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Glyburide inhibits the bone resorption induced by traumatic occlusion in rats
Author(s) -
Arita Yoichi,
Yoshinaga Yasunori,
Kaneko Takashi,
Kawahara Yuri,
Nakamura Keiko,
Ohgi Kimiko,
Arita Seiichi,
Ryu Takanori,
Takase Minoru,
Sakagami Ryuji
Publication year - 2020
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1111/jre.12731
Subject(s) - medicine , occlusion , rankl , bone resorption , molar , resorption , dentistry , receptor , activator (genetics)
Objective To examine whether glyburide inhibits bone destruction caused by traumatic occlusion in a rat occlusal trauma model. Background Excessive mechanical stress, such as traumatic occlusion, induces expression of IL‐1β and may be involved in bone resorption. NLRP3 inflammasomes have been linked to IL‐1β expression, but it is currently unclear whether glyburide, the inhibiter of NLRP3 inflammasome, suppresses occlusal trauma in rats. Methods Male SD rats aged 7 weeks were used. In the trauma group, the occlusal surface of the maxillary first right molar was raised by attaching a metal wire to apply occlusal trauma to the mandibular first right molar. In the trauma + glyburide group, the NLRP3 inhibitor glyburide was administered orally every 24 hours from 1 day before induction of occlusal trauma. Rats were euthanized after 5 or 10 days, and the maxillary first molars were harvested with the adjacent tissues for histopathological investigation. Immunohistochemical expression of IL‐1β, NLRP3, and RANKL was also assessed. Results On day 5, bone resorption was significantly greater in the trauma group compared with the control group or the trauma + glyburide group, and there were significantly higher numbers of osteoclasts and cells positive for IL‐1β, NLRP3, and RANKL in the trauma group. Conclusion In this study, glyburide inhibits bone resorption by traumatic occlusion in rats. It suggests that the NLRP3/IL‐1β pathway might be associated with bone resorption induced by traumatic occlusion.