Abstract

This study was designed to assess the functional role of interleukin-18 (IL-18) in periodontal tissues. IL-18 transgenic (IL-18Tg) mice and wild-type (WT) mice were inoculated intraorally with Porphyromonas gingivalis. Alveolar bone loss, gingival cytokine levels, and gingival gene expression were assessed using morphometric analysis, enzyme-linked immunosorbent assay (ELISA), and semiquantitative reverse transcription polymerase chain reaction, respectively. P. gingivalis-infection induced periodontal bone loss in IL-18Tg mice, whereas bone loss did not occur in WT mice. Interferon gamma was downregulated only in IL-18Tg mice by P. gingivalis-infection. P. gingivalis-infection upregulated the expression of receptor activator of nuclear factor kappa B ligand (RANKL) in IL-18Tg mice vs. WT-type mice.These results suggest that IL-18Tg mice are highly susceptible to bone loss induced by the periodontal pathogen P. gingivalis, which may be mediated via RANKL-dependent pathway.

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