Periodontitis, a chronic infectious disease in periodontal tissues, is characterized by an imbalance of alveolar bone resorption and remodeling, which eventually results in tooth loosening and even tooth loss. The etiology of periodontitis is polymicrobial synergy and dysbiosis, in which Porphyromonas gingivalis (P. gingivalis) is one of the primary pathogens responsible for periodontitis progression. The interplay of EphrinB2/EphB4 is crucial for osteoblast–osteoclast communication during bone remodeling and healing. This study investigates the mechanism of EphB4/EphrinB2 transduction modulating osteogenesis inhibition and bone resorption in periodontitis induced by P. gingivalis. An in vivo model of chronic periodontitis provoked by P. gingivalis was constructed, the inflammation and bone resorption were evaluated. The expression of EphB4 and EphrinB2 proteins in periodontal tissues was detected, which was also evaluated, respectively, in osteoblasts and osteoclasts infected with P. gingivalis in vitro. Then, a simulated coculture model of osteoblasts and osteoclasts was established to activate the forward and reverse pathways of EphB4/EphrinB2 with P. gingivalis infection. This study showed that P. gingivalis infection promoted alveolar bone resorption in rats and enhanced EphB4 and EphrinB2 expression in periodontal tissues. EphB4 and molecules associated with osteogenesis in osteoblasts infected with P. gingivalis were inhibited, while EphrinB2 and osteoclast differentiation-related markers in osteoclasts were activated. In conclusion, this study suggested that EphB4/EphrinB2 proteins were involved in alveolar bone remodeling in the process of periodontitis induced by P. gingivalis infection. Moreover, attenuated EphB4/EphrinB2 with P. gingivalis infection weakened osteoblast activity and enhanced osteoclast activity.

中文翻译：

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不平衡的 EphB4/EphrinB2 信号调节牙龈卟啉单胞菌引起的牙周炎的骨吸收

牙周炎是牙周组织的一种慢性感染性疾病，其特点是牙槽骨吸收和重塑失衡，最终导致牙齿松动甚至脱落。牙周炎的病因是多种微生物协同作用和菌群失调，其中牙龈卟啉单胞菌（P.gingivalis）是导致牙周炎进展的主要病原体之一。 EphrinB2/EphB4 的相互作用对于骨重塑和愈合过程中成骨细胞与破骨细胞的通讯至关重要。本研究探讨EphB4/EphrinB2转导调节牙龈卟啉单胞菌诱导的牙周炎成骨抑制和骨吸收的机制。构建牙龈卟啉单胞菌引起的慢性牙周炎体内模型，评价炎症和骨吸收情况。检测牙周组织中EphB4和EphrinB2蛋白的表达，并分别在体外感染牙龈卟啉单胞菌的成骨细胞和破骨细胞中进行评估。然后，建立了成骨细胞和破骨细胞的模拟共培养模型，以激活牙龈卟啉单胞菌感染的EphB4/EphrinB2的正向和反向通路。本研究表明，牙龈卟啉单胞菌感染促进大鼠牙槽骨吸收，并增强牙周组织中 EphB4 和 EphrinB2 的表达。感染牙龈卟啉单胞菌的成骨细胞中EphB4和与成骨相关的分子受到抑制，而破骨细胞中的EphrinB2和破骨细胞分化相关标志物被激活。总之，本研究提示EphB4/EphrinB2蛋白参与牙龈卟啉单胞菌感染引起的牙周炎过程中的牙槽骨重塑。此外，牙龈卟啉单胞菌感染减弱的EphB4/EphrinB2减弱了成骨细胞活性，增强了破骨细胞活性。