Plasmin-Mediated Fibrinolysis in Periodontitis Pathogenesis

The hemostatic and inflammatory systems work hand in hand to maintain homeostasis at mucosal barrier sites. Among the factors of the hemostatic system, fibrin is well recognized for its role in mucosal homeostasis, wound healing, and inflammation. Here, we present a basic overview of the fibrinolytic system, discuss fibrin as an innate immune regulator, and provide recent work uncovering the role of fibrin-neutrophil activation as a regulator of mucosal/periodontal homeostasis. We reason that the role of fibrin in periodontitis becomes most evident in individuals with the Mendelian genetic defect, congenital plasminogen (PLG) deficiency, who are predisposed to severe periodontitis in childhood due to a defect in fibrinolysis. Consistent with plasminogen deficiency being a risk factor for periodontitis, recent genomics studies uncover genetic polymorphisms in PLG, encoding plasminogen, being significantly associated with periodontal disease, and suggesting PLG variants as candidate risk indicators for common forms of periodontitis.

Automated summary

The hemostatic and inflammatory systems cooperate to maintain homeostasis at mucosal barrier sites. Fibrin plays a crucial role in this process and acts as an immune regulator, influencing mucosal homeostasis, wound healing, and inflammation. Recent studies have revealed the role of fibrin-neutrophil activation in regulating mucosal and periodontal homeostasis. Individuals with congenital plasminogen deficiency, a genetic defect affecting fibrinolysis, are predisposed to severe periodontitis in childhood, highlighting the importance of fibrin in periodontal health. Genomic studies have also identified polymorphisms in the PLG gene, encoding plasminogen, as associated with periodontal disease, suggesting PLG variants as potential risk indicators.