Effect of HMGB1 on bone resorption induced by traumatic occlusion

2023 Fiscal Year Final Research Report

• Project/Area Number: 19K10154
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Review Section: Basic Section 57030:Conservative dentistry-related
• Research Institution: Nagasaki University
• Principal Investigator: UKAI TAKASHI 長崎大学, 病院(歯学系), 教授 (20295091)
• Co-Investigator(Kenkyū-buntansha): 吉村 篤利 長崎大学, 医歯薬学総合研究科(歯学系), 教授 (70253680)
• Project Period (FY): 2019-04-01 – 2024-03-31
• Keywords: HMGB1 / 破骨細胞 / 外傷性咬合

Outline of Final Research Achievements

Periodontal disease is caused by bacteria in plaque and is accelerated by an abnormal bite called traumatic occlusion. In the present study, it was confirmed histopathologically using immunohistological techniques that the molecule HMGB1 is strongly expressed in the periodontal ligament when the teeth of mice are subjected to traumatic occlusion. It was also confirmed that the function of this molecule could be suppressed by systemic administration of antibodies to HMGB1, thereby reducing the bone resorption caused by traumatic occlusion. It was also confirmed that the expression of factors that promote the induction of osteoclast differentiation, which causes bone resorption, was reduced. It is suggested that suppressing HMGB1 may suppress the expression of factors that induce osteoclast differentiation, thereby reducing the bone resorption seen with traumatic occlusion.

Free Research Field

歯周病学

Academic Significance and Societal Importance of the Research Achievements

成人の多くが歯周病により歯を失っている。その促進要因の一つである外傷性咬合による骨吸収を抑制することは歯を守るための戦略の一つとなるであろう。今回、外傷性咬合を付与した際に増加するHMGB1という分子に注目し、これが促進的に関与することを確認した。今回の結果から考えると外傷性咬合による歯肉の腫れや骨吸収が進行した際に、HMGB1を抑制する製剤を歯肉に注入することで骨吸収の進行を抑えられる可能性がある。今回の研究では全身投与の効果を示したのみであるので、局所投与でも効果があることを示し、臨床応用に向けて研究を進めていくのは国民の歯を守ることに役立つものと考えられる。