{"title":"Effects of Experimental Periodontitis and Periodontal Treatment on Alzheimer-Like Pathology in Rats.","authors":"Sedanur Yavuz, Birsen Elibol, Esra Demir, Beyza Kinsiz, Ozlem Toluk, Sadiye Gunpinar","doi":"10.1111/odi.70001","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>This study investigated the effects of periodontitis (P) and non-surgical periodontal therapy (NSPT) on behavior, neurodegeneration, and neuroinflammation in rats with Alzheimer's disease (AD)-like pathology.</p><p><strong>Methods: </strong>AD-like pathology was induced in rats (n = 28) using STZ neurodegeneration model. Periodontitis was experimentally induced (n = 32), and half of which received NSPT with Chlorhexidine (CHX) gel. Behavioral assessment included the passive avoidance task (PA) and Morris water maze (MWM). Levels of NLRP3, phosphorylated tau (p-tau), and tau in the hippocampus, cerebrospinal fluid (CSF), and serum were measured by ELISA, while BACE1, IL1β, iNOS, and NF-κβ proteins were assessed by Western blotting.</p><p><strong>Results: </strong>Rats in the AD and AD + P groups performed worse in behavioral tests compared to controls (p < 0.05), whereas the NSPT group showed similar performance to controls (p > 0.05). CSF p-tau levels were comparable between AD and AD + P groups, but the hippocampal p-tau/tau ratio was significantly higher in the AD + P group (p < 0.05). BACE1 levels were similar in P and AD groups. NLRP3 and iNOS levels did not show significant differences across groups. Notably, the NSPT group exhibited reduced NF-κβ levels (p < 0.05).</p><p><strong>Conclusions: </strong>Periodontitis may exacerbate AD-like molecular pathology, particularly by promoting tau hyperphosphorylation, while NSPT appears to mitigate disease progression and improve behavioral outcomes.</p>","PeriodicalId":19615,"journal":{"name":"Oral diseases","volume":" ","pages":""},"PeriodicalIF":2.9000,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Oral diseases","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1111/odi.70001","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"DENTISTRY, ORAL SURGERY & MEDICINE","Score":null,"Total":0}
引用次数: 0
Abstract
Objective: This study investigated the effects of periodontitis (P) and non-surgical periodontal therapy (NSPT) on behavior, neurodegeneration, and neuroinflammation in rats with Alzheimer's disease (AD)-like pathology.
Methods: AD-like pathology was induced in rats (n = 28) using STZ neurodegeneration model. Periodontitis was experimentally induced (n = 32), and half of which received NSPT with Chlorhexidine (CHX) gel. Behavioral assessment included the passive avoidance task (PA) and Morris water maze (MWM). Levels of NLRP3, phosphorylated tau (p-tau), and tau in the hippocampus, cerebrospinal fluid (CSF), and serum were measured by ELISA, while BACE1, IL1β, iNOS, and NF-κβ proteins were assessed by Western blotting.
Results: Rats in the AD and AD + P groups performed worse in behavioral tests compared to controls (p < 0.05), whereas the NSPT group showed similar performance to controls (p > 0.05). CSF p-tau levels were comparable between AD and AD + P groups, but the hippocampal p-tau/tau ratio was significantly higher in the AD + P group (p < 0.05). BACE1 levels were similar in P and AD groups. NLRP3 and iNOS levels did not show significant differences across groups. Notably, the NSPT group exhibited reduced NF-κβ levels (p < 0.05).
Conclusions: Periodontitis may exacerbate AD-like molecular pathology, particularly by promoting tau hyperphosphorylation, while NSPT appears to mitigate disease progression and improve behavioral outcomes.
期刊介绍:
Oral Diseases is a multidisciplinary and international journal with a focus on head and neck disorders, edited by leaders in the field, Professor Giovanni Lodi (Editor-in-Chief, Milan, Italy), Professor Stefano Petti (Deputy Editor, Rome, Italy) and Associate Professor Gulshan Sunavala-Dossabhoy (Deputy Editor, Shreveport, LA, USA). The journal is pre-eminent in oral medicine. Oral Diseases specifically strives to link often-isolated areas of dentistry and medicine through broad-based scholarship that includes well-designed and controlled clinical research, analytical epidemiology, and the translation of basic science in pre-clinical studies. The journal typically publishes articles relevant to many related medical specialties including especially dermatology, gastroenterology, hematology, immunology, infectious diseases, neuropsychiatry, oncology and otolaryngology. The essential requirement is that all submitted research is hypothesis-driven, with significant positive and negative results both welcomed. Equal publication emphasis is placed on etiology, pathogenesis, diagnosis, prevention and treatment.