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Immunocytochemical Distribution of Human PMN Elastase and Cathepsin-G in Dental Pulp

Department of Endodontics and Microbiology, Baltimore College of Dental Surgery, University of Maryland Dental School, 666 W. Baltimore St., Baltimore, Maryland 21201

C.R. Rauschenberger

Department of Endodontics and Microbiology, Baltimore College of Dental Surgery, University of Maryland Dental School, 666 W. Baltimore St., Baltimore, Maryland 21201

R.K. Nauman

Department of Endodontics and Microbiology, Baltimore College of Dental Surgery, University of Maryland Dental School, 666 W. Baltimore St., Baltimore, Maryland 21201

Components of primary (azurophilic) granules of polymorphonuclear leukocytes (PMNs) have been implicated as important mediators in pulpal inflammation. This anatomical study used ultracryoimmunocytochemical techniques and characterized and contrasted the subcellular distributions of human PMN elastase (PMN-E), PMN cathepsin-G (PMN-CG), and alpha-2 macroglobulin (a-2M) in healthy and inflamed dental pulps. Inflamed pulpal tissue sections revealed an intense distribution of PMN-E in the extracellular domain throughout the collagen matrix. PMN-E was also localized in the perinuclear cytoplasm of PMNs and distributed in a random fashion. PMN-CG was localized intensely in the intracellular granules of PMNs and observed moderately within the extracellular matrix. Healthy pulpal tissues exposed to PMN-E and PMN-CG antibodies revealed no evidence of PMN infiltration and no specific labeling. a-2M, a natural serum inhibitor of PMN-E and PMN-CG, was distributed in an intense fashion within the intravascular compartments of both inflamed and healthy pulpal samples. Immunogold-labeling for a-2M was observed in moderate amounts within the extravascular domain of inflamed pulpal samples but only in mild amounts within the same area of healthy tissues. These results suggest that PMN-E and PMN-CG are released to the extracellular matrix of irreversibly inflamed teeth, enabling them to facilitate pulpal connective tissue destruction. Conversely, moderate extravascular labeling for a-2M within inflamed samples suggests a physiological attempt at inhibiting the pulpal connective tissue destruction mediated by human PMN-E and PMN-CG.

Journal of Dental Research, Vol. 72, No. 11, 1485-1490 (1993)
DOI: 10.1177/00220345930720110501


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