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Remineralizing capacity of zinc oxide eugenol sealer following the addition of nanohydroxyapatite-tyrosine amino acid: An in vivo animal study. 添加纳米羟基磷灰石-酪氨酸氨基酸后氧化锌丁香酚封闭剂的再矿化能力:活体动物研究。
IF 2.6 Q1 DENTISTRY, ORAL SURGERY & MEDICINE Pub Date : 2024-10-15 DOI: 10.1016/j.job.2024.09.006
Rasha M Al-Shamaa, Raghad A Al-Askary

Objective: Although several sealers have been developed, the zinc oxide eugenol (ZOE) sealer is still used in many private dental clinics. This study aimed to compare the biocompatibility and remineralizing capacity οf ZOE sealer with the addition of nanohydroxyapatite-tyrosine amino acid.

Methods: This study was conducted on Twenty rabbits. The rabbits were divided into four groups based on the test observation period (3, 7, 21, and 28 days) following surgical implantation. General anesthesia was administered to each rabbit, and a subcutaneous incision of approximately 1±0.5 cm was made along the symphyseal area of the mandible of each rabbit. Four bone cavities were generated in the interdental space of the lower jaw between the central and molar teeth of each rabbit, with one longitudinal subcutaneous incision. The ZOE sealers were mixed according to the manufacturer's guidelines and directly inserted within the cavities generated at the end of each test period. The animals were sacrificed, and bone biopsy was carried out at the site of testing. The biopsy samples were obtained and subjected to histological analysis using a low-power light microscope (Olympus C ⅹ 21, Japan) and immunohistochemistry using Ki67 antibody.

Results: The collected information was examined by parametric statistical tests using SPSS software version ''22." One-way ANOVA and post-hoc Duncan's tests were used to measure the significance among various groups, with statistical significance set, when "P≤0.01".

Conclusion: The 20% mixed endodontic sealer displayed excellent outcomes compared to other experimental groups, as identified by higher new bone formation at every evaluation period.

目的:尽管已开发出多种封闭剂,但许多私人牙科诊所仍在使用氧化锌丁香酚(ZOE)封闭剂。本研究旨在比较添加纳米羟基磷灰石-酪氨酸氨基酸的氧化锌封闭剂的生物相容性和再矿化能力:本研究以 20 只兔子为对象。根据手术植入后的试验观察期(3、7、21 和 28 天)将兔子分为四组。对每只兔子进行全身麻醉,沿每只兔子下颌骨的骨骺区做一个约 1±0.5 厘米的皮下切口。在每只兔子下颌中牙和磨牙之间的牙间隙生成四个骨腔,其中一个为纵向皮下切口。按照制造商的指导原则混合 ZOE 密封剂,并在每个测试期结束时直接将其插入生成的骨腔中。动物被处死,并在测试部位进行骨活检。获得活检样本后,使用低倍光学显微镜(日本奥林巴斯 C ⅹ 21)进行组织学分析,并使用 Ki67 抗体进行免疫组化:使用 SPSS 软件版本''22 "对收集的信息进行参数统计检验。采用单因素方差分析和事后邓肯检验来衡量各组间的显著性,当 "P≤0.01 "时,统计学意义成立:结论:与其他实验组相比,20% 混合根管封闭剂的效果非常好,在每个评估阶段都有较高的新骨形成。
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引用次数: 0
Reactivation of Epstein-Barr virus by n-butyric acid from Pseudoramibacter alactolyticus induces inflammatory cytokines in periapical granulomas. 溶乳假杆菌产生的正丁酸使 Epstein-Barr 病毒重新活化,诱导根尖周炎肉芽肿中的炎性细胞因子。
IF 2.6 Q1 DENTISTRY, ORAL SURGERY & MEDICINE Pub Date : 2024-10-12 DOI: 10.1016/j.job.2024.10.001
Taiki Miyata, Osamu Takeichi, Kenichi Imai, Masayuki Okano, Seiya Inoue, Takuya Yasukawa, Yusuke Suzuki

Objectives: This study investigates whether latent Epstein-Barr virus (EBV) can be reactivated by n-butyric acid from Pseudoramibacter alactolyticus, and if such reactivation induces expression of interleukin (IL)-1β and IL-6 in periapical granulomas.

Methods: We analyzed periapical granulomas and healthy gingival tissues to detect the presence of EBV and P. alactolyticus. The concentration of n-butyric acid in P. alactolyticus culture supernatants was measured. BZLF-1 luciferase assays were conducted with or without these supernatants. Immunohistochemical detection of ZEBRA-, IL-1β-, and IL-6-expressing cells was performed in the tissue samples. Additionally, mRNA expression levels of BZLF-1, IL-1β, and IL-6 were quantified and statistically analyzed for correlation. The expression of these mRNAs was also measured in Daudi cells treated with or without the culture supernatants.

Results: Both EBV and P. alactolyticus were detected in periapical granulomas, but not in healthy tissues. The concentration of n-butyric acid in the culture supernatants was ∼3.58 mmol/L. BZLF-1 luciferase activity in the presence of the culture supernatants was comparable to that of commercially available butyric acid, whereas no activity was detected without the supernatants. Cells expressing ZEBRA co-expressed IL-1β and IL-6. The mRNA levels of BZLF-1, IL-1β, and IL-6 in periapical granulomas were correlated with the number of EBV DNA copies. Daudi cells treated with the culture supernatants expressed BZLF-1, IL-1β, and IL-6 mRNA, while those without the supernatants did not.

Conclusions: The study concludes that EBV can be reactivated by n-butyric acid produced by P. alactolyticus, leading to the induction of IL-1β and IL-6 expression in periapical granulomas.

研究目的本研究探讨了潜伏的爱泼斯坦-巴氏病毒(EBV)能否被溶乳假杆菌的正丁酸重新激活,以及这种重新激活能否诱导根尖周炎肉芽肿中白细胞介素(IL)-1β和IL-6的表达:我们分析了根尖周炎肉芽肿和健康牙龈组织,以检测是否存在 EBV 和溶乳杆菌。测量溶乳杆菌培养上清液中的正丁酸浓度。用或不用这些上清液进行 BZLF-1 荧光素酶检测。对组织样本中的 ZEBRA-、IL-1β 和 IL-6 表达细胞进行免疫组化检测。此外,还对 BZLF-1、IL-1β 和 IL-6 的 mRNA 表达水平进行了量化和相关性统计分析。在使用或不使用培养上清液处理的 Daudi 细胞中也检测了这些 mRNA 的表达:结果:在根尖周炎肉芽肿中检测到 EBV 和溶乳杆菌,而在健康组织中未检测到。培养上清液中的正丁酸浓度为 3.58 mmol/L。在有培养上清存在的情况下,BZLF-1荧光素酶的活性与市售丁酸的活性相当,而在没有培养上清的情况下则检测不到任何活性。表达 ZEBRA 的细胞同时表达 IL-1β 和 IL-6。根尖周炎肉芽肿中 BZLF-1、IL-1β 和 IL-6 的 mRNA 水平与 EBV DNA 拷贝数相关。用培养上清液处理的 Daudi 细胞表达 BZLF-1、IL-1β 和 IL-6 mRNA,而未用培养上清液处理的细胞则不表达:本研究得出结论:EBV 可被溶乳杆菌产生的正丁酸重新激活,从而诱导根尖周炎肉芽肿中 IL-1β 和 IL-6 的表达。
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引用次数: 0
ED-71 promotes osseointegration of titanium implants in a rat model of GIOP by alleviating the effects of dexamethasone on bone remodeling in a SIRT1-dependent manner. ED-71 可通过 SIRT1 依赖性方式减轻地塞米松对骨重塑的影响,从而促进钛植入物在大鼠 GIOP 模型中的骨结合。
IF 2.6 Q1 DENTISTRY, ORAL SURGERY & MEDICINE Pub Date : 2024-10-10 DOI: 10.1016/j.job.2024.10.003
Chunying Li, Pengfei Xue, Guanglin Duan, Ailing Song, Runbing Zhai, Jie Ma, Minqi Li

Objective: Glucocorticoid-induced osteoporosis (GIOP), a common complication of glucocorticoid usage, plays a critical role in the success of dental implant restoration by affecting osseointegration. Eldecalcitol (ED-71) prevents GIOP; however, its role in the osseointegration of implants under GIOP conditions remains elusive.

Methods: Dexamethasone was used to establish a rat model of GIOP. Subsequently, mini-implant surgery was performed on the femur. GIOP rats were administered ED-71 via gavage to assess its role in the osseointegration of titanium implants under GIOP conditions. MC3T3-E1 and RAW264.7 cells were utilized to explore the molecular mechanism of ED-71 in ameliorating disorder of bone remodeling caused by dexamethasone.

Results: The administration of ED-71 promoted the formation of newly formed woven bone and the resolution of inflammation around titanium implants. In vitro experiments indicated that ED-71 ameliorated dexamethasone-induced dysfunction of osteoblasts and osteoclasts by increasing the expression level of sirtuin 1 (SIRT1). Inhibition of SIRT1 by selisistat counteracts the regulatory effects of ED-71 on dexamethasone-induced disorder of bone remodeling. Molecular docking and Western blotting revealed that the neurogenic locus notch homolog protein and nuclear factor kappa B signaling pathways are essential for the effects of ED-71 on dexamethasone-induced disorder of bone remodeling.

Conclusion: ED-71 promoted implant osseointegration in a rat model of GIOP by alleviating the effects of dexamethasone on bone remodeling in a SIRT1-dependent manner.

目的:糖皮质激素诱导的骨质疏松症(GIOP)是使用糖皮质激素的常见并发症,它通过影响骨结合对牙科种植修复的成功起着至关重要的作用。艾地卡骨化醇(ED-71)可预防 GIOP,但它在 GIOP 条件下对种植体骨结合的作用仍不明确:方法:使用地塞米松建立大鼠 GIOP 模型。方法:使用地塞米松建立 GIOP 大鼠模型,随后在股骨上进行微型植入手术。给 GIOP 大鼠灌胃 ED-71,以评估其在 GIOP 条件下对钛植入物骨结合的作用。利用 MC3T3-E1 和 RAW264.7 细胞探讨 ED-71 改善地塞米松引起的骨重塑紊乱的分子机制:结果:服用ED-71可促进新形成的编织骨的形成,并缓解钛种植体周围的炎症。体外实验表明,ED-71通过提高sirtuin 1(SIRT1)的表达水平,改善了地塞米松诱导的成骨细胞和破骨细胞功能障碍。塞利司他对SIRT1的抑制抵消了ED-71对地塞米松诱导的骨重塑障碍的调节作用。分子对接和Western印迹显示,ED-71对地塞米松诱导的骨重塑障碍的影响离不开神经原位点缺口同源蛋白和核因子卡巴B信号通路:结论:ED-71以SIRT1依赖的方式减轻了地塞米松对骨重塑的影响,从而促进了大鼠GIOP模型中种植体的骨结合。
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引用次数: 0
Development of a new antibody drug to treat congenital tooth agenesis 开发治疗先天性牙齿缺失的新型抗体药物。
IF 2.6 Q1 DENTISTRY, ORAL SURGERY & MEDICINE Pub Date : 2024-10-09 DOI: 10.1016/j.job.2024.10.002
K. Takahashi , H. Kiso , E. Mihara , J. Takagi , Y. Tokita , A. Murashima-Suginami

Background

This study aimed to develop a therapeutic agent promoting teeth regeneration from autologous tissues for congenital tooth agenesis, specifically for hypodontia (≤5 missing congenital teeth, 10% prevalence) and oligodontia (≥6 missing congenital teeth, 0.1% prevalence).

Highlight

We studied mice genetically deficient in the USAG-1 protein, an antagonist of BMP/Wnt which forms excessive teeth. We identified USAG-1 as a target molecule for increasing the number of teeth. Crossing USAG-1-deficient mice with a congenital tooth agenesis model restored tooth formation. We produced anti-USAG-1 neutralizing antibodies as potential therapeutic agents for the treatment of congenital tooth agenesis. Mice anti-USAG-1 neutralizing antibodies can potentially rescue the developmentally arrested tooth germ programmed to a certain tooth type. A humanized anti-USAG-1 antibody was developed as the final candidate.

Conclusion

Targeting USAG-1 shows promise for treating missing congenital tooth. Anti-USAG-1 neutralizing antibodies have been developed and will progress towards clinical trials, which may regenerate missing congenital teeth in conditions, such as hypodontia and oligodontia. The protocol framework for a phase 1 study has been finalized, and preparation for future studies is underway.
研究背景本研究旨在开发一种促进自体组织牙齿再生的治疗剂,用于治疗先天性牙齿缺失,特别是牙列不齐(先天性牙齿缺失≤5颗,发病率为10%)和少牙症(先天性牙齿缺失≥6颗,发病率为0.1%):我们研究了基因缺失 USAG-1 蛋白的小鼠,它是 BMP/Wnt 的拮抗剂,会形成过多的牙齿。我们发现 USAG-1 是增加牙齿数量的目标分子。将 USAG-1 缺失小鼠与先天性牙齿缺失模型杂交,可恢复牙齿的形成。我们制备了抗 USAG-1 中和抗体,作为治疗先天性牙齿缺失的潜在药物。小鼠抗USAG-1中和抗体有可能挽救发育停滞的牙胚,使其形成某种牙型。结论:靶向USAG-1有望用于治疗先天性牙齿缺失:结论:以 USAG-1 为靶点有望治疗先天性牙齿缺失。抗USAG-1中和抗体已经开发出来,并将进入临床试验阶段,这可能会使缺失的先天性牙齿再生,如牙列不齐和少牙症。第一阶段研究的方案框架已经确定,未来研究的准备工作正在进行中。
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引用次数: 0
Herbal medicine Ninjinyoeito inhibits RANKL-induced osteoclast differentiation and bone resorption activity by regulating NF-κB and MAPK pathway 中药 Ninjinyoeito 通过调节 NF-kB 和 MAPK 通路,抑制 RANKL 诱导的破骨细胞分化和骨吸收活性。
IF 2.6 Q1 DENTISTRY, ORAL SURGERY & MEDICINE Pub Date : 2024-10-02 DOI: 10.1016/j.job.2024.09.007
Kaung Htike , Kunihiro Yoshida , Takanori Eguchi , Katsuki Takebe , Xueming Li , Yaxin Qu , Eiko Sakai , Takayuki Tsukuba , Kuniaki Okamoto

Objectives

Osteoporosis is a systemic bone metabolism disorder characterized by decreased bone mass and strength. Osteoclasts (OCs) are giant multinucleated cells that regulate bone homeostasis by degrading bone matrix. Excessive OC differentiation and activity can lead to serious bone metabolic disorders including osteoporosis. Current treatments, including antiresorptive drugs, exert considerable adverse effects, including jaw osteonecrosis. Herbal medicines, such as Ninjinyoeito (NYT), may also offer efficacy, but with fewer adverse effects. In this study, we investigated NYT's effects on osteoclastogenesis.

Methods

Tartrate-resistant acid phosphatase (TRAP) staining and bone resorption assays were performed to examine NYT's effects on OC differentiation and function. OC-related gene expression at mRNA and protein levels was investigated to confirm NYT's inhibitory action against osteoclastogenesis. We also demonstrated involvement of signaling pathways mediated by IκBα and mitogen-activated protein kinases (MAPK) [extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38] and showed nuclear translocation of nuclear factor of activated T-cell cytoplasmic 1 (NFATc1) and nuclear factor kappa B (NF-κB) p65 during osteoclastogenesis.

Results

TRAP staining and bone resorption assays confirmed that NYT significantly inhibited OC differentiation and function. Western blot and RT-PCR results showed that NYT ameliorated osteoclastogenesis by suppressing mRNA and protein level expression of OC-related genes. Moreover, blots and immunocytochemistry (ICC) data clarified that NYT abrogates signaling pathways mediated by IκBα and MAPK (ERK, JNK, p38), and demonstrated nuclear translocation of NFATc1 and NF-κB p65 during OC differentiation.

Conclusions

These findings suggest NYT is an alternative therapeutic candidate for treating osteoporosis.
目的:骨质疏松症是一种全身性骨代谢疾病,以骨量和骨强度下降为特征。破骨细胞(OC)是一种巨大的多核细胞,通过降解骨基质来调节骨平衡。过度的 OC 分化和活动可导致严重的骨代谢紊乱,包括骨质疏松症。目前的治疗方法,包括抗骨质吸收药物,会产生相当大的不良影响,包括颌骨骨坏死。中药,如九节鞭(NYT),也可能具有疗效,但不良反应较少。在这项研究中,我们调查了NYT对破骨细胞生成的影响:方法:采用耐酒石酸磷酸酶(TRAP)染色法和骨吸收测定法研究 NYT 对 OC 分化和功能的影响。研究了OC相关基因在mRNA和蛋白质水平上的表达,以证实NYT对破骨细胞生成的抑制作用。我们还证明了IκBα和丝裂原活化蛋白激酶(MAPK)[细胞外信号调节激酶(ERK)、c-Jun N-末端激酶(JNK)和p38]介导的信号通路的参与,并显示了在破骨细胞生成过程中活化T细胞胞浆核因子1(NFATc1)和核因子卡巴B(NF-κB)p65的核转位:结果:TRAP染色和骨吸收试验证实,NYT能显著抑制OC的分化和功能。Western印迹和RT-PCR结果显示,NYT通过抑制OC相关基因的mRNA和蛋白水平表达,改善了破骨细胞的生成。此外,印迹和免疫细胞化学(ICC)数据表明,NYT抑制了由IκBα和MAPK(ERK、JNK、p38)介导的信号通路,并证明了在OC分化过程中NFATc1和NF-κB p65的核转位:这些研究结果表明,NYT是治疗骨质疏松症的另一种候选疗法。
{"title":"Herbal medicine Ninjinyoeito inhibits RANKL-induced osteoclast differentiation and bone resorption activity by regulating NF-κB and MAPK pathway","authors":"Kaung Htike ,&nbsp;Kunihiro Yoshida ,&nbsp;Takanori Eguchi ,&nbsp;Katsuki Takebe ,&nbsp;Xueming Li ,&nbsp;Yaxin Qu ,&nbsp;Eiko Sakai ,&nbsp;Takayuki Tsukuba ,&nbsp;Kuniaki Okamoto","doi":"10.1016/j.job.2024.09.007","DOIUrl":"10.1016/j.job.2024.09.007","url":null,"abstract":"<div><h3>Objectives</h3><div>Osteoporosis is a systemic bone metabolism disorder characterized by decreased bone mass and strength. Osteoclasts (OCs) are giant multinucleated cells that regulate bone homeostasis by degrading bone matrix. Excessive OC differentiation and activity can lead to serious bone metabolic disorders including osteoporosis. Current treatments, including antiresorptive drugs, exert considerable adverse effects, including jaw osteonecrosis. Herbal medicines, such as Ninjinyoeito (NYT), may also offer efficacy, but with fewer adverse effects. In this study, we investigated NYT's effects on osteoclastogenesis.</div></div><div><h3>Methods</h3><div>Tartrate-resistant acid phosphatase (TRAP) staining and bone resorption assays were performed to examine NYT's effects on OC differentiation and function. OC-related gene expression at mRNA and protein levels was investigated to confirm NYT's inhibitory action against osteoclastogenesis. We also demonstrated involvement of signaling pathways mediated by IκBα and mitogen-activated protein kinases (MAPK) [extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38] and showed nuclear translocation of nuclear factor of activated T-cell cytoplasmic 1 (NFATc1) and nuclear factor kappa B (NF-κB) p65 during osteoclastogenesis.</div></div><div><h3>Results</h3><div>TRAP staining and bone resorption assays confirmed that NYT significantly inhibited OC differentiation and function. Western blot and RT-PCR results showed that NYT ameliorated osteoclastogenesis by suppressing mRNA and protein level expression of OC-related genes. Moreover, blots and immunocytochemistry (ICC) data clarified that NYT abrogates signaling pathways mediated by IκBα and MAPK (ERK, JNK, p38), and demonstrated nuclear translocation of NFATc1 and NF-κB p65 during OC differentiation.</div></div><div><h3>Conclusions</h3><div>These findings suggest NYT is an alternative therapeutic candidate for treating osteoporosis.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"66 4","pages":"Pages 49-57"},"PeriodicalIF":2.6,"publicationDate":"2024-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142376160","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Potassium nitrate suppresses hyperactivities of Vc neurons of the model with dentin hypersensitivity 硝酸钾可抑制牙本质过敏模型 Vc 神经元的过度活动。
IF 2.6 Q1 DENTISTRY, ORAL SURGERY & MEDICINE Pub Date : 2024-09-19 DOI: 10.1016/j.job.2024.09.005
Shiori Sugawara , Koichi Iwata , Toshiki Takamizawa , Masashi Miyazaki , Masayuki Kobayashi

Objective

Potassium nitrate (KNO3) suppresses nociception induced by dental hypersensitivity (HYS). We aimed to examine the effects of KNO3 on the neural activity of the trigeminal spinal subnucleus caudalis (Vc) in HYS model rats.

Methods

KNO3 or vehicle was applied to the exposed dentin of HYS rats for 3 days. c-Fos expression and neuronal activity in the Vc after acetone treatment for cold stimulation were examined to evaluate the effects of KNO3 application on dentin.

Results

The number of c-Fos-immunoreactive cells in the Vc was lower in the group that received KNO3 (KNO3 group) than in the group that received vehicle (control group). Spike firing of Vc neurons in response to cold stimulation of the dentin was recorded before and after KNO3 application to the cavity, and the increased neural activity was effectively suppressed by KNO3 application. Scanning electron microscopy revealed that the dentin tubules were not occluded by deposits in any of the groups.

Conclusions

KNO3-induced suppression of Vc neuronal activity does not involve physical occlusion of the dentin tubules but likely involves suppression of Aδ or C-fiber activities in the tooth pulp, resulting in the suppression of Vc neuronal activities.
目的硝酸钾(KNO3)能抑制牙科超敏反应(HYS)引起的痛觉。我们旨在研究 KNO3 对 HYS 模型大鼠三叉神经脊髓尾下核(Vc)神经活动的影响:方法:在 HYS 大鼠暴露的牙本质上涂抹 KNO3 或载体 3 天,检测丙酮处理冷刺激后 Vc 中 c-Fos 的表达和神经元活性,以评估涂抹 KNO3 对牙本质的影响:结果:接受 KNO3 治疗组(KNO3 组)的 Vc 中 c-Fos 免疫反应细胞数量低于接受药物治疗组(对照组)。在龋洞中施用 KNO3 之前和之后,记录了 Vc 神经元对牙本质冷刺激的尖峰点燃反应,施用 KNO3 有效地抑制了神经活动的增加。扫描电子显微镜显示,各组的牙本质小管均未被沉积物堵塞:结论:KNO3 诱导的 Vc 神经元活动抑制并不涉及牙本质小管的物理闭塞,而可能涉及牙髓中 Aδ 或 C 纤维活动的抑制,从而导致 Vc 神经元活动的抑制。
{"title":"Potassium nitrate suppresses hyperactivities of Vc neurons of the model with dentin hypersensitivity","authors":"Shiori Sugawara ,&nbsp;Koichi Iwata ,&nbsp;Toshiki Takamizawa ,&nbsp;Masashi Miyazaki ,&nbsp;Masayuki Kobayashi","doi":"10.1016/j.job.2024.09.005","DOIUrl":"10.1016/j.job.2024.09.005","url":null,"abstract":"<div><h3>Objective</h3><div>Potassium nitrate (KNO<sub>3</sub>) suppresses nociception induced by dental hypersensitivity (HYS). We aimed to examine the effects of KNO<sub>3</sub> on the neural activity of the trigeminal spinal subnucleus caudalis (Vc) in HYS model rats.</div></div><div><h3>Methods</h3><div>KNO<sub>3</sub> or vehicle was applied to the exposed dentin of HYS rats for 3 days. c-Fos expression and neuronal activity in the Vc after acetone treatment for cold stimulation were examined to evaluate the effects of KNO<sub>3</sub> application on dentin.</div></div><div><h3>Results</h3><div>The number of c-Fos-immunoreactive cells in the Vc was lower in the group that received KNO<sub>3</sub> (KNO<sub>3</sub> group) than in the group that received vehicle (control group). Spike firing of Vc neurons in response to cold stimulation of the dentin was recorded before and after KNO<sub>3</sub> application to the cavity, and the increased neural activity was effectively suppressed by KNO<sub>3</sub> application. Scanning electron microscopy revealed that the dentin tubules were not occluded by deposits in any of the groups.</div></div><div><h3>Conclusions</h3><div>KNO<sub>3</sub>-induced suppression of Vc neuronal activity does not involve physical occlusion of the dentin tubules but likely involves suppression of Aδ or C-fiber activities in the tooth pulp, resulting in the suppression of Vc neuronal activities.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"66 4","pages":"Pages 41-48"},"PeriodicalIF":2.6,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142298231","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Comparison of rhythmic jaw muscle activities induced by electrical stimulations of the corticobulbar tract during rapid eye movement sleep with those during wakefulness and non-rapid eye movement sleep in freely moving Guinea pigs 自由活动的豚鼠在快速眼动睡眠时与清醒和非快速眼动睡眠时通过电刺激皮质束诱发的下颌肌肉节律性活动的比较。
IF 2.6 Q1 DENTISTRY, ORAL SURGERY & MEDICINE Pub Date : 2024-09-18 DOI: 10.1016/j.job.2024.09.004
Makoto Higashiyama , Yuji Masuda , Ayano Katagiri , Hiroki Toyoda , Masaharu Yamada , Atsushi Yoshida , Takafumi Kato

Objective

Rhythmic jaw muscle activities (RJMAs) occur during rapid eye movement (REM) sleep in humans and animals even though motoneurons are inhibited. The present study compared the characteristics of jaw muscle activities induced by electrical microstimulations of the corticobulbar tract (CT) during REM sleep with those during wakefulness and non-REM sleep.

Methods

Eleven guinea pigs were surgically prepared for polygraphic recordings with the implantation of a stimulating electrode. Long- and short-train repetitive electrical microstimulations were applied to the CT under freely moving conditions. The response rate, latency, burst amplitude, and cycle length in the digastric muscle were calculated and cortical and cardiac activities were quantified.

Results

Long-train microstimulations induced RJMAs in the digastric muscle followed by masseter muscle activity during wakefulness and non-REM sleep and only induced rhythmic digastric muscle activity during REM sleep. The response rate of RJMAs and the burst amplitude of digastric muscles were significantly lower during REM sleep than during wakefulness and non-REM sleep. However, response latency did not significantly differ between REM sleep and wakefulness. Transient cortical and cardiac changes were associated with RJMAs induced during non-REM sleep, but not during REM sleep. Short-train microstimulations induced a short-latency digastric response, the amplitude of which was significantly lower during REM sleep than during non-REM sleep and wakefulness.

Conclusions

These results suggest that the masticatory CPG was activated by electrical CT stimulations independently of the motoneuron inhibitory system during REM sleep.
目的:人类和动物在快速眼动睡眠(REM)期间会出现有节奏的下颌肌肉活动(RJMA),即使运动神经元受到抑制。本研究比较了快速眼动睡眠期与清醒和非快速眼动睡眠期皮质束(CT)电微刺激诱发的下颌肌肉活动的特征:方法:对 11 只豚鼠进行手术准备,植入一个刺激电极以进行多图记录。在自由移动的条件下,对 CT 进行长程和短程重复微电刺激。结果:结果:在清醒状态和非快速眼动睡眠状态下,长程微刺激可诱发掘胸肌的 RJMAs,随后是咀嚼肌活动,而在快速眼动睡眠状态下仅诱发有节律的掘胸肌活动。在快速动眼期睡眠中,RJMA 的反应率和指阔肌的爆发振幅明显低于清醒和非快速动眼期睡眠。然而,快速动眼期睡眠和清醒时的反应潜伏期并无明显差异。短暂的皮层和心脏变化与非快速动眼期睡眠时诱导的 RJMAs 有关,但与快速动眼期睡眠时无关。短程微刺激诱发了短时咀嚼反应,其振幅在快速动眼期睡眠中明显低于非快速动眼期睡眠和清醒时:这些结果表明,在快速动眼睡眠期间,咀嚼CPG是由CT电刺激激活的,与运动神经元抑制系统无关。
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引用次数: 0
Antihypertensive agent losartan promotes tongue squamous cell carcinoma cell proliferation via EGFR/ERK1/2/cyclin D1 signaling axis 降压药洛沙坦通过表皮生长因子受体/ERK1/2/环素D1信号轴促进舌鳞状细胞癌细胞增殖
IF 2.6 Q1 DENTISTRY, ORAL SURGERY & MEDICINE Pub Date : 2024-09-07 DOI: 10.1016/j.job.2024.09.003
Luo-Yun Wu , Bor-Chyuan Su , Hsin-Hsien Yu , Chih-Cheng Cheng , Chia-Chi Tsai , Pei-Ling Hsu , Chu-Wan Lee

Objective

To study the effects of losartan, an angiotensin II receptor blocker, in the SCC4 and SCC25 human tongue squamous cell carcinoma cell lines.

Methods

Cell proliferation was measured by MTS/PMS activity and trypan blue exclusion assays. The levels of the cell proliferation marker, cyclin D1, were analyzed by western blotting. Apoptosis was assessed by caspase-3 activation and Annexin V-FITC/propidium iodide double staining. Activation of epidermal growth factor receptor (EGFR) and ERK1/2 was validated by western blotting.

Results

Moderate concentrations of losartan enhanced the proliferation of SCC4 and SCC25 cells. However, high losartan concentrations induced apoptosis in SCC4 cells. Losartan activated the EGFR/ERK1/2/cyclin D1 signaling axis, which in turn promoted cell proliferation. Afatinib (EGFR inhibitor) and U0126 (ERK1/2 inhibitor) abolished losartan-induced cell proliferation. In contrast, UC2288 (p21 inhibitor) enhanced it.

Conclusions

Losartan exhibited dual effects on tongue squamous cell carcinoma cells. Moderate losartan concentrations facilitated cell proliferation, whereas high concentrations induced cytotoxicity in tongue carcinoma cells.
目的研究血管紧张素 II 受体阻滞剂洛沙坦对 SCC4 和 SCC25 人舌鳞癌细胞系的影响:方法:细胞增殖通过 MTS/PMS 活性和胰蓝排除试验进行测定。细胞增殖标记物细胞周期蛋白 D1 的水平通过 Western 印迹法进行分析。细胞凋亡通过 caspase-3 活化和 Annexin V-FITC/ 碘化丙啶双染色进行评估。表皮生长因子受体(EGFR)和ERK1/2的活化通过Western印迹进行验证:结果:中等浓度的洛沙坦能增强 SCC4 和 SCC25 细胞的增殖。然而,高浓度的洛沙坦可诱导 SCC4 细胞凋亡。洛沙坦激活了表皮生长因子受体/ERK1/2/环素D1信号轴,进而促进了细胞增殖。阿法替尼(表皮生长因子受体抑制剂)和 U0126(ERK1/2 抑制剂)抑制了洛沙坦诱导的细胞增殖。与此相反,UC2288(p21 抑制剂)却能促进细胞增殖:结论:洛沙坦对舌鳞癌细胞具有双重作用。结论:洛沙坦对舌鳞癌细胞具有双重作用,适度浓度的洛沙坦可促进细胞增殖,而高浓度的洛沙坦可诱导舌癌细胞产生细胞毒性。
{"title":"Antihypertensive agent losartan promotes tongue squamous cell carcinoma cell proliferation via EGFR/ERK1/2/cyclin D1 signaling axis","authors":"Luo-Yun Wu ,&nbsp;Bor-Chyuan Su ,&nbsp;Hsin-Hsien Yu ,&nbsp;Chih-Cheng Cheng ,&nbsp;Chia-Chi Tsai ,&nbsp;Pei-Ling Hsu ,&nbsp;Chu-Wan Lee","doi":"10.1016/j.job.2024.09.003","DOIUrl":"10.1016/j.job.2024.09.003","url":null,"abstract":"<div><h3>Objective</h3><div>To study the effects of losartan, an angiotensin II receptor blocker, in the SCC4 and SCC25 human tongue squamous cell carcinoma cell lines.</div></div><div><h3>Methods</h3><div>Cell proliferation was measured by MTS/PMS activity and trypan blue exclusion assays. The levels of the cell proliferation marker, cyclin D1, were analyzed by western blotting. Apoptosis was assessed by caspase-3 activation and Annexin V-FITC/propidium iodide double staining. Activation of epidermal growth factor receptor (EGFR) and ERK1/2 was validated by western blotting.</div></div><div><h3>Results</h3><div>Moderate concentrations of losartan enhanced the proliferation of SCC4 and SCC25 cells. However, high losartan concentrations induced apoptosis in SCC4 cells. Losartan activated the EGFR/ERK1/2/cyclin D1 signaling axis, which in turn promoted cell proliferation. Afatinib (EGFR inhibitor) and U0126 (ERK1/2 inhibitor) abolished losartan-induced cell proliferation. In contrast, UC2288 (p21 inhibitor) enhanced it.</div></div><div><h3>Conclusions</h3><div>Losartan exhibited dual effects on tongue squamous cell carcinoma cells. Moderate losartan concentrations facilitated cell proliferation, whereas high concentrations induced cytotoxicity in tongue carcinoma cells.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"66 4","pages":"Pages 74-80"},"PeriodicalIF":2.6,"publicationDate":"2024-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142157193","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Productions of Th2 cytokines, IL-4 and IL-10, were enhanced via the function of IL-2 from anti-CD3 antibody-stimulated mouse spleen cells treated with caffeic acid phenethyl ester 经咖啡酸苯乙酯处理的抗 CD3 抗体刺激的小鼠脾细胞通过 IL-2 的功能增强了 Th2 细胞因子(IL-4 和 IL-10)的产生。
IF 2.6 Q1 DENTISTRY, ORAL SURGERY & MEDICINE Pub Date : 2024-09-04 DOI: 10.1016/j.job.2024.09.001
Moe Takahashi , Masako Mizuno-Kamiya , Shifa Rahman , Hanemi Tsuruta , Kumiko Ikeno , Harumi Kawaki , Genjiro Nakamura , Yasunori Muramatsu , Toru Nikaido , Hisakazu Fujita , Nobuo Kondoh

Objectives

Interleukin (IL)-2 production by mouse spleen cells stimulated with an anti-CD3 antibody is significantly enhanced by caffeic acid phenethyl ester (CAPE), a major constituent of Chinese propolis (CP). In this study, we evaluated the functional significance of IL-2 in CAPE-treated activated spleen cells.

Methods

Mouse spleen cells were stimulated with an anti-CD3 monoclonal antibody in the presence of CAPE. Cytokine production was examined using an enzyme-linked immunosorbent assay (ELISA). Messenger RNA expression was examined via reverse transcription quantitative polymerase chain reaction (RT-PCR). IL-2 function was assessed using IL-2 and a neutralizing antibody. Spleen cell subsets were identified and characterized using flow cytometry.

Results

CAPE treatment of anti-CD3 antibody-stimulated spleen cells reduced IFN-γ production, then enhanced IL-2 production, followed by enhancement of IL-4 and IL-10 production. The Th2 cytokine production enhancing effects of CAPE were completely abolished by addition of an anti-IL-2 neutralizing antibody. In the absence of CAPE, exogenously added IL-2 could enhance IL-4 production to a lesser degree, but did not stimulate IL-10 production, in stimulated spleen cells. Interestingly, CAPE significantly reduced the proportions of CD4+ and CD8+ cells, and increased those of CD4CD8 cells among anti-CD3 stimulated spleen cells, in the presence or absence of anti-IL-2 neutralizing antibody treatment.

Conclusion

CAPE reduced IFN-γ production, then enhanced IL-4 and IL-10 production via the activity of specifically elevated IL-2 in stimulated spleen cells. CAPE exerted these effects in a CD4 CD8 cell specific manner.
目的用抗CD3抗体刺激小鼠脾脏细胞产生的白细胞介素(IL)-2在中国蜂胶(CP)的主要成分咖啡酸苯乙酯(CAPE)的作用下明显增强。本研究评估了经 CAPE 处理的活化脾细胞中 IL-2 的功能意义:方法:在 CAPE 存在的情况下,用抗 CD3 单克隆抗体刺激小鼠脾脏细胞。使用酶联免疫吸附试验(ELISA)检测细胞因子的产生。通过逆转录定量聚合酶链反应(RT-PCR)检测信使 RNA 水平的表达。使用 IL-2 和中和抗体评估 IL-2 功能。使用流式细胞术鉴定和描述脾脏细胞亚群:结果:CAPE 处理抗 CD3 抗体刺激的脾细胞可减少 IFN-γ 的产生,然后增强 IL-2 的产生,接着增强 IL-4 和 IL-10 的产生。加入抗 IL-2 中和抗体后,CAPE 增强 Th2 细胞因子产生的作用完全消失。在没有CAPE的情况下,外源添加的IL-2能在较小程度上促进受刺激脾细胞中IL-4的产生,但不能刺激IL-10的产生。有趣的是,无论有无抗IL-2中和抗体处理,CAPE都能显著降低抗CD3刺激的脾细胞中CD4+和CD8+细胞的比例,并增加CD4-CD8-细胞的比例:结论:CAPE可减少IFN-γ的产生,然后通过特异性升高的IL-2活性增强受刺激脾细胞中IL-4和IL-10的产生。CAPE 以 CD4- CD8- 细胞特异性的方式发挥这些作用。
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引用次数: 0
STAT3 interactome predicts presence of proteins that regulate immune system in oral squamous cell carcinoma STAT3相互作用组预测了口腔鳞状细胞癌中调节免疫系统的蛋白质的存在。
IF 2.6 Q1 DENTISTRY, ORAL SURGERY & MEDICINE Pub Date : 2024-09-03 DOI: 10.1016/j.job.2024.09.002
Rajdeep Chakraborty , Pallavi Khodlan , Aidan Tay , Fei Liu

Objectives

Signal transducer and activator of transcription 3 (STAT3) is one of the key proliferation mechanism–related proteins that helps in oral squamous cell carcinoma (OSCC) progression. Immune evasion by STAT3 is mediated by the JAK2/STAT3/PDL1 signaling axis. Based on previous findings, we hypothesized that STAT3-binding partners participate in the inhibition of anti-tumor activity in OSCC.

Methods

A 3D cancer-immune co-culture model was constructed using oral cancer cell lines SCC4, SCC9, SCC25, and CAL27 and normal oral cell line OKF6. The cells were co-cultured with natural killer (NK-92) and Jurkat cells. The target protein STAT3 was chosen based on SWATH data, and co-immunoprecipitation (Co-IP)-based proteomics was conducted. The Co-IP LC-MS/MS output was analysed to determine the protein interaction network, gene ontology, pathway analysis, and protein cluster annotation.

Results

STAT3 in oral cancer cell lines interacts with the epidermal growth factor receptor (EGFR) and other proteins that participate in proliferation and immune mechanisms. Proteome analysis showed that some STAT3-binding proteins found in this study are known immune system regulators.

Conclusion

Overall, STAT3 interactive proteins regulate the immune system in oral squamous cell carcinoma cells.
目的:信号转导和转录激活因子 3(STAT3)是与增殖机制相关的关键蛋白之一,有助于口腔鳞状细胞癌(OSCC)的进展。STAT3 的免疫逃避是由 JAK2/STAT3/PDL1 信号轴介导的。基于之前的研究结果,我们假设 STAT3 结合伙伴参与了 OSCC 抗肿瘤活性的抑制:方法:我们利用口腔癌细胞系 SCC4、SCC9、SCC25 和 CAL27 以及正常口腔细胞系 OKF6 构建了三维癌症-免疫共培养模型。细胞与自然杀伤细胞(NK-92)和Jurkat细胞共培养。根据 SWATH 数据选择了目标蛋白 STAT3,并进行了基于共免疫沉淀(Co-IP)的蛋白质组学研究。对共沉淀 LC-MS/MS 产物进行分析,以确定蛋白质相互作用网络、基因本体、通路分析和蛋白质集群注释:结果:口腔癌细胞系中的 STAT3 与表皮生长因子受体(EGFR)及其他参与增殖和免疫机制的蛋白质相互作用。蛋白质组分析表明,本研究发现的一些 STAT3 结合蛋白是已知的免疫系统调节因子:总之,STAT3 交互蛋白可调节口腔鳞状细胞癌细胞的免疫系统。
{"title":"STAT3 interactome predicts presence of proteins that regulate immune system in oral squamous cell carcinoma","authors":"Rajdeep Chakraborty ,&nbsp;Pallavi Khodlan ,&nbsp;Aidan Tay ,&nbsp;Fei Liu","doi":"10.1016/j.job.2024.09.002","DOIUrl":"10.1016/j.job.2024.09.002","url":null,"abstract":"<div><h3>Objectives</h3><div>Signal transducer and activator of transcription 3 (STAT3) is one of the key proliferation mechanism–related proteins that helps in oral squamous cell carcinoma (OSCC) progression. Immune evasion by STAT3 is mediated by the JAK2/STAT3/PDL1 signaling axis. Based on previous findings, we hypothesized that STAT3-binding partners participate in the inhibition of anti-tumor activity in OSCC.</div></div><div><h3>Methods</h3><div>A 3D cancer-immune co-culture model was constructed using oral cancer cell lines SCC4, SCC9, SCC25, and CAL27 and normal oral cell line OKF6. The cells were co-cultured with natural killer (NK-92) and Jurkat cells. The target protein STAT3 was chosen based on SWATH data, and co-immunoprecipitation (Co-IP)-based proteomics was conducted. The Co-IP LC-MS/MS output was analysed to determine the protein interaction network, gene ontology, pathway analysis, and protein cluster annotation.</div></div><div><h3>Results</h3><div>STAT3 in oral cancer cell lines interacts with the epidermal growth factor receptor (EGFR) and other proteins that participate in proliferation and immune mechanisms. Proteome analysis showed that some STAT3-binding proteins found in this study are known immune system regulators.</div></div><div><h3>Conclusion</h3><div>Overall, STAT3 interactive proteins regulate the immune system in oral squamous cell carcinoma cells.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"66 4","pages":"Pages 67-73"},"PeriodicalIF":2.6,"publicationDate":"2024-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142141360","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
期刊
Journal of Oral Biosciences
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