Department of Orthodontics, Center of Dento-Maxillo-Facial Medicine, University of Bonn, Bonn 53111, Germany.
Department of Orthodontics, Center of Dento-Maxillo-Facial Medicine, University of Bonn, Bonn 53111, Germany; Section of Experimental Dento-Maxillo-Facial Medicine, Center of Dento-Maxillo-Facial Medicine, University of Bonn, Bonn 53111, Germany.
Ann Anat. 2021 Mar;234:151648. doi: 10.1016/j.aanat.2020.151648. Epub 2020 Nov 20.
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.
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.
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 1d.
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.
本研究旨在评估趋化因子 CXCL5、CXCL8 和 CXCL10 在牙周细胞和组织中对微生物信号和/或生物机械力的反应表达。
使用来自炎症和健康部位的人牙龈活检组织，通过实时 PCR 和免疫组织化学检测趋化因子的表达和蛋白水平。还研究了经历实验性牙周炎和/或牙齿移动的大鼠牙龈活检组织中的趋化因子。此外，通过实时 PCR 和 ELISA 检测牙周成纤维细胞在牙周病原体福赛斯坦纳菌和/或持续张力 (CTS) 刺激下的趋化因子水平。此外，还通过实时 PCR 评估了在 MAPK 抑制剂存在或不存在的情况下，牙周成纤维细胞暴露于福赛斯坦纳菌和/或 CTS 时的基因表达。
与牙周健康相比，来自炎症部位的人牙龈和大鼠牙龈中的 CXCL5、CXCL8 和 CXCL10 水平升高。大鼠实验性牙周炎导致牙槽骨吸收显著增加（p<0.05），当与牙齿移动结合时，牙槽骨吸收进一步增加。在体外，福赛斯坦纳菌在第 1 天引起 CXCL5、CXCL8 和 CXCL10 的显著上调。一旦细胞同时暴露于福赛斯坦纳菌和 CTS，趋化因子的调节明显增强。转录发现也在蛋白质水平上得到观察。MEK1/2 抑制剂的预孵育显著（p<0.05）抑制了福赛斯坦纳菌单独或与 CTS 联合作用于 CXCL5、CXCL8 和 CXCL10 表达水平的刺激作用。
我们的数据提供了原始证据，表明生物力学应变进一步增强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更多的免疫炎症细胞募集到牙周组织，从而可能导致牙周炎和破坏的加重。
