We have performed studies aimed at elucidating the nature of the humoral immune response in rapidly progressive periodontitis (RPP). We analyzed the sera of 36 periodontally normal subjects and 36 RPP patients for titers and avidities of IgG antibodies reactive with the antigens of Porphyromonas gingivalis using ELISA, prior to and following treatment. We used whole‐cell sonicate, purified lipopolysaccharide (LPS), and total extractable protein as plate antigens. Twelve of the patients had antibody titers at least 2‐fold greater than the median of the controls and were designated as seropositive. The remaining 24 patients had titers that did not exceed twice the median titer of the controls and were designated as seronegative. For both patient groups, antibody titers were highest when whole‐cell antigen was used, intermediate for LPS, and lowest for the protein fraction. Following treatment, median titer for seropositive patients decreased from pretreatment values of 241.7 to 76.5, while median titer for seronegative patients increased from 39.5 to 80.1. Avidities of pretreatment sera from both patient groups for all 3 antigen preparations were lower than the median avidities of the control sera. Avidity significantly increased following treatment to levels greater than those for control sera in both patient groups. Thus, some young adults with severe periodontitis mount a humoral immune response and produce high levels of serum IgG antibodies reactive with antigens of P. gingivalis, while others do not. The antibodies produced are of relatively low avidity, and may therefore be relatively ineffective biologically. Therapy, which greatly reduces antigen load, appears to stimulate production of higher avidity IgG antibodies in both patient groups; in the seropositive group, low avidity antibodies appear to be replaced by antibodies of higher avidity. Both the purified LPS and protein fractions contain reactive antigen(s), although LPS binds more antibody. Our data are consistent with the idea that many RPP patients do not produce protective levels of biologically functional antibody during the course of their natural infection, but they may be stimulated to do so by treatment. J Periodontol 1991; 62:781–791.

ActinobaciUus actinomycetemcomitans has been closely associated with early-onset, severe periodontitis, and such patients often have serum immunoglobulin G (IgG) antibodies reactive with antigens of this gram-negative pathogen. We examined the functionality and potential importance of these antibodies. The opsonic activity against A. actinomycetemcomians of sera from 30 patients with rapidly progressive periodontitis (RPP) and from 28 periodontally normal subjects was tested by using polymorphonuclear leukocyte (PMN) chemiluminescence and bactericidal assays. Peak chemiluminescence values correlated strongly with kllUing observed in the PMN-dependent bactericidal assay (r = 0.88; P < 0.001). Neither the mean IgG titer nor the mean peak chemiluminescence differed significantly between the two groups. However, when the relationship between chemiluminescence and titer was examined, regression analysis showed that antibodies present in low-titer normal sera were significantly more effective at opsonizing A. actinomycetemcomians than antibodies present in low-titer RPP patient sera (P = 0.04). Thus, periodontally normal individuals may be better able than RPP patients to dear A. actinomycetemcomitans in early stages of colonization, and anti-A. actinomycetemcomitans antibodies in RPP patients may be relatively ineffective in preventing infection by this organism.

Although periodontal treatment by scaling and root planing (SCRP) is known to induce bacteremia, the effect of this procedure on the host immune response is not known. We have determined pre-and post-SCRP immunoglobulin G antibody titers to antigens ofActinobacilus actinomycetemcomitans in the sera of 22 patients with rapidly progressive periodontitis. We also assessed the ability of these sera to enhance phagocytosis and killing of A. actinomycetemcomitans by human polymorphonuclear leukocytes by using a polymorphonuclear leukocyte chemiluminescence (CL) assay. Specific anti-A. actinomycetemcomitans antibody titers were significantly increased at 6 and 12 months after beginning treatment, and CL values were significantly increased at 12 months, whereas mean interproximal pocket depths were significantly decreased at 12 months after beginning treatment. When patients were classified as either seropositive (twice the median titer of control subjects; n = 10) or seronegative (n = 12), both median titers and CL values were significantly increased for the seronegative group at 6 and 12 months after treatment. In the seropositive group, only the median titer was significantly increased at 12 months. Western blot (immunoblot) patterns for six seronegative and six seropositive patients differed remarkably at the baseline. Before treatment, all of the seropositive patients recognized high-molecular-mass lipopolysaccharide (LPS) and a large number of protein components. Patterns were virtually unaffected by therapy. Before treatment, only one of the seronegative patients recognized the LPS smear and none reacted strongly with protein components. Following treatment, slight LPS staining was observed for five of six seronegative patients and detection of protein bands was enhanced in all cases. We conclude that treatment by SCRP induces a humoral immune response, especially in seronegative patients, and that response may play a role in the observed beneficial effects of periodontal treatment.

W studied 4 isolates of Porphyromonas gingivalis, ATCC 33277, 381, A7A1-28, and W50, to identify major cell surface antigens and select the best strain from which to obtain antigen for a test vaccine. Immunoglobulin G (IgG) titers measured by enzyme-linked immunosorbent assay using whole-cell sonicates as antigen were significantly elevated for the sera of 64 rapidly progressive periodontitis patients relative to sera of 30 normal control subjects for each of the 4 strains studied. Western blots were prepared for all 4 strains and developed using sera from 22 patients and 20 control subjects to identify and determine the frequency of antibody-binding components. The intensity of binding by patient sera was greatest for the 75-kDa and 55-kDa components. The 43-kDa component was also widely recognized. Strains ATCC 33277 and 381 appeared to be antigenically similar. Because of the higher serum antibody titers, the larger proportion of seropositive patients and higher frequency of binding to specific protein components in Western blots, our efforts were focussed on strain ATCC 33277. Whole-cell sonicates, proteinase K-digested sonicate, lipopolysaccharide, capsular polysaccharide, and whole-cell protein fractions were prepared and evaluated for antigenic activity. By dot immunoblot, most of the antibody binding activity was found in the whole-cell protein fraction, with much lesser amounts in lipopolysaccharide and none in capsular polysaccharide. The antibody-binding activity was accessible on the cell surface, since 98.9% of P. gingivalis-specific antibody, including antibody binding to the 43-kDa, 55-kDa components on Western blot, was removed by whole-cell adsorption. Furthermore, the 43-kDa and 55-kDa but not the 75-kDa component on intact cells were accessible for labeling with 125I, confirming their cell surface location and accessibility.

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