| First Author | Baker PJ | Year | 2000 |
| Journal | Infect Immun | Volume | 68 |
| Issue | 6 | Pages | 3103-7 |
| PubMed ID | 10816450 | Mgi Jnum | J:62266 |
| Mgi Id | MGI:1858657 | Doi | 10.1128/iai.68.6.3103-3107.2000 |
| Citation | Baker PJ, et al. (2000) Adhesion molecule deficiencies increase Porphyromonas gingivalis-induced alveolar bone loss in mice. Infect Immun 68(6):3103-7 |
| abstractText | 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. |
