Harding Alice, Kanagasingam Shalini, Welbury Richard, Singhrao Sim K
Brain and Behavior Centre, Faculty of Clinical and Biomedical Sciences, School of Dentistry, University of Central Lancashire, Preston, UK.
Adv Exp Med Biol. 2022;1373:241-260. doi: 10.1007/978-3-030-96881-6_13.
Periodontitis and Alzheimer's disease (AD) exist globally within the adult population. Given that the risk of AD incidence doubles within 10 years from the time of periodontal disease diagnosis, there is a window of opportunity for slowing down or preventing AD by risk-reduction-based intervention. Literature appraisal on the shared risk factors of these diseases suggests a shift to a healthy lifestyle would be beneficial. Generalised (chronic) periodontitis with an established dysbiotic polymicrobial aetiology affects the tooth supporting tissues with eventual tooth loss. The cause of AD remains unknown, however two neurohistopathological lesions - amyloid-beta plaques and neurofibrillary tangles, together with the clinical history, provide AD diagnosis at autopsy. Historically, prominence was given to the two hallmark lesions but now emphasis is placed on cerebral inflammation and what triggers it. Low socioeconomic status promotes poor lifestyles that compromise oral and personal hygiene along with reliance on poor dietary intake. Taken together with advancing age and a declining immune protection, these risk factors may negatively impact on periodontitis and AD. These factors also provide a tangible solution to controlling pathogenic bacteria indigenous to the oral and gastrointestinal tract microbioes in vulnerable subjects. The focus here is on Porphyromonas gingivalis, one of several important bacterial pathogens associated with both periodontitis and AD. Recent research has enabled advances in our knowledge of the armoury of P. gingivalis via reproduction of all clinical and neuropathological hallmark lesions of AD and chronic periodontal disease in vitro and in vivo experimental models, thus paving the way for better future management.
牙周炎和阿尔茨海默病（AD）在全球成年人群中均有存在。鉴于从牙周疾病诊断之时起，AD发病风险在10年内会翻倍，因此存在通过基于降低风险的干预措施来减缓或预防AD的机会之窗。对这些疾病共同风险因素的文献评估表明，转向健康的生活方式会有益处。具有已确定的生态失调多微生物病因的广泛性（慢性）牙周炎会影响牙齿支持组织，最终导致牙齿脱落。AD的病因尚不清楚，然而两种神经组织病理学病变——β-淀粉样蛋白斑块和神经原不清楚，然而两种神经组织病理学病变——β-淀粉样蛋白斑块和神经原纤维缠结，连同临床病史，可在尸检时做出AD诊断。从历史上看，人们关注的是这两种标志性病变，但现在重点放在了脑炎症及其触发因素上。社会经济地位低下会导致不良的生活方式，损害口腔和个人卫生，同时依赖不良的饮食摄入。再加上年龄增长和免疫保护下降，这些风险因素可能会对牙周炎和AD产生负面影响。这些因素也为控制易感人群口腔和胃肠道微生物群中的本土致病细菌提供了切实可行的解决方案。这里的重点是牙龈卟啉单胞菌，它是与牙周炎和AD相关的几种重要细菌病原体之一。最近的研究通过在体外和体内实验模型中再现AD和慢性牙周疾病的所有临床和神经病理学标志性病变，使我们对牙龈卟啉单胞菌的致病机制有了进一步的了解，从而为未来更好的治疗铺平了道路。
