Affiliation:
1. The State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases, Department of Prosthodontics, West China Hospital of Stomatology Sichuan University Sichuan China
2. The State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases, Department of General Clinic, West China Hospital of Stomatology Sichuan University Sichuan China
3. The State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases, Department of Oral Implantology, West China Hospital of Stomatology Sichuan University Sichuan China
Abstract
AbstractObjectivesPeriodontitis 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.Materials and MethodsThis 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.ResultsOcclusal 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.ConclusionOcclusal trauma promotes excessive fibrin deposition by suppressing the plasminogen/plasmin system, thus exacerbating periodontitis.