T cell knockout mice have diminished alveolar bone loss after oral infection with Porphyromonas gingivalis.

Document Type


Publication Date



Animals, Bacteroidaceae-Infections, Disease-Models-Animal, Female, Genes-T-Cell-Receptor-alpha, Immunocompetence, Mice, Mice-Inbred-C57BL, Mice-Knockout, Periodontal-Diseases, Porphyromonas-gingivalis, SUPPORT-NON-U-S-GOVT, SUPPORT-U-S-GOVT-P-H-S, T-Lymphocytes

JAX Source

FEMS Immunol Med Microbiol 2002 Sep; 34(1):45-50.


Periodontal diseases are chronic inflammatory diseases that can result in resorption of the alveolar bone of the jaw. We have developed a murine model in which alveolar bone loss is induced by oral infection with Porphyromonas gingivalis, an oral anaerobic bacterium associated with periodontal disease in humans. Here we compared a strain of immunocompetent mice (C57BL/6J) to the same strain of mice made T cell deficient by genetic deletion of the alpha chain of their T cell receptors (C57BL/6J-Tcra). T cell deficiency did not affect the ability of P. gingivalis to implant in the oral cavity. The two strains of mice had equal percentages of P. gingivalis among their cultivable anaerobes 7 weeks after infection. The same bacterial load led to much less bone resorption in the T cell deficient mice than in the immune normal mice, measured as either the number of sites with significant loss, or as the total amount of bone resorbed. T cell deficient mice lost bone at only three out of 14 measurement sites, compared with eight out of 14 sites in the wild-type mice. The total amount of bone lost was 70% less in the T cell deficient mice. T cell deficient mice had lower titers of P. gingivalis-specific IgG than the wild-type mice after oral infection did, but the same titers of specific IgA. Lower titers did not correlate with greater bone loss. Antigen-activated T lymphocytes are known to induce osteoclastogenesis; here we demonstrate that T cell deletion decreases the amount of alveolar bone loss induced by infection of the murine oral cavity.

Please contact the Joan Staats Library for information regarding this document.