{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,19]],"date-time":"2026-07-19T00:45:56Z","timestamp":1784421956635,"version":"3.55.0"},"reference-count":34,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2007,7,1]],"date-time":"2007-07-01T00:00:00Z","timestamp":1183248000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Periodontology"],"published-print":{"date-parts":[[2007,7]]},"abstract":"<jats:p><jats:bold>Background:<\/jats:bold> Tissue plasminogen activator (t\u2010PA) and plasminogen activator inhibitor type 1 (PAI\u20101) are involved in the pathogenesis of periodontitis by controlling proteolytic events in the extracellular matrix. This study was designed to investigate the association of t\u2010PA and PAI\u20101 gene polymorphisms with chronic periodontitis (CP).<\/jats:p><jats:p><jats:bold>Methods:<\/jats:bold> One hundred eighty\u2010nine subjects were included. Genomic DNA was obtained from the peripheral blood of 84 patients with CP and 105 periodontally healthy subjects. Polymerase chain reaction and endonuclease digestion was used to genotype the 4G\/5G polymorphism in the promoter region of the PAI\u20101 gene and the Alu\u2010repeat insertion (I)\/deletion (D) polymorphism in intron 8 of the t\u2010PA gene.<\/jats:p><jats:p><jats:bold>Results:<\/jats:bold> The genotype distributions and allele frequencies of t\u2010PA polymorphism were not different between patients with CP and healthy subjects (24.7% I\/I, 45.7% I\/D, and 29.6% D\/D and 30.3% I\/I, 45.5% I\/D, and 24.2% D\/D, respectively; <jats:italic>P<\/jats:italic> &gt;0.05). The t\u2010PA D allele frequency was similar in patients with CP (52.4%) and healthy subjects (46.5%). PAI\u20101 genotype distribution in patients with CP (30.9% 4G\/4G, 35.8% 4G\/5G, and 33.3% 5G\/5G) and healthy subjects (36.2% 4G\/4G, 41.9% 4G\/5G, and 21.9% 5G\/5G) was also similar. The 4G allele frequency was not different between patients with CP (48.8%) and healthy subjects (57.1%) (<jats:italic>P<\/jats:italic> &gt;0.05). The 4G allele frequency in non\u2010smoking CP patients was significantly lower than in non\u2010smoking, healthy subjects (\u03c7<jats:sup>2<\/jats:sup> = 4.201; <jats:italic>P<\/jats:italic> = 0.040). Non\u2010smoking CP patients also had a significantly lower percentage of 4G\u2010positive genotypes compared to non\u2010smoking healthy subjects (\u03c7<jats:sup>2<\/jats:sup> = 5.046; <jats:italic>P<\/jats:italic> = 0.025).<\/jats:p><jats:p><jats:bold>Conclusions:<\/jats:bold> t\u2010PA or PAI\u20101 genotypes are not associated with susceptibility to CP in Turkish subjects. Conversely, the 4G allele of the PAI\u20101 gene could be related to a decreased susceptibility to CP in non\u2010smokers.<\/jats:p>","DOI":"10.1902\/jop.2007.060383","type":"journal-article","created":{"date-parts":[[2007,7,3]],"date-time":"2007-07-03T08:26:29Z","timestamp":1183451189000},"page":"1256-1263","source":"Crossref","is-referenced-by-count":13,"title":["Tissue Plasminogen Activator and Plasminogen Activator Inhibitor\u20101 Gene Polymorphisms in Patients With Chronic Periodontitis"],"prefix":"10.1002","volume":"78","author":[{"given":"Ali","family":"G\u00fcrkan","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"G\u00fclnur","family":"Emingil","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Buket 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