Costa Moan Jéfter Fernandes, de Araújo Isabela Dantas Torres, da Rocha Alves Luana, da Silva Romerito Lins, Dos Santos Calderon Patricia, Borges Boniek Castillo Dutra, de Aquino Martins Ana Rafaela Luz, de Vasconcelos Gurgel Bruno Cesar, Lins Ruthineia Diogenes Alves Uchoa
Department of Dentistry, Federal University of Rio Grande do Norte, Av. Sen. Salgado Filho, 1787 - Lagoa Nova, Natal, RN, 59056-000, Brazil.
Clin Oral Investig. 2021 Mar;25(3):797-806. doi: 10.1007/s00784-020-03764-w. Epub 2021 Jan 20.
This study aimed to analyze the following PICO question: Are animals infected with Porphyromonas gingivalis (P. gingivalis) or bacterial lipopolysaccharide (Pg-LPS) more affected by neurodegeneration, similar to the pathogenesis generated by Alzheimer's disease (AD), compared with non-infected animals?
Databases PubMed, Lilacs, SciELO, Science Direct, Scopus, Web of Science, and Cochrane were searched for pre-clinical in vivo studies in which mice were infected with P. gingivalis or received Pg-LPS, in order to assess the brain tissue and cognitive impairment. No limit for date or publication language was imposed and this study was registered at the International Prospective Register of Systematic Reviews (PROSPERO), with nine articles included. Syrcle's protocol was used to evaluate bias in the selected studies.
Nine articles were included. Infection by P. gingivalis or the administration of Pg-LPS increased the production of the inflammatory mediators, TNF-α (tumor necrosis factor-alpha), IL-6 (interleukin-6), and IL-1β (interleukin-1beta), augmented Aβ (amyloid beta) production, and activated the complement system, causing inflammation, brain tissue degeneration, and cognitive impairment, consistent with the damage in AD.
Infection by P. gingivalis and Pg-LPS administration appears to be in relation with the pathogenesis of AD by activating the complement cascade, increasing Aβ production and augmenting pro-inflammatory cytokine expression, causing age-dependent brain inflammation, neuroinflammation, and neurodegeneration.
Taking into account the importance of holistic treatment in the dental office, this study focuses on identifying highly prevalent oral diseases, such as periodontal disease, as risk factors for the aggravation of degenerative diseases in the elderly population.
本研究旨在分析以下PICO问题:与未感染的动物相比,感染牙龈卟啉单胞菌(P. gingivalis)或细菌脂多糖(Pg-LPS)的动物是否更易受到神经退行性变的影响,类似于阿尔茨海默病(AD)所产生的发病机制?
检索了PubMed、Lilacs、SciELO、Science Direct、Scopus、Web of Science和Cochrane数据库,以查找小鼠感染牙龈卟啉单胞菌或接受Pg-LPS的临床前体内研究,以评估脑组织和认知障碍。对日期或出版语言没有限制,本研究已在国际系统评价前瞻性注册库(PROSPERO)注册,纳入了9篇文章。使用Syrcle的方案评估所选研究中的偏倚。
纳入9篇文章。牙龈卟啉单胞菌感染或Pg-LPS给药增加了炎症介质肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)和白细胞介素-1β(IL-1β)的产生,增加了β淀粉样蛋白(Aβ)的产生,并激活了补体系统,导致炎症、脑组织变性和认知障碍,这与AD中的损伤一致。
牙龈卟啉单胞菌感染和Pg-LPS给药似乎与AD的发病机制有关,通过激活补体级联反应、增加Aβ产生和增强促炎细胞因子表达,导致年龄依赖性脑炎症、神经炎症和神经退行性变。
考虑到综合治疗在牙科诊所的重要性,本研究着重于确定高度流行的口腔疾病,如牙周病,作为老年人群退行性疾病加重的危险因素。