Polymorphonuclear neutrophil chemiluminescence in periodontal disease

Abstract

The oxidative metabolism of polymorphonuclear leukocytes (PMNs) in rapidly progressive periodontitis (RPP, n = 19), localized juvenile periodontitis (LJP, n = 10), adults periodontitis (AP, n = 10) and healthy control subjects (HS, n = 39) was compared using the luminol chemiluminescence (CL) method. Possible influences of the isolation procedure on CL were circumvented by replacing starch with Haemaccell 35 as the sedimentation agent. In all groups, CL was significantly higher with autologous serum than with normal pooled serum (NPS) and there was a significant linear relationship between the two values. Comparisons of both pooled and autologous serum between patient groups and their matched controls were not statistically significant. There was a suggestion of serum-induced defects in 2 patients and 1 control. The range of individual values within each group was very heterogeneous, probably because of the many factors that are able to influence both the production of CL and the basal levels of CL observed.

Oxidative Injury and Inflammatory Periodontal Diseases : the Challenge of Anti-Oxidants to Free Radicals and Reactive Oxygen Species

“…In AP, only a slight increase in CL was observed (Whyte et al, 1989), while there were minor differences (Zafiropoulos et al, 1991), no differences (Mouynet et al, 1994), or a CL decrease (Gomez et al, 1994) among healthy subjects or patients with gingivitis, juvenile periodontitis, or AP PMN from AP patients have higher CL after Fcgreceptor stimulation than do those from healthy subjects (Gustafsson and Asman, 1996). In RPP patients was found a lowering of CL (Zafiropoulos et al, 1988), and only minor differences in the CL responses between PE patients and healthy controls were found in terms of the oxidative metabolism of PMN (Zafiropoulos et al, 1991). The RB of PMN in the peripheral blood of patients with various types of PE (evaluated by fluorescence/flow cytometry) indicated that all groups contained variable populations of subjects with normal and increased DCF formation, while the control subjects exhibited DCF formation as a single population.…”

“…PMN from both PLS patients and controls produced similar amounts of 02'-when stimulated with opsonized bacteria or PMA, but both resting PMN and PMN stimulated with polyhistidine from the PLS patients released larger amounts of 02' than PMN from the controls (Bimstein et al, 1990). In AP, only a slight increase in CL was observed (Whyte et al, 1989), while there were minor differences (Zafiropoulos et al, 1991), no differences (Mouynet et al, 1994), or a CL decrease (Gomez et al, 1994) among healthy subjects or patients with gingivitis, juvenile periodontitis, or AP PMN from AP patients have higher CL after Fcgreceptor stimulation than do those from healthy subjects (Gustafsson and Asman, 1996). In RPP patients was found a lowering of CL (Zafiropoulos et al, 1988), and only minor differences in the CL responses between PE patients and healthy controls were found in terms of the oxidative metabolism of PMN (Zafiropoulos et al, 1991).…”

“…PMN from young patients with PE generate increased CL (Asman et al, 1984;Asman, 1988;Shapira et al, 1991;Leino et al, 1994), but PMN from localized juvenile periodontitis patients (LIP) display a normal oxidative capacity (Ellegard et al, 1984;Van Dyke et al, 1986;Zafiropoulos et al, 1991). Release by PMN was low in subjects suffering from Papillon-Lefevre syndrome (PLS), as measured by a ferri-cytochrome c reduction assay (Bullon et al, 1993).…”

Constitutionally Hyperreactive Neutrophils in Periodontitis

“…This agrees with our previous findings and those of others (Table 1). [5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22] We tried to avoid possible interference by inflammation with a careful examination to confirm good general health and excluding cigarette smokers to clarify the pathogenesis of periodontitis.…”

“…However, Fcγ-receptor (FcγR)-mediated stimulation has consistently shown an increase in the generation of oxygen radicals from activated neutrophils of patients with periodontitis (Table 1). [5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22] The primary aim of this study was to compare the neutrophil generation of oxygen radicals from patients with chronic periodontitis and matched controls after stimulation via various activating pathways. We therefore activated the neutrophils via FcγR (IgG-opsonized Staphylococcus aureus), complement receptor CR3, (complement-opsonized zymosan), and directly using activation of the intra-cellular protein kinase C enzyme (PKC) by phorbol myristate acetate (PMA).…”