P. gingivalis OMVs Attenuate the Osteogenesis of PDLSCs by Activating PERK Signaling.

IF 2.9 3区医学 Q1 DENTISTRY, ORAL SURGERY & MEDICINE

Oral diseases Pub Date : 2025-08-01 Epub Date: 2025-03-27 DOI:10.1111/odi.15320

Yingying Huang, Xiaoning He, Jiangwei Liao, Dihao Tao, Hanzhe Wang, Bei Li, Zhiwei Dong, Junjie Wu

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引用次数: 0

Abstract

Objective: The Porphyromonas gingivalis outer membrane vesicles (P. gingivalis OMVs) carry toxins that contribute to the onset and progression of periodontitis. These OMVs have been implicated in host cell invasion and damage. This study aimed to determine the role and potential mechanisms of P. gingivalis OMVs on periodontal inflammation.

Methods: A model of PDLSCs induced by P. gingivalis OMVs was developed, and changes in their biological functions were examined. We established a rat periodontitis model to confirm whether P. gingivalis OMV promotes the periodontal inflammatory phenotype. Additionally, the potential mechanisms by which P. gingivalis OMVs impair the osteogenic differentiation capacity of PDLSCs were investigated.

Results: P. gingivalis OMVs inhibited the proliferation, promoted apoptosis and suppressed the osteogenesis of PDLSCs, while promoting periodontal inflammatory phenotype in vivo. Furthermore, mechanistic studies revealed that pretreatment of PDLSCs with 4-phenylbutyric acid (4-PBA) prevented the P. gingivalis OMVs-induced activation of the PERK pathway and restored the osteogenesis of PDLSCs.

Conclusions: We demonstrate that P. gingivalis OMV exacerbates the periodontitis phenotype and inhibits the regenerative function of PDLSCs, potentially through mechanisms involving endoplasmic reticulum dysfunction.

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牙龈卟啉卟啉omv通过激活PERK信号减弱PDLSCs的成骨作用。

目的：牙龈卟啉单胞菌外膜囊（P. gingivalis OMVs）携带毒素，有助于牙周炎的发生和进展。这些omv参与了宿主细胞的侵袭和损伤。本研究旨在确定牙龈假单胞菌omv在牙周炎症中的作用及其潜在机制。方法：建立牙龈假单胞菌omv诱导的PDLSCs模型，观察其生物学功能的变化。我们建立大鼠牙周炎模型，以证实牙龈假单胞菌OMV是否促进牙周炎症表型。此外，我们还研究了牙龈卟啉卟啉omv损害PDLSCs成骨分化能力的潜在机制。结果：牙龈假单胞菌omv在体内抑制PDLSCs增殖、促进细胞凋亡、抑制成骨，同时促进牙周炎症表型。此外，机制研究表明，4-苯基丁酸（4-PBA）预处理PDLSCs可以阻止牙龈卟啉卟啉omvs诱导的PERK通路激活，恢复PDLSCs的成骨功能。结论：我们证明牙龈卟啉单胞菌OMV会加剧牙周炎表型并抑制PDLSCs的再生功能，可能通过涉及内质网功能障碍的机制。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Oral diseases 医学-牙科与口腔外科

CiteScore

7.60

自引率

5.30%

发文量

325

审稿时长

4-8 weeks

期刊介绍： Oral Diseases is a multidisciplinary and international journal with a focus on head and neck disorders, edited by leaders in the field, Professor Giovanni Lodi (Editor-in-Chief, Milan, Italy), Professor Stefano Petti (Deputy Editor, Rome, Italy) and Associate Professor Gulshan Sunavala-Dossabhoy (Deputy Editor, Shreveport, LA, USA). The journal is pre-eminent in oral medicine. Oral Diseases specifically strives to link often-isolated areas of dentistry and medicine through broad-based scholarship that includes well-designed and controlled clinical research, analytical epidemiology, and the translation of basic science in pre-clinical studies. The journal typically publishes articles relevant to many related medical specialties including especially dermatology, gastroenterology, hematology, immunology, infectious diseases, neuropsychiatry, oncology and otolaryngology. The essential requirement is that all submitted research is hypothesis-driven, with significant positive and negative results both welcomed. Equal publication emphasis is placed on etiology, pathogenesis, diagnosis, prevention and treatment.