| Project/Area Number |
12470470
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Periodontal dentistry
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| Research Institution | OKAYAMA UNIVERSITY |
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Principal Investigator |
MURAYAMA Yoji Graduate School of Medicine and Dentistry, Okayama University, Professor, 大学院・医歯学総合研究科, 教授 (50029972)
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| Co-Investigator(Kenkyū-buntansha) |
SHIKATA Kenichi Medical School Hospital, Okayama University, Assistant Professor, 医学部・附属病院, 講師 (00243452)
MAKINO Hirofumi Graduate School of Medicine and Dentistry, Okayama University, Professor, 大学院・医歯学総合研究科, 教授 (50165685)
NISHIMURA Fusanori Dental School Hospital, Okayama University, Assistant Professor, 歯学部・附属病院, 講師 (80208222)
FUKUDA Tetsuya Medical School Hospital, Okayama University, Assistant, 医学部・附属病院, 助手 (00304345)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥14,500,000 (Direct Cost: ¥14,500,000)
Fiscal Year 2001: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 2000: ¥12,700,000 (Direct Cost: ¥12,700,000)
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| Keywords | type 2 diabetes / obesity / insulin resistance / TNF-α / periodontitis / type 1 diabetes / sero-diagnosis / GAD antibody / 生活習慣病 / 歯周病 / 疑陽性 |
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| Research Abstract |
The number of diabetes increased markedly due possibly to the rapid change of our lifestyle, and to the increase in obese subjects with insulin resistance. Tumor necrosis factor-α (TNF-α) produced from adipocytes in the adipose tissues has been suggested to be affect insulin resistance in obese subjects. Apart from adipocytes, activated macrophages infiltrated in inflammatory lesion also produce large quantity of TNF-α. Based on these backgrounds, we hypothesized that successful periodontal treatment in diabetes patients may result in decrease in circulating TNF-α and subsequent metabolic control of diabetes. The results indicated that anti-microbial periodontal treatment resulted in marked decrease in 1) the number of microorganism in periodontal pockets and 2) circulating TNF-α concentration, and in significant improvement in 3) insulin resistance and 4) subsequent metabolic control.
We also found that some periodontitis patients exhibited increased anti-GAD antibody which is widely used as a sero-diagnostic marker in patients with type 1 diabetes. Generally, GAD is known to be produced in pancreatic β-cells and some nerve cells. However, we also found that fibroblastic cells including gingival fibroblasts express GAD both at gene and protein level. Thus, we thought that periodontal inflammation which destruct periodontal connective tissues resulted in the release of GAD and in exposure of such GAD to immune cells, led to the production of anti-GAD antibodies. Therefore, it is possible that periodontal inflammation influences sero-diagnosis of type 1 diabetes.
These results indicate that diabetes not only influence the susceptibility and progression of periodontitis, but periodontal inflammation also influences diabetic status. Thus, it can be concluded that periodontitis is an important complication of diabetes modulating the clinical course and diagnostic procedure of diabetes.
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