{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,11]],"date-time":"2026-06-11T16:54:18Z","timestamp":1781196858553,"version":"3.54.1"},"reference-count":59,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2011,12,7]],"date-time":"2011-12-07T00:00:00Z","timestamp":1323216000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Molecular Oral Microbiology"],"published-print":{"date-parts":[[2012,2]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p>In periodontitis, an effective host\u2010response is primarily related to neutrophils loaded with serine proteases, including elastase (NE) and protease 3 (PR3), the extracellular activity of which is tightly controlled by endogenous inhibitors. <jats:italic>In vitro<\/jats:italic> these inhibitors are degraded by gingipains, cysteine proteases produced by <jats:italic>Porphyromonas gingivalis.<\/jats:italic> The purpose of this study was to determine the level of selected protease inhibitors in gingival crevicular fluid (GCF) in relation to periodontal infection. The GCF collected from 31 subjects (nine healthy controls, seven with gingivitis, five with aggressive periodontitis and 10 with chronic periodontitis) was analyzed for the levels of elafin and secretory leukocyte protease inhibitor (SLPI), two main tissue\u2010derived inhibitors of neutrophil serine proteases. In parallel, activity of NE, PR3 and arginine\u2010specific gingipains (Rgps) in GCF was measured. Finally loads of <jats:italic>P.\u00a0gingivalis<\/jats:italic>, <jats:italic>Aggregatibacter actinomycetemcomitans<\/jats:italic>, <jats:italic>Tannerella forsythia<\/jats:italic> and <jats:italic>Treponema denticola<\/jats:italic> were determined. The highest values of elafin were found in aggressive periodontitis and the lowest in controls. The quantity of elafin correlated positively with the load of <jats:italic>P.\u00a0gingivalis<\/jats:italic>, <jats:italic>Ta.\u00a0forsythia<\/jats:italic> and <jats:italic>Tr.\u00a0denticola<\/jats:italic>, as well as with Rgps activity. In addition, NE activity was positively associated with the counts of those bacterial species, but not with the amount of elafin. In contrast, the highest concentrations of SLPI were found in periodontally healthy subjects whereas amounts of this inhibitor were significantly decreased in patients infected with <jats:italic>P.\u00a0gingivalis<\/jats:italic>. Periodontopathogenic bacteria stimulate the release of NE and PR3, which activities escape the control through degradation of locally produced inhibitors (SLPI and elafin) by host\u2010derived and bacteria\u2010derived proteases.<\/jats:p>","DOI":"10.1111\/j.2041-1014.2011.00631.x","type":"journal-article","created":{"date-parts":[[2011,12,7]],"date-time":"2011-12-07T07:41:27Z","timestamp":1323243687000},"page":"45-56","source":"Crossref","is-referenced-by-count":33,"title":["Periodontal pathogens affect the level of protease inhibitors in gingival crevicular 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