Epidermal downgrowth around percutaneous devices produce sinus tracts, which then accumulate bacteria becoming foci of infection. This mode to failure is epidermal‐centric, and is accelerated by changes in the chemokines and cytokines of the underlying periprosthetic granulation tissue (GT). In order to more fully comprehend the mechanism of downgrowth, in this 28‐day study, percutaneous devices were placed in 10 Zucker diabetic fatty rats; 5 animals were induced with diabetes mellitus II (DM II) prior to the surgery and 5 animals served as a healthy, nondiabetic cohort. At necropsy, periprosthetic tissues were harvested, and underwent histological and polymerase chain reaction (PCR) studies. After isolating GTs from the surrounding tissue and extracting ribonucleic acids, PCR array and quantitative‐PCR (qPCR) analyses were carried‐out. The PCR array for 84 key wound‐healing associated genes showed a five‐fold or greater change in 31 genes in the GTs of healthy animals compared to uninjured healthy typical skin tissues. Eighteen genes were overexpressed and these included epidermal growth factor (EGF) and epidermal growth factor receptor (EGFR). Thirteen genes were underexpressed. When GTs of DM II animals were compared to healthy animals, there were 8 genes overexpressed and 25 genes underexpressed; under expressed genes included EGF and EGFR. The qPCR and immunohistochemistry data further validated these observations. Pathway analysis of genes up‐regulated 15‐fold or more indicated two, EGFR and interleukin‐10, centric clustering effects. It was concluded that EGFR could be a key player in exacerbating the epidermal downgrowth, and might be an effective target for preventing downgrowth.

中文翻译：

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表皮生长因子受体基因在经皮装置周围的假体周围软组织中过度表达：一项初步研究。

经皮装置周围的表皮向下生长产生窦道，然后积聚细菌成为感染病灶。这种失败模式是以表皮为中心的，并且会因潜在假体周围肉芽组织 (GT) 的趋化因子和细胞因子的变化而加速。为了更全面地理解向下生长的机制，在这项为期 28 天的研究中，在 10 只 Zucker 糖尿病肥胖大鼠中放置了经皮装置；5 只动物在手术前接受糖尿病 II (DM II) 诱导，5 只动物作为健康的非糖尿病组。在尸检时，收获假体周围组织，并进行组织学和聚合酶链反应 (PCR) 研究。从周围组织中分离出 GTs 并提取核糖核酸后，进行 PCR 阵列和定量 PCR (qPCR) 分析。84 个关键伤口愈合相关基因的 PCR 阵列显示，与未受伤的健康典型皮肤组织相比，健康动物 GT 中的 31 个基因发生了 5 倍或更大的变化。18 个基因过度表达，其中包括表皮生长因子 (EGF) 和表皮生长因子受体 (EGFR)。13 个基因表达不足。DM II 动物的 GT 与健康动物相比，有 8 个基因过表达，25 个基因表达不足；表达不足的基因包括 EGF 和 EGFR。qPCR 和免疫组织化学数据进一步验证了这些观察结果。对上调 15 倍或更多基因的通路分析表明 EGFR 和白细胞介素 10 两种中心聚类效应。结论是 EGFR 可能是加剧表皮向下生长的关键因素，