Immunohistochemical analysis of the gingiva with periodontitis of type I plasminogen deficiency compared to gingiva with gingivitis and periodontitis and healthy gingiva

Serum, salivary, and tissue levels of plasminogen in familial Mediterranean fever, amyloidosis, and chronic periodontitis

“…As stated above, none of our patients with LP were also characterized by a PLG deficiency in this study. Although similar subgingival microbiological flora was observed in cases of periodontitis with a type 1 PLG deficiency as in other periodontal diseases, strong staining of elastase, matrix metalloproteinase (MMP)‐3 and MMP‐7 and weak staining of PLG in gingival tissues of patients with type 1 PLG deficiency support independent PLG fibrin clearance . Clearance of the PLG‐independent enzymatic fibrin through elastase and MMPs could also be responsible for the destruction of periodontal tissues in patients with FMF and/or amyloidosis.…”

“…Clearance of the PLG‐independent enzymatic fibrin through elastase and MMPs could also be responsible for the destruction of periodontal tissues in patients with FMF and/or amyloidosis. This hypothesis was supported by our histopathologic findings demonstrating severe periodontal inflammation, epithelial hyperplasia (n = 9), dystrophic calcification (n = 1), and stromal fibrosis (n = 2) in our patients with FMF.…”

Plasmin inhibition by bacterial serpin: Implications in gum disease

“…Pathological fibrin deposits in plasmin activity-deficient mice 13 and in cases of ligneous periodontitis in humans 11 suggest that these activities of miropin would have deleterious effects. The high in vivo expression of miropin at periodontitis sites 45 further argues that miropin may have significant effects on the pathobiological events during the initiation and progression of periodontitis.…”

“…Control of plasmin activity may prevent excessive activation of matrix metalloproteases, 11 which can degrade the collagen in periodontal ligament fibers. Control of plasmin activity may prevent excessive activation of matrix metalloproteases, 11 which can degrade the collagen in periodontal ligament fibers.…”

“…9 These receptors bind plasminogen, facilitate its activation, and protect surface-bound plasmin from inactivation. 11 Furthermore, antifibrinolytic therapy based on the use of tranexemic acid to block the binding of plasminogen to fibrin can occasionally lead to progressive periodontitis. 7 In humans, a rare (1 out of 1 million births) congenital plasminogen deficiency, referred to as type 1 plasminogen deficiency or hypoplasminogenemia, is defined by reduced levels of functional plasminogen in the circulation and is clinically manifested by mucous membrane thickening.…”