Trial study for the establishment of the new therapeutical method for periodontal disease that targets oxidation LDL receptor LOX-1.
| Project/Area Number |
26670895
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Periodontology
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| Research Institution | Meikai University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
OKAYASU Mari 東京大学, 医学部付属病院, 特任臨床医 (10610941)
SHIN Kitetsu 明海大学, 歯学部, 教授 (40187555)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 炎症性骨吸収 / 破骨細胞 / 歯周病 / 炎症性骨破壊 / 実験的歯周炎モデル / LOX-1 |
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| Outline of Final Research Achievements |
Increasing epidemiological studies indicate the close relationship between arteriosclerosis and periodontitis. Lectin-like oxidized LDL receptor-1 (LOX-1) was originally discovered as a responsible gene for atherosclerosis. In vitro osteoclast formation assay showed that LOX-1 negatively regulates osteoclasts differentiation by suppressing the cell-cell fusion of preosteoclasts. In this study, we attempted to develop an in vivo periodontitis model using mice. However, the development unfortunately does not still establish. Alternatively, we employed an in vivo inflammatory bone destruction model induced by daily lipopolysaccharide-injection into mouse calvariae. The inflammation-induced bone destruction was reduced by LOX-1 deficiency, in parallel with decreased expression of RANKL, a trigger molecule for osteoclast differentiation, in inflamed bones. Thus, the LOX-1 targeting could open a new therapeutical method for inflammatory periodontitis.
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Report
(3 results)
Research Products
(5 results)
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[Journal Article] Lectin-like oxidized low-density lipoprotein receptor-1 abrogation causes resistance to inflammatory bone destruction in mice, despite promoting osteoclastogenesis in the steady state.2015
Author(s)
Nakayachi M, Ito J, Hayashida C, Ohyama Y, Kakino A, Okayasu M, Sato T, Ogasawara T, Kaneda T, Suda N, Sawamura T, Hakeda Y
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Journal Title
Bone. 75:170-182
Volume: 75
Pages: 170-182
DOI
Related Report
Peer Reviewed / Open Access
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