高功率微波暴露抑制小鼠牙周组织成骨能力的效应与机制
党高鹏 , 朱轶娜 , 王雨竹 , 李婧 , 李翠侠 , 郭友祥 , 牛丽娜 , 顾俊婷
空军军医大学学报 ›› 2026, Vol. 47 ›› Issue (6) : 882 -888.
高功率微波暴露抑制小鼠牙周组织成骨能力的效应与机制
High-power microwave exposure impairs the osteogenic capacity of periodontal tissues in mice
目的 分析高功率微波(HPM)暴露对小鼠口腔牙周组织成骨能力的影响, 重点关注骨形态发生蛋白2(BMP-2)、骨钙素(OCN)及Runt相关转录因子2(Runx2)的表达变化, 初步阐明HPM暴露致口腔牙周组织损伤的具体机制。方法 选用8周龄SPF级雄性C57BL/6N小鼠, 随机分为对照组(假辐射处理)和HPM暴露组[采用微波源(2.856 GHz, 峰值功率密度200 W/cm2, 平均功率密度8 mW/cm2)单次辐射小鼠15 min, 4次/d]。第7日辐射处理后, 采集两组小鼠口腔牙周组织样本。通过HE染色观察牙周组织病理形态学改变; 采用qRT-PCR检测BMP-2、OCN、Runx2的mRNA表达水平; 使用ELISA、免疫组化、免疫荧光染色检测样本中BMP-2、OCN、Runx2的蛋白表达情况。结果 与对照组相比, HPM暴露组小鼠牙周膜纤维束松散、断裂, 排列方向紊乱, 与骨组织连接面可见间隙, 骨小梁变细、稀疏, 部分区域可见骨吸收陷窝; BMP-2、OCN的mRNA及蛋白表达显著下调, 而Runx2的表达情况与对照组相比差异无统计学意义。结论 本研究证实HPM辐射可导致小鼠口腔牙周组织发生病理损伤, 其机制与下调牙周膜及牙槽骨表面BMP-2、OCN的表达, 以及抑制牙周组织修复及骨代谢平衡有关。本研究为HPM暴露环境下作业人员的口腔健康风险评估提供了实验基础, 也为后续相关防治策略提供了新的方向。
Objective To analyze the effects of high-power microwave (HPM) exposure on the osteogenic capacity of oral periodontal tissues in mice, with a focus on the expression changes of bone morphogenetic protein-2 (BMP-2), osteocalcin (OCN), and runt-related transcription factor 2 (Runx2), thereby preliminarily elucidating the specific mechanisms by which HPM exposure causes damage to oral periodontal tissues. Methods Eight-week-old SPF-grade male C57BL/6N mice were selected and randomly divided into a control group (pseudo-radiation treatment) and an HPM exposure group [using a microwave source (2.856 GHz, peak power density 200 W/cm2, average power density 8 mW/cm2) for 15 min at a single time, 4 times a day]. Oral periodontal tissue samples were collected from both groups after the 7th day of radiation exposure. HE staining was used to observe pathological morphological changes in periodontal tissues. qRT-PCR was employed to detect mRNA expression levels of BMP-2, OCN, and Runx2. ELISA, immunohistochemistry, and immunofluorescence staining were used to assess protein expression of BMP-2, OCN, and Runx2 in the samples. Results Compared with the control group, HPM-exposed mice exhibited loosened and fractured periodontal ligament fiber bundles with disordered alignment. Gaps appeared at the bone attachment surfaces, accompanied by thinner and sparser trabeculae, with resorption pits visible in some areas. The mRNA and protein expressions of BMP-2 and OCN were significantly down-regulated, while the expression of Runx2 showed no statistical significance compared with the control group. Conclusion This study confirms that HPM radiation induces pathological damage in mouse oral periodontal tissues. The mechanism involves downregulation of BMP-2 and OCN expression on the periodontal ligament and alveolar bone surfaces, coupled with inhibition of periodontal tissue repair and bone metabolic balance. This study provides an experimental basis for assessing the oral health risks of workers exposed to HPM, and also offers a new direction for subsequent related prevention and control strategies.
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国家自然科学基金杰出青年科学基金(82325012)
国家自然科学基金青年科学基金(82301043)
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