We have reviewed the recent literature on the humoral immune responses to a variety of subgingival plaque bacterial species in patients with destructive periodontal diseases. We do not feel that the information presently available on the specific antibody responses to proposed pathogens such as Bacteroides gingivalis and Actinobacillus actinomycetemcomitans allows antibody responses to be diagnostic. All control subjects without periodontal destruction have antibodies to candidate pathogens but the generally higher levels in patients are not sufficiently elevated to be diagnostic. Nor can they be used to predict the initiation of disease or the onset of new episodes of destruction where disease had previously occurred. Successful treatment of patients may lead to lower levels of antibodies to some organisms, including possible pathogens, and thus support a given species in the aetiopathogenesis of disease. It appears that unsuccessful treatment may be accompanied by continuing high antibody levels to some organisms and further studies may enable this observation to be used to monitor therapy. There is some evidence from serological studies that each destructive episode may be induced by a different bacterial species or consortium. The start of studies using single antigens and the techniques of molecular biology will provide not only antibody-based diagnostic methods but also allow us to determine which bacterial antigens are virulence factors and thus the role of the antibody responses, whether protective or damaging, in the periodontal diseases.
SUMMARY IgM rheumatoid factor (RF) was measured in the sera of 48 rheumatoid patients and of 48 age and sex-matched normal controls by the Rose-Waaler and latex agglutination tests, a rate nephelometer, and an enzyme-linked immunosorbent assay (ELISA). Good correlation was obtained between all assays. The rate nephelometer assay was the easiest and quickest to perform and gave results in international units/ml. The Rose-Waaler was the least sensitive assay and the most difficult to perform and interpret. Both the latex agglutination and the ELISA were sensitive, though some overlap of patient and control sera was seen with all the assays. In addition to IgM RF the ELISA was used to measure IgG RF and IgA RF in both rheumatoid and control sera. Although some normal sera had detectable amounts of IgG and IgA RF, the levels of both were significantly raised in the rheumatoid sera. IgG RF levels were lower after pepsin digestion of the sera, suggesting that IgM RF interfered with the assay for IgG RF unless this treatment was included.
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