Periodontitis, a chronic, inflammatory disease, induces systemic inflammation and contributes to the development of neurodegenerative diseases. The precise etiology of the most common neurodegenerative disorders, such as sporadic Alzheimer’s, Parkinson’s diseases and multiple sclerosis (AD, PD, and MS, respectively), remains to be revealed. Chronic neuroinflammation is a well-recognized component of these disorders, and evidence suggests that systemic inflammation is a possible stimulus for neuroinflammation development. Systemic inflammation can lead to deleterious consequences on the brain if the inflammation is sufficiently severe or if the brain shows vulnerabilities due to genetic predisposition, aging, or neurodegenerative diseases. It has been proposed that periodontal disease can initiate or contribute to the AD pathogenesis through multiple pathways, including key periodontal pathogens. Dysbiotic oral bacteria can release bacterial products into the bloodstream and eventually cross the brain-blood barrier; these bacteria can also cause alterations to gut microbiota that enhance inflammation and potentially affect brain function via the gut–brain axis. The trigeminal nerve has been suggested as another route for connecting oral bacterial products to the brain. PD and MS are often preceded by gastrointestinal symptoms or aberrant gut microbiome composition, and alterations in the enteric nervous system accompany the disease. Clinical evidence has suggested that patients with periodontitis are at a higher risk of developing PD and MS. This nexus among the brain, periodontal disease, and systemic inflammation heralds new ways in which microglial cells, the main innate immune cells, and astrocytes, the crucial regulators of innate and adaptive immune responses in the brain, contribute to brain pathology. Currently, the lack of understanding of the pathogenesis of neurodegeneration is hindering treatment development. However, we may prevent this pathogenesis by tackling one of its possible contributors (periodontitis) for systemic inflammation through simple preventive oral hygiene measures.

牙周炎是一种慢性炎症性疾病，可诱发全身炎症并导致神经退行性疾病的发展。最常见的神经退行性疾病，如散发性阿尔茨海默病、帕金森病和多发性硬化症（分别为 AD、PD 和 MS）的确切病因仍有待揭示。慢性神经炎症是这些疾病中公认的组成部分，有证据表明全身炎症可能是神经炎症发展的刺激因素。如果炎症足够严重或大脑因遗传易感性、衰老或神经退行性疾病而表现出脆弱性，全身性炎症可能会对大脑造成有害后果。已经提出牙周病可以通过多种途径引发或促成 AD 发病机制，包括关键的牙周病原体。不益生菌的口腔细菌可以将细菌产物释放到血液中，最终穿过脑血屏障；这些细菌还可以引起肠道菌群的改变，从而增强炎症并可能通过肠-脑轴影响大脑功能。三叉神经已被建议作为将口腔细菌产品连接到大脑的另一种途径。PD 和 MS 通常先于胃肠道症状或肠道微生物组组成异常，并且伴随疾病发生的肠神经系统发生改变。临床证据表明，牙周炎患者发生 PD 和 MS 的风险更高。大脑之间的这种联系，牙周病和全身性炎症预示着小胶质细胞（主要的先天免疫细胞）和星形胶质细胞（大脑中先天性和适应性免疫反应的关键调节因子）促成脑病理学的新途径。目前，对神经退行性变的发病机制缺乏了解正在阻碍治疗的发展。然而，我们可以通过简单的预防性口腔卫生措施来解决全身炎症的可能因素之一（牙周炎），从而预防这种发病机制。对神经退行性病变的发病机制缺乏了解阻碍了治疗的发展。然而，我们可以通过简单的预防性口腔卫生措施来解决全身炎症的可能因素之一（牙周炎），从而预防这种发病机制。对神经退行性病变的发病机制缺乏了解阻碍了治疗的发展。然而，我们可以通过简单的预防性口腔卫生措施来解决全身炎症的可能因素之一（牙周炎），从而预防这种发病机制。