Detection of human IL-2 in normal and inflamed dental pulps.

Irreversible pulpitis has been associated with an increase in the number of pulpal T-cells. Interleukin-2 (IL-2) stimulates T-cell proliferation and signals the release of other proinflammatory mediators associated with connective tissue degradation. IL-2 has been suggested to be a useful marker of pathologic inflammatory activity in periodontal and systemic disease conditions. The purpose of this study was to analyze normal and inflamed dental pulps for the presence of immunoreactive IL-2 (iIL-2). Normal healthy pulpal tissue was obtained from 17 impacted third molars and inflamed samples were obtained from 12 symptomatic carious molars clinically diagnosed with irreversible pulpitis. Pulpal tissues were collected, prepared, and analyzed for histological status and iIL-2 concentration by a modified ELISA technique. iIL-2 was detected in all vital pulpal tissues. A t-test revealed significant differences in iIL-2 concentrations when inflamed pulpal tissues were compared to normal healthy samples (T = -2.75, p < 0.05). These results suggest that iIL-2 may serve as a marker of pathologic inflammatory activity in irreversible pulpitis.

Immunocytochemical distribution of human PMN elastase and cathepsin-G in dental pulp.

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 (alpha-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. alpha-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 alpha-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 alpha-2M within inflamed samples suggests a physiological attempt at inhibiting the pulpal connective tissue destruction mediated by human PMN-E and PMN-CG.