DMD, Private Practice, San Francisco, California, USA.
Department of Medicine, University of Fribourg.
Curr Opin Neurol. 2020 Apr;33(2):230-238. doi: 10.1097/WCO.0000000000000797.
The review article discusses the association between periodontal disease and the development of dementia.
In the last decade, increasing evidence has pointed to a microbial and inflammatory origin for Alzheimer's disease with the discovery of oral and airway bacteria, viruses, and fungal species in the brain of patients with Alzheimer's disease. Furthermore, recognized as the culprit of neural network dysfunction, β-amyloid oligomeric species have antimicrobial properties reinforcing the idea that dysbiosis in the host-microbiota interaction can be at the origin of dementia. Periodontitis (gum disease), a persistent low-grade inflammatory condition, caused by pathogenic microorganisms, has been linked to an increased β-amyloid burden and cognitive disabilities later in life.
The pathogens of periodontal disease and the subsequent chronic inflammatory responses have significant implications on the development of Alzheimer's disease. The exact molecular mechanism by which Porphyromonas gingivalis and periodontal disease are involved in the pathogenicity of Alzheimer's disease is not currently evident. Understanding this causality can be instrumental in the development of treatments for this yet uncurable disease.
本文讨论了牙周病与痴呆发展之间的关系。
在过去的十年中,越来越多的证据表明阿尔茨海默病的发病机制与微生物和炎症有关,在阿尔茨海默病患者的大脑中发现了口腔和气道细菌、病毒和真菌。此外,被认为是神经网络功能障碍的罪魁祸首的β-淀粉样寡聚体具有抗菌特性,这进一步证实了宿主-微生物相互作用中的失调可能是痴呆症的根源。牙周炎(牙龈疾病)是一种由致病性微生物引起的持续低度炎症状态,与β-淀粉样蛋白负担增加和晚年认知障碍有关。
牙周病的病原体及其随后的慢性炎症反应对阿尔茨海默病的发展有重要影响。目前还不清楚牙龈卟啉单胞菌和牙周病如何参与阿尔茨海默病的发病机制。了解这种因果关系有助于开发治疗这种尚未治愈的疾病的方法。