Wang Xiaoyu, Hu Jiangqi, Jiang Qingsong
Department of Prosthodontics, Beijing Stomatology Hospital, School of Stomatology, Capital Medical University, Beijing, China.
Front Neurosci. 2022 Feb 10;16:811335. doi: 10.3389/fnins.2022.811335. eCollection 2022.
There is a dose-response relationship between tooth loss and cognitive impairment, while tooth loss can be an independent risk factor for Alzheimer's disease (AD) and vascular dementia (VaD). Tooth loss can also accelerate nerve damage and neurodegeneration. However, the associated mechanisms remain poorly understood.
To conduct a systematic review of animal experiments on cognitive decline caused by the loss of occlusal support performed over the past 10 years and summarize the possible underlying mechanisms.
"Tooth Loss," "Edentulous," "Tooth Extraction and Memory Loss," "Cognition Impairment," and "Dementia" were used as keywords to search PubMed, Embase, SCI, ScienceDirect, and OpenGrey. A total of 1,317 related articles from 2010 to 2021 were retrieved, 26 of which were included in the review after screening according to predetermined inclusion and exclusion criteria. Comprehensiveness was evaluated using ARRIVE guidelines and the risk of bias was assessed using SYCLE'S risk of bias tool.
The putative mechanisms underlying the cognitive impairment resulting from the loss of occlusal support are as follows: (1) The mechanical pathway, whereby tooth loss leads to masticatory motor system functional disorders. Masticatory organ activity and cerebral blood flow decrease. With reduced afferent stimulation of peripheral receptors (such as in the periodontal membrane) the strength of the connections between neural pathways is decreased, and the corresponding brain regions degenerate; (2) the aggravation pathway, in which tooth loss aggravates existing neurodegenerative changes. Tooth loss can accelerates nerve damage through apoptosis and mitochondrial autophagy, increases amyloid deposition in the brain; and (3) the long-term inflammatory stress pathway, which involves metabolic disorders, microbial-gut-brain axis, the activation of microglia and astrocytes, and inflammatory cascade effect in central nervous system.
The loss of occlusal support may lead to cognitive dysfunction through the reduction of chewing-related stimuli, aggravation of nerve damage, and long-term inflammatory stress.
牙齿缺失与认知障碍之间存在剂量反应关系，牙齿缺失可能是阿尔茨海默病（AD）和血管性痴呆（VaD）的独立危险因素。牙齿缺失还会加速神经损伤和神经退行性变。然而，相关机制仍知之甚少。
对过去10年进行的关于咬合支持丧失导致认知衰退的动物实验进行系统综述，并总结可能的潜在机制。
以“牙齿缺失”“无牙”“拔牙与记忆丧失”“认知障碍”和“痴呆”作为关键词，检索PubMed、Embase、SCI、ScienceDirect和OpenGrey。共检索到2010年至2021年的1317篇相关文章，根据预先设定的纳入和排除标准筛选后，其中26篇纳入综述。使用ARRIVE指南评估全面性，使用SYCLE偏倚风险工具评估偏倚风险。
咬合支持丧失导致认知障碍的潜在机制如下：（1）机械途径，牙齿缺失导致咀嚼运动系统功能障碍。咀嚼器官活动和脑血流量减少。随着外周感受器（如牙周膜中的感受器）传入刺激减少，神经通路之间的连接强度降低，相应脑区发生退化；（2）加重途径，牙齿缺失加剧现有的神经退行性变化。牙齿缺失可通过细胞凋亡和线粒体自噬加速神经损伤，增加大脑中淀粉样蛋白沉积；（3）长期炎症应激途径，涉及代谢紊乱、微生物-肠道-脑轴、小胶质细胞和星形胶质细胞的激活以及中枢神经系统中的炎症级联效应。
咬合支持丧失可能通过减少咀嚼相关刺激、加重神经损伤和长期炎症应激导致认知功能障碍。
