재발성 아프타성 궤양 환자에서 Helicobacter pylori의 발현정도 및 병인과의 상관성
Incidence of Helicobacter pylori detected by PCR and its Relation to the Potential Etiology of Recurrent Aphthous Ulcerations
소속 상세정보
김현철/Kim HC
김재홍/이상섭/신경진/최종훈/김종열/Kim JH/Lee SS/Shin KJ/Choi JH/Kim CY
KMID : 0355220020270040401
Abstract
Patients, referred to the Department of Oral Diagnosis & Oral Medicine, College of Dentistry, Yonsei University, for recurrent aphthous ulcer(RAU), were subjected to analysis and evaluation of the presence and the detection rate of H. pylori, obtained from ulcer lesion on buccal mucosa, from normal buccal mucosa, and from supraginival plaques, with the use of polymerase chain reaction(PCR), to assess the role of H. pylori as an oral reservoir as well as an etiologic factor for RAU. The results are summarized as follows.
1. In a sample of the RAU group (RAU patients), 32.5% was H. pylori positive, of which ulcer lesion on buccal mucosa and plaques showed 35.0% and 30.0% of positivity respectively. In a sample of the history group (patients with history of RAU), 15.0% proved positive of H. pylori, in which buccal mucosa and plaques indicated 5.0% and 25.0% respectively.
Finally, in a sample of the control group, only 7.5% tested positive for H. pylori, in which buccal mucosa and plaque were positively identified with 10.0% and 5.0% respectively.
2. The RAU group and the control group showed statistically significant difference (P<0.01), whereas no difference was found between the RAU and the history group, or between the history and the control group.
3. Significant difference (P<0.05) was found when the buccal mucosa of the RAU group and that of the history group were compared. However, there was no evidence of significant difference between the RAU group and the control group, or between the history and the control group.
4. Significant difference (P<0.05) was also shown between plaques of the RAU group and those of the control group, when there was no difference between the RAU and the history group, or between the history and the control group.
Based on the data stated above, this investigation supports the hypothesis that H. pylori can be considered as a possible etiological factor for RAU, and that plaques play a role as an oral reservoir of H. pylori. However, need for more profound and comprehensive study (such as immunology, microbiology, molecular cell biology, etc.) can be required, using more subjects. Additionally, the investigation of the relationship between the RAU and the gastric ulcer, of which H. pylori is the cause, is considered to be of value.
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