These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


PUBMED FOR HANDHELDS

Search MEDLINE/PubMed


  • Title: The role of RgpA in the pathogenicity of Porphyromonas gingivalis in the murine periodontitis model.
    Author: Wilensky A, Polak D, Houri-Haddad Y, Shapira L.
    Journal: J Clin Periodontol; 2013 Oct; 40(10):924-32. PubMed ID: 23909600.
    Abstract:
    AIM: To investigate the in vivo role of gingipains in Porphyromonas gingivalis' virulence, and suggest a possible host mechanisms through which the bacteria cause alveolar bone loss. MATERIALS AND METHODS: Mice were orally infected with P. gingivalis wild type, or the gingipains mutants (RgpA⁻, Kgp⁻, RgpA⁻/Kgp⁻). Mice were analysed for alveolar bone loss using micro-computed tomography. The molecular effects of the proteases were evaluated using the subcutaneous chamber model. Mice were infected with P. gingivalis wild type or mutants. Exudates were analysed for cytokine and leukocytes levels, in vivo phagocytosis, P. gingivalis survival and serum anti-P. gingivalis IgG titres. RESULTS: Only RgpA-expressing bacteria induced significantly alveolar bone loss, and suppressed phagocytosis resulting in increased survival of P. gingivalis in the chamber exudates. In addition, RgpA-expressing bacteria induced higher levels of leukocytes and cytokines 2 h post-infection, and reduced levels of serum anti-P. gingivalis IgG titres 7 days post-infection. CONCLUSIONS: Our findings showed that elimination of RgpA from P. gingivalis diminished inflammation, but augmented phagocytosis and antibody titres, coincidental with reduced alveolar bone loss. These findings support the hypothesis that RgpA is a critical virulence factor in the pathogenesis of experimental periodontitis in mice.
    [Abstract] [Full Text] [Related] [New Search]