Antiphosphorylcholine antibody levels are elevated in humans with periodontal diseases

Human immunoglobulin G2 (IgG2) serum concentrations and the IgG2 antibody r esponse to Actinobacillus actinomycetemcomitans can be influenced by genes, by environmental factors such as smoking, and by periodontal disease statu s. Examination of the IgG2 response to phosphorylcholine (PC), a response t hought to be mainly induced by the C polysaccharide of Streptococcus pneumo niae, suggested that periodontal disease status was also associated with th is response. This prompted the hypothesis that PC is an important oral anti gen associated with organisms in the periodontal flora and that anti-PC ant ibody is elevated as a consequence of periodontal disease. Subjects in vari ous periodontal disease diagnostic categories in which attachment loss is e xhibited were tested for anti-PC in serum. Those with adult periodontitis, localized juvenile periodontitis, generalized early onset periodontitis, an d gingival recession all had similar levels of anti-PC IgG2 serum antibody which were significantly greater than in the group of subjects with no atta chment loss. Analysis of plaque samples from subgingival and supragingival sites in all diseases categories for reactivity with the anti-PC specific m onoclonal antibody TEPC-15 revealed that a substantial proportion of the ba cteria in dental plaque (30 to 40%) bear PC antigen; this antigen was not r estricted to morphotypes resembling only cocci but was also present on rods and branched filamentous organisms. We found that S. mitis, S, oralis, and S, sanguis, as well as oral actinomycetes, including A. viscosus, A. odont olyticus, and A. israelii, incorporated substantial amounts of [H-3]choline from culture media. Further analysis of antigens derived from these organi sms by Western blot indicated that S. oralis, S. sanguis, A. viscosus, A. o dontolyticus, and A. israelii contained TEPC-15-reactive antigens, The data show that many commonly occurring bacterial species found in dental plaque contain PC antigen and that immunization with plaque-derived PC antigens a s a consequence of inflammation and periodontal attachment loss may influen ce systemic anti-PC antibody concentrations.