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The effects of local immunization with periodontopathic microorganisms on periodontal bone loss in gnotobiotic rats
Author(s) -
Crawford John M.,
Taubman Martin A.,
Smith Daniel J.
Publication year - 1978
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1111/j.1600-0765.1978.tb00198.x
Subject(s) - saliva , antibody , streptococcus mutans , delayed hypersensitivity , immunology , immunization , medicine , actinomyces naeslundii , immune system , homologous chromosome , microbiology and biotechnology , biology , bacteria , biochemistry , gene , genetics
Experiments were performed to study the effect of stimulation of salivary antibody on the progress of periodontal bone loss in monoinfected rats. Animals were immunized with formalin‐killed S. mutans , A. naeslundii or A. viscosus in the region of each major salivary gland and then inoculated orally with live homologous organism. Salivary and serum antibody activities were measured by microagglutination. The contribution of IgA to the activity in saliva was further assessed by antiglobulin augmentation with class specific antiglobulin eagents directed to rat immunoglobulins. In certain experiments the presence of delayed hypersensitivity was investigated by skin testing. Periodontal bone loss was assessed by measurement of both horizontal and vertical bone loss. Estimation of the number of bacteria colonizing the teeth at the termination of each experiment was also made. Inexperiments with S. mutans or A. naeslundii , when relatively high levels of salivary antibody directed to the homologous organism were elicited by local injection, definite trends toward reductions in periodontal bone loss occurred. Serum antibody was also present in immunized animals. Fewer bacteria were generally recovered from immunized rats than from sham‐immunized rats. Delayed hypersensitivity to A. viscosus was accompanied by an increase in vertical bone loss. It is suggested that inflammatory lesions contributing to periodontal disease might be modified by manipulation of the host's immune system.