Zhiwu Wu, Shaoying Duan, Mingming Li, Aopeng Zhang, Hui Yang, Jingjing Luo, Ran Cheng, Tao Hu
{"title":"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。","authors":"Zhiwu Wu, Shaoying Duan, Mingming Li, Aopeng Zhang, Hui Yang, Jingjing Luo, Ran Cheng, Tao Hu","doi":"10.1111/iej.14103","DOIUrl":null,"url":null,"abstract":"<div>\n \n \n <section>\n \n <h3> Aim</h3>\n \n <p>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.</p>\n </section>\n \n <section>\n \n <h3> Methodology</h3>\n \n <p>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 (<i>p</i> < .05).</p>\n </section>\n \n <section>\n \n <h3> Results</h3>\n \n <p>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) (<i>p</i> < .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 (<i>p</i> < .01) and OPG (<i>p</i> < .05), more intense expression of RANK (<i>p</i> < .01) and RANKL (<i>p</i> < .01), and a higher RANKL/OPG ratio (<i>p</i> < .05).</p>\n </section>\n \n <section>\n \n <h3> Conclusion</h3>\n \n <p>Autophagy may exert a protective effect against AP by regulating the RANKL/RANK/OPG axis, thereby inhibiting excessive bone loss.</p>\n </section>\n </div>","PeriodicalId":13724,"journal":{"name":"International endodontic journal","volume":null,"pages":null},"PeriodicalIF":5.4000,"publicationDate":"2024-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Autophagy regulates bone loss via the RANKL/RANK/OPG axis in an experimental rat apical periodontitis model\",\"authors\":\"Zhiwu Wu, Shaoying Duan, Mingming Li, Aopeng Zhang, Hui Yang, Jingjing Luo, Ran Cheng, Tao Hu\",\"doi\":\"10.1111/iej.14103\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div>\\n \\n \\n <section>\\n \\n <h3> Aim</h3>\\n \\n <p>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.</p>\\n </section>\\n \\n <section>\\n \\n <h3> Methodology</h3>\\n \\n <p>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 (<i>p</i> < .05).</p>\\n </section>\\n \\n <section>\\n \\n <h3> Results</h3>\\n \\n <p>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) (<i>p</i> < .05). Inflammatory cell infiltration was observed in the EAP + saline and EAP + 3-MA groups. 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Autophagy regulates bone loss via the RANKL/RANK/OPG axis in an experimental rat apical periodontitis model
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.
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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