Objective To study the histological change of microscrew-bone interface, detect the relative cytokine of gingival crevicular fluid, and explore the impossible mechanism of peri-implantitis. Methods Four male Beagles were collected. Randomly select one side of animals jaw as the experimental group to induce the peri-implantitis,and another side as the controll group. Four microscrews were implanted on each side. In the 1st, 2nd, 3rd, 4th weeks after implantation, collect peri-implant sulcular fluid(PISF) and detect tumor necrosis factor-α (TNF-α) levels before sacrificed, and the harvest tissue were observed in histological ways. Results According to the extension of time after implantation, the experimental group showed visible progress of interface destruction: 1st week after implantation showed large numbers inflammatory cells collected at the neck but did not undermine the cortical bone; 2nd week after implantation, cortical bone were observed angular absorption; Bone resorption continued to develop and at the 4th week, bone resorption were enlarged to the second thread of microscrew and the interface was filled with a large number of collagen fibers. Conclusion The destruction of interface began at the neck of microscrew, and the further development was along the interface in depth.Both microscrews with peri-implantitis and the healthy controls showed the presence of TNF-α. Inflammation accumulation might trigger the up-regulation of TNF-α level, and the onset of inflammation would enhance the up-trend.%目的 研究微种植体周围炎对微种植体-骨界面的组织学改变,同时对龈沟液相关细胞因子进行检测,从而探讨微种植体周围炎的发生机制.方法健康雄性Beagle纯种犬4只,采用自身对照,随机选定实验动物一侧为对照组,一侧为实验组,每侧植入4枚微种植体.实验组种植体颈部结扎丝线,诱导微种植体周围炎.在植入后第1、2、3、4周分别处死动物,处死前收集种植体周围龈沟液(PISF),酶联免疫吸附试验(EIJSA)检测肿瘤坏死因子-α(TNF-α)含量,收集标本做硬组织切片观察.结果 根据植入后时间的延长,实验组微种植体颈部表现明显的进展性破坏:植入1周微种植体颈部聚集大量炎性细胞,但并没有破坏皮质骨:植入2周微种植体颈部皮质骨已经出现少量角形吸收:植入3周表现骨吸收进一步向纵深发展:植入4周表现骨吸收已经至第二螺纹,充满火量胶原纤维.植入后1、2、3、4周,实验组与对照组PISF和TNF-α相比均有显著性差异(P<0.05),实验组高于对照组:实验组植入后4周PISF和TNF-α显著高于其余各阶段(P<0.05).结论 微种植体周围炎首先破坏结合界面颈部,并沿界面进一步纵深发展.无论是健康或者炎症的微种植体周围都有TNF-α吨表现,炎症的发生可能是造成TNF-α吨含量上调的始动因素,炎症的发生进一步加剧了TNF-α表达的上调.
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