| Project/Area Number |
10671778
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
病態科学系歯学(含放射線系歯学)
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| Research Institution | TOKYO DENTAL COLLEGE |
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Principal Investigator |
EBIHARA Yoko TOKYO DENT.COLL.,DEPT.,PROFESSOR, 歯学部, 教授 (00129355)
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| Co-Investigator(Kenkyū-buntansha) |
OKUDA Katsuji TOKYO DENT.COLL.,DEPT.DENTISTRY,PROFESSOR, 歯学部, 教授 (40085741)
ISHIHARA Kazuyuki TOKYO DENT.COLL.,DEPT.DENTISTRY,LECTURER, 歯学部, 講師 (00212910)
MIURA Tadashi TOKYO DENT.COLL.,DEPT.DENTISTRY,ASSISTANT, 歯学部, 助手 (10266570)
NOMA Hiroyasu TOKYO DENT.COLL.,DEPT.DENTISTRY,PROFESSOR, 歯学部, 教授 (40085791)
水野 嘉夫 東京歯科大学, 歯学部, 教授 (40051750)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥3,800,000 (Direct Cost: ¥3,800,000)
Fiscal Year 1999: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 1998: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Keywords | helicobacter pylori / oral cancer / transient bacteria |
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| Research Abstract |
We detected Helicobacter pylori (IL pylori) by the PCR method from the intraoral palaque, tongue, and saliva in patients with inraoral cancer and established a detection method. IL pylori was found at the gastic mucosa in 21 of 53 patients with intraoral cancer (36%). In the group of patients positive for H. pylori in the stomach, intraoral H. pylori was detected at a rate as high as 52% (11 patients). When the antagonism of intraoral normal bacteria flora to H. pylori was investigated, H. pylori inhibited the growth of most of the bacteria flora. When we looked at cocoagulation with H. pylori the organism was coagulated with only Fusobacterium nucleatum and porphyromonas gingivalis, but not other bacteria. In separate experiments, DNA amplified by PCR was cut by restriction enzymes such as Hae III, Ras I, Hiu fi, or Tag I in order to investigate its multiformation. This confirmed that both IL. Pylori in the mouth and gastric mucosa were genetically identical.
Although the presence of H. pylori in the mouth is clear from this finding, condition leading to the migration of H. pylori to the mouth and their growth there are poor and it was thus assumed that H. pylori might be present in there only temporarily by gastric reflux. However, in patients with intraoral cancer in whom the immunecompetence is decreased, while some H. pylori may be eliminated by the antagonism of intraoral normal bacteria flora, but remaining H. pylori may be trapped by other bacteria and thus be present at a high rate in the mouth. H. pylori was detected from the mucosa on the surface of intraoral cancer in three of 11 patients in whom H. pylori was found in the mouth. The bacteria were localized in the marginal epithelium of the cancer lesion, which was shown by postoperative H. E. staining. However, the number of the bacteria was so small that their direct involvement in the development of intraoral cancer was considered unlikely.
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