Abstract：
OBJECTIVE: Periodontitis is a common oral disease that is aggravated by occlusal trauma. Fibrin is a protein that participates in blood clotting and is involved in several human diseases. The deposition of fibrin in periodontal tissues can induce periodontitis, while mechanical forces may regulate the degradation of fibrin. Our study investigated how occlusal trauma aggravating periodontitis through regulating the plasminogen/plasmin system and fibrin deposition.
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.
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.
摘要：
目的：牙周炎是一种常见的口腔疾病，因咬合创伤而加重。纤维蛋白是一种参与血液凝固的蛋白质，与几种人类疾病有关。牙周组织中纤维蛋白的沉积可以诱发牙周炎,而机械力可以调节纤维蛋白的降解。我们的研究调查了咬合创伤如何通过调节纤溶酶原/纤溶酶系统和纤维蛋白沉积来加重牙周炎。
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。
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。
