Earl Fu, Kuo‐Feng Huang, Hsi‐Hsien Chang, Hui‐Hwa Tseng, Stephen Shei‐Dei Yang
{"title":"Periodontitis Increases Gingival, Serum and Hippocampus β‐Amyloid Expressions but Reduces Neurovascular Coupling in Basilar Artery of Rats","authors":"Earl Fu, Kuo‐Feng Huang, Hsi‐Hsien Chang, Hui‐Hwa Tseng, Stephen Shei‐Dei Yang","doi":"10.1111/jcpe.14110","DOIUrl":null,"url":null,"abstract":"AimNeurodegenerative diseases are characterized by early increased beta‐amyloid (Aβ) and decreased cerebrovascular reactivity. We investigated Aβ in gingiva, serum or hippocampus and neurovascular reactivity in basilar artery (BA) of periodontitis rats, to test the impact of Aβ on BA vasoreactivity ex vivo.Materials and MethodsPeriodontitis was induced in 32 rats using silk‐ligation. Rats were sacrificed at weeks 0, 1, 2 and 4. Gingival TNF‐α, IL‐1β and Aβ were quantified via immunoblotting. Alveolar bone destruction was examined by micro‐computed tomography. Serum and hippocampus Aβ values were measured by enzyme‐linked immunosorbent assay and fluorescence staining, respectively. Vasoreactivity was measured by myography on isolated BA.ResultsFrom Week 1, gingival TNF‐α and IL‐1β and bone destruction increased. Gingiva, serum and hippocampus Aβ values increased from Week 2. Nicotine‐induced BA relaxation declined from Week 2, while acetylcholine‐induced relaxation decreased by Week 4. Bone loss correlated with Aβ and nicotine‐induced relaxation. Correlations were observed between Aβs in tissues, between two induced BA relaxations and between Aβ expressions and the induced relaxations. Ex vivo, Aβ reduced nicotine‐ and isoproterenol‐induced relaxations but not electrical stimulated relaxation.ConclusionsPeriodontitis may increase Aβ expressions and reduce BA neurovascular reactivity, with Aβ contributing to this abnormal neurovascular coupling.","PeriodicalId":15380,"journal":{"name":"Journal of Clinical Periodontology","volume":"84 1","pages":""},"PeriodicalIF":5.8000,"publicationDate":"2025-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Clinical Periodontology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1111/jcpe.14110","RegionNum":1,"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
AimNeurodegenerative diseases are characterized by early increased beta‐amyloid (Aβ) and decreased cerebrovascular reactivity. We investigated Aβ in gingiva, serum or hippocampus and neurovascular reactivity in basilar artery (BA) of periodontitis rats, to test the impact of Aβ on BA vasoreactivity ex vivo.Materials and MethodsPeriodontitis was induced in 32 rats using silk‐ligation. Rats were sacrificed at weeks 0, 1, 2 and 4. Gingival TNF‐α, IL‐1β and Aβ were quantified via immunoblotting. Alveolar bone destruction was examined by micro‐computed tomography. Serum and hippocampus Aβ values were measured by enzyme‐linked immunosorbent assay and fluorescence staining, respectively. Vasoreactivity was measured by myography on isolated BA.ResultsFrom Week 1, gingival TNF‐α and IL‐1β and bone destruction increased. Gingiva, serum and hippocampus Aβ values increased from Week 2. Nicotine‐induced BA relaxation declined from Week 2, while acetylcholine‐induced relaxation decreased by Week 4. Bone loss correlated with Aβ and nicotine‐induced relaxation. Correlations were observed between Aβs in tissues, between two induced BA relaxations and between Aβ expressions and the induced relaxations. Ex vivo, Aβ reduced nicotine‐ and isoproterenol‐induced relaxations but not electrical stimulated relaxation.ConclusionsPeriodontitis may increase Aβ expressions and reduce BA neurovascular reactivity, with Aβ contributing to this abnormal neurovascular coupling.
期刊介绍:
Journal of Clinical Periodontology was founded by the British, Dutch, French, German, Scandinavian, and Swiss Societies of Periodontology.
The aim of the Journal of Clinical Periodontology is to provide the platform for exchange of scientific and clinical progress in the field of Periodontology and allied disciplines, and to do so at the highest possible level. The Journal also aims to facilitate the application of new scientific knowledge to the daily practice of the concerned disciplines and addresses both practicing clinicians and academics. The Journal is the official publication of the European Federation of Periodontology but wishes to retain its international scope.
The Journal publishes original contributions of high scientific merit in the fields of periodontology and implant dentistry. Its scope encompasses the physiology and pathology of the periodontium, the tissue integration of dental implants, the biology and the modulation of periodontal and alveolar bone healing and regeneration, diagnosis, epidemiology, prevention and therapy of periodontal disease, the clinical aspects of tooth replacement with dental implants, and the comprehensive rehabilitation of the periodontal patient. Review articles by experts on new developments in basic and applied periodontal science and associated dental disciplines, advances in periodontal or implant techniques and procedures, and case reports which illustrate important new information are also welcome.