Section of Periodontology, Department of Odontology, Fukuoka Dental College, Fukuoka, Japan.
Oral Medicine Research Center, Fukuoka Dental College, Fukuoka, Japan.
J Periodontal Res. 2020 Jun;55(3):464-471. doi: 10.1111/jre.12731. Epub 2020 Mar 10.
To examine whether glyburide inhibits bone destruction caused by traumatic occlusion in a rat occlusal trauma model.
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.
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.
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.
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.
研究格列本脲是否能抑制创伤性咬合大鼠咬合创伤模型中的骨破坏。
过度的机械应力,如创伤性咬合,会诱导白细胞介素-1β(IL-1β)的表达,并可能参与骨吸收。NLRP3 炎性小体与 IL-1β 的表达有关,但目前尚不清楚作为 NLRP3 炎性小体抑制剂的格列本脲是否能抑制大鼠的咬合创伤。
选用 7 周龄雄性 SD 大鼠。在创伤组中,通过在上颌第一右侧磨牙的咬合面上附加金属丝,施加咬合创伤于下颌第一右侧磨牙。在创伤+格列本脲组中,从诱导咬合创伤前 1 天开始,每天 24 小时口服给予 NLRP3 抑制剂格列本脲。在 5 天或 10 天后处死大鼠,取上颌第一磨牙及其邻近组织进行组织病理学研究。还评估了 IL-1β、NLRP3 和 RANKL 的免疫组织化学表达。
第 5 天,与对照组或创伤+格列本脲组相比,创伤组的骨吸收明显增加,且创伤组的破骨细胞数量和 IL-1β、NLRP3 和 RANKL 阳性细胞数量明显增加。
本研究表明,格列本脲抑制了大鼠因创伤性咬合导致的骨吸收。这提示 NLRP3/IL-1β 通路可能与创伤性咬合诱导的骨吸收有关。