种植体周围上皮的组织病理学和免疫组织化学研究

Yoshikazu Nakayama, Chieko Taguchi, Mitsuko Nakayama, Masaaki Suemitsu, Kayo Kuyama
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引用次数: 0

摘要

背景:人β -防御素(HBDs),上皮来源的抗菌肽,有助于牙龈健康和牙周病。特别是,在牙周组织中上调HBD-3表达有助于牙周组织再生。具体来说,HBD-3在牙周组织中的表达上调有助于牙周组织再生。但是关于种植体周围炎的内上皮,特别是HBD表达模式对口腔感染的保护作用的研究还不够充分。目的:应用组织病理学和免疫组织化学方法研究种植体周炎种植体内上皮的组织病理学特征,并与牙周炎种植体内缘上皮进行比较。材料与方法:植周炎10例,牙周炎11例,对照组10例。进行HE观察、内上皮厚度测定、Ki-67、HBD-3免疫组化分析。结果:牙周炎组内上皮厚度(156.2 [138.0,186.4]μm)显著高于种植周炎组(70.7 [67.5,97.5]μm)和对照组(80.7 [76.6,89.4]μm) (p < 0.001)。内上皮和外上皮的Ki-67阳性率依次为:牙周炎、种植周炎和对照组(p < 0.001)。牙周炎患者的内上皮明显升高(p < 0.001)。对于HBD-3,在所有病例中,内上皮的强度和区域评分(IRS)均显著高于外上皮(浅层)(p < 0.001)。牙周炎内上皮的IRS值明显高于种植周炎(p < 0.001)。结论:组成种植体内上皮的角化细胞HBD-3分泌减少可能是影响种植体周围炎组织修复的因素之一。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Histopathological and Immunohistochemical Study of Peri-Implant Epithelium
Background: Human beta-defensins (HBDs), epithelial-derived antimicrobial peptides, contribute to gingival health and periodontal disease. Particularly, the upregulation of HBD-3 expression in periodontal tissues is described to contribute to periodontal tissue regeneration. Specifically, the upregulation of HBD-3 expression in periodontal tissues is described to contribute to periodontal tissue regeneration. But there has been insufficient investigation of the inner epithelium in peri-implantitis, especially the HBD expression patterns as protection against oral infection. Objectives: The purpose of this study was to investigate the histopathological characteristics of the inner implant epithelium in peri-implantitis using histopathological and immunohistochemical methods and to compare it with the inner marginal epithelium in periodontitis. Materials and Methods: The biopsied cases consisted of 10 peri-implantitis, 11 periodontitis, and 10 controls. HE observation, measurement of the thickness of the inner epithelium, and immunohistochemical analysis for Ki-67 and HBD-3 were conducted. Results: Concerning the thickness of the inner epithelium, it was significantly higher in periodontitis (156.2 [138.0, 186.4] μm) than in peri-implantitis and control, 70.7 [67.5, 97.5] μm and 80.7 [76.6, 89.4] μm, respectively (p < 0.001). The Ki-67 positivity rates, both for inner epithelium and outer epithelium, were significantly higher in the following order: periodontitis, peri-implantitis, and control (p < 0.001). The inner epithelium is significantly elevated in the case of periodontitis (p < 0.001). For HBD-3, the intensity and region score (IRS) was significantly higher for inner epithelium than for outer epithelium (superficial layer) (p < 0.001) in all cases. The comparisons of IRS, significantly higher values were seen in inner epithelium of periodontitis than that of peri-implantitis (p < 0.001). Conclusion: Decreased production of HBD-3 in keratinocytes composing the inner implant epithelium may be one of the factors affecting tissue repair in peri-implantitis.
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