A study of molecular mechanisms of jaw bone resorption by tumors: Focousing on regulation of RANKL expression.

2019 Fiscal Year Final Research Report

• Project/Area Number: 16K11682
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Surgical dentistry
• Research Institution: Osaka University
• Principal Investigator: Aikawa Tomonao 大阪大学, 歯学研究科, 准教授 (00362674)
• Co-Investigator(Kenkyū-buntansha): 宮川 和晃 大阪大学, 歯学部附属病院, 医員 (50635381)
• Project Period (FY): 2016-04-01 – 2020-03-31
• Keywords: 骨吸収 / 顎骨 / 腫瘍 / RANKL / TGF-b / IL-6

Outline of Final Research Achievements

The odontogenic tumor, odontogenic cyst, and oral cancer are the representative diseases which grow with resorption and destruction of the jaw bone. However, the mechanisms of bone resorption and destruction by those disease are still unclear.
We focused on Transforming growth factor beta (TGF-b) which were produced by odontogenic tumor, cyst, and oral cancer, we studied the mechanisms of induction of RANKL, an osteoclast inducing factor, in stromal fibroblasts. Furthermore, we successfully made the mouse experimental model which mimic the findings of clinical bone resorption by oral cancer, one was severe bone resorption by cancer cells, and the other was mild bone resorption by the same cell line cells but cells from different strain. We studied the mechanisms of bone resorption using the experimental model.

Free Research Field

歯学、外科系歯学、口腔外科学

Academic Significance and Societal Importance of the Research Achievements

歯原性腫瘍、歯原性嚢胞は口腔がんは骨吸収と骨破壊をしながら増大しますが、どのように骨吸収されるかの分子機序がわかっていないため、どの分子を標的に治療するのかが明らかではありません。今回の研究ではTransforming growth factor beta, Interleukin-1, Interleukin-6の相互作用で破骨細胞活性化因子であるRANKL発現の調整を研究しました。これらの基礎研究の成果の蓄積で、新たな治療標的となる分子が明らかになることが期待される。