ID | 55408 |
フルテキストURL | |
著者 |
Yamada, Chiaki
Department of Oral and Maxillofacial Reconstructive Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Aikawa, Tomonao
Department of Oral and Maxillofacial Surgery, Graduate School of Dentistry, Osaka University
Okuno, Emi
Department of Oral and Maxillofacial Surgery, Graduate School of Dentistry, Osaka University
Miyagawa, Kazuaki
Department of Oral and Maxillofacial Surgery, Graduate School of Dentistry, Osaka University
Amano, Katsuhiko
Department of Oral and Maxillofacial Surgery, Graduate School of Dentistry, Osaka University
Takahata, Sosuke
Department of Oral and Maxillofacial Surgery, Graduate School of Dentistry, Osaka University
Kimata, Masaaki
Department of Oral and Maxillofacial Surgery, Graduate School of Dentistry, Osaka University
Okura, Masaya
Department of Oral and Maxillofacial Surgery, Graduate School of Dentistry, Osaka University
Iida, Seiji
Department of Oral and Maxillofacial Reconstructive Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Kaken ID
publons
researchmap
Kogo, Mikihiko
Department of Oral and Maxillofacial Surgery, Graduate School of Dentistry, Osaka University
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抄録 | Odontogenic tumors and cysts, arising in the jawbones, grow by resorption and destruction of the jawbones. However, mechanisms underlying bone resorption by odontogenic tumors/cysts remain unclear. Odontogenic tumors/cysts comprise odontogenic epithelial cells and stromal fibroblasts, which originate from the developing tooth germ. It has been demonstrated that odontogenic epithelial cells of the developing tooth germ induce osteoclastogenesis to prevent the tooth germ from invading the developing bone to maintain its structure in developing bones. Thus, we hypothesized that odontogenic epithelial cells of odontogenic tumors/cysts induce osteoclast formation, which plays potential roles in tumor/cyst outgrowth into the jawbone. The purpose of this study was to examine osteoclastogenesis by cytokines, focusing on transforming growth factor-β (TGF-β), produced by odontogenic epithelial cells. We observed two pathways for receptor activator of NF-κB ligand (RANKL) induction by keratocystic odontogenic tumor fluid: the cyclooxygenase-2 (COX-2)/prostaglandin E2 (PGE2) pathway through interleukin-1α (IL-1α) signaling and non-COX-2/PGE2 pathway through TGF-β receptor signaling. TGF-β1 and IL-1α produced by odontogenic tumors/cysts induced osteoclastogenesis directly in the osteoclast precursor cells and indirectly via increased RANKL induction in the stroma.
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発行日 | 2016-05-31
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出版物タイトル |
International Journal of Oncology
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巻 | 49巻
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号 | 2号
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出版者 | Spandidos
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開始ページ | 499
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終了ページ | 508
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ISSN | 1019-6439
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NCID | AA10992511
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資料タイプ |
学術雑誌論文
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言語 |
英語
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OAI-PMH Set |
岡山大学
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著作権者 | https://creativecommons.org/licenses/by-nc-nd/4.0/deed.ja
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論文のバージョン | publisher
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PubMed ID | |
DOI | |
Web of Science KeyUT | |
関連URL | isVersionOf https://doi.org/10.3892/ijo.2016.3548
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