T-cell contributions to alveolar bone loss in response to oral infection with Porphyromonas gingivalis

• Published in: Acta odontologica Scandinavica Vol. 59; no. 4; p. 222
• Main Authors: Baker, P J, Garneau, J, Howe, L, Roopenian, D C
• Format: Journal Article
• Language: English
• Published: England 01.08.2001
• Subjects: Alveolar Bone Loss - immunology; Alveolar Bone Loss - microbiology; Animals; Bacteroidaceae Infections - immunology; Carrier Proteins - biosynthesis; Carrier Proteins - immunology; CD4-Positive T-Lymphocytes - immunology; CD4-Positive T-Lymphocytes - metabolism; Histocompatibility Antigens Class II - immunology; Interferon-gamma - immunology; Interleukin-6 - biosynthesis; Interleukin-6 - immunology; Membrane Glycoproteins - biosynthesis; Membrane Glycoproteins - immunology; Mice; Mice, Inbred C57BL; Mice, Knockout; Porphyromonas gingivalis - pathogenicity; RANK Ligand; Receptor Activator of Nuclear Factor-kappa B; Receptors, Antigen, T-Cell, alpha-beta - immunology
• ISSN: 0001-6357; 1502-3850
• DOI: 10.1080/00016350152509247

We have previously shown that mice lacking CD4+, but not CD8+, T cells lose less alveolar bone loss in response to oral infection with Porphyromonas gingivalis than do immunocompetent mice of the same genetic background, indicating that CD4+ T cells contribute to bone resorption. The CD4+ and CD8+ T-cell knockouts were produced by targeted deletions of, respectively, major histocompatibility complex II (MHCII) or beta2-microglobulin (producing non-expression of MHCI). Because MHC deletions can have other effects in addition to those on T-cell selection, we wanted to confirm that the lessened bone loss was truly an effect of the lack of T cells. Consequently, we repeated our experiments with C57B1 /6J-Tcra mice that have a targeted deletion of the alpha chain of the T-cell receptor (Tcra). Six weeks after oral infection with P. gingivalis ATCC 53977 the total bone loss at buccal maxillary sites was 0.28 mm in infected immunocompetent mice (P=0.002 compared with sham-infected mice), whereas in Tcra knockouts the bone loss was only 0.08 mm (P=0.04 compared with shams). The T-cell-deficient mice thus lost 70% less bone after infection than did genetically matched immunocompetent mice (P =0.003). These experiments confirm that T cells, and their responses to oral infection with P. gingivalis, help to push bone remodeling in the direction of net loss of bone.