METHODS: This study included 84 C57BL/6 mice in which periodontitis was induced with or without occlusal trauma. Micro-computed tomography was used to assess bone resorption. Fibrin, fibrinogen, plasminogen, plasmin, tissue plasminogen activator (t-PA), and urokinase plasminogen activator (u-PA) levels were measured using Frazer-Lendrum staining, quantitative reverse transcription polymerase chain reaction, enzyme-linked immunosorbent assay, western blotting, immunofluorescence staining, and immunohistochemistry staining.
RESULTS: Occlusal trauma aggravated inflammation and bone resorption. The periodontitis group showed significant fibrin deposition. Occlusal trauma increased fibrin deposition and neutrophil aggregation. The periodontitis with occlusal trauma group had decreased fibrinogen, t-PA, and u-PA expression and plasmin and fibrin degradation product levels, as well as increased plasminogen levels.
CONCLUSIONS: Occlusal trauma promotes excessive fibrin deposition by suppressing the plasminogen/plasmin system, thus exacerbating periodontitis.
方法:这项研究包括84只C57BL/6小鼠,其中有或没有咬合创伤引起牙周炎。显微计算机断层扫描用于评估骨吸收。纤维蛋白,纤维蛋白原,纤溶酶原,纤溶酶,组织纤溶酶原激活剂(t-PA),和尿激酶纤溶酶原激活物(u-PA)水平测量使用Frazer-Lendrum染色,定量逆转录聚合酶链反应,酶联免疫吸附测定,西方印迹,免疫荧光染色,和免疫组织化学染色。
结果:咬合创伤加重炎症和骨吸收。牙周炎组显示显著的纤维蛋白沉积。咬合创伤增加了纤维蛋白沉积和中性粒细胞聚集。牙周炎伴咬合创伤组纤维蛋白原降低,t-PA,和u-PA表达和纤溶酶和纤维蛋白降解产物水平,以及增加的纤溶酶原水平。
结论:咬合创伤通过抑制纤溶酶原/纤溶酶系统促进过度的纤维蛋白沉积,从而加剧牙周炎。