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Journal of Dental Research
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Localization of Active and Inactive Elastase, Alpha-1-Proteinase Inhibitor, and Alpha-2-Macroglobulin in Human Gingiva

C.N. Kennett

Department of Periodontology, King's College School of Medicine and Dentistry, London, SE5 9RW, United Kingdom

S.W. Cox

Department of Periodontology, King's College School of Medicine and Dentistry, London, SE5 9RW, United Kingdom

B.M. Eley

Department of Periodontology, King's College School of Medicine and Dentistry, London, SE5 9RW, United Kingdom

Biochemically, there is usually much less elastase activity in gingival tissue than in crevicular fluid. The tissue distributions of active and inactive elastase and the endogenous inhibitors alpha-1-proteinase inhibitor ({alpha} 1PI) and alpha-2-macroglobulin ({alpha}2M) were therefore compared. Inflamed tissue was obtained from chronic periodontitis patients, and cryostat sections were incubated with the histochemical elastase substrate MeOSuc-Ala-Ala-Pro-Val-MNA. Adjacent sections were examined immunocytochemically with antibodies to neutrophil elastase, {alpha}1PI, {alpha}2M, and leukocyte differentiation antigens. Antigenic elastase was widely distributed in CD15-positive granulocytes in both the epithelium and lamina propria as well as in granulomatous tissue from infrabony defects. However, there was very limited histochemical staining of these cells, and biochemical activity against the equivalent substrate MeOSuc-Ala-Ala-Pro-Val-AFC could be extracted only from sections with such staining. The pH optimum and effector response of the activity in the extracts were, nevertheless, consistent with those of leukocyte elastase. The large difference between the total elastase content of the tissue, as determined immunocytochemically, and the limited amount of active enzyme, as demonstrated histochemically, indicated that the majority was in an inactive form. The involvement of tissue inhibitors was suggested by the fact that extracts from sections with no histochemical staining reduced biochemical elastase activity in crevicular fluid. {alpha}2M was found in many fibroblasts and also some CD68-positive macrophages, which additionally contained {alpha}1PI. Both inhibitors appeared to be present extracellularly, since there was significant background staining. Thus, {alpha}1PI and {alpha}2M could contribute to the regulation of elastase activity in the gingiva.

Key Words: elastase • alpha-1-proteinase inhibitor • alpha-2-macroglobulin • gingiva • periodontitis.

Journal of Dental Research, Vol. 74, No. 2, 667-674 (1995)
DOI: 10.1177/00220345950740020701
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