Evaluation of the effect of experimental periodontitis and periodontal treatment on neurodegeneration and neuroinflamation in brain of rats

Neuroinflammation plays an important role in the pathology of Alzheimer's disease (AD) and may occur due to systemic inflammation. Inflammation due to periodontal disease may increase neuroinflammation associated with AD. The aim of this study was to investigate the effects of periodontal disease and nonsurgical periodontal treatment (NSPT) on behavioral parameters, neurodegeneration and neuroinflammation in rats with experimental periodontitis and AD. 64 Sprague Dawley rats were used in this study. AH was induced in 28 of them by intracranial streptozocin injection. Experimental periodontitis was induced by placing the 4/0 silk sutur around the upper left second molars in 32 rats. NSPT was performed with CHX gel application to 16 of 32 rats with periodontitis. The periodontal parameters of all rats were evaluated before the establishment of experimental periodontitis (Day 0), before sutures were removed (Day 21), and after NSPT (Day 41). Behavioral parameters were evaluated by passive avoidance and Morris water maze test on all rats. Half of the rats were sacrificed on the 21st day and the other half on the 41st day, and following hippocampus, cerebrospinal fluid (CSF) and serum samples were collected. Nod-like Receptor Protein 3 (NLRP3) and hyperphosphorylated tau (p-tau) levels in the samples were evaluated by ELISA method. Alveolar bone loss was measured by morphometric analysis in maxilla samples. It was determined that passive avoidance test results in rats with alzheimer and alzheimer+periodontitis were shorter than the control group (p<0.05), and Morris water maze test results were longer (p<0.05). On the other hand, it was determined that there was no difference between the rats with alzheimer+periodontitis and the groups with only alzheimer (p>0.05). In addition, the results of passive avoidance and Morris water maze test of the groups treated with CHX gel and NSPT were found to be similar to the control group (p>0.05). CSF p-tau levels were not different between only alzheimer and alzheimer+periodontitis groups (p>0.05), while hippocampus p-tau levels were higher in alzheimer+periodontitis groups than only alzheimer groups (p<0.05). On the other hand, CSF, hippocampus and serum NLRP3 levels were not different between the study groups (p>0.05). Within the limits of our study, it can be concluded that periodontitis does not exacerbate AD, on the other hand, treatment of existing periodontal disease may slow the progression of AD by improving behavioral parameters.