[Phagocytosis, intracellular killing and interleukin 1 production of polymorphonuclear leukocytes in human periodontal diseases].

Abstract

The role of the polymorphonuclear leukocyte (PMNL) as a primary protective cell in periodontal diseases has been well recognized. Functional abnormalities of PMNL chemotaxis have been implicated in the pathogenesis of some types of periodontitis. However, no consistent correlation with other PMNL functions has been reported. In the present study, phagocytosis and intracellular killing (oxidative product formation) of the PMNL from the patients with various forms of periodontal disease were evaluated by flow cytometry. Moreover, interleukin 1 (IL-1) production by the PMNL was determined by means of the enzyme-linked immunosorbent assay (ELISA) with monoclonal antibodies against rIL-1 alpha and rIL-1 beta. In order to examine these functions of peripheral (p-PMNL) and/or gingival crevicular PMNL (g-PMNL), 15 patients with localized juvenile periodontitis (LJP), 13 patients with generalized juvenile periodontitis (GJP) and 52 patients with adult periodontitis (AP) served as subjects. About 50% of the patients in LJP and GJP group exhibited depressed p-PMNL phagocytosis. While only a minimal number of the AP patients and no healthy subjects showed any reduction of p-PMNL phagocytosis. The reduction of phagocytosis was not related to the clinical periodontal status, and no detectable improvement of p-PMNL phagocytosis could be observed after periodontal therapy. In addition, it was suggested that complement receptors on the p-PMNL might be closely related with the reduction. Compared to p-PMNL, g-PMNL from the same individual have a lower phagocytic capacity in all subjects. However, no significant difference in g-PMNL phagocytosis could be demonstrated among three patient groups. Incremental oxidative responses in p-PMNL were observed in LJP, GJP and AP patients without any significant difference being found among these three groups. The increased rate of oxidative product formation was related to the clinical periodontal status, and it followed that periodontal therapy had significant effect on the improvement of this p-PMNL function. In IL-1 production assay of PMNL, a significant amount of IL-1, especially IL-1 beta, was observed in g-PMNL, but not in p-PMNL. The g-PMNL of the patients was found to produce greater amounts of IL-1 alpha and IL-1 beta than did the healthy controls. In addition, IL-1 production of p-PMNL was induced by the stimulation with some pathogenic bacteria including Bacteroides gingivalis. These results suggest that impaired PMNL phagocytosis may contribute to the early onset of periodontal deterioration in some young patients.(ABSTRACT TRUNCATED AT 400 WORDS)