periodontal bacteria ( Porphyromonas gingivalis, Treponema denticola, Tannerella forsythia, and Fusobacterium nucleatum ) as polybacterial infection for 12wks (inoculating 4 times per week every third week) to induce periodontitis. Sham-infected mice was inoculated with vehicle. At the end of the 12wks infection period, mice were subjected to 60min of transient ischemia. Mice were tested for PD [bacterial infection, periodontal inflammation, alveolar bone resorption (ABR)] and functional and anatomical stroke outcomes at 48h post-stroke. Results: All bacteria were colonized/infected in the mice gingival surface (83-100%). Polybacterial-infected mice developed mild periodontal inflammation with a trend to increased ABR. We also observed that the neurological deficit score in PD group increased by 32.4018.56% (p<0.01). Similarly, the infarction volume in the infected mice (n=7) also increased significantly by 44.2626.04% (p<0.05) as compared with controls (n=8). We also observed a significant difference in parenchymal bleeding in infected mice as compared with the sham-infected mice (30% vs 11%; p<0.001). Conclusion: This is the first report demonstrating that oral bacteria induced significant neurological deficits, infarction volume, and parenchymal bleeding resulting in enhanced ischemic stroke damages.
