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Cell-mediated immunity (CMI) and humoral immunity (HI) against oral bacteria (Streptococcus sanguis strain 2A, ATCC 10556, Streptococcus sanguis group H1, Neisseria subflava and Staphylococcus) and adult human oral mucosa (AHOM) antigens were investigated in relation to exacerbation of recurrent aphthous stomatitis (RAS). The material consisted of 10 patients with RAS and 10 controls. The CMI and HI were assessed by means of the leukocyte migration test (LMT) and a double-layer immunofluorescence (IF) technique. Compared with normal controls the leukocyte migration inhibition against Strep. 2A and AHOM was significantly increased in patients with exacerbation of RAS and the reactivity seemed to develop in relation to the exacerbation of RAS. The leukocyte migration inhibition was not significantly increased when Strep. H1, Neisseria subflava, Staphylococcus or fetal human kidney extracts were used as antigens. The IgG antibodies against Strep. 2A and Strep. H1 were significantly raised in sera from patients with exacerbation of RAS. However, the endpoint titers (EPT) did not increase significantly in relation to the exacerbation of RAS. The distribution of EPT against Neisseria subflava, Staphylococcus and AHOM did not differ significantly when sera from patients with exacerbation of RAS were related to sera from controls. The present investigations support the hypothesis that CMI against streptococcal and AHOM antigens may be involved in the immunopathogenesis of RAS. [ABSTRACT FROM AUTHOR]

Immunologic cross-reactions between Strep. 2A, fetal human oral mucosa (FHOM), and adult human oral mucosa (AHOM) were investigated by the use of a double layer immunofluorescence staining technique. Rabbit sera were prepared against Strep. 2A and FHOM. Seventeen sera from patients with recurrent aphthous stomatitis (RAS) and with known antibodies against Strep. 2A and AHOM were examined for anti- bodies against FHOM. The distribution of endpoint titers against FROM in the sera from RAS differed significantly from the distribution in 17 controls. The immune absorptions in the rabbit sera and in the 17 sera from patients with RAS indicate that some cross-reacting antigenic determinants are shared between Strep. 2A, FHOM, and AHOM. Furthers the present results indicate that antibodies are produced against antigenic determinants which are not shared by Strep. 2A, FHOM, and AHOM. The role of cross-reacting antigens in the pathogenesis of RAS is discussed but remains obscure. [ABSTRACT FROM AUTHOR]