Akademik Veri Yönetim Sistemi
JOURNAL OF PERIODONTAL RESEARCH, cilt.56, sa.6, ss.1154-1162, 2021 (SCI-Expanded)
Background and aim The hippocampus, which has a central role in cognitive and behavioral activities, is one of the most sensitive parts of the brain to systemic inflammatory diseases. This animal study aims to comprehensively investigate the possible inflammatory, oxidative, and apoptotic effects of periodontitis on the hippocampus. Methods Sixteen male Sprague-Dawley rats were randomly assigned to two groups: control and experimental periodontitis (Ep). In the Ep group, periodontitis was induced by placing 3.0 sutures sub-paramarginally around the necks of right and left mandibular first molars and maintaining the ligatures in place for 5 weeks. Following the euthanasia, mandibula and hippocampus samples were collected bilaterally. Alveolar bone loss was measured histomorphometrically and radiologically on the right and left mandibles. On the right hippocampal sections histological (Caspase-3, TNF-alpha, and 8-OHdG) and the left hippocampal sections, biochemical (IL-1 beta, A beta(1-42), MDA, GSH, and TAS levels) evaluations were performed. Results Histopathological changes associated with periodontitis were limited (p > .05). A slight increase in caspase-3 positive neuron density in EP rats showed that apoptotic changes were also limited (p > .05). 8-OHdG activity, on the other hand, was significantly higher compared to controls (p < .05). In biochemical analysis, there was a significant increase in IL-1 beta levels and oxidative membrane damage (MDA) (p < .05) whereas A beta(1-42) and antioxidant marker (GSH and TAS) levels were slightly increased (p > .05). Conclusion Periodontitis causes marked increases in IL-1 beta levels and oxidative stress in the hippocampus, but limited degenerative and apoptotic changes.