The interleukin-10 knockout mouse is highly susceptible toPorphyromonas gingivalis-induced alveolar bone loss.

Sasaki H, Okamatsu Y, Kawai T, Kent R, Taubman M, Stashenko P. The interleukin-10 knockout mouse is highly susceptible toPorphyromonas gingivalis-induced alveolar bone loss. J Periodont Res 2004; doi: 10.1111/j.1600-0765.2004.00760.x.© Blackwell Munksgaard 2004Interleukin-10 is an anti-inflammatory cytokine that reduces periapical bone loss, but its role in periodontal bone loss is unclear. In the present study, we tested the hypothesis that endogenous interleukin-10 is a potent suppressor ofPorphyromonas gingivalis-induced alveolar bone lossin vivo.Interleukin-10 knockout (–/–) and wild-type mice were inoculated intraorally withP. gingivalis. Non-infected animals served as negative controls. 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 (RT–PCR), respectively.P. gingivalis-infected interleukin-10^–/– mice exhibited severe alveolar bone loss compared to non-infected interleukin-10^–/– and wild-type mice by day 42. Surprisingly, bone resorptive cytokines interleukin-1α and tumor necrosis factor alpha (TNF-α) were not up-regulated in gingival tissues byP. gingivalis-infection. Although interleukin-1β was marginally increased, blockade of both interleukin-1 isoforms or interleukin-1 receptor type I with neutralizing antisera failed to reduce alveolar bone loss in interleukin-10^–/– mice, indicating the operation of an interleukin-1-independent mechanism. No strong correlations between bone loss and other cytokines was observed, although interferon gamma (IFNγ), interleukin-6, interleukin-4, and prostaglandin E2 were modestly up-regulated in infected interleukin-10^–/– mice.P. gingivalisinfection reduced the expression of cell markers in gingival tissue on days 7 and 14 in both interleukin-10^–/– and wild-type animals, suggestive of bacteria-induced cytotoxicity or apoptosis. This was followed by up-regulated expression of receptor activator of nuclear factor kappa B ligand (RANKL) and CD40 ligand (CD40L on days 28 and 70 in infected interleukin-10^–/– mice only.The interleukin-10^–/– mouse is highly susceptible to bone loss induced by the periodontal pathogenP. gingivalis, which is mediated via an interleukin-1-independent pathway. [ABSTRACT FROM AUTHOR]

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