Efforts to control inflammation and achieve better tissue repair in the treatment of periodontitis have been ongoing for years. Human β-defensin 3, a broad-spectrum antimicrobial peptide has been proven to have a variety of biological functions in periodontitis; however, relatively few reports have addressed the effects of human periodontal ligament cells (hPDLCs) on osteogenic differentiation. In this study, we evaluated the osteogenic effects of hPDLCs with an adenoviral vector encoding human β-defensin 3 in an inflammatory microenvironment. Then human β-defensin 3 gene-modified rat periodontal ligament cells were transplanted into rats with experimental periodontitis to observe their effects on periodontal bone repair. We found that the human β-defensin 3 gene-modified hPDLCs presented with high levels of osteogenesis-related gene expression and calcium deposition. Furthermore, the p38 MAPK pathway was activated in this process. In vivo, human β-defensin 3 gene-transfected rat PDLCs promoted bone repair in SD rats with periodontitis, and the p38 mitogen-activated protein kinase (MAPK) pathway might also have been involved. These findings demonstrate that human β-defensin 3 accelerates osteogenesis and that human β-defensin 3 gene modification may offer a potential approach to promote bone repair in patients with periodontitis.

中文翻译：

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人β-防御素3基因修饰可促进人牙周膜细胞的成骨分化和牙周炎的骨修复。

在牙周炎的治疗中控制炎症和实现更好的组织修复的努力已经进行了多年。人类β-防御素3是一种广谱抗菌肽，已被证明在牙周炎中具有多种生物学功能。然而，相对较少的报道涉及人牙周膜细胞（hPDLC）对成骨分化的影响。在这项研究中，我们评估了hPDLC在炎性微环境中与编码人β-防御素3的腺病毒载体的成骨作用。然后将人β-防御素3基因修饰的大鼠牙周膜细胞移植到实验性牙周炎大鼠中，观察其对牙周骨修复的作用。我们发现，人类β-防御素3基因修饰的hPDLC具有高水平的成骨相关基因表达和钙沉积。此外，在此过程中激活了p38 MAPK途径。在体内，人β-防御素3基因转染的大鼠PDLC促进了牙周炎SD大鼠的骨修复，并且可能还涉及了p38丝裂原活化蛋白激酶（MAPK）途径。这些发现表明，人β-防御素3可加速成骨作用，而人β-防御素3基因修饰可为促进牙周炎患者的骨修复提供潜在的途径。并且可能还涉及了p38丝裂原活化蛋白激酶（MAPK）途径。这些发现表明，人β-防御素3可加速成骨作用，而人β-防御素3基因修饰可为促进牙周炎患者的骨修复提供潜在的途径。并且可能还涉及了p38丝裂原活化蛋白激酶（MAPK）途径。这些发现表明，人β-防御素3可加速成骨作用，而人β-防御素3基因修饰可为促进牙周炎患者的骨修复提供潜在的途径。