Open AccessAdhesion Molecule Deficiencies IncreasePorphyromonas gingivalis-Induced Alveolar Bone Loss in Mice
Author(s) -
Pamela J. Baker,
L Dufour,
Mark Dixon,
Derry C. Roopenian
Publication year - 2000
Publication title -
infection and immunity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.508
H-Index - 220
eISSN - 1070-6313
pISSN - 0019-9567
DOI - 10.1128/iai.68.6.3103-3107.2000
Subject(s) - porphyromonas gingivalis , dental alveolus , bone resorption , biology , intercellular adhesion molecule 1 , immunology , cell adhesion molecule , periodontitis , microbiology and biotechnology , medicine , endocrinology , dentistry
Alveolar bone resorption can be induced in specific-pathogen-free mice by oral infection withPorphyromonas 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 toP. 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 β2 -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 decreaseP. gingivalis -specific serum immunoglobulin G responses, but lower antibody titers did not lead to increased bone loss in partially β2 -integrin-deficient mice. In conclusion, P-selectin and ICAM-1 deficiencies increase susceptibility to and severity of alveolar bone loss afterP. gingivalis infection. This finding underscores the importance of innate immunity in protection againstP. gingivalis -induced alveolar bone resorption.