The relationship of serum IgG antibody titers to periodontal pathogens to indicators of the host response in crevicular fluid.

In this study; the relationship of indicators of the local host response in gingival crevicular fluid (GCF) to the serum antibody titer to periodontal pathogens was examined. 15 patients with chronic adult periodontitis were studied. GCF was collected and analyzed for the total amount of IgG, IgM, the lysosomal enzyme B-glucuronidase (BG) and alpha-2-macroglobulin (alpha 2M). At the same examination, serum from these patients was collected, and enzyme-linked immunosorbent assays used to determine the serum IgG antibody titer to a panel of 17 periodontal pathogens (Actinobacillus actinomycetemcomitans (3 strains), Bacteroides gingivalis (4), Eikenella corrodens (2), Wolinella recta, Bacteroides intermedius (3), Fusobacterium nucleatum, and 3 Capnocytophaga species). Using Spearman rank order correlation analysis, correlation coefficients were calculated to relate the 4 indicators of host response in GCF to the serum IgG antibody titer to each of the 17 micro-organisms. The mean correlation between total IgG in GCF and the serum IgG antibody titer was positive (r = +0.30), and statistically significant correlations between total IgG in GCF and serum IgG antibody titer were observed for one strain of B. intermedius and C. ochracea. A weaker positive correlation was observed for IgM (r = 0.18). In contrast, the mean correlation between total BG in GCF and the serum antibody titer was negative (r = -0.34). Statistically significant negative correlations were observed for all 3 strains of A. actinomycetemcomitans, one strain of E. corrodens and W. recta. The mean correlation for alpha 2M was r = -0.06. These data suggest that elevated BG activity in GCF, believed to be a marker for lysosomal enzyme released from polymorphonuclear leukocytes in the crevicular environment, may be associated with a reduced serum IgG antibody response to suspected periodontal pathogens. Furthermore, these findings imply that the development of a serum IgG antibody response to suspected periodontal pathogens is consistent with a protective host response.