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Prevalence and virulence factors of haemolytic Enterococcus faecalis isolated from root filled teeth associated with periradicular lesions: A laboratory investigation in Thailand 从牙根充填并伴有根周病变的牙齿中分离出的溶血性粪肠球菌的流行率和毒力因素：泰国实验室调查。
IF 5 1区 医学 Q1 Dentistry
International endodontic journal
Pub Date : 2024-03-14 DOI: 10.1111/iej.14059
Kewalin Thammasitboon, Rawee Teanpaisan, Nuntiya Pahumunto

Aim

Previous endodontic research has provided limited understanding of the prevalence and roles of haemolytic and non-haemolytic Enterococcus faecalis strains in root filled teeth. This study aimed to determine the prevalence of these strains in root filled teeth with periradicular lesions and investigate their associated virulence factors.

Methodology

A total of 36 root canal samples were collected from 36 subjects. The prevalence of E. faecalis was determined using culture and PCR methods. Antibiotic susceptibility of haemolytic and non-haemolytic E. faecalis strains was assessed using the broth dilution assay. The cytokine stimulation in periodontal ligament (PDL) cells and neutrophil migration were evaluated using real-time PCR and migration assay, respectively. Cell invasion ability of the strains was assessed using a cell culture model. Additionally, the virulence gene expression of the haemolytic and non-haemolytic strains was investigated using real-time PCR. The Mann–Whitney U and Spearman's ρ tests were used to examine the significant difference between the two strains and to analyse the correlation between phenotype and gene expression, respectively.

Results

Enterococcus faecalis was detected in 33.3% and 88.9% of samples by culture and real-time PCR, respectively. Haemolytic strains were found in 36.4% of subjects. Non-haemolytic strains exhibited susceptibility to erythromycin and varying susceptibility to tetracycline, while all haemolytic strains were resistant to both antibiotics. Haemolytic strains significantly upregulated the expression of IL-8, OPG and RANKL in PDL cells (p < .05). Notably, the fold increases in these genes were higher: IL-8 (556.1 ± 82.9 vs. 249.6 ± 81.8), OPG (2.2 ± 0.5 vs. 1.3 ± 0.2) and RANKL (1.8 ± 0.3 vs. 1.2 ± 0.1). Furthermore, haemolytic strains had a greater effect on neutrophil migration (68.7 ± 15.2% vs. 46.9 ± 11.4%) and demonstrated a higher level of internalization into oral keratinocyte cells (68.6 ± 0.4% vs. 33.8 ± 0.5%) (p < .05). They also showed enhanced expression of virulence genes associated with haemolysin, surface proteins, collagen-binding and aggregation substances. Gelatinase activity was only detectable in non-haemolytic strains.

Conclusions

This study revealed that haemolytic strains E. faecalis possessed enhanced abilities in host invasion and a higher abundance of virulence factors, suggesting their potential contribution to more severe disease manifestat

目的：以往的牙髓病学研究对溶血性和非溶血性粪肠球菌菌株在根充牙中的流行情况和作用了解有限。本研究旨在确定这些菌株在根充牙根周病变中的流行率，并调查其相关的致病因素：方法：共收集了 36 名受试者的 36 份根管样本。方法：共收集了 36 名受试者的 36 份根管样本，采用培养和 PCR 方法确定了粪大肠杆菌的流行率。采用肉汤稀释法评估溶血性和非溶血性粪大肠杆菌菌株的抗生素敏感性。实时 PCR 和迁移试验分别评估了细胞因子对牙周韧带（PDL）细胞的刺激作用和中性粒细胞的迁移。使用细胞培养模型评估了菌株的细胞侵袭能力。此外，还利用实时 PCR 技术研究了溶血菌株和非溶血菌株的毒力基因表达。曼-惠特尼 U 检验和斯皮尔曼 ρ 检验分别用于检验两种菌株之间的显著差异，以及分析表型和基因表达之间的相关性：结果：通过培养和实时 PCR 检测，分别有 33.3% 和 88.9% 的样本检出了粪肠球菌。在 36.4% 的受试者中发现了溶血性菌株。非溶血性菌株对红霉素有敏感性，对四环素也有不同程度的敏感性，而所有溶血性菌株对这两种抗生素都有耐药性。溶血菌株能明显上调 PDL 细胞中 IL-8、OPG 和 RANKL 的表达（p 结论：溶血菌株能明显上调 PDL 细胞中 IL-8、OPG 和 RANKL 的表达：本研究发现，溶血性菌株具有更强的宿主侵袭能力和更丰富的毒力因子，这表明它们可能会导致更严重的疾病表现。
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引用次数: 0
In-depth investigation of FAM20A insufficiency effects on deciduous dental pulp cells: Altered behaviours, osteogenic differentiation, and inflammatory gene expression 深入研究 FAM20A 不足对脱落牙髓细胞的影响：行为、成骨分化和炎症基因表达的改变
IF 5 1区 医学 Q1 Dentistry
International endodontic journal
Pub Date : 2024-03-13 DOI: 10.1111/iej.14056
Kanokwan Sriwattanapong, Thanakorn Theerapanon, Chompak Khamwachirapitak, Pannagorn Sae-ear, Noppadol Sa-Ard-Iam, Vorasuk Shotelersuk, Thantrira Porntaveetus

Aim

Loss-of-function mutations in FAM20A result in amelogenesis imperfecta IG (AI1G) or enamel-renal syndrome, characterized by hypoplastic enamel, ectopic calcification, and gingival hyperplasia, with some cases reporting spontaneous tooth infection. Despite previous reports on the consequence of FAM20A reduction in gingival fibroblasts and transcriptome analyses of AI1G pulp tissues, suggesting its involvement in mineralization and infection, its role in deciduous dental pulp cells (DDP) remains unreported. The aim of this study was to evaluate the properties of DDP obtained from an AI1G patient, providing additional insights into the effects of FAM20A on the mineralization of DDP.

Methodology

DDP were obtained from a FAM20A-AI1G patient (mutant cells) and three healthy individuals. Cellular behaviours were examined using flow cytometry, MTT, attachment and spreading, colony formation, and wound healing assays. Osteogenic induction was applied to DDP, followed by alizarin red S staining to assess their osteogenic differentiation. The expression of FAM20A-related genes, osteogenic genes, and inflammatory genes was analysed using real-time PCR, Western blot, and/or immunolocalization. Additionally, STRING analysis was performed to predict potential protein–protein interaction networks.

Results

The mutant cells exhibited a significant reduction in FAM20A mRNA and protein levels, as well as proliferation, migration, attachment, and colony formation. However, normal FAM20A subcellular localization was maintained. Additionally, osteogenic/odontogenic genes, OSX, OPN, RUNX2, BSP, and DSPP, were downregulated, along with upregulated ALP. STRING analysis suggested a potential correlation between FAM20A and these osteogenic genes. After osteogenic induction, the mutant cells demonstrated reduced mineral deposition and dysregulated expression of osteogenic genes. Remarkably, FAM20A, FAM20C, RUNX2, OPN, and OSX were significantly upregulated in the mutant cells, whilst ALP, and OCN was downregulated. Furthermore, the mutant cells exhibited a significant increase in inflammatory gene expression, that is, IL-1β and TGF-β1, whereas IL-6 and NFκB1 expression was significantly reduced.

Conclusion

The reduction of FAM20A in mutant DDP is associated with various cellular deficiencies, including delayed proliferation, attachment, spreading, and migration as well as altered oste

目的：FAM20A的功能缺失突变导致釉质发育不全IG（AI1G）或釉肾综合征，其特征是釉质发育不全、异位钙化和牙龈增生，部分病例报告有自发性牙齿感染。尽管之前有报道称 FAM20A 在牙龈成纤维细胞中的减少以及 AI1G 牙髓组织的转录组分析表明其参与矿化和感染，但其在脱落牙髓细胞（DDP）中的作用仍未见报道。本研究旨在评估从一名 AI1G 患者体内获得的 DDP 的特性，从而进一步了解 FAM20A 对 DDP 矿化的影响：方法：从一名 FAM20A-AI1G 患者（突变细胞）和三名健康人身上获取 DDP。使用流式细胞仪、MTT、附着和扩散、集落形成和伤口愈合试验检测细胞行为。对 DDP 进行成骨诱导，然后进行茜素红 S 染色，以评估其成骨分化情况。使用实时 PCR、Western 印迹和/或免疫定位分析了 FAM20A 相关基因、成骨基因和炎症基因的表达。此外，还进行了STRING分析，以预测潜在的蛋白质-蛋白质相互作用网络：结果：突变细胞的FAM20A mRNA和蛋白水平以及增殖、迁移、附着和集落形成均显著降低。然而，FAM20A亚细胞定位保持正常。此外，OSX、OPN、RUNX2、BSP 和 DSPP 等成骨/牙生成基因下调，ALP 上调。STRING分析表明，FAM20A与这些成骨基因之间存在潜在的相关性。诱导成骨后，突变细胞显示出矿物质沉积减少和成骨基因表达失调。值得注意的是，FAM20A、FAM20C、RUNX2、OPN 和 OSX 在突变细胞中明显上调，而 ALP 和 OCN 则下调。此外，突变体细胞的炎症基因（即IL-1β和TGF-β1）表达明显增加，而IL-6和NFκB1的表达则明显减少：结论：突变 DDP 中 FAM20A 的减少与各种细胞缺陷有关，包括增殖、附着、扩散和迁移延迟以及成骨和炎症反应改变。这些发现为牙髓细胞中 FAM20A 的生物学特性提供了新的见解，并揭示了 AI1G 病理学的分子机制。
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引用次数: 0
Influence of dental bleaching on the pulp tissue: A systematic review of in vivo studies 牙齿漂白对牙髓组织的影响：体内研究的系统回顾。
IF 5 1区 医学 Q1 Dentistry
International endodontic journal
Pub Date : 2024-03-12 DOI: 10.1111/iej.14061
Mariana Viana Donato, Alexandre Henrique dos Reis-Prado, Lucas Guimarães Abreu, Lara Cancella de Arantes, Juliana Goto, Hebertt Gonzaga dos Santos Chaves, Luciano Tavares Angelo Cintra, André Luiz Fraga Briso, Isabella Faria da Cunha Peixoto, Francine Benetti

Background

Although several studies indicate the harmful effects of bleaching on pulp tissue, the demand for this procedure using high concentrations of hydrogen peroxide (HP) is high.

Objectives

To investigate the influence of bleaching on the pulp tissue.

Methods

Electronic searches were conducted (PubMed/MEDLINE, Scopus, Cochrane Library and grey literature) until February 2021. Only in vivo studies that evaluated the effects of HP and/or carbamide peroxide (CP) bleaching gels on the inflammatory response in the pulp tissue compared with a non-bleached group were included. Risk of bias was performed according to a modified Methodological Index for Non-Randomized Studies scale for human studies and the Systematic Review Centre for Laboratory Animal Experimentation's RoB tool for animal studies. Meta-analysis was unfeasible.

Results

Of the 1311 studies, 30 were eligible. Of these, 18 studies evaluated the inflammatory response in animal models. All these studies reported a moderate-to-strong inflammatory response in the superficial regions of pulp, characterized by cell disorganization and necrotic areas, particularly during the initial periods following exposure to 35%–38% HP, for 30–40 min. In the evaluation of human teeth across 11 studies, seven investigated inflammatory responses, with five observing significant inflammation in the pulp of bleached teeth. In terms of tertiary dentine deposition, 11 out of 12 studies noted its occurrence after bleaching with 35%–38% HP in long-term assessments. Additionally, three studies reported significant levels of osteocalcin/osteopontin at 2 or 10 days post-treatment. Other studies indicated an increase in pro-inflammatory cytokines ranging from immediately up to 10 days after bleaching. Studies using humans' teeth had a low risk of bias, whereas animal studies had a high risk of bias.

Discussion

Despite the heterogeneity in bleaching protocols among studies, High-concentrations of HP shows the potential to induce significant pulp damage.

Conclusions

High-concentrations of bleaching gel increases inflammatory response and necrosis in the pulp tissue at short periods after bleaching, mainly

背景：尽管一些研究表明漂白对牙髓组织有害，但使用高浓度过氧化氢（HP）进行漂白的需求量很大：研究漂白对牙髓组织的影响：方法：进行电子检索（PubMed/MEDLINE、Scopus、Cochrane Library 和灰色文献），直至 2021 年 2 月。仅纳入了评估HP和/或过氧化卡巴酰胺（CP）漂白凝胶与未漂白组相比对牙髓组织炎症反应影响的体内研究。对于人类研究，根据修改后的非随机研究方法指数表进行偏倚风险分析；对于动物研究，根据实验动物实验系统性审查中心的 RoB 工具进行偏倚风险分析。元分析不可行：在 1311 项研究中，有 30 项符合条件。其中 18 项研究评估了动物模型的炎症反应。所有这些研究都报告了牙髓表层区域的中度至强烈炎症反应，其特点是细胞紊乱和坏死区域，尤其是在暴露于 35%-38% HP 30-40 分钟后的初期。在对人类牙齿进行的 11 项评估研究中，有 7 项研究调查了炎症反应，其中 5 项研究观察到漂白牙齿的牙髓有明显炎症。在牙本质三级沉积方面，12 项研究中有 11 项指出，在使用 35%-38% HP 漂白后的长期评估中出现了牙本质三级沉积。此外，有三项研究报告称，在治疗后 2 天或 10 天，骨钙素/osteopontin 的水平显著升高。其他研究表明，漂白后的促炎细胞因子会在短短10天内增加。使用人类牙齿进行的研究偏倚风险较低，而动物研究的偏倚风险较高：讨论：尽管各研究的漂白方案不尽相同，但高浓度漂白剂有可能诱发严重的牙髓损伤：结论：高浓度漂白凝胶会在漂白后短时间内增加牙髓组织的炎症反应和坏死，主要是在大鼠磨牙和人类门牙中，此外，随着时间的推移，硬组织沉积也会增加。然而，由于这些研究在方法上的局限性，我们鼓励进一步开展长期跟踪的组织学研究：PROCROPERO（CRD42021230937）。
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引用次数: 0
Biocompatibility and bioactive potential of NeoPUTTY calcium silicate-based cement: An in vivo study in rats NeoPUTTY 硅酸钙水泥的生物相容性和生物活性潜力：大鼠体内研究。
IF 5 1区 医学 Q1 Dentistry
International endodontic journal
Pub Date : 2024-03-11 DOI: 10.1111/iej.14054
Evelin Carine Alves Silva, Jéssica Arielli Pradelli, Guilherme Ferreira da Silva, Paulo Sérgio Cerri, Mario Tanomaru-Filho, Juliane Maria Guerreiro-Tanomaru

Aim

To evaluate the inflammatory reaction and the ability to induce mineralization activity of a new repair material, NeoPUTTY (NPutty; NuSmile, USA), in comparison with Bio-C Repair (BC; Angelus, Brazil) and MTA Repair HP (MTA HP; Angelus, Brazil).

Methodology

Polyethylene tubes were filled with materials or kept empty (control group, CG) and implanted in subcutaneous tissue of rats for 7, 15, 30, and 60 days (n = 6/group). Capsule thickness, number of inflammatory cells (ICs), fibroblasts, collagen content, and von Kossa analysis were performed. Unstained sections were evaluated under polarized light and by immunohistochemistry for osteocalcin (OCN). Data were submitted to two-way anova followed by Tukey's test (p ≤ .05), except for OCN. OCN data were submitted to Kruskal–Wallis and Dunn and Friedman post hoc tests followed by the Nemenyi test at a significance level of 5%.

Results

At 7, 15, and 30 days, thick capsules containing numerous ICs were seen around the materials. At 60 days, a moderate inflammatory reaction was observed for NPutty, BC while MTA HP presented thin capsules with moderate inflammatory cells. In all periods, NPutty specimens contained the highest values of ICs (p < .05). From 7 to 60 days, the number of ICs reduced significantly while an increase in the number of fibroblasts and birefringent collagen content was observed. At 7 and 15 days, no significant difference was observed in the immunoexpression of OCN (p > .05). At 30 and 60 days, NPutty showed the lowest values of OCN (p < .05). At 60 days, a similar immunoexpression was observed for BC and MTA HP (p > .05). In all time intervals, capsules around NPutty, BC, and MTA HP showed von Kossa-positive and birefringent structures.

Conclusions

Despite the greater inflammatory reaction promoted by NeoPutty than BC and MTA HP, the reduction in the thickness of capsules, the increase in the number of fibroblasts, and the reduction in the number of ICs indicate that this bioceramic material is biocompatible Furthermore, NeoPutty presents the ability to induce mineralization activity.

目的：评估一种新型修复材料 NeoPUTTY（NPutty；NuSmile，美国）与 Bio-C Repair（BC；Angelus，巴西）和 MTA Repair HP（MTA HP；Angelus，巴西）的炎症反应和诱导矿化活性的能力：方法：在聚乙烯管中填充材料或保持空管（对照组，CG），并植入大鼠皮下组织 7、15、30 和 60 天（n = 6/组）。进行蒴果厚度、炎症细胞（IC）数量、成纤维细胞、胶原蛋白含量和 von Kossa 分析。未染色的切片在偏振光下进行评估，并通过免疫组织化学检测骨钙素（OCN）。除 OCN 外，其他数据均进行双向 anova 后的 Tukey's 检验（p ≤ .05）。OCN数据进行Kruskal-Wallis、Dunn和Friedman事后检验，然后进行Nemenyi检验，显著性水平为5%：7天、15天和30天时，材料周围出现了含有大量集成电路的厚囊。在 60 天时，NPutty 和 BC 出现中度炎症反应，而 MTA HP 则出现带有中度炎症细胞的薄囊。在所有时期，NPutty 试样的 IC 值最高（p .05）。在 30 天和 60 天时，NPutty 的 OCN 值最低（p .05）。在所有时间间隔内，NPutty、BC 和 MTA HP 周围的胶囊都显示出 von Kossa 阳性和双折射结构：尽管与 BC 和 MTA HP 相比，NeoPutty 引发的炎症反应更大，但囊肿厚度的减少、成纤维细胞数量的增加以及 IC 数量的减少都表明这种生物陶瓷材料具有生物相容性。
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引用次数: 0
New associate editor for case reports and launch of opinion/perspective articles 新设副主编，负责病例报告，并推出观点/前瞻性文章。
IF 5 1区 医学 Q1 Dentistry
International endodontic journal
Pub Date : 2024-03-06 DOI: 10.1111/iej.14037
Henry F. Duncan

As part of the continued evolution of the Editorial Board to reflect current trends in submission and publication in the journal, the International Endodontic Journal is delighted to announce the appointment of a new Associate Editor Professor Zhi Chen who will be responsible for case reports and opinion/perspective articles. Professor Chen will replace Paul McCabe who served as an Associate Editor handling case reports and clinical techniques for many years. I would like to take this opportunity to thank Paul for all the work he has done for the IEJ over the years and wish him well in his future endeavours.

Professor Chen will lead along with the Editor-in-Chief a new invitation-only section called ‘Perspective/Leading Opinion articles’. These are designed to opinionated or perspective articles that explore important clinical and scientific issues that are designed to stimulate further discussion and the development of Endodontology. The contributions will generally emanate from leaders in our discipline or related scientific, clinical or educational fields.

Professor Chen currently serves as the LuoJia Distinguished Professor at Wuhan University, China. He earned both his D.D.S. and Ph.D. from Wuhan University and has been an integral part of the School & Hospital of Stomatology since 1990. Professor Chen has further enriched his expertise by serving as a visiting scholar at multiple renowned institutions: University Paris Descartes under Professor Michel Goldberg in 1994–1995, University of Strasbourg with Dr. Herve Lesot in 2001 and University of Missouri Kansas City with Professor Jerry Feng in 2004. Professor Chen's research mainly focuses on dental pulp biology. This encompasses odontoblast differentiation, dentinogenesis and dental pulp repair and regeneration. His significant contributions have garnered support from the Natural Science Foundation of China (NSFC), with him leading Key Projects, International Cooperation Projects and General Projects. He is the executive member of Chinese Stomatological Association; Vice Chairman of Chinese Society of Cariology and Endodontics. He is the Chief Editor of Chinese textbook Cariology and Endodontics. He services as the Editor-in-Chief of the Chinese Journal of Oral Science Research (2016-), Associate Editor of Chines Journal of Stomatology (2023-), Associate Editor of Oral Diseases (2017-), Associate Editor of Frontiers in Physiology—Craniofacial Biology and Dental Research (2020-) as well as an Editorial Board member of J Dent Res (2018–2022).

The author has no conflict of interest to report.

国际牙髓病学杂志》很高兴地宣布任命陈志教授为新的副主编，负责病例报告和观点/前瞻性文章。陈教授将接替保罗-麦凯布（Paul McCabe）担任副主编，后者多年来一直负责病例报告和临床技术。我想借此机会感谢保罗多年来为 IEJ 所做的一切工作，并祝愿他在今后的工作中一切顺利。陈教授将与主编一起领导一个新的受邀栏目，名为 "观点/领导性意见文章"。这些文章旨在探讨重要的临床和科学问题，以激发进一步的讨论，促进牙髓病学的发展。陈教授目前是中国武汉大学珞珈特聘教授。自 1990 年以来，他一直是武汉大学口腔医学院和口腔医院不可或缺的一员。陈教授曾在多所知名学府担任访问学者，进一步丰富了自己的专业知识：1994-1995年，陈教授在巴黎笛卡尔大学师从Michel Goldberg教授；2001年，在斯特拉斯堡大学师从Herve Lesot博士；2004年，在密苏里大学堪萨斯城分校师从Jerry Feng教授。陈教授的研究主要集中于牙髓生物学。其中包括牙本质母细胞分化、牙本质生成和牙髓修复与再生。他的重大贡献获得了国家自然科学基金委员会（NSFC）的支持，主持了重点项目、国际合作项目和一般项目。他是中华口腔医学会常务理事、中国牙体牙髓病学会副主任委员。担任《口腔龋病与牙髓病学》教材主编。担任《中华口腔科学研究杂志》主编（2016-）、《中华口腔医学杂志》副主编（2023-）、《口腔疾病》副主编（2017-）、《生理学前沿-颅面生物学与牙科研究》副主编（2020-）以及《J Dent Res》编委（2018-2022）。
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引用次数: 0
Editor-in-Chief thanks the associate editors, editorial board and referees 主编感谢副主编、编委会和审稿人。
IF 5 1区 医学 Q1 Dentistry
International endodontic journal
Pub Date : 2024-03-06 DOI: 10.1111/iej.14039
Henry F. Duncan

On behalf of the Editor-in-Chief and the editorial team in Wiley, I would like to thank those who have contributed to the continued success of the IEJ in 2023. I would like to start by acknowledging and thanking the Associate Editors for their outstanding contribution during the year and their ongoing support to me as Editor-in-Chief:

Sebastian Bürklein, Gustavo De-Deus, Ikhlas El-karim, Michael Hülsmann, Francesco Mannocci, Paul McCabe, Venkateshbabu Nagendrababu, Ronald Ordinola-Zapata, Ove Peters and Emi Shimizu. I would also like to specially thank Christopher Sexton (consultant statistical advisor) for his statistical support throughout the year and Ronald Ordinola-Zapata, Prasanna Neelakantan and Maria Teresa Arias-Moliz for their guest editorship on the ‘Next-generation antimicrobial strategies in endodontics’ special issue.

I would also like to thank all the other members of the Editorial Board:

Vivek Aggarwal, Ana Arias, Hany Ahmed, Vasudev Ballal, Lars Bjørndal, Christos Boutsioukis, Bruno Cavalcanti, Luis Chavez de Pas, Zhi Chen, Bunsan Chong, Gary Cheung, Elizabetta Cotti, Roeland De Moor, Ashraf ElAyouti, Jose de Figueiredo, Giampiero Rossi-Fedele, Kerstin Galler, Brenda Gomes, Markus Haapasalo, Jiiang-Huei Jeng, Aleksandar Jakovljevic, Lise-Lotte Kirkevang, Anil Kishen, Gabriel Krastl, Thomas Kvist, Paul Lambrechts, Chun-Pin Lin, Teresa Arias-Moliz, Prasanna Neelakantan, Mohammad Nekoofar, Takashi Okiji, Shanon Patel, Masoud Parirokh, Carlo Prati, Dan Rechenberg, Tina Rödig, Francesc Abella Sans, Edgar Schäfer, Juanjo Segura-Egea, Hagay Shemesh, Ya Shen, Emmanuel Silva, Erick Souza, Nessrin Taha, H. Tao, Leo Tjäderhane, Phil Tomson, Marco Versiani, Ronald Weiger, Matthias Widbiller, John Whitworth, Victoria Yu, Matt Zehnder, and Chengfei Zhang.

I would also like to acknowledge and thank the panel of referees for their critical appraisal of manuscripts and expert insight:

Silva, Emmanuel; Segura-Egea, Juan; Jakovljevic, Aleksandar; Ballal, Vasudev; Aggarwal, Vivek; Marka, Nicholas; Rossi-Fedele, Giampiero; Versiani, Marco; Al-Nuaimi, Nassr; Huang, Dingming; Palma, Paulo; Parirokh, Masoud; Jeng, Jiiang-Huei; Nosrat, Ali; Widbiller, Matthias; Yu, Victoria; Arias-Moliz, Maria Teresa; Arias, Ana; Gaudin, Alexis; Chen, Zhi; Meng, Liuyan; Cushley, Siobhan; El-Karim, Ikhlas; Krastl, Gabriel; Okiji, Takashi; Abella Sans, Francesc; Ahmed, Hany Mohamed Aly; Gomes Brenda; Sousa-Neto, Manoel; Weiger, Roland; Bhuva, Bhavin; Bjørndal, Lars; Fransson, Helena; Kahler, William; Shen, Ya; Donnermeyer, David; Keles, Ali; Neelakantan, Prasanna; Rahim, Noushad; Zhang, Chengfei; Boutsioukis, Christos; Del Fabbro, Massimo; Fouad, Ashraf; Hosseinpour, Sepanta; Kawashima, Nobuyuki; Schäfer, Edgar; Shemesh, Hagay; Silva, Lea; Souza, Erick; Taha, Nessrin; Cotti, Elisabetta; Dissanayaka, Waruna; Kvist, Thomas; Martins, Jorge; Saber, Shehabeldin; Tsesis, Igor; Adorno, Carlos; Cavalcanti, Bruno; Donnelly, Aisling; Haug, Sivakami;

在此，我还要感谢并感谢评审小组对稿件的严格评审和专家的真知灼见：Silva, Emmanuel; Segura-Egea, Juan; Jakovljevic, Aleksandar; Ballal, Vasudev; Aggarwal, Vivek; Marka, Nicholas; Rossi-Fedele, Giampiero; Versiani, Marco; Al-Nuaimi, Nassr; Huang, Dingming; Palma, Paulo; Parirokh, Masoud; Jeng, Jiiang-Huei; Nosrat, Ali；Widbiller, Matthias; Yu, Victoria; Arias-Moliz, Maria Teresa; Arias, Ana; Gaudin, Alexis; Chen, Zhi; Meng, Liuyan; Cushley, Siobhan; El-Karim, Ikhlas; Krastl, Gabriel; Okiji, Takashi; Abella Sans, Francesc; Ahmed, Hany Mohamed Aly; Gomes Brenda；Sousa-Neto, Manoel; Weiger, Roland; Bhuva, Bhavin; Bjørndal, Lars; Fransson, Helena; Kahler, William; Shen, Ya; Donnermeyer, David; Keles, Ali; Neelakantan, Prasanna; Rahim, Noushad; Zhang, Chengfei; Boutsioukis, Christos; Del Fabbro, Massimo; Fouad, Ashraf；Hosseinpour, Sepanta; Kawashima, Nobuyuki; Schäfer, Edgar; Shemesh, Hagay; Silva, Lea; Souza, Erick; Taha, Nessrin; Cotti, Elisabetta; Dissanayaka, Waruna; Kvist, Thomas; Martins, Jorge; Saber, Shehabeldin; Tsesis, Igor; Adorno, Carlos; Cavalcanti, Bruno；Donnelly, Aisling; Haug, Sivakami; Jayaraman, Jayakumar; Keskin, Cangul; Lin, Fei; Meire, Maarten; Patel, Neha; Patel, Shanon; Sexton, Christopher; Shah, Pratik; Tomson, Phillip; Tzanetakis, Giorgos; Zehnder, Matthias; Zheng, Lisha; Ali, Ahmed；Alovisi, Mario; Aminoshariae, Anita; Chevalier, Valérie; Elnaghy, Amr; Hashem, Ahmed; Herbst, Sascha; Lima, Bruno; Schmalz, Gottfried; Silva, Renato; Tanalp, Jale; Taşdemir, Tamer; Testarelli, Luca; van der Waal, Suzette; Virdee, Satnam; Ye, Zhou；Amin, Suzan; Awawdeh, Lama; Chang, Mei-Chi; Connert, Thomas; Dammaschke, Till; Dong, Yanmei; Grande, Nicola Maria; He, Wen-Xi; Hülsmann, Michael; Jacinto, Rogério; Kannan, Thirumulu; Karataş, Ertuğrul; Kim, Hyeon Cheol; Kirkevang, Lise-Lotte；Kruse, Casper; Li, Zehan; Love, Robert; Martinho, Frederico; Milasin, Jelena; Murray, Peter; Olivieri, Juan; Osathanon, Thanaphum; Primus, Carolyn; Rhodes, John; Rosa, Vinicius; Taschieri, Silvio; Xu, Chun; Yassen, Ghaeth; Zamparini, Fausto; Ahmad, Paras；Aksel, Hacer; Andrukhov, Oleh; Barthel-Zimmer, Claudía; Bitter, Kerstin; Bottino, Marco; Chen, Fa-Ming; Chompu-inwai, Papimon; Chong, Bun San; Cintra, Luciano; Dhar, Vineet; Faria, Gisele; Farmakis, Eleftherios Terry; Fernandez, Eduardo; Foschi, Federico；Haapasalo，Markus；Han，Dr Pingping；Kaval，Mehmet；Kim，Sunil；Koller，Garrit；Min，Kyung-San；Natanasabapathy，Velmurugan；Ordinola-Zapata，Ronald；Ormiga，Fabíola；Petridis，Xenos；Rödig，Tina；Rosen，Eyal；Saavedra，Flavia；Shibukawa，Yoshiyuki；Spin-Neto, Rubens; Suresh, Nandini; Takahashi, Yusuke; Tanomaru-Filho, Mário; Tordik, Patricia; Umer, Fahad; Whitworth, John; Zahran, Shatha; Abramovitz, Itzhak; Al-Qudah, Aladdin; Alcalde, Murilo; Allihaibi, Marwa; Alves, Flávio; Aral, Kubra; Ather, Amber；Austin, Rupert; Bakhsh, Abdulaziz; Belladonna, Felipe; Bose, Rahul; Botero, Tatiana; Bürklein, Sebastian; Camilleri, Josette; Cathro, Peter; Caviedes-Bucheli, Javier; Chawla, Amrita; Cui, Li; Diegritz, Christian; Doğramacı, Esma; Duarte
{"title":"Editor-in-Chief thanks the associate editors, editorial board and referees","authors":"Henry F. Duncan","doi":"10.1111/iej.14039","DOIUrl":"10.1111/iej.14039","url":null,"abstract":"<p>On behalf of the Editor-in-Chief and the editorial team in Wiley, I would like to thank those who have contributed to the continued success of the IEJ in 2023. I would like to start by acknowledging and thanking the Associate Editors for their outstanding contribution during the year and their ongoing support to me as Editor-in-Chief:</p><p>Sebastian Bürklein, Gustavo De-Deus, Ikhlas El-karim, Michael Hülsmann, Francesco Mannocci, Paul McCabe, Venkateshbabu Nagendrababu, Ronald Ordinola-Zapata, Ove Peters and Emi Shimizu. I would also like to specially thank Christopher Sexton (consultant statistical advisor) for his statistical support throughout the year and Ronald Ordinola-Zapata, Prasanna Neelakantan and Maria Teresa Arias-Moliz for their guest editorship on the ‘Next-generation antimicrobial strategies in endodontics’ special issue.</p><p>I would also like to thank all the other members of the Editorial Board:</p><p>Vivek Aggarwal, Ana Arias, Hany Ahmed, Vasudev Ballal, Lars Bjørndal, Christos Boutsioukis, Bruno Cavalcanti, Luis Chavez de Pas, Zhi Chen, Bunsan Chong, Gary Cheung, Elizabetta Cotti, Roeland De Moor, Ashraf ElAyouti, Jose de Figueiredo, Giampiero Rossi-Fedele, Kerstin Galler, Brenda Gomes, Markus Haapasalo, Jiiang-Huei Jeng, Aleksandar Jakovljevic, Lise-Lotte Kirkevang, Anil Kishen, Gabriel Krastl, Thomas Kvist, Paul Lambrechts, Chun-Pin Lin, Teresa Arias-Moliz, Prasanna Neelakantan, Mohammad Nekoofar, Takashi Okiji, Shanon Patel, Masoud Parirokh, Carlo Prati, Dan Rechenberg, Tina Rödig, Francesc Abella Sans, Edgar Schäfer, Juanjo Segura-Egea, Hagay Shemesh, Ya Shen, Emmanuel Silva, Erick Souza, Nessrin Taha, H. Tao, Leo Tjäderhane, Phil Tomson, Marco Versiani, Ronald Weiger, Matthias Widbiller, John Whitworth, Victoria Yu, Matt Zehnder, and Chengfei Zhang.</p><p>I would also like to acknowledge and thank the panel of referees for their critical appraisal of manuscripts and expert insight:</p><p>Silva, Emmanuel; Segura-Egea, Juan; Jakovljevic, Aleksandar; Ballal, Vasudev; Aggarwal, Vivek; Marka, Nicholas; Rossi-Fedele, Giampiero; Versiani, Marco; Al-Nuaimi, Nassr; Huang, Dingming; Palma, Paulo; Parirokh, Masoud; Jeng, Jiiang-Huei; Nosrat, Ali; Widbiller, Matthias; Yu, Victoria; Arias-Moliz, Maria Teresa; Arias, Ana; Gaudin, Alexis; Chen, Zhi; Meng, Liuyan; Cushley, Siobhan; El-Karim, Ikhlas; Krastl, Gabriel; Okiji, Takashi; Abella Sans, Francesc; Ahmed, Hany Mohamed Aly; Gomes Brenda; Sousa-Neto, Manoel; Weiger, Roland; Bhuva, Bhavin; Bjørndal, Lars; Fransson, Helena; Kahler, William; Shen, Ya; Donnermeyer, David; Keles, Ali; Neelakantan, Prasanna; Rahim, Noushad; Zhang, Chengfei; Boutsioukis, Christos; Del Fabbro, Massimo; Fouad, Ashraf; Hosseinpour, Sepanta; Kawashima, Nobuyuki; Schäfer, Edgar; Shemesh, Hagay; Silva, Lea; Souza, Erick; Taha, Nessrin; Cotti, Elisabetta; Dissanayaka, Waruna; Kvist, Thomas; Martins, Jorge; Saber, Shehabeldin; Tsesis, Igor; Adorno, Carlos; Cavalcanti, Bruno; Donnelly, Aisling; Haug, Sivakami; ","PeriodicalId":13724,"journal":{"name":"International endodontic journal","volume":null,"pages":null},"PeriodicalIF":5.0,"publicationDate":"2024-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/iej.14039","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140039259","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Nlrp3 inflammasome drives regulatory T cell depletion to accelerate periapical bone erosion Nlrp3 炎性体驱动调节性 T 细胞耗竭，加速根尖周骨质侵蚀。
IF 5.4 1区 医学 Q1 DENTISTRY, ORAL SURGERY & MEDICINE
International endodontic journal
Pub Date : 2024-03-05 DOI: 10.1111/iej.14062
Konghuai Wang, Jiayi Liu, Junli Yue, Lu Zhou, Hanqing Mao, Jiaqi Li, Zhijun Sun, Zhi Chen, Lu Zhang

Aim

Apical periodontitis is an inflammatory disorder triggered by an immune response to bacterial infection, leading to the periapical tissue damage and alveolar resorption. However, the underlying mechanisms driving this process remain elusive, due to the complex and interconnected immune microenvironment within the local lesion site. In this study, the influence of Nlrp3 inflammasome-mediated immune response on the apical periodontitis was investigated.

Methodology

RNA sequencing, immunohistochemistry and ELISA assay were performed to investigate the activation of Nlrp3 inflammasome signalling pathways in the human periapical tissues, including radicular cysts, periapical granulomas and healthy oral mucosa. A mouse model of apical periodontitis was established to study the role of Nlrp3 knockout in periapical bone resorption and Treg cell stability, and the underlying mechanism was explored through in vitro experiments. In vivo Treg cell adoptive transfer was performed to investigate the effects of Treg cells on the progression of apical periodontitis.

Results

Our findings find that the hyperactivated Nlrp3 inflammasome is present in human periapical lesions and plays a vital role in the immune-related periapical bone loss. Using a mouse model of apical periodontitis, we observe that Nlrp3 deficiency is resistant to bone resorption. This protection was accompanied by elevated generation and infiltration of local Treg cells that displayed a notable ability to suppress RANKL-dependent osteoclast differentiation. In terms of the mechanism of action, Nlrp3 deficiency directly inhibits the osteoclast differentiation and bone loss through JNK/MAPK and NF-κB pathways. In addition, Nlrp3 induces pyroptosis in the stem cells from apical papilla (SCAPs), and the subsequent release of cytokines affects the stability of Treg cell in periapical lesions, leading indirectly to enhanced bone resorption. In turn, adoptive transfer of both Nlrp3-deficient and wild-type Treg cells effectively prevent the bone erosion during apical periodontitis.

Conclusions

Together, our data identify that the Nlrp3 inflammasome modulates the Treg cell stability and osteoclastogenesis in the periapical inflammatory microenvironment, thus determining the progression of bone erosion.

目的：根尖牙周炎是由细菌感染引起的免疫反应引发的炎症性疾病，导致根尖周组织损伤和牙槽骨吸收。然而，由于局部病变部位的免疫微环境复杂且相互关联，驱动这一过程的潜在机制仍然难以捉摸。本研究探讨了Nlrp3炎性体介导的免疫反应对根尖牙周炎的影响：方法：通过RNA测序、免疫组织化学和ELISA检测，研究Nlrp3炎性体信号通路在人类根尖周组织（包括根尖囊肿、根尖周肉芽肿和健康口腔黏膜）中的激活情况。为了研究 Nlrp3 基因敲除在根尖周骨吸收和 Treg 细胞稳定性中的作用，我们建立了根尖周炎小鼠模型，并通过体外实验探索其潜在机制。体内Treg细胞收养性转移研究了Treg细胞对根尖周炎进展的影响：我们的研究结果发现，人类根尖周炎病变中存在过度激活的 Nlrp3 炎性体，并在与免疫相关的根尖周炎骨质流失中发挥着重要作用。我们利用小鼠根尖牙周炎模型观察到，Nlrp3 缺乏会抑制骨吸收。这种保护作用伴随着局部 Treg 细胞的生成和浸润的增加，这些细胞具有显著的抑制 RANKL 依赖性破骨细胞分化的能力。在作用机制方面，Nlrp3 缺乏可通过 JNK/MAPK 和 NF-κB 通路直接抑制破骨细胞分化和骨质流失。此外，Nlrp3 还能诱导根尖乳头干细胞（SCAPs）发生热凋亡，随后释放的细胞因子会影响根尖周病变中 Treg 细胞的稳定性，从而间接导致骨吸收增强。反过来，Nlrp3缺陷型和野生型Treg细胞的收养性转移可有效防止根尖牙周炎期间的骨侵蚀：综上所述，我们的数据表明，Nlrp3 炎性体可调节根尖周炎微环境中 Treg 细胞的稳定性和破骨细胞的生成，从而决定骨侵蚀的进展。
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引用次数: 0
Harnessing antimicrobial peptides in endodontics 在牙髓治疗中利用抗菌肽。
IF 5 1区 医学 Q1 Dentistry
International endodontic journal
Pub Date : 2024-03-05 DOI: 10.1111/iej.14043
Xinzi Kong, Vijetha Vishwanath, Prasanna Neelakantan, Zhou Ye

Endodontic therapy includes various procedures such as vital pulp therapy, root canal treatment and retreatment, surgical endodontic treatment and regenerative endodontic procedures. Disinfection and tissue repair are crucial for the success of these therapies, necessitating the development of therapeutics that can effectively target microbiota, eliminate biofilms, modulate inflammation and promote tissue repair. However, no current endodontic agents can achieve these goals. Antimicrobial peptides (AMPs), which are sequences of amino acids, have gained attention due to their unique advantages, including reduced susceptibility to drug resistance, broad-spectrum antibacterial properties and the ability to modulate the immune response of the organism effectively. This review systematically discusses the structure, mechanisms of action, novel designs and limitations of AMPs. Additionally, it highlights the efforts made by researchers to overcome peptide shortcomings and emphasizes the potential applications of AMPs in endodontic treatments.

牙髓治疗包括各种程序，例如活髓治疗、根管治疗和再治疗、外科牙髓治疗和再生牙髓治疗程序。消毒和组织修复对这些疗法的成功至关重要，因此有必要开发能有效针对微生物群、消除生物膜、调节炎症和促进组织修复的疗法。然而，目前还没有一种牙髓治疗药物能够实现这些目标。抗菌肽（AMPs）是由氨基酸组成的序列，因其独特的优势而备受关注，包括降低耐药性、广谱抗菌特性以及有效调节机体免疫反应的能力。本综述系统地讨论了 AMPs 的结构、作用机制、新型设计和局限性。此外，它还着重介绍了研究人员为克服多肽的缺点所做的努力，并强调了 AMPs 在牙髓治疗中的潜在应用。
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引用次数: 0
Ginsenoside Rb1 alleviates lipopolysaccharide-induced inflammation in human dental pulp cells via the PI3K/Akt, NF-κB, and MAPK signalling pathways 人参皂苷Rb1通过PI3K/Akt、NF-κB和MAPK信号通路减轻脂多糖诱导的人牙髓细胞炎症。
IF 5 1区 医学 Q1 Dentistry
International endodontic journal
Pub Date : 2024-03-04 DOI: 10.1111/iej.14058
Ok Hyung Nam, Jae-Hwan Kim, Si Won Kang, Yong Kwon Chae, Myeong-Kwan Jih, Hyekyoung Hannah You, Jeong-Tae Koh, Young Kim

Aim

Among numerous constituents of Panax ginseng, a constituent named Ginsenoside Rb1 (G-Rb1) has been studied to diminish inflammation associated with diseases. This study investigated the anti-inflammatory properties of G-Rb1 on human dental pulp cells (hDPCs) exposed to lipopolysaccharide (LPS) and aimed to determine the underlying molecular mechanisms.

Methodology

The KEGG pathway analysis was performed after RNA sequencing in G-Rb1- and LPS-treated hDPCs. Reverse-transcription polymerase chain reaction (RT–PCR) and western blot analysis were used for the assessment of cell adhesion molecules and inflammatory cytokines. Statistical analysis was performed with one-way ANOVA and the Student–Newman–Keuls test.

Results

G-Rb1 did not exhibit any cytotoxicity within the range of concentrations tested. However, it affected the levels of TNF-α, IL-6 and IL-8, as these showed reduced levels with exposure to LPS. Additionally, less mRNA and protein expressions of vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) were shown. With the presence of G-Rb1, decreased levels of PI3K/Akt, phosphorylated IκBα and p65 were also observed. Furthermore, phosphorylated ERK and JNK by LPS were diminished within 15, 30 and 60 min of G-Rb1 exposure; however, the expression of non-phosphorylated ERK and JNK remained unchanged.

Conclusions

G-Rb1 suppressed the LPS-induced increase of cell adhesion molecules and inflammatory cytokines, while also inhibiting PI3K/Akt, phosphorylation of NF–κB transcription factors, ERK and JNK of MAPK signalling in hDPCs.

目的：在人参的众多成分中，一种名为人参皂苷Rb1（G-Rb1）的成分被研究用于减少与疾病相关的炎症。本研究调查了 G-Rb1 对暴露于脂多糖（LPS）的人牙髓细胞（hDPCs）的抗炎特性，并旨在确定其潜在的分子机制：在对G-Rb1和LPS处理过的hDPCs进行RNA测序后，进行KEGG通路分析。逆转录聚合酶链反应（RT-PCR）和免疫印迹分析用于评估细胞粘附分子和炎症细胞因子。统计分析采用单因素方差分析和Student-Newman-Keuls检验：在测试的浓度范围内，G-Rb1 没有表现出任何细胞毒性。然而，它影响了 TNF-α、IL-6 和 IL-8 的水平，因为这些物质的水平随着暴露于 LPS 而降低。此外，血管细胞粘附分子-1（VCAM-1）和细胞间粘附分子-1（ICAM-1）的 mRNA 和蛋白质表达也有所减少。随着 G-Rb1 的存在，还观察到 PI3K/Akt、磷酸化 IκBα 和 p65 水平下降。此外，在 G-Rb1 暴露于 LPS 的 15、30 和 60 分钟内，磷酸化 ERK 和 JNK 均有所减少；然而，非磷酸化 ERK 和 JNK 的表达保持不变：结论：G-Rb1 能抑制 LPS 诱导的细胞粘附分子和炎症细胞因子的增加，同时还能抑制 hDPCs 中的 PI3K/Akt、NF-κB 转录因子磷酸化、ERK 和 JNK 的 MAPK 信号传导。
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引用次数: 0
Anti-inflammatory cerium-containing nano-scaled mesoporous bioactive glass for promoting regenerative capability of dental pulp cells 用于促进牙髓细胞再生能力的抗炎含铈纳米鳞片介孔生物活性玻璃。
IF 5 1区 医学 Q1 Dentistry
International endodontic journal
Pub Date : 2024-03-04 DOI: 10.1111/iej.14055
Yiyuan Duan, Kai Zheng, Wenzhu Hu, Jake Jinkun Chen, Xiaolin Lu, Mingxin Wang, Yuxin Yang, Jingyao Guo, Yanlai Lu, Qian Ma

Aims

This study aimed to investigate the anti-inflammatory and odontoblastic effects of cerium-containing mesoporous bioactive glass nanoparticles (Ce-MBGNs) on dental pulp cells as novel pulp-capping agents.

Methodology

Ce-MBGNs were synthesized using a post-impregnation strategy based on the antioxidant properties of Ce ions and proposed the first use of Ce-MBGNs for pulp-capping application. The biocompatibility of Ce-MBGNs was analysed using the CCK-8 assay and apoptosis detection. Additionally, the reactive oxygen species (ROS) scavenging ability of Ce-MBGNs was measured using the 2,7-Dichlorofuorescin Diacetate (DCFH-DA) probe. The anti-inflammatory effect of Ce-MBGNs on THP-1 cells was further investigated using flow cytometry and quantitative real-time polymerase chain reaction (RT-qPCR). Moreover, the effect of Ce-MBGNs on the odontoblastic differentiation of the dental pulp cells (DPCs) was assessed by combined scratch assays, RT-qPCR, western blotting, immunocytochemistry, Alizarin Red S staining and tissue-nonspecific alkaline phosphatase staining. Analytically, the secretions of tumour necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were detected with enzyme-linked immunosorbent assay (ELISA).

Results

Ce-MBGNs were confirmed to effectively scavenge ROS in THP-1-derived macrophages and DPCs. Flow cytometry and RT-qPCR assays revealed that Ce-MBGNs significantly inhibited the M1 polarization of macrophages (Mφ). Furthermore, the protein levels of TNF-α and IL-1β were downregulated in THP-1-derived macrophages after stimulation with Ce-MBGNs. With a step-forward virtue of promoting the odontoblastic differentiation of DPCs, we further confirmed that Ce-MBGNs could regulate the formation of a conductive immune microenvironment with respect to tissue repair in DPCs, which was mediated by macrophages.

Conclusions

Ce-MBGNs protected cells from self-produced oxidative damage and exhibited excellent immunomodulatory and odontoblastic differentiation effects on DPCs. As a pulp-capping agent, this novel biomaterial can exert anti-inflammatory effects and promote restorative dentine regeneration in clinical treatment. We believe that this study will stimulate further correlative research on the development of advanced pulp-capping agents.

目的：本研究旨在探讨作为新型牙髓覆盖剂的含铈介孔生物活性玻璃纳米粒子（Ce-MPGNs）对牙髓细胞的抗炎和牙髓形成作用：根据铈离子的抗氧化特性，采用后浸渍策略合成了Ce-MPGNs，并首次提出将Ce-MPGNs用于牙髓覆盖剂。利用 CCK-8 试验和细胞凋亡检测分析了 Ce-MBGNs 的生物相容性。此外，还使用 2,7-Dichlorofuorescin Diacetate（DCFH-DA）探针测量了 Ce-MBGNs 清除活性氧（ROS）的能力。使用流式细胞术和实时定量聚合酶链反应（RT-qPCR）进一步研究了 Ce-MBGNs 对 THP-1 细胞的抗炎作用。此外，还通过划痕试验、RT-qPCR、Western 印迹、免疫细胞化学、茜素红 S 染色和组织非特异性碱性磷酸酶染色等方法，评估了 Ce-MBGNs 对牙髓细胞（DPCs）牙髓分化的影响。用酶联免疫吸附试验（ELISA）检测了肿瘤坏死因子-α（TNF-α）和白细胞介素-1β（IL-1β）的分泌物：结果：证实 Ce-MBGNs 能有效清除 THP-1 巨噬细胞和 DPCs 中的 ROS。流式细胞术和 RT-qPCR 检测显示，Ce-MBGNs 能显著抑制巨噬细胞的 M1 极化（Mφ）。此外，经 Ce-MBGNs 刺激后，THP-1 衍生巨噬细胞中 TNF-α 和 IL-1β 蛋白水平下调。我们进一步证实，Ce-MBGNs具有促进DPCs牙骨质分化的作用，它可以调节DPCs组织修复方面的传导性免疫微环境的形成，而这种微环境是由巨噬细胞介导的：结论：Ce-MBGNs能保护细胞免受自身产生的氧化损伤，并对DPCs表现出良好的免疫调节和牙本质分化作用。作为一种牙髓覆盖剂，这种新型生物材料可在临床治疗中发挥抗炎作用并促进牙本质再生修复。我们相信，这项研究将激励人们进一步开展相关研究，开发先进的牙髓覆盖剂。
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