| Project/Area Number |
10470405
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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 |
Conservative dentistry
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| Research Institution | Osaka University |
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Principal Investigator |
SHIMAUCHI Hidetoshi Faculty of Dentistry, Osaka University. Associate Professor, 歯学部, 助教授 (70187425)
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| Co-Investigator(Kenkyū-buntansha) |
KITAMURA Masahiro Dental Hospital, Osaka University. Assistant professor, 歯学部・附属病院, 講師 (10243247)
SHIMABUKURO Yoshio Faculty of Dentistry, Osaka University. Instructor, 歯学部, 助手 (50231361)
OKADA Hiroshi Faculty of Dentistry, Osaka University. Professor, 歯学部, 教授 (40038865)
NOZAKI Takenori Faculty of Dentistry, Osaka University. Instructor, 歯学部, 助手 (30263304)
SAHO Teruyuki Dental Hospital, Osaka University. Instructor, 歯学部・附属病院, 助手 (10263295)
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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 |
¥7,600,000 (Direct Cost: ¥7,600,000)
Fiscal Year 1999: ¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 1998: ¥6,000,000 (Direct Cost: ¥6,000,000)
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| Keywords | periapical periodontitis / pro-inflammatory cytokine / anti-inflammatory cytokine / superoxide / nitric oxide / growth factor / LPS-tolerance / cyclooxygenase-2 / 根尖性歯周病 / 活性酸素 / プロスタグランディン合成 / 調節性サイトカイン / 慢性化 / 免疫応答制御機構 / 根管浸出液 / IL-1β / IL-1ra / 単球 / マクロファージ / LPSトレランス / IL-10 |
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| Research Abstract |
Chronic periapical periodontitis is a chronic destructive disease characterized by an interaction of bacteria infected in the root canal system and the host immune cells. The local host response results in the release of wide array of the pro-and anti-inflammatory cytokines and mediators in the periapical lesion. We quantified the levels of IL-1β and IL-1ra in periapical exudates, and indicated that IL-1ra-mediated antagonism occurred to block locally produced IL-1 activity. Decreased IL-1ra : IL-1β ratio resulted in an acute and higher inflammatory activity in periapical lesion. Our quantitative analysis also revealed increased IL-8 production in the periapical exudate from symptomatic periapical lesion. A significantly positive correlation was found between IL-8 and nitric oxide levels. Semi-quantitative RT-PCR analysis was performed to determine the expression of pro- and anti-inflammatory cytokine and growth factor messages in the periapical tissue specimen. Results showed that COX
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-2 and IL-8 messages were present in all samples tested, and suggested up-regulated production of pro-inflammatory mediators in periapical lesions. On the other hand, anti-inflammatory cytokines, IL-10 and TGF-β1 mRNA was detected in most samples. We also showed the presence of IGF-1 and EGF messages in the majority of test specimens. In vitro studies also revealed that the chronic exposure of human monocytes to Porphyromonas gingivalis LPS resulted in the induction of LPS tolerance that resulted in the selective up-or down-regulation of cell functions. Our data also suggested that IL-10 mediate IL-6 down-regulation in P. gingivalis LPS-tolerant monocytes in an autocrine manner. These results suggest the potential involvement of both the pro-and anti-inflammatory cytokines and mediators in the regulation of chronic inflammatory disease periapical periodontitis. In conclusion, dissection of the precise role of these cytokines and mediators that have an impact on perapical pathogenesis may provide opportunities for the development of new diagnostic procedures and therapeutic agents. Less
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