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失衡的EphB4/EphrinB2信号传导调节由……诱导的牙周炎中的骨吸收。 (注:原文中“by”后面内容缺失)

Imbalanced EphB4/EphrinB2 Signaling Modulates Bone Resorption in Periodontitis Induced by .

作者信息

Fu Ying, Zhang Shuwei, Liu Junchao, Lu Ze, Li Yuchao, Liu Jinwen, Pan Yaping

机构信息

Oral Medicine Department, The Second Affiliated Hospital of Jinzhou Medical University, Jinzhou 121000, China.

Department of Periodontics, Liaoning Provincial Key Laboratory of Oral Diseases, School and Hospital of Stomatology, China Medical University, Shenyang 110002, China.

出版信息

ACS Infect Dis. 2024 Apr 12;10(4):1152-1161. doi: 10.1021/acsinfecdis.3c00459. Epub 2024 Mar 5.

Abstract

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 () 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 . An in vivo model of chronic periodontitis provoked by 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 in vitro. Then, a simulated coculture model of osteoblasts and osteoclasts was established to activate the forward and reverse pathways of EphB4/EphrinB2 with infection. This study showed that 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 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 infection. Moreover, attenuated EphB4/EphrinB2 with infection weakened osteoblast activity and enhanced osteoclast activity.

摘要

牙周炎是牙周组织的一种慢性感染性疾病,其特征是牙槽骨吸收与重塑失衡,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生态失调,其中()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破骨细胞与成骨细胞的通讯至关重要。本研究探讨EphB4/EphrinB2信号转导调节由()诱导的牙周炎中骨生成抑制和骨吸收的机制。构建了由()引发的慢性牙周炎体内模型,评估炎症和骨吸收情况。检测牙周组织中EphB4和EphrinB2蛋白的表达,体外感染()的成骨细胞和破骨细胞中也分别进行评估。然后,建立成骨细胞和破骨细胞的模拟共培养模型,通过感染()激活EphB4/EphrinB2的正向和反向信号通路。本研究表明,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()的成骨细胞中与骨生成相关的EphB4及分子受到抑制,而破骨细胞中的EphrinB2及破骨细胞分化相关标志物被激活。总之,本研究表明EphB4/EphrinB2蛋白参与了由()感染诱导的牙周炎过程中的牙槽骨重塑。此外,感染()使EphB4/EphrinB2信号减弱,削弱了成骨细胞活性并增强了破骨细胞活性。

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