摘要： 目的探讨CXCR2在小鼠种植体周围炎发病机制中的作用。方法将小鼠的右上颌第一磨牙拔除后即刻植入种植体，愈合4周达骨结合后，随机分为对照组、模型组和治疗组。通过结扎浸有热灭活牙龈卟啉单胞菌的丝线诱导种植体周围炎，治疗组腹腔注射CXCR2抑制剂SB225002，对照组及模型组注射生理盐水。连续注射14 d后，肉眼观察牙龈大体形态；应用Micro-CT检测种植体周围骨丧失情况；HE染色、免疫荧光染色分别检测牙龈总炎症细胞、中性粒细胞浸润情况；TRAP染色观察牙槽嵴顶破骨细胞数量差异；RT-PCR检测Cxcl1 （人白细胞介素-8小鼠功能同源物）及骨吸收相关因子Rankl mRNA表达情况。结果与对照组相比，模型组的骨吸收程度、中性粒细胞及破骨细胞数量、Cxcl1及Rankl mRNA表达水平显著升高。治疗组的骨吸收程度、中性粒细胞及破骨细胞数量、Cxcl1及Rankl mRNA表达水平较模型组显著降低。结论 CXCR2在小鼠种植体周围炎中参与中性粒细胞募集和破骨细胞生成，可能是种植体周围炎潜在的治疗靶点。

CXCR2参与调控小鼠种植体周围炎发病机制的研究

王少磊^1,2, 张倩¹, 宋续军^1,2, 李雪¹, 王丽喆^1,2, 刘杰¹

1. 青岛大学附属医院口腔修复科, 山东 青岛 266003;
2. 青岛大学口腔医学院口腔修复学教研室, 山东 青岛 266003

收稿日期:2021-11-29出版日期:2022-05-30发布日期:2022-05-28
通讯作者:刘杰
作者简介:王少磊(1994-),男,医师,硕士.
基金资助:山东省自然科学基金青年基金（ZR202102280377）；青岛市民生科技计划（19-6-1-51-nsh）


关键词: 种植体周围炎, CXCR2, 破骨细胞, 中性粒细胞
Abstract: Objective To investigate the role of the CXCR2 in the pathogenesis of peri-implantitis in mice. Methods Mice were implanted with titanium implants immediately after extraction of the right maxillary first molars. After achieving osseointegration,the mice were randomly divided into control,model,and treatment groups. Size'5-0' silk thread was then soaked with inactivated Porphyromonas gingivalis and ligated at the neck of the implant to induce peri-implantitis. The treatment group was intraperitoneally injected with the CXCR2 inhibitor SB225002. The control and model groups were injected with normal saline. After 14 days of continuous injection,the morphology of the peri-implant gingival tissue was visually observed,and bone resorption around the implant was detected using micro-computed tomography (Micro-CT). The infiltration of inflammatory cells and neutrophils was examined via hematoxylin-eosin and immunofluorescence staining,respectively. The number of osteoclasts in the alveolar crest was evaluated via tartrate-resistant acid phosphatase (TRAP) staining. The mRNA expression level of Cxcl1 and Rankl in the gingival tissue was detected via reverse transcription polymerase chain rection (RT-PCR). Results Micro-CT demonstrated that bone resorption around the implant was substantially decreased upon the administration of the CXCR2 inhibitor. Additionally,histology and TRAP staining showed less neutrophils and osteoclasts in the peri-implant tissues after the application of the CXCR2 inhibitor. Moreover,RT-PCR analysis showed that gingival mRNA expression of Cxcl1 and Rankl were significantly reduced by the CXCR2 inhibitor treatment. Conclusion Our study suggests that the CXCR2 is involved in neutrophil recruitment and osteoclastogenesis in mouse peri-implantitis and that it may be a potential therapeutic target for this process.
Key words: peri-implantitis, CXCR2, osteoclasts, neutrophils
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