Periodontitis can lead to an Initial Process of Neuroinflammation in Experimental Models

Abstract

Introduction: Recent evidence shows 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. Objectives: Evaluate the influence of ligature-induced experimental periodontitis on the inflammation of the hippocampus of rats. Materials and Methods: Twenty male Wistar rats, divided into Control Group (GC) and Periodontal Disease Group (GDP). GDP was induced to experimental periodontitis by placing a ligature on the lower molars for 30 days. The study performed three behavioral tests during the experiment in two stages: before and after the induction of periodontitis; at the end, the rats underwent euthanasia and the collection of the hippocampus (histological and immunological analysis) and hemimandibles (histological and radiographic analysis), with subsequent performance of Student's T-tests and Two-Way ANOVA to analyze the results. Results: GDP showed a higher level of anxiety, less habituation and reduced time to explore the new object compared to GC (p<0.05). Besides, GDP had a lower number of osteocytes and osteoblasts, and higher osteoclastic activity, as well as more significant alveolar bone loss compared to GC (p<0.05). Senile plaques were noted in the hippocampus in addition to positive beta-amyloid, tau, and CD68 markings on GDP. Conclusions: Therefore, it can be concluded that periodontitis triggered the presence of senile plaques, beta-amyloid, tau, and CD68 markings, which, together, manifested an initial neuroinflammation process in these animals. Clinical Relevance: Periodontitis can be a risk factor in neuroinflammation process