| 研究生: |
吳牧恒 Wu, Mu-Heng |
|---|---|
| 論文名稱: |
口腔菌相與口腔衰弱臨床因素之間的相關性研究 An Association Study Between Oral Microbiota and Clinical Factors of Oral Frailty |
| 指導教授: |
劉宗霖
Liu, Tsung-Lin |
| 學位類別: |
碩士 Master |
| 系所名稱: |
生物科學與科技學院 - 生物科技與產業科學系 Department of Biotechnology and Bioindustry Sciences |
| 論文出版年: | 2023 |
| 畢業學年度: | 111 |
| 語文別: | 英文 |
| 論文頁數: | 62 |
| 中文關鍵詞: | 口腔衰弱 、口腔菌相 、生物資訊 、宏觀基因組分析 、16S rRNA 定序 |
| 外文關鍵詞: | Oral frailty, Oral microbiota, Bioinformatics, Metagenomics analysis, 16S rRNA sequencing |
| 相關次數: | 點閱:123 下載:0 |
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口腔是具有咀嚼、吞咽和溝通等功能的重要器官,而這些功能下降被定義為口腔衰弱。口腔衰弱可能導致食物殘留和累積進而影響口腔衛生,造成包括口臭、牙周病、蛀牙和口腔發炎等口腔疾病。另一方面,口腔衰弱可能會影響口腔微生物。然而,口腔衰弱是否與特定的口腔細菌有關連,並且這些細菌與口腔疾病是否有關尚不清楚。為了瞭解口腔衰弱與口腔菌相的關聯性,在本研究中,我們收集了口腔衰弱患者和健康人的唾液樣本進行16S rRNA定序,並探討口腔菌相與口腔功能指標的關聯性。結果顯示,口腔衰弱導致口腔微生物群落的多樣性減少。具體而言,咀嚼能力低下組的口腔細菌多樣性比健康組低。β多樣性分析還顯示,咀嚼能力低下組及口腔衰弱組在細菌組成上與健康對照組有著顯著的差異。在多樣性分析之後,我們接著找出異常和健康對照組之間豐富度有差異的細菌,如乳酸菌和奈瑟氏菌屬而這些菌有在過去的文獻中被報導與口腔疾病有關。總結來說,口腔衰弱和咀嚼能力低下可能導致口腔細菌多樣性降低,且口腔衰弱和咀嚼能力與口腔細菌組成有關係。根據我們的分析的結果,我們推測口腔衰弱有可能透過改變口腔菌相組成來造成口腔疾病,這對未來口腔衰弱患者預防口腔疾病的方法有一個新的見解。
The human oral cavity is involved in chewing, swallowing, and speech. The impaired of oral functions, defined as oral frailty, may result in the accumulation of food residue or decreased oral hygiene, therefore causing many oral diseases including bad breath, periodontal disease, dental caries, and oral inflammation, etc. However, the relationship between oral frailty, oral microbiota, and their association with oral diseases remains unclear. Clarifying the connection between oral frailty and oral microbiota can pave the way to treating, diagnosing, and preventing oral frailty-related disease by changing oral microbiota. In this study, we collected saliva samples from patients with oral frailty and healthy individuals for sequencing. We performed a metagenomic and bioinformatic analysis combined with clinical factors information. Our findings indicate that oral frailty is associated with a lower in the diversity of the oral microbiota. Specifically, patients with poor chewing ability had significantly lower divers of oral microbiota than the normal group. Although other clinical factors were not statistically significant, the normal group's diversity was generally higher than that of the abnormal group. Our beta diversity analysis also showed that the chewing and oral frailty groups had distinct bacterial compositions between normal and abnormal groups. Following the diversity analysis, we investigated bacterial abundances that had differences between abnormal and normal groups, such as the Lactobacillus genera which has been reported associated with oral disease. In conclusion, our study reveals that oral frailty can influence the oral microbiota. In particular, chewing ability is the key clinical factor affecting the oral microbiota. Additionally, we found different abundance genera between oral frailty groups and within oral frailty clinical factor, these different abundance genera have been report has associated with oral disease. Suggests that oral frailty may cause oral disease by changing the oral microbiota. Our findings contribute to new insights into the treatment and prevention of oral diseases in patients with oral frailty.
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