Elastase and α‐ 1 ‐Proteinase Inhibitor in Gingival Crevicular Fluid and Gingival Tissue in Adult and Juvenile Periodontitis
- 1 July 1994
- journal article
- research article
- Published by Wiley in The Journal of Periodontology
- Vol. 65 (7) , 702-709
- https://doi.org/10.1902/jop.1994.65.7.702
Abstract
The presence and localization of PMN/neutrophil elastase and its endogenous inhibitor α1-proteinase inhibitor (α1PI) were studied immunohistochemically in gingival tissue specimens collected from 9 adult periodontitis (AP) patients during flap surgery after the initial phase of periodontal therapy, and from 6 healthy controls with clinicallyhealthy periodontium upon surgical extraction of impacted third molars. In order to evaluate how periodontal tissue destructive events are reflected in gingival crevicular fluid (GCF), GCF samples were collected from the AP patients before any periodontal treatment and prior to flap surgery, from 5 localized juvenile periodontitis (LJP) patients, and from the controls. Elastase activity in the GCF was measured with the SAAVNA-assay and the molecular forms and amount of α1PI by Western- and dot-blotting. Immunohistochemical staining for PMN elastase was strongly positive in the connective tissue, but not in the epithelium, of the AP patients' gingival tissue specimens. In the healthy gingival tissue specimens only a few elastase-positive cells were present. Both in AP and in control gingival specimens, α1PI was detected in the connective tissue and in the keratinized layer of the epithelium, however, its amount was markedly lower in the control specimens. Elevated levels of α1PI and PMN elastase were detected in the GCF of all periodontitis patients when compared to controls. Based on the present findings we conclude that: 1) PMN elastase activity is associated with periodontal inflammation in situ, and increased activities are detected in AP GCF, but not in LJP GCF, and 2) α1PI is present both in healthy and in inflamed periodontal tissues, but during periodontal inflammation its amount is increased, probably due to a compensatory extracellular matrix (ECM) -protective mechanisms of the host's defense system. J Periodontol 1994;65:702–709.Keywords
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