Periodontal diseases are infections of the structures that surround and support teeth; they are characterized by local inflammation and alveolar bone loss. Most treatment used to focus on only one aspect, inhibiting inflammation, or promoting osteoblasts. We set out to develop a new method that would intervene in the two aspects simultaneously. Adiponectin (APN), secreted by adipocytes, inhibits the inflammatory response and promotes osteogenesis. However, its role in human periodontal ligament cells (hPDLCs) is unclear. Therefore, we aim to investigate whether adiponectin could suppress lipopolysaccharide-induced inflammation and promote osteogenesis in hPDLCs. In this study, we stimulated hPDLCs with lipopolysaccharide in the presence or absence of adiponectin. Real-time PCR and western blotting results demonstrated that adiponectin partially inhibited the activation of the classical nuclear factor kappa-B (NF-κB) pathway. These results were confirmed by a change of expressions of NF-κB downstream inflammatory genes, such as decreased cyclooxygenase-2 and tumor necrosis factor-alpha, along with increased interleukin-10. As for the role of adiponectin in osteogenesis, alizarin red S staining showed that APN treatment induced more calcium deposition nodules than controls. We also found that adiponectin enhanced the expression of osteoblast-related genes (osteopontin, collagen 1, osteocalcin, alkaline phosphatase, runt-related transcription factor 2, and bone morphogenetic protein 2) in hPDLCs via the APPL1/p38 signal transduction pathway. Therefore, adiponectin inhibits LPS-induced inflammation and promotes osteogenesis in hPDLCs and may have potential therapeutic value in treating periodontitis by inhibiting the inflammatory lesions and contributing to bone tissue regeneration.

中文翻译：

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脂联素抑制脂多糖诱导的炎症并促进 hPDLCs 的成骨。

牙周病是围绕和支撑牙齿的结构的感染；它们的特点是局部炎症和牙槽骨丢失。大多数治疗过去只关注一个方面，抑制炎症或促进成骨细胞。我们着手开发一种新方法，可以同时干预这两个方面。脂肪细胞分泌的脂联素 (APN) 抑制炎症反应并促进成骨。然而，其在人类牙周膜细胞 (hPDLCs) 中的作用尚不清楚。因此，我们的目的是研究脂联素是否可以抑制脂多糖诱导的炎症并促进 hPDLCs 的成骨。在这项研究中，我们在存在或不存在脂联素的情况下用脂多糖刺激 hPDLC。实时 PCR 和蛋白质印迹结果表明，脂联素部分抑制了经典核因子 kappa-B (NF-κB) 通路的激活。这些结果通过 NF-κB 下游炎症基因表达的变化得到证实，例如环加氧酶-2 和肿瘤坏死因子-α 的减少，以及白细胞介素-10 的增加。至于脂联素在成骨中的作用，茜素红 S 染色显示 APN 处理比对照诱导更多的钙沉积结节。我们还发现脂联素通过 APPL1/p38 信号转导通路增强 hPDLCs 中成骨细胞相关基因（骨桥蛋白、胶原蛋白 1、骨钙素、碱性磷酸酶、runt 相关转录因子 2 和骨形态发生蛋白 2）的表达。所以，