Adhesion molecule deficiencies increase Porphyromonas gingivalis-induced alveolar bone loss in mice.

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Animal, Antibodies-Bacterial, Antigens-CD18, Bacteroidaceae-Infections, Cell-Adhesion-Molecules, IgG, Immune-Tolerance, Immunity-Natural, Intercellular-Adhesion-Molecule-1, Mice, Mice-Inbred-C57BL, Mice-Mutant-Strains, P-Selectin, Porphyromonas-gingivalis, SUPPORT-NON-U-S-GOVT, SUPPORT-U-S-GOVT-P-H-S

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Infect Immun 2000 Jun; 68(6):3103-7.


R29DE10728/DE/NIDCR, RO1


Alveolar bone resorption can be induced in specific-pathogen-free mice by oral infection with Porphyromonas gingivalis (P. J. Baker, R. T. Evans, and D. C. Roopenian, Arch. Oral Biol. 39:1035-1040, 1994). Here we used a mouse strain, C57BL/6J, which is relatively resistant to P. gingivalis-induced bone loss to examine whether partial or complete deletion of various adhesion molecules would increase susceptibility. Complete deletion of P-selectin or nearly complete lack of expression of intercellular adhesion molecule 1 (ICAM-1) led to increased susceptibility to bone resorption after oral infection, while a hypomorphic defect in beta(2)-integrins did not. Both the total amount of bone lost and the number of sites at which there was significant loss were increased in mice deficient in either ICAM-1 or P-selectin. Each of the three adhesion molecule deficiencies was sufficient to decrease P. gingivalis-specific serum immunoglobulin G responses, but lower antibody titers did not lead to increased bone loss in partially beta(2)-integrin-deficient mice. In conclusion, P-selectin and ICAM-1 deficiencies increase susceptibility to and severity of alveolar bone loss after P. gingivalis infection. This finding underscores the importance of innate immunity in protection against P. gingivalis-induced alveolar bone resorption.

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