| Project/Area Number |
21791927
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Prosthetic dentistry
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| Research Institution | Fukuoka College of Health Sciences (2010-2011)
Fukuoka Dental College (2009) |
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Principal Investigator |
GOTO-T Kazuko (2010-2011) 福岡医療短期大学, 歯科衛生学科, 准教授 (60389418)
後藤 加寿子 (2009) Fukuoka Dental College, 歯学部, 助教 (60389468)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2011: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2010: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2009: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
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| Keywords | ケモカイン / 咬合性外傷 / メカニカルストレス / CCL2 / CCL3 / CCL5 / 歯槽骨吸収 / 破骨細胞 / 顎骨 |
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| Research Abstract |
Excessive mechanical stress(MS) during hyperocclusion is known to result in disappearance of the alveolar hard line, enlargement of the periodontal ligament(PDL) space, and destruction of alveolar bone, leading to occlusal traumatism. We hypothesized that MS induces expression of osteoclastogenesis-associated chemokines in PDL tissue, resulting in chemotaxis and osteoclastogenesis during occlusal traumatism. We examined the effect of MS on relationships between chemokine expression and osteoclastogenesis using in vivo and in vitro hyperocclusion models. Using an in vitro model, intermittent stretching-induced MS was shown to upregulate the expression of CC chemokine ligand(CCL) 2, CCL3 and CCL5 in PDL cells. The expression levels of CCL2 in PDL tissues, its receptor CCR2 in preosteoclasts, and tartrate-resistant acid phosphatase-positive cells in alveolar bone were significantly upregulated 4.7 days after excessive MS during hyperocclusion in in vivo rodent models. Hyperocclusion predominantly induced CCL2 expression in PDL tissues and promoted chemotaxis and osteoclastogenesis, leading to MS-dependent alveolar bone destruction during occlusal traumatism.
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