Identification of novel mechanisms of direct bone demineralization by ameloblastoma

2015 Fiscal Year Final Research Report

• Project/Area Number: 24592991
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Surgical dentistry
• Research Institution: Fukuoka Dental College (2014-2015); Kyushu University (2012-2013)
• Principal Investigator: Morita Hiromitsu 福岡歯科大学, 歯学部, 准教授 (30380463)
• Co-Investigator(Kenkyū-buntansha): MITSUYASU Takeshi 九州大学, 大学病院, 助教 (00380519) ; NAKAMURA Seiji 九州大学, 歯学研究院, 教授 (60189040) ; ITO Yushi 久留米大学, 医学部, 教授 (80037506)
• Co-Investigator(Renkei-kenkyūsha): HIRATA Masato 九州大学, 歯学研究院, 教授 (60136471)
• Project Period (FY): 2012-04-01 – 2016-03-31
• Keywords: 口腔外科学一般 / エナメル上皮腫 / 骨吸収 / V-ATPase / CLC-7

Outline of Final Research Achievements

Ameloblastoma is the most common benign odontogenic tumor in Japan. It is believed that it expands in the jaw bone through peritumoral activation of osteoclasts by RANKL released from the ameloblastoma. However, we found that ameloblastoma cells (AM-1) formed resorption pits on calcium phosphate-coated plates by activation of V-ATPase and CLC-7 like osteoclasts. This demineralization activity was inhibited by application of bafilomycin A1, a typical V-ATPase blocker. Furthermore, V-ATPase and CLC-7 were detected on the surface of AM-1 cells by plasma membrane biotinylation and immunofluorescence analysis. Immunohistochemical analysis of clinical samples of ameloblastoma also showed plasma membrane-localized V-ATPase and CLC-7 in the epithelium of plexiform, follicular and basal cell types. These results suggest that the expansion of several typical types of ameloblastomas in jaw bone is attributable to its demineralization ability.

Free Research Field

イオンチャネル病態生理学