阻断P2X7受体激活可减轻结扎所致大鼠牙周炎模型的骨质流失。

IF 2.4 4区 医学 Q2 NEUROSCIENCES
Nadine Linhares, Marco Aurelio Teófilo, Juliane Fernandes, Maria Jennifer Bernardino, Rachel Solidonio, Vanessa Sousa, Gisele Barreto, Everton da Silva, Ariana Maria Soares, Sthefane Feitosa, Denis Gonçalves, Delane Gondim, Renata Leitão, Mirna Marques, Paula Goes
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引用次数: 0

摘要

牙周炎是一种非常普遍的免疫炎症性疾病,它损害牙齿的支撑组织,特别是牙周韧带和牙槽骨。在疾病进展过程中,炎症反应导致ATP的释放,ATP与嘌呤能受体如P2X7R相互作用,可能影响骨重塑。尽管P2X7R已经在骨细胞中进行了研究,但其在牙周炎中的具体作用仍不清楚。本研究旨在评估P2X7R调控对成骨细胞活性和实验性骨质流失的影响。在体外,P2X7R在OFCOL II成骨细胞中被证实表达。使用BzATP激活受体可显著降低细胞活力,改变细胞形态,降低碱性磷酸酶(ALP)活性
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Blockage of P2X7 receptor activation attenuated bone loss in ligature-induced model of periodontitis in rats.

Periodontitis is a highly prevalent immunoinflammatory disease that compromises the supporting tissues of the teeth, especially the periodontal ligament and alveolar bone. During disease progression, inflammatory responses lead to the release of ATP, which interacts with purinergic receptors such as P2X7R, potentially influencing bone remodeling. Although P2X7R has been studied in bone cells, its specific role in periodontitis remains poorly characterized. This study aimed to evaluate the effects of P2X7R modulation on osteoblastic activity and experimental bone loss. In vitro, P2X7R expression was confirmed in OFCOL II osteoblastic cells. Receptor activation using BzATP significantly reduced cell viability, altered cell morphology, and decreased alkaline phosphatase (ALP) activity (p < 0.05). In vivo, periodontitis was induced in Wistar rats via ligature. Animals were allocated into four groups: (1) Naïve; (2) Periodontitis (saline-treated); (3) BzATP-treated (P2X7R agonist); and (4) BBG-treated (P2X7R antagonist). BzATP aggravated periodontal damage, with increased inflammation, loss of osteoblasts, and disorganization of periodontal ligament fibers. In contrast, BBG improved tissue architecture, reduced inflammatory infiltrate, and increased osteoblast numbers and ALP activity, possibly via the Wnt signaling pathway. These results suggest that P2X7R activation contributes to inflammation-driven bone loss, impairing osteoblast viability and function. Therefore, P2X7R inhibition may serve as a promising pharmacological strategy to preserve bone and periodontal integrity in the context of periodontitis.

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来源期刊
Purinergic Signalling
Purinergic Signalling 医学-神经科学
CiteScore
6.60
自引率
17.10%
发文量
75
审稿时长
6-12 weeks
期刊介绍: Nucleotides and nucleosides are primitive biological molecules that were utilized early in evolution both as intracellular energy sources and as extracellular signalling molecules. ATP was first identified as a neurotransmitter and later as a co-transmitter with all the established neurotransmitters in both peripheral and central nervous systems. Four subtypes of P1 (adenosine) receptors, 7 subtypes of P2X ion channel receptors and 8 subtypes of P2Y G protein-coupled receptors have currently been identified. Since P2 receptors were first cloned in the early 1990’s, there is clear evidence for the widespread distribution of both P1 and P2 receptor subtypes in neuronal and non-neuronal cells, including glial, immune, bone, muscle, endothelial, epithelial and endocrine cells.
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