| Project/Area Number |
17592129
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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 |
Orthodontic/Pediatric dentistry
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
KANNO Zuisei Tokyo Medical and Dental University Graduate School, Orthodontic Science, Assistant Professor, 大学院医歯学総合研究科, 助手 (40345301)
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| Co-Investigator(Kenkyū-buntansha) |
SOMA Kunimichi Tokyo Medical and Dental University Graduate School, Orthodontic Science, Professor & Chairman, 大学院医歯学総合研究科, 教授 (10014200)
MATSUMOTO Yoshiro Tokyo Medical and Dental University Graduate School, Orthodontic Science, Associate Professor, 大学院医歯学総合研究科, 講師 (20292980)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2006: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2005: ¥2,100,000 (Direct Cost: ¥2,100,000)
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| Keywords | autotransplantation / hypofunctional PDL / inflammatory cytokine / ankylosis / root resorption / regeneration of PDL |
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| Research Abstract |
While many studies reported the structural changes in the periodontal ligament (PDL) under hypofunctional conditions, the associations of cytokine growth factors are still unclear. They are known to take part in inflammation, and may affect the biological properties of hypofunctional tooth. To investigate the hypofunctional PDL and the recovery from this condition, we focused on interleukin-1 beta (IL-1) and basic fibroblast growth factor (FGF-2). The lack of occlusal stimuli caused atrophic changes in the PDL with the upregulation of IL-1 and decreased expression of FGF-2, while decreased IL-1 and enhanced FGF-2 expression were observed in the recovery process. These results suggest that occlusal stimuli regulate IL-1 and FGF-2 expression, and the nature of this regulation may differ from that in the healing process of an inflammatory reaction.
Our study also revealed that the occlusal stimuli promote the proliferation and differentiation of PDL cells with enhanced nitric oxide (NO) synthesis, while the lack of occlusal stimuli reduced the NO synthesis and induced atrophic changes in PDL which resulted in the dentoalveolar ankylosis.
Those results clarified that the mechanical stimulus, such as occlusal force, is an important factor for the regeneration of PDL, which could be regulated by NO and cytokine growth factors.
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