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Tissue plasminogen activator (t‐PA) and placental plasminogen activator inhibitor (PAI‐2) in gingival crevicular fluid from patients with Papillon–Lefèvre syndrome
Author(s) -
Ullbro Christer,
Kinnby Bertil,
Lindberg Pia,
Matsson Lars
Publication year - 2004
Publication title -
journal of clinical periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.456
H-Index - 151
eISSN - 1600-051X
pISSN - 0303-6979
DOI - 10.1111/j.1600-051x.2004.00551.x
Subject(s) - plasminogen activator , medicine , gingivitis , tissue plasminogen activator , pathological , periodontitis , inflammation , plasminogen activator inhibitor 1 , fibrin , gastroenterology , pathogenesis , clinical attachment loss , pathology , dentistry , immunology
Objectives: Numerous patients with Papillon–Lefèvre syndrome (PLS) express a severe periodontal inflammation that results in premature loss of deciduous and permanent teeth. The plasminogen activating (PA) system is involved in physiological and pathological processes including epithelial healing, extracellular proteolysis and local inflammatory reactions. The aim of the study was to explore a possible role of the PA system in patients with PLS. Material and Methods: Samples of gingival crevicular fluid (GCF) were collected from areas with gingival infection in 20 patients with PLS and in 20 healthy controls. The concentration of tissue plasminogen activator (t‐PA) and inhibitor (PAI‐2) was measured with ELISA. Results: The median level of PAI‐2 was significantly higher ( p <0.01) in PLS patients than in the controls, while the median value of t‐PA did not differ between the groups. No difference in t‐PA or PAI‐2 levels was found regarding age, gender or presence of active periodontal disease. Conclusion: The findings indicate an atypical activity of the PA system with a disturbed epithelial function in PLS patients, suggesting that the periodontal destruction seen in patients with PLS is secondary to a hereditary defect in the defense system.