Analysis of the relationship between HMGB1 and necroptosis in dental pulpitis

2022 Fiscal Year Final Research Report

• Project/Area Number: 20K18499
• Research Category: Grant-in-Aid for Early-Career Scientists
• Allocation Type: Multi-year Fund
• Review Section: Basic Section 57030:Conservative dentistry-related
• Research Institution: Tokyo Medical and Dental University
• Principal Investigator: Hashimoto Kentaro 東京医科歯科大学, 大学院医歯学総合研究科, 助教 (80825662)
• Project Period (FY): 2020-04-01 – 2023-03-31
• Keywords: HMGB1

Outline of Final Research Achievements

To investigate the induction of inflammatory mediator production by HMGB1 and the expression of HMGB1 in inflamed dental pulp, mouse dental papilla cells (MDP) were treated at various temperatures, and the resulting cell supernatants were added to MDP. As a result, an increase in the release of HMGB1 protein and the upregulation of Interleukin-6 (IL6), an inflammatory cytokine, gene expression were observed at 52°C treatment. Additionally, an enhancement of NF-κB p65 phosphorylation was observed. These findings suggest that even temporary exposure of dental pulp tissue to high temperatures induces the production of DAMPs, including HMGB1, and the produced HMGB1 may induce the production of inflammatory mediators through the phosphorylation of NF-κB.

Free Research Field

歯髄

Academic Significance and Societal Importance of the Research Achievements

健康寿命の伸ばすためには歯の保存が必要である。歯を長期にわたって口腔内で保存するためには歯髄の保存が重要である。歯髄炎・歯髄壊死は歯髄を失う原因である。通常の歯髄炎ではう蝕によっておこるが、う蝕のない歯においても歯髄炎や歯髄壊死を認めることがある。High mobility group box 1(HMGB1)と呼ばれる核内タンパク質はダメージを受けた細胞から放出され炎症を修飾する。この研究ではHMGB1と歯髄細胞の炎症との関連について調べた。この研究は歯髄における非感染性の炎症のメカニズムの一端を解明する一助となり将来歯髄炎を抑制する治療戦略の創生につながることが期待できる。