Mechanisms of bone resorption in alveolar bone of IL-1 transgenic mice

牙周病是一种感染性慢性炎症性疾病，可导致牙槽骨丢失和牙周区域结缔组织破坏。骨吸收是通过免疫反应触发的，并且是针对牙周病细菌的炎症反应的结果。破骨细胞是骨吸收细胞，从巨噬细胞/单核细胞谱系细胞分化而来，并被NF-κB配体受体激活剂（RANKL）激活。针对牙周病细菌的活化的抗原特异性CD 4阳性T细胞产生RANKL，RANKL已被证明在牙周病的骨吸收中起关键作用。RANKL表达于成骨细胞/基质细胞的细胞膜上，刺激破骨细胞生成。在本研究中，RANKL mRNA的表达水平在牙槽骨进行了检查。IL-1转基因小鼠牙槽骨RANKL mRNA表达水平与野生型小鼠无明显差异。相反，IL-1转基因小鼠股骨中RANKL mRNA表达显著增加。而牙槽骨骨密度不受IL-1过量产生的影响。这些结果表明，牙槽骨吸收是由不同的机制，发生在长骨的调节。

Periodontal diseases are infectious, chronic inflammatory diseases that result both in loss of alveolar bone and destruction of connective tissue in periodontal regions. The bone resorption is triggered through immune responses, and results from inflammatory reactions directed against periodontopathic bacteria. Osteoclasts, bone resorbing cells, differentiate from macrophage/monocyte lineage cells, and are activated by receptor activator of NF-κB ligand (RANKL). Activated antigen-specific CD4 positive T-cells directed against periodontopathic bacteria produce RANKL, which has been shown to play a critical role in bone resorption in periodontal diseases.RANKL, which is expressed on the cell membrane of osteoblasts/stromal cells, stimulates osteoclastogenesis. In the present study, the expression level of RANKL mRNA in alveolar bone was examined. The expression level of RANKL mRNA in alveolar bone in IL-1 transgenic mice was not different from wild one. In contrast, RANKL mRNA expression was significantly increased in the femur of IL-1 transgenic mice. However, bone mineral density of alveolar bone did not influence by the overproduction of IL-1. These results indicate that alveolar bone resorption was regulated by the different mechanisms which occurred in the long bone.