Immunohistlogical study of mouse periodontal burst model

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It has been reported that bacterial lipopolysaccharide (LPS) induces alveolar bone resorption and that the host immune system especially activated T cells, plays a crucial role in osteoclastogenesis. On the other hand, interferon-gamma (IFN-γ), which is produced by activated T cells, suppresses bone resorption both in vitro and in vivo. Thus, the question arises as to whether or not IFN-γ production increases with increasing bone resorption. We previously demonstrated that repeated injections of Escherichia coli LPS into mouse gingiva causes osteoclast formation in alveolar bone. In the present study we observed changes in the IFN-γ production of infiltrating cells in concurrence with bone resorption. Mice were repeatedly injected with 5μg LPS 26times every 48h. After the 16th injection when the alveolar bone resorption reached a plateau, the concentration of LPS was altered (25μg LPS or PBS alone). The level of active resorption became significantly elevated, and the number of IFN-γ- and interleukin-1 beta (IL-1 β)- bearing cells also increased significantly, in relation to bone resorption within the 25γg LPS injected group. On the other hand, few tartrate-resistant acid phosphatase positive cells, or IFN-γ- and IL-1 β- bearing cells, were seen in the PBS injected group. These results suggest that alteration in IFN-γ-bearing cells might play arole in counterbalancing LPS induced bone resorption resulting from osteoclast activating cytokines such as IL-1 β.