Periodontal disease (PD), as an age-related disease, prevalent in middle-aged and elderly population, is characterized as inflammatory periodontal tissue loss, including gingival inflammation and alveolar bone resorption. However, the definite mechanism of aging-related inflammation in PD pathology needs further investigation. Our study is aimed at exploring the effect of inflamm-aging-related cytokines of interleukin-17 (IL-17) and interferon-γ (IFN-γ) on osteoclastogenesis in vitro and periodontal destruction in vivo. For receptor activator of nuclear factor-κB ligand- (RANKL-) primed bone marrow macrophages (BMMs), IL-17 and IFN-γ enhanced osteoclastogenesis, with the expression of osteoclastogenic mRNA (TRAP, c-Fos, MMP-9, Ctsk, and NFATc1) and protein (c-Fos and MMP-9) upregulated. Ligament-induced rat models were established to investigate the role of IL-17 and IFN-γ on experimental periodontitis. Both IL-17 and IFN-γ could enhance the local inflammation in gingival tissues. Although there might be an antagonistic interaction between IL-17 and IFN-γ, IL-17 and IFN-γ could facilitate alveolar bone loss and osteoclast differentiation.

中文翻译：

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IL-17 和 IFN-γ 的炎症衰老相关细胞因子加速破骨细胞生成和牙周破坏

牙周病（PD）作为一种与年龄相关的疾病，多见于中老年人群，其特点是炎症性牙周组织缺损，包括牙龈炎症和牙槽骨吸收。然而，PD病理学中衰老相关炎症的明确机制需要进一步研究。我们的研究旨在探索炎症衰老相关细胞因子白细胞介素 17 (IL-17) 和干扰素-γ (IFN- γ ) 对体外破骨细胞生成和体内牙周破坏的影响。对于核因子受体活化κ乙配体（RANKL-）引发的骨髓巨噬细胞（两种BMM），IL-17和IFN- γ破骨细胞生成增强，破骨细胞生成 mRNA（TRAP、c-Fos、MMP-9、Ctsk 和 NFATc1）和蛋白质（c-Fos 和 MMP-9）的表达上调。建立韧带诱导的大鼠模型以研究IL-17和IFN- γ对实验性牙周炎的作用。IL-17和IFN- γ都可以增强牙龈组织的局部炎症。尽管 IL-17 和 IFN- γ之间可能存在拮抗作用，但 IL-17 和 IFN- γ可以促进牙槽骨丢失和破骨细胞分化。