Objective

The aim of the present study was to evaluate the expressions of CXCL5, CXCL8, and CXCL10 in periodontal cells and tissues in response to microbial signals and/or biomechanical forces.

Methods

Human gingival biopsies from inflamed and healthy sites were used to examine the chemokine expressions and protein levels by real-time PCR and immunohistochemistry. The chemokines were also investigated in gingival biopsies from rats submitted to experimental periodontitis and/or tooth movement. Furthermore, chemokine levels were determined in human periodontal fibroblasts stimulated by the periodontopathogen Fusobacterium nucleatum and/or constant tensile forces (CTS) by real-time PCR and ELISA. Additionally, gene expressions were evaluated in periodontal fibroblasts exposed to F. nucleatum and/or CTS in the presence and absence of a MAPK inhibitor by real-time PCR.

Results

Increased CXCL5, CXCL8, and CXCL10 levels were observed in human and rat gingiva from sites of inflammation as compared with periodontal health. The rat experimental periodontitis caused a significant (p < 0.05) increase in alveolar bone resorption, which was further enhanced when combined with tooth movement. In vitro, F. nucleatum caused a significant upregulation of CXCL5, CXCL8, and CXCL10 at 1 day. Once the cells were exposed simultaneously to F. nucleatum and CTS, the chemokines regulation was significantly enhanced. The transcriptional findings were also observed at protein level. Pre-incubation with the MEK1/2 inhibitor significantly (p < 0.05) inhibited the stimulatory actions of F. nucleatum either alone or in combination with CTS on the expression levels of CXCL5, CXCL8, and CXCL10 at 1 d.

Conclusions

Our data provide original evidence that biomechanical strain further increases the stimulatory actions of periodontal bacteria on the expressions of these chemokines. Therefore, biomechanical loading in combination with periodontal infection may lead to stronger recruitment of immunoinflammatory cells to the periodontium, which might result in an aggravation of periodontal inflammation and destruction.

中文翻译：

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牙周组织中细菌和机械力对 CXCL5、CXCL8 和 CXCL10 的调节

客观的

本研究的目的是评估 CXCL5、CXCL8 和 CXCL10 在牙周细胞和组织中的表达，以响应微生物信号和/或生物力学力。

方法

来自发炎和健康部位的人类牙龈活检用于通过实时 PCR 和免疫组织化学检查趋化因子表达和蛋白质水平。还在接受实验性牙周炎和/或牙齿移动的大鼠的牙龈活检中研究了趋化因子。此外，通过实时 PCR 和 ELISA测定了由牙周病原体具核梭杆菌和/或恒定张力 (CTS)刺激的人牙周成纤维细胞中的趋化因子水平。此外，在存在和不存在 MAPK 抑制剂的情况下，通过实时 PCR 在暴露于具核梭菌和/或 CTS 的牙周成纤维细胞中评估基因表达。

结果

与牙周健康相比，在人和大鼠牙龈炎症部位观察到 CXCL5、CXCL8 和 CXCL10 水平升高。大鼠实验性牙周炎导致 牙槽骨吸收显着增加（ p < 0.05），当与牙齿移动相结合时进一步增强。在体外，F. nucleatum在 1 天引起 CXCL5、CXCL8 和 CXCL10 的显着上调。一旦细胞同时暴露于F. nucleatum和 CTS，趋化因子调节显着增强。在蛋白质水平上也观察到转录结果。与 MEK1/2 抑制剂预孵育显着 ( p  < 0.05) 抑制F. nucleatum的刺激作用单独或与 CTS 联合使用对 CXCL5、CXCL8 和 CXCL10 在 1 d 表达水平的影响。

结论

我们的数据提供了原始证据，表明生物力学应变进一步增加了牙周细菌对这些趋化因子表达的刺激作用。因此，生物力学负荷与牙周感染相结合可能导致免疫炎症细胞更强地募集到牙周组织，这可能导致牙周炎症和破坏的恶化。