Efeitos da periodontite experimental sobre a morfofisiologia cognitiva do hipocampo

Abstract

Late evidence demonstrates a possible causal relationship between periodontitis and neurodegenerative diseases. Changes in the hippocampus can result in reduced cognitive functions, such as behaviors associated with memory and emotions. This study aimed to evaluate changes in the hippocampus and associated behaviors of rats with ligature-induced experimental periodontitis. Twenty 12-week-old male Wistar rats were used, divided into two groups: Control Group (CG) and Periodontal Disease Group (PDG). PDG received a bandage around the left and right first molars for 30 days, causing experimentally induced periodontitis. The animals of both groups were submitted to three behavioral tests (Open Field, Elevated Plus Maze, and Object Recognition) to assess locomotor and exploratory activities, anxiety, and memory, in two stages, being these: before and on the 27th day of the experiment, and 28 and 29 days after periodontitis induction. After 30 days, the rats underwent euthanasia and collection of the hippocampus (histological and immunological analysis) and hemimandibles (histological and radiographic analysis). The results were analyzed through the GraphPad software, using the Shapiro-Wilk test and the Student‟s t-test (p<0.05). Behavioral tests were analyzed using the Two-Way ANOVA test. PDG showed more considerable anxiety (Elevated Plus Maze Test), less habituation (Open Field Test), and reduced time to explore the new object (Object Recognition Test) compared to CG (p<0.05). Besides, PDG had a lower number of osteocytes and osteoblasts, and higher osteoclastic activity (p<0.05), as well as more significant alveolar bone loss morphometrically and radiographically (p<0.05) compared to CG. In the hippocampus, senile plaques were noted, in addition to positive beta-amyloid, tau, and CD68 markings on PDG. Therefore, it can be concluded that PD triggered the presence of senile plaques, beta-amyloid, tau, and CD68 positive markings, which, together, manifested an initial neuroinflammation process in these animals.