從類澱粉-β胜肽含量之觀點探討牙周疾病與阿茲海默症之關聯性：系統性回顧與統合分析

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题名:	從類澱粉-β胜肽含量之觀點探討牙周疾病與阿茲海默症之關聯性：系統性回顧與統合分析 Association Between Periodontal Disease and Alzheimer’s Disease--From Amyloid-β Peptide Loading：A Systematic Review and Meta-Analysis
作者:	饒佳艾 Jao, Chia-Ai
贡献者:	牙醫學系碩博士班呂炫堃
关键词:	牙周感染;牙齒喪失;失智症;類澱粉途徑 periodontitis;tooth loss;dementia;amyloidogenic pathway
日期:	2019-01-03
上传时间:	2020-01-21 09:40:23 (UTC+8)
摘要:	Background: Periodontal disease (PD) is an oral chronic infection/inflammatory condition; it has been identified as a source of mediators of inflammation into the blood circulation which may contribute to exacerbating several diseases. Periodontitis is also one of the main reasons for tooth loss. Alzheimer’s disease (AD) is a chronic neurodegenerative disease that is responsible for 60-70% of dementia cases. The pathogenesis of AD is widely believed to be driven by the production and deposition of amyloid-β peptide (Aβ). In the last decade, several studies have suggested that there existed an association between periodontitis/tooth loss and AD. However, at this time the pathogenesis between periodontitis/tooth loss and AD remains unresolved. Purpose: The aim of this systematic review is to investigate if periodontitis/tooth loss increases Aβ deposition in the brain/serum and to confirm that periodontitis/tooth loss increases the risk of AD. Materials and Methods: A literature search (until the end of Nov 2018) was carried out using various databases (Medline/PubMed, Embase, Google Scholar and Cochrane Library) with language restriction to English. Two independent reviewers extracted data and assessed the risk bias (Newcastle–Ottawa scale and modified CAMARADES 10-item checklist). Meta-analyses were performed by: (1) using the levels of Aβ in serum in participants with or without periodontitis; (2) using the concentration of Aβ deposition in brain in animals with or without tooth loss. The mean difference was analyzed (P <0.05). Results: Twenty articles remained for full text reading. Finally, ten articles met the inclusion criteria. There were three parts: (1) three animal studies of Aβ deposition in brain for P. gingivalis (Pg)-infection; (2) one human study of Aβ deposition in the brain and two human studies of Aβ levels in serum for periodontitis; (3) tooth loss: four animal studies of Aβ deposition in brain and one human study of Aβ levels in serum. The included studies show that there is statistically more Aβ deposition in the brains of animals infected by P.gingivalis (Pg) and periodontitis patients (p = 0.002). However, there is no significant difference in the Aβ serum levels of periodontitis patients (overall: p = 0.34). There is also no difference between the concentration of Aβ deposition in the brains of animals with and without tooth extraction. (overall: p = 0.10) Furthermore, there is no significant difference in Aβ levels in the human study when comparing the different numbers of remaining teeth [Aβ40 (p = 0.559) and Aβ42 (p = 0.354)]. Conclusion: In this study, the included literature indicated that (1) Pg-infected animals show a significantly higher Aβ deposition in brain, which is the main pathogenesis of AD; (2) there is no relationship between levels of Aβ accumulation and periodontitis in human serum; (3) tooth loss may not be an indicator for increased Aβ loading. The present evidence shows that the correlation for increasing Aβ levels between periodontal infection and AD are inconclusive. Therefore, we speculate that the infection of periodontal pathogen through blood-brain barrier (BBB) would be a main issue for further research. To make the evidence stronger, more RCTs or epidemiological studies including a high number of participants are warranted.
描述:	碩士指導教授：呂炫堃委員：鄭景暉委員：陳立昇
数据类型:	thesis
显示于类别:	[牙醫學系] 博碩士論文

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