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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
Kogo, Mikihiko Department of Oral and Maxillofacial Surgery, Graduate School of Dentistry, Osaka University
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.
発行日
2016-05-31
出版物タイトル
International Journal of Oncology
49巻
2号
出版者
Spandidos
開始ページ
499
終了ページ
508
ISSN
1019-6439
NCID
AA10992511
資料タイプ
学術雑誌論文
言語
English
OAI-PMH Set
岡山大学
著作権者
https://creativecommons.org/licenses/by-nc-nd/4.0/deed.ja
論文のバージョン
publisher
PubMed ID
DOI
Web of Sience KeyUT
関連URL
isVersionOf https://doi.org/10.3892/ijo.2016.3548