Immunohistlogical study of mouse periodontal burst model

据报道，细菌脂多糖（LPS）诱导牙槽骨吸收，宿主免疫系统特别是活化的T细胞在破骨细胞发生中起着至关重要的作用。另一方面，干扰素γ (IFN-γ)，由活化的T细胞产生，在体外和体内都抑制骨吸收。因此，问题是IFN-γ的产生是否随着骨吸收的增加而增加。我们之前的研究表明，在小鼠牙龈中反复注射大肠杆菌LPS可引起牙槽骨中破骨细胞的形成。在本研究中，我们观察到了骨吸收过程中浸润细胞IFN-γ产生的变化。小鼠每48h重复注射5μg LPS 26次。第16次注射后，当牙槽骨吸收达到平台期时，改变LPS浓度（25μg LPS或单独PBS）。25γg LPS注射组骨吸收水平显著升高，IFN-γ-和白细胞介素-1 β (IL-1 β)-承载细胞数量也显著增加。另一方面，PBS注射组很少见抗酒石酸酸性磷酸酶阳性细胞或携带IFN-γ和IL-1 β的细胞。这些结果表明，IFN-γ承载细胞的改变可能在平衡LPS诱导的破骨细胞激活因子（如IL-1 β）引起的骨吸收中起作用。

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.