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Activity and inhibition of elastase in GCF
Author(s) -
Figueredo C. M. S.,
Gustafsson A.
Publication year - 1998
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.1998.tb02483.x
Subject(s) - elastase , pancreatic elastase , chemistry , periodontitis , neutrophil elastase , alpha (finance) , slpi , enzyme , biochemistry , medicine , inflammation , surgery , construct validity , patient satisfaction
. The aim of this study was to investigate the presence of free elastase in GCF. Samples were taken from inflamed sites in 12 subjects with gingivitis alone and from inflamed sites with and without tissue destruction in 19 patients having periodontitis. Elastase activity was measured with a low molecular weight substrate. To distinguish between free elastase and elastase bound to α‐2‐macroglobulin (A2MG), an excess of α‐1‐antitrypsin (AlAT) was added to the samples. The activity that could be inhibited by AlAT was considered as free elastase, and the uninhibited activity as derived from the elastase‐A2MG complex. The elastase‐ A1AT complex was measured with an ELISA. Free elastase was found in almost all samples, but both the total amount and the proportion of free elastase were higher in samples from sites showing destruction. The elastase‐A2MG complex was also increased in sites with tissue destruction, while there was no significant difference in the amount of AlAT complex between the 3 categories of sites. In conclusion , our study clearly reveals free elastase in GCF. The elevated levels of free elastase in sites showing tissue destruction seem to be due to a combination of increased release of elastase and an inactivation of AlAT.