2012 Fiscal Year Final Research Report
The elucidation of sharing roles of periodontal ligament cells and alveolar bone osteoblasts in orthodontic-force responsive osteoclast formation.
| Project/Area Number |
22592298
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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 | Nihon University |
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Principal Investigator |
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| Research Collaborator |
KOTOEMAYAHARA Kotoe 日本大学, 歯学部, 助教 (60440046)
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| Project Period (FY) |
2010 – 2012
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| Keywords | メカニカルストレス / 破骨細胞 / RANKL / 歯根膜細胞 / 骨芽細胞 / PGE_2 |
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| Research Abstract |
Periodontal ligament cells (PDLs) produce PGE_2 during orthodontic tooth movement. PGE_2 is a potent osteoclast-inducing factor that induces RANKL. In this study, we compared the functional difference in osteoclastogenesis between human PDLs (HPDLs) and normal human osteoblasts (HOBs) as a direct effect of PGE_2 exposure.We examined the expression of RANKL with or without PGE_2 in HPDLs and HOBs. Then, RAW264.7 cells were co-cultured on HPDLs or HOBs pretreated with PGE_2. PGE_2 exposure increased significantly RANKL expression in HOBs compared with HPDLs. The number of tartrate-resistant acid phosphatase staining osteoclast-like cells from RAW264.7 cells increased significantly by PGE_2 pretreatment in HOBs and was reduced by small interfering RNA knockdown of RANKL. These results suggest that osteoblasts strongly influence the stimulation of osteoclastogenesis via RANKL, induced byPGE2 in periodontal tissues, compared with PDLs.
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