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

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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.