IL⁃17A对小鼠实验性牙周炎骨破坏作用研究
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国家自然科学基金(81470749,81771074);江苏省高校自然科学研究重大项目(16KJA320001);江苏省高层次卫生人才“六个一工程”(LGY2016048);江苏省高校优势学科建设工程资助项目(2018?87);江苏省卫生健康委科研课题(H2018044);江苏省高校自然科学研究项目面上项目(18KJB320012)


Effects of IL⁃17A on bone destruction in experimental periodontitis of mice
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    摘要:

    目的:通过构建白介素-17A(interleukin-17A,IL-17A)基因敲除小鼠实验性牙周炎模型,初探IL-17A参与调控牙周炎骨破坏的机制。方法:选用雄性IL-17A基因敲除(knock out,KO)的C57BL/6小鼠和相同基因背景的野生型(wild type,WT)C57BL/6小鼠,通过结扎和喂菌诱导小鼠实验性牙周炎,WT小鼠及KO小鼠均分为正常对照组和牙周炎组。确认结扎4周后处死小鼠收集上颌骨,进行Micro-CT断层成像、HE染色、抗酒石酸酸性磷酸酶(tartrate-resistant acid phosphatase,TRAP)染色、免疫组化和组织病理学分析。结果:在喂菌和结扎诱导的小鼠实验性牙周炎模型中,在Micro-CT的三维重建及近远中向截面上,KO小鼠较WT小鼠牙槽骨吸收减少,KO小鼠上颌第二磨牙牙槽嵴顶到釉牙骨质界的近中线性距离为(0.51 ± 0.11)mm,远中为(0.45 ± 0.04)mm,显著低于WT小鼠的近中(0.61 ± 0.09)mm和远中(0.65 ± 0.08)mm(P < 0.05);KO小鼠骨体积分数比为41.88 ± 1.82,显著高于WT小鼠的36.55 ± 2.08(P < 0.05);KO小鼠骨密度为84.39 ± 2.11,显著高于WT小鼠的76.90 ± 2.55(P < 0.05);HE染色中可见牙槽骨吸收减少;TRAP染色中可见TRAP染色阳性细胞减少;免疫组化结果显示牙周组织核因子κB受体活化因子配体(receptor activator of nuclear factor κB ligand,RANKL)的表达降低。结论:牙周炎中IL-17A可能有促进牙周炎发生发展及促进牙槽骨吸收的作用。

    Abstract:

    Objective:This study aimed to investigate the role of interleukin 17A(IL-17A) in the regulation of bone destruction in experimental periodontitis model. Methods:Male IL-17A knockout C57BL/6 mice and C57BL/6 wild type mice induced with ligation and Porphyromonasgingivalis infection were used to establish experimental periodontitis model in this study. Wild type mice and IL-17A knockout mice were divided into the normal group and the periodontitis group,respectively. The experimental periodontitis model mice were sacrificed 4 weeks after ligation to collect maxillary bones. Micro-computed tomography(Micro-CT),HE staining,TRAP staining,immunohistochemistry and histopathological analysis were performed to reveal the role of IL-17A on bone destruction and inflammation. Results:In the experimental periodontitis mice model induced with Porphyromonasgingivalis infection and ligation,IL-17A knockout mice showed less alveolar bone resorption in the three-dimensional reconstruction of Micro-CT than wild-type mice did. The mesial and distal linear distance from the alveolar bone crest(ABC) to the cementoenamel junction(CEJ) of maxillary second molars in the IL-17A knockout mice was(0.51 ± 0.11)mm and (0.45 ± 0.04)mm respectively,significantly less than those in wild-type mice(P < 0.05),which was(0.61 ± 0.09)mm and(0.65 ± 0.08)mm respectively. In addition,compared to wild-type mice,the mean bone volume fraction in IL-17A knockout mice was 41.88 ± 1.82,significantly higher than that in wild-type mice(36.55 ± 2.08,P < 0.05),and the bone mineral density in IL-17A knockout mice was 84.39 ± 2.11,significantly higher than that in wild-type mice(76.90 ± 2.55,P < 0.05). On the other hand,IL-17A knockout mice exhibited significantly less alveolar bone resorption in periodontal tissue in HE staining than wild-type mice;TRAP-positive cells and the expression of receptor activator of nuclear factor κB ligand(RANKL) in periodontal tissue were reduced as well. Conclusion:IL-17A may promote the development of periodontitis and alveolar bone resorption.

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吴偲偲,李 璐,徐 艳,王晓茜. IL⁃17A对小鼠实验性牙周炎骨破坏作用研究[J].南京医科大学学报(自然科学版),2019,(9):1376-1382

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  • 收稿日期:2019-01-20
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  • 在线发布日期: 2019-09-29
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