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  • 學位論文

牙菌斑及胃中幽門螺旋桿菌之探討

Helicobacter pylori in the dental plaque and the stomach

指導教授 : 何坤炎
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摘要


目的:幽門螺旋桿菌(Helicobacter pylori)是世界上最常見的病菌之一,與十二指腸潰瘍、胃潰瘍、胃炎關係密切,且會使潰瘍癒合延遲、潰瘍再發,與胃癌的發生也有一定的關係。牙菌斑提供只需少量氧氣即能生長的環境,有利於幽門螺旋桿菌之生長,但口腔是否為其永久的藏身之處還是莫衷一是。本研究的目的在探討胃部及牙菌斑中之幽門螺旋桿菌的關係。 材料與方法:本研究對象為至高雄醫學大學胃腸內科胃鏡檢查之患者152位,排除條件包括曾接受過腸胃道手術、無牙、以及一個月內曾接受藥物治療(包括質子幫浦抑制劑、抗生素、鉍鹽)者。所有患者均接受胃鏡檢查並同時於胃竇及胃體部切片,施行快速尿素酉每測試、細菌培養、組織學檢查及13C尿素呼氣試驗,並以幽門螺旋桿菌培養陽性或其他三項中二項陽性為胃部幽門螺旋桿菌陽性。胃鏡檢查當天收集牙菌斑樣本並記錄患者之牙菌斑指數及牙齦指數,以快速尿素酉每測試及聚合酉每鏈鎖反應檢測cagA基因。這些患者經藥物治療四個月後,再取胃黏膜切片及牙菌斑做同樣的檢測,以確定幽門螺旋桿菌根除治療的結果。 結果:分別以聚合酉每鏈鎖反應及快速尿素酉每測試檢測患者治療前牙菌斑中的狀況,與胃中感染情形之間的odds ratio分別為2.5及2.9,顯示牙菌斑有幽門螺旋桿菌存在確為胃部感染的危險因子之一。在根除治療後,牙菌斑中仍有幽門螺旋桿菌存在,顯示抗生素可能無法如在胃中有效根除牙菌斑中的細菌。胃中幽門螺旋桿菌陽性者之牙齦指數明顯高於陰性者,顯示口腔衛生對胃部的感染與否具有影響。 結論:牙菌斑中有幽門螺旋桿菌的存在,且於根除治療後仍存在牙菌斑中之幽門螺旋桿菌,可能為胃部感染再發的來源之一。

並列摘要


Objective. Helicobacter pylori is one of the most common pathogens worldwide. Many investigators had reported strong correlation between H. pylori and duodenal ulcer, gastric ulcer, gastritis, and even gastric cancer. The presence of H. pylori is also associated with delayed healing of ulcer and ulcer recurrence. Microaerophilic acidic environment of dental plaque can be an ideal environment for growth of H pylori. However, whether dental plaque is a potential reservoir for H. pylori remains controversial. The aim of this study is to investigate the relationship of H. pylori in the stomach and dental plaque. Material & Methods. One hundred and fifty-two patients who received gastric endoscopic biopsy in Kaohsiung Medical University Hospital were enrolled in our study. Patients were excluded if they were edentulous or had received gastrointestinal tract surgery and medical therapy that may alter the results (include proton pump inhibitors, antibiotics and compounds containing bismuth) within one month. Gastric specimens were obtained from gastric antrum and body, and were assessed by rapid urease test, culture, histology and 13C urea breath test. Gastric H. pylori infection was confirmed when the culture was positive or a concordance of two of the other three tests was positive. At the same day of endoscopy, dental plaque specimens were collected after recording the plaque index and gingival index of patients, and then assessed by rapid urease test (RUT) and polymerase chain reaction (PCR) (cagA gene). Four months after H. pylori eradication therapy for 4 months, above assessments were repeated to confirm the outcome of therapy. Results. The plaque before the eradication therapy was assessed by PCR and RUT respectively. Compared with the gastric infection status, the odds ratios were 2.5 and 2.9. It shows that the presence of H. pylori in dental plaque is one of the risk factors of gastric infection. The existence of H. pylori in the dental plaque after the eradication therapy indicated that the antibiotics might not be as effective in such a biofilm as in the stomach. The fact that the gingival index of gastric H. pylori (+) patients were significantly higher than gastric H. pylori (-) patients suggested that oral hygiene is important to gastric H. pylori infection status. Conclusions. Oral cavity is a reservoir of H. pylori, and the existence of H. pylori in the dental plaque after the eradication therapy infers that the recolonization of H. pylori from dental plaque may be a source of the transmission and recrudescence of gastsric infection.

參考文獻


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