Autophagy regulates bone loss via the RANKL/RANK/OPG axis in an experimental rat apical periodontitis model

IF 5.4 1区 医学 Q1 DENTISTRY, ORAL SURGERY & MEDICINE
Zhiwu Wu, Shaoying Duan, Mingming Li, Aopeng Zhang, Hui Yang, Jingjing Luo, Ran Cheng, Tao Hu
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引用次数: 0

Abstract

Aim

Autophagy is involved in human apical periodontitis (AP). However, it is not clear whether autophagy is protective or destructive in bone loss via the receptor activator of nuclear factor-κB ligand (RANKL)/RANK/osteoprotegerin (OPG) axis. This study aimed to investigate the involvement of autophagy via the RANKL/RANK/OPG axis during the development of AP in an experimental rat model.

Methodology

Twenty-four female Sprague–Dawley rats were divided into control, experimental AP (EAP) + saline, and EAP + 3-methyladenine (An autophagy inhibitor, 3-MA) groups. The control group did not receive any treatment. The EAP + saline group and the EAP + 3-MA group received intraperitoneal injections of saline and 3-MA, respectively, starting 1 week after the pulp was exposed. Specimens were collected for microcomputed tomography (micro-CT) scanning, histological processing, and immunostaining to examine the expression of light chain 3 beta (LC3B), RANK, RANKL, and OPG. Data were analysed using one-way analysis of variance (p < .05).

Results

Micro-CT showed greater bone loss in the EAP + 3-MA group than in the EAP + saline group, indicated by an elevated trabecular space (Tb.Sp) (p < .05). Inflammatory cell infiltration was observed in the EAP + saline and EAP + 3-MA groups. Compared with EAP + saline group, the EAP + 3-MA group showed weaker expression of LC3B (p < .01) and OPG (p < .05), more intense expression of RANK (p < .01) and RANKL (p < .01), and a higher RANKL/OPG ratio (p < .05).

Conclusion

Autophagy may exert a protective effect against AP by regulating the RANKL/RANK/OPG axis, thereby inhibiting excessive bone loss.

在实验性大鼠根尖牙周炎模型中,自噬通过 RANKL/RANK/OPG 轴调节骨质流失。
目的:自噬参与人类根尖牙周炎(AP)。然而,尚不清楚自噬是通过核因子κB配体受体激活剂(RANKL)/RANK/骨保护素(OPG)轴对骨质流失起保护作用还是起破坏作用。本研究旨在探讨自噬通过 RANKL/RANK/OPG 轴参与实验大鼠模型中 AP 的形成:24只雌性Sprague-Dawley大鼠被分为对照组、实验性AP(EAP)+生理盐水组和EAP+3-甲基腺嘌呤(一种自噬抑制剂,3-MA)组。对照组不接受任何治疗。EAP + 生理盐水组和 EAP + 3-MA 组分别在暴露牙髓一周后开始腹腔注射生理盐水和 3-MA。采集标本进行微型计算机断层扫描(micro-CT)、组织学处理和免疫染色,以检测轻链 3 beta(LC3B)、RANK、RANKL 和 OPG 的表达。数据采用单因素方差分析(P 结果):显微 CT 显示,EAP + 3-MA 组比 EAP + 生理盐水组的骨质流失更严重,表现为骨小梁间隙(Tb.Sp)升高(p 结论:自噬可能会对骨质流失起到保护作用:自噬可通过调节 RANKL/RANK/OPG 轴对 AP 发挥保护作用,从而抑制骨质过度流失。
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
International endodontic journal
International endodontic journal 医学-牙科与口腔外科
CiteScore
10.20
自引率
28.00%
发文量
195
审稿时长
4-8 weeks
期刊介绍: The International Endodontic Journal is published monthly and strives to publish original articles of the highest quality to disseminate scientific and clinical knowledge; all manuscripts are subjected to peer review. Original scientific articles are published in the areas of biomedical science, applied materials science, bioengineering, epidemiology and social science relevant to endodontic disease and its management, and to the restoration of root-treated teeth. In addition, review articles, reports of clinical cases, book reviews, summaries and abstracts of scientific meetings and news items are accepted. The International Endodontic Journal is essential reading for general dental practitioners, specialist endodontists, research, scientists and dental teachers.
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