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Y-27632 enables long-term expansion of mouse submandibular gland epithelial cells via inactivation of TGF-β1/CTGF/p38 and ROCK2/JNK signaling pathway Y-27632 通过抑制 TGF-β1/CTGF/p38 和 ROCK2/JNK 信号通路,实现小鼠下颌下腺上皮细胞的长期扩增。
IF 2.6 Q1 DENTISTRY, ORAL SURGERY & MEDICINE Pub Date : 2024-09-01 DOI: 10.1016/j.job.2024.08.005
Kichul Kim , Naeun Oh , Hyewon Kim , Sangho Roh

Objectives

This study aimed to investigate the effects of Y-27632 on the long-term maintainence of mouse submandibular epithelial cells (SG-Epis) in vitro and to elucidate the underlying mechanisms.

Methods

The role of the Rho-associated kinase (ROCK) inhibitor Y-27632 in maintaining SG-Epis and its underlying mechanisms were evaluated by examining the in vitro expansion of mouse SG-Epis. Changes in key cellular characteristics, such as proliferation, long-term expansion, and mRNA and protein expression, were assessed in the presence or absence of Y-27632.

Results

Treatment with Y-27632 significantly enhanced the proliferative potential of SG-Epis, preserving Krt8 and Krt14 expression over 17 passages. In the absence of Y-27632, SG-Epis lost their epithelial morphology. However, Y-27632 treatment maintained the epithelial morphology and downregulated mRNA levels of Tgf-β1, Ctgf, and Rock2. Treatment with TGF-β1 indicated that TGF-β/CTGF/p38 signaling is responsible for the maintenance of SG-Epis, while RNA interference studies revealed that ROCK2/c-Jun N-terminal kinase (JNK) signaling is also crucial for SG-Epis proliferation and maintenance.

Conclusions

The TGF-β1/CTGF/p38 and ROCK2/JNK signaling pathways are responsible for SG-Epis proliferation, and Y-27632 treatment effectively inactivates these pathways, enabling long-term in vitro maintenance of SG-Epis. The culture method utilizing Y-27632 provides an effective approach for the in vitro expansion of SG-Epis.
研究目的本研究旨在探讨Y-27632对小鼠颌下腺上皮细胞(SG-Epis)体外长期维持的影响,并阐明其潜在机制:方法:通过研究小鼠SG-Epis的体外扩增,评估了Rho相关激酶(ROCK)抑制剂Y-27632在维持SG-Epis中的作用及其内在机制。在有无Y-27632存在的情况下,对增殖、长期扩增、mRNA和蛋白质表达等关键细胞特征的变化进行了评估:结果:用Y-27632处理可显著增强SG-Epis的增殖潜力,并在17次传代中保持Krt8和Krt14的表达。在没有 Y-27632 的情况下,SG-Epis 会失去上皮形态。然而,Y-27632 处理可维持上皮形态,并下调 Tgf-β1、Ctgf 和 Rock2 的 mRNA 水平。用TGF-β1处理表明,TGF-β/CTGF/p38信号转导是维持SG-Epis的原因,而RNA干扰研究表明,ROCK2/c-Jun N-末端激酶(JNK)信号转导对SG-Epis的增殖和维持也至关重要:结论:TGF-β1/CTGF/p38和ROCK2/JNK信号通路是SG-Epis增殖的原因,Y-27632能有效地使这些通路失活,从而实现SG-Epis的体外长期维持。利用 Y-27632 的培养方法为 SG-Epis 的体外扩增提供了一种有效的方法。
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引用次数: 0
Role of fimbriae variations in Porphyromonas gulae biofilm formation 古拉卟啉单胞菌生物膜形成过程中菌丝变化的作用
IF 2.6 Q1 DENTISTRY, ORAL SURGERY & MEDICINE Pub Date : 2024-08-30 DOI: 10.1016/j.job.2024.08.003
Sho Yoshida , Hiroaki Inaba , Ryota Nomura , Kazuhiko Nakano , Michiyo Matsumoto-Nakano

Objectives

Porphyromonas gulae is a major causative agent of periodontal disease in companion animals that possesses various virulence factors, including fimbriae, lipopolysaccharides, and proteases. P. gulae fimbriae are classified into three genotypes (A, B, and C) based on their nucleotide sequences. Type C fimbrial isolates have been reported to be more virulent than other fimA types, suggesting that different fimA types may aid in the regulation of periodontal pathogenesis. Detailed findings regarding the ability of P. gulae to form biofilms have yet to be reported. Here, we investigated the contributions of fimbrial genotypes in P. gulae biofilm formation.

Methods

P. gulae and P. gingivalis biofilms were generated on plates and analyzed using confocal laser microscopy. Additionally, the biofilms formed were assessed by staining with crystal violet. Furthermore, the physical strength of P. gulae biofilms was examined by ultrasonication.

Results

Biofilms formed by P. gulae type C were denser than those formed by types A and B. Moreover, the amount of biofilm formed by type C strains was significantly greater than that formed by type A and B strains, which was similar to the biofilms formed by P. gingivalis with type II fimbriae. Additionally, the physical strength of the type C biofilm was significantly greater than that of the other strains.

Conclusions

These results suggest that FimA variation may coordinate for biofilm formation. This is the first report on the observation and characterization of P. gulae biofilm formation.
目的:古拉卟啉单胞菌是伴侣动物牙周病的主要致病菌,具有多种毒力因子,包括缘膜、脂多糖和蛋白酶。根据核苷酸序列,P. gulae 菌膜可分为三种基因型(A、B 和 C)。据报道,C型缘核膜分离物比其他fimA型的毒性更强,这表明不同的fimA型可能有助于调节牙周致病机理。有关 P. gulae 形成生物膜能力的详细研究结果尚未见报道。在此,我们研究了fimbrial基因型在P. gulae生物膜形成中的贡献:方法:在平板上生成 P. gulae 和 P. gingivalis 生物膜,并使用激光共聚焦显微镜进行分析。此外,还通过水晶紫染色法对形成的生物膜进行了评估。此外,还用超声波检测了 P. gulae 生物膜的物理强度:此外,C 型菌株形成的生物膜数量明显多于 A 型和 B 型菌株形成的生物膜,这与带有 II 型指状体的牙龈球菌形成的生物膜相似。此外,C 型生物膜的物理强度明显高于其他菌株:这些结果表明,FimA 的变异可能会协调生物膜的形成。这是第一份关于古拉痢疾杆菌生物膜形成的观察和特征描述的报告。
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引用次数: 0
Invasion of human dental pulp fibroblasts by Porphyromonas gingivalis leads to autophagy via the phosphoinositide 3-kinase/Akt/mammalian target of rapamycin signaling pathway 牙龈卟啉单胞菌侵入人牙髓成纤维细胞后,会通过磷脂酰肌醇3-激酶/Akt/哺乳动物雷帕霉素靶标信号通路导致自噬。
IF 2.6 Q1 DENTISTRY, ORAL SURGERY & MEDICINE Pub Date : 2024-08-22 DOI: 10.1016/j.job.2024.08.004
Ying Feng , Mingxiang Liu , Yi Liu , Hong Li

Objectives

Porphyromonas gingivalis is a pathogenic bacterium that causes periodontitis and dental pulp infection. Autophagy is a potential mechanism involved in inflammatory disease. This study established an in vitro model of P. gingivalis intracellular infection in human dental pulp fibroblasts (HDPFs) to investigate the effects of live P. gingivalis on HDPFs.

Methods

Morphological and quantification techniques such as fluorescence microscopy, transmission electron microscopy (TEM), indirect immunofluorescence analysis, enzyme-linked immunosorbent assay (ELISA), real-time polymerase chain reaction (PCR), and western blotting were used in this study.

Results

After cell invasion, P. gingivalis is mainly localized in the cytoplasm and lysosomes. Additionally, P. gingivalis activates autophagy in HDPFs by upregulating the expression of autophagy-related gene Beclin-1, activate autophagy-related gene12 (ATG12), and microtubule-associated protein light chain 3 (LC3). Furthermore, the invasion of P. gingivalis leads to increased phosphorylation of PI3K, Akt, and mTOR with the addition of rapamycin, whereas the addition of wortmannin decreased phosphorylation. This invasion of P. gingivalis, also causes an inflammatory response, leading to the upregulation of IL-1β, IL-6, and TNF-α. Rapamycin helps decrease levels of pro-inflammatory cytokines, but the addition of wortmannin increases them. These results show that the invasion of P. gingivalis can cause excessive inflammation and promote the autophagy of HDPFs, which is regulated by PI3K/Akt/mTOR.

Conclusions

P. gingivalis escapes the immune system by inducing autophagy in the host cells, causing excessive inflammation. P. gingivalis regulates autophagy in HDPFs through the phosphoinositide 3-kinase/Akt/mammalian target of rapamycin pathway.
目的:牙龈卟啉单胞菌是一种致病细菌,可导致牙周炎和牙髓感染。自噬是参与炎症性疾病的一种潜在机制。本研究在人牙髓成纤维细胞(HDPFs)中建立了牙龈卟啉单胞菌胞内感染的体外模型,以研究活的牙龈卟啉单胞菌对 HDPFs 的影响:方法:采用荧光显微镜、透射电子显微镜(TEM)、间接免疫荧光分析、酶联免疫吸附试验(ELISA)、实时聚合酶链反应(PCR)和免疫印迹等形态学和定量技术进行研究:结果:牙龈球菌侵入细胞后主要定位于细胞质和溶酶体。此外,牙龈狰狞梭菌通过上调自噬相关基因 Beclin-1、激活自噬相关基因 12(ATG12)和微管相关蛋白轻链 3(LC3)的表达,激活 HDPFs 的自噬。此外,加入雷帕霉素后,牙龈脓疱病菌的入侵会导致 PI3K、Akt 和 mTOR 的磷酸化增加,而加入沃特曼素则会减少磷酸化。牙龈脓胞的入侵还会引起炎症反应,导致 IL-1β、IL-6 和 TNF-α 的上调。雷帕霉素有助于降低促炎细胞因子的水平,但加入沃特曼素则会提高这些水平。这些结果表明,牙龈脓胞杆菌的入侵可导致过度炎症并促进 HDPFs 的自噬,而自噬是由 PI3K/Akt/mTOR 调节的:结论:牙龈脓毒性鹅膏菌通过诱导宿主细胞自噬来逃避免疫系统的攻击,从而引起过度炎症。牙龈脓疱病通过磷酸肌醇3-激酶/Akt/哺乳动物雷帕霉素靶途径调控HDPFs的自噬。
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引用次数: 0
PLAG1 overexpression in salivary gland duct-acinar units results in epithelial tumors with acinar-like features: Tumorization of luminal stem/progenitor cells may result in the development of salivary gland tumors consisting of only luminal cells PLAG1 在唾液腺导管-针状单元中的过表达会导致具有针状特征的上皮肿瘤:管腔干细胞/祖细胞的肿瘤化可能导致仅由管腔细胞组成的唾液腺肿瘤的发生。
IF 2.6 Q1 DENTISTRY, ORAL SURGERY & MEDICINE Pub Date : 2024-08-17 DOI: 10.1016/j.job.2024.08.002
Yunosuke Ikeda , Rika Yasuhara , Junichi Tanaka , Hiroko Ida-Yonemochi , Haruhiko Akiyama , Keishi Otsu , Ikuya Miyamoto , Hidemitsu Harada , Hiroyuki Yamada , Toshiyuki Fukada , Tarou Irié

Objectives

Details about salivary gland tumor histogenesis remain unknown. Here, we established a newly generated murine salivary gland tumor model that could overexpress pleomorphic adenoma gene 1 (PLAG1) and attempted to clarify the events that occur during the early phase of salivary gland tumor histogenesis.

Methods

Salivary gland tumors were generated using murine models (Sox9IRES-CreERT2; ROSA26-PLAG1). Lineage tracing of Sox9-expressing cells was performed using Sox9IRES-CreERT2; ROSA26-tdTomato mice, which were generated by crossing Sox9CreERT2/- and ROSA26-tdTomato mice (expressing the tdTomato fluorescent protein). Organ-cultured embryonic salivary glands from the murine model were morphologically analyzed, and mRNA sequencing was conducted two days after tumor induction for gene enrichment and functional annotation analysis.

Results

Salivary gland tumors exhibited epithelial features with acinar-like structures because of gene rearrangements in the luminal cells. Structural disturbances in the duct-acinar unit of the salivary gland were observed and cancer-related pathways were enriched among the differentially upregulated genes in the early phase of tumor induction in an organ-cultured embryonic salivary gland tumor model.

Conclusions

The newly generated murine salivary gland tumor model may show that the tumorization of luminal stem/progenitor cells can result in the development of salivary gland tumors comprising only luminal cells.
目的:唾液腺肿瘤组织发生的细节仍不清楚。在此,我们建立了一种新生成的可过表达多形性腺瘤基因 1(PLAG1)的小鼠涎腺肿瘤模型,并试图阐明涎腺肿瘤组织发生早期阶段发生的事件:方法:利用小鼠模型(Sox9IRES-CreERT2;ROSA26-PLAG1)生成唾液腺肿瘤。利用Sox9IRES-CreERT2; ROSA26-tdTomato小鼠进行Sox9表达细胞的系谱追踪,该小鼠是通过杂交Sox9CreERT2/-和ROSA26-tdTomato小鼠(表达tdTomato荧光蛋白)产生的。对小鼠模型的器官培养胚胎唾液腺进行了形态学分析,并在肿瘤诱导两天后进行了 mRNA 测序,以进行基因富集和功能注释分析:结果:由于管腔细胞中的基因重排,唾液腺肿瘤表现出具有类针状结构的上皮特征。在器官培养的胚胎唾液腺肿瘤模型中,观察到唾液腺导管-针状单元的结构紊乱,肿瘤诱导早期的差异上调基因中富集了与癌症相关的通路:结论:新建立的小鼠涎腺肿瘤模型表明,管腔干细胞/祖细胞肿瘤化可导致仅由管腔细胞组成的涎腺肿瘤的发生。
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引用次数: 0
Anti-Streptococcus mutans and anti-inflammatory effects of ginsenoside Compound K and enzyme-treated red ginseng extract (BTEX-K) 人参皂苷化合物 K 和酶处理红参提取物(BTEX-K)的抗变异链球菌和抗炎作用。
IF 2.6 Q1 DENTISTRY, ORAL SURGERY & MEDICINE Pub Date : 2024-08-09 DOI: 10.1016/j.job.2024.08.001
Jin-Hwan Oh , SangJoon Mo , Le Thi Nhu Ngoc , Jonghyuk Lee , Moon-Young Kim , Hae-Seo Park , Jin-Hee Kim , Yu-Jin Ha , Lee Sung , Young-Chul Lee , Youl Hour

Objectives

Dental caries, or tooth decay, is an oral health issue worldwide. Oral healthcare researchers are considering how to develop safe and effective preventive measures and treatments for dental caries. This study evaluated the potential applications of Compound K and BTEX-K, a Compound K–rich red ginseng extract, for the prevention and treatment of dental caries. Moreover, this study briefly confirmed its inhibitory effect on inflammation, an important factor in dental health.

Methods

The amount of organic acids produced by bacteria in biofilm was determined using in vitro and in vivo assays. The ability of these extracts to promote tooth remineralization and microhardness was evaluated using an in vivo mouse assay. We evaluated their anti-inflammatory potential by inhibiting proinflammatory cytokine expression and lipopolysaccharide-induced nitrous oxide production in cell lines.

Results

Compound K (10–20 μg/mL) and BTEX-K (50–100 μg/mL) effectively inhibited the growth of Streptococcus mutans bacteria, demonstrating significant antibacterial properties. They can potentially prevent biofilm formation by reducing lactic acid production in the teeth. These compounds showed a strong ability to promote tooth remineralization and improve the microhardness of acid-producing bacteria. They also possess potent anti-inflammatory properties that downregulate proinflammatory cytokine (interleukin-6, interleukin-1β, inducible nitric oxide synthase) expression, suppress nuclear factor-kappa B transcription factor activation (∼1.6 times), and reduce nitrous oxide production in lipopolysaccharide-induced RAW264.7 cells.

Conclusions

Compounds K and BTEX-K may provide a novel approach to dental caries prevention as well as inflammation prevention and treatment.
目的:龋齿或蛀牙是全世界的口腔健康问题。口腔保健研究人员正在考虑如何开发安全有效的龋齿预防措施和治疗方法。本研究评估了化合物 K 和 BTEX-K(一种富含化合物 K 的红参提取物)在预防和治疗龋齿方面的潜在应用。此外,本研究还简要证实了其对炎症的抑制作用,而炎症是影响牙齿健康的一个重要因素:方法:使用体外和体内试验测定了生物膜中细菌产生的有机酸量。使用小鼠体内试验评估了这些提取物促进牙齿再矿化和微硬度的能力。我们通过抑制细胞系中促炎细胞因子的表达和脂多糖诱导的一氧化二氮的产生,评估了这些提取物的抗炎潜力:结果:化合物 K(10-20 μg/mL)和 BTEX-K(50-100 μg/mL)有效抑制了变异链球菌的生长,显示出显著的抗菌特性。它们可以通过减少牙齿中乳酸的产生来防止生物膜的形成。这些化合物具有很强的促进牙齿再矿化和改善产酸细菌微硬度的能力。它们还具有强大的抗炎特性,能下调促炎细胞因子(白细胞介素-6、白细胞介素-1β、诱导型一氧化氮合酶)的表达,抑制核因子卡巴 B 转录因子的活化(1.6 倍),并减少脂多糖诱导的 RAW264.7 细胞中一氧化氮的产生:化合物 K 和 BTEX-K 可为龋齿预防以及炎症预防和治疗提供一种新方法。
{"title":"Anti-Streptococcus mutans and anti-inflammatory effects of ginsenoside Compound K and enzyme-treated red ginseng extract (BTEX-K)","authors":"Jin-Hwan Oh ,&nbsp;SangJoon Mo ,&nbsp;Le Thi Nhu Ngoc ,&nbsp;Jonghyuk Lee ,&nbsp;Moon-Young Kim ,&nbsp;Hae-Seo Park ,&nbsp;Jin-Hee Kim ,&nbsp;Yu-Jin Ha ,&nbsp;Lee Sung ,&nbsp;Young-Chul Lee ,&nbsp;Youl Hour","doi":"10.1016/j.job.2024.08.001","DOIUrl":"10.1016/j.job.2024.08.001","url":null,"abstract":"<div><h3>Objectives</h3><div>Dental caries, or tooth decay, is an oral health issue worldwide. Oral healthcare researchers are considering how to develop safe and effective preventive measures and treatments for dental caries. This study evaluated the potential applications of Compound K and BTEX-K, a Compound K–rich red ginseng extract, for the prevention and treatment of dental caries. Moreover, this study briefly confirmed its inhibitory effect on inflammation, an important factor in dental health.</div></div><div><h3>Methods</h3><div>The amount of organic acids produced by bacteria in biofilm was determined using in vitro and in vivo assays. The ability of these extracts to promote tooth remineralization and microhardness was evaluated using an in vivo mouse assay. We evaluated their anti-inflammatory potential by inhibiting proinflammatory cytokine expression and lipopolysaccharide-induced nitrous oxide production in cell lines.</div></div><div><h3>Results</h3><div>Compound K (10–20 μg/mL) and BTEX-K (50–100 μg/mL) effectively inhibited the growth of <em>Streptococcus mutans</em> bacteria, demonstrating significant antibacterial properties. They can potentially prevent biofilm formation by reducing lactic acid production in the teeth. These compounds showed a strong ability to promote tooth remineralization and improve the microhardness of acid-producing bacteria. They also possess potent anti-inflammatory properties that downregulate proinflammatory cytokine (interleukin-6, interleukin-1β, inducible nitric oxide synthase) expression, suppress nuclear factor-kappa B transcription factor activation (∼1.6 times), and reduce nitrous oxide production in lipopolysaccharide-induced RAW264.7 cells.</div></div><div><h3>Conclusions</h3><div>Compounds K and BTEX-K may provide a novel approach to dental caries prevention as well as inflammation prevention and treatment.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"66 4","pages":"Pages 19-27"},"PeriodicalIF":2.6,"publicationDate":"2024-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141917734","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
Molecular microbiological profiling of bottled unsweetened tea beverages: A screening experiment 瓶装不加糖茶饮料的分子微生物分析:筛选实验。
IF 2.6 Q1 DENTISTRY, ORAL SURGERY & MEDICINE Pub Date : 2024-07-26 DOI: 10.1016/j.job.2024.07.006
Nagara Kaku , Miho Kawachi , Anna Wakui , Misato Miyazawa , Manami Imai , Nanase Takahashi , Aya Sato , Takashi Abe , Haruna Sato , Yuki Kato , Rika Okabe , Yuka Naruse , Nao Sato , Nanami Asano , Momoko Morohashi , Hiroto Sano , Jumpei Washio , Yuki Abiko , Kaori Tanaka , Nobuhiro Takahashi , Takuichi Sato

To explore the potential storage and safety of drinking leftover bottled tea beverages from various manufacturers after direct drinking from bottles, we conducted a screening experiment on the growth of salivary bacteria in plastic bottles of tea. The diluted saliva samples from 10 participants were inoculated into the test bottled beverages, which resulted in bacteria, particularly former members of the genus Lactobacillus, growing in some green tea beverages with a neutral pH. In contrast, tea beverages with less bacterial growth contained Streptococcus spp., and the leftovers may be safe to store and drink again.

为了探索直接饮用不同厂家生产的瓶装茶饮料后残留物的潜在储存和饮用安全性,我们对塑料瓶装茶饮料中唾液细菌的生长情况进行了筛选实验。将 10 位参与者的稀释唾液样本接种到测试的瓶装饮料中,结果在一些 pH 值为中性的绿茶饮料中生长出了细菌,尤其是乳酸杆菌属的前成员。相比之下,细菌生长较少的茶饮料中含有链球菌属,剩下的茶饮料可以安全储存并再次饮用。
{"title":"Molecular microbiological profiling of bottled unsweetened tea beverages: A screening experiment","authors":"Nagara Kaku ,&nbsp;Miho Kawachi ,&nbsp;Anna Wakui ,&nbsp;Misato Miyazawa ,&nbsp;Manami Imai ,&nbsp;Nanase Takahashi ,&nbsp;Aya Sato ,&nbsp;Takashi Abe ,&nbsp;Haruna Sato ,&nbsp;Yuki Kato ,&nbsp;Rika Okabe ,&nbsp;Yuka Naruse ,&nbsp;Nao Sato ,&nbsp;Nanami Asano ,&nbsp;Momoko Morohashi ,&nbsp;Hiroto Sano ,&nbsp;Jumpei Washio ,&nbsp;Yuki Abiko ,&nbsp;Kaori Tanaka ,&nbsp;Nobuhiro Takahashi ,&nbsp;Takuichi Sato","doi":"10.1016/j.job.2024.07.006","DOIUrl":"10.1016/j.job.2024.07.006","url":null,"abstract":"<div><p>To explore the potential storage and safety of drinking leftover bottled tea beverages from various manufacturers after direct drinking from bottles, we conducted a screening experiment on the growth of salivary bacteria in plastic bottles of tea. The diluted saliva samples from 10 participants were inoculated into the test bottled beverages, which resulted in bacteria, particularly former members of the genus <em>Lactobacillus</em>, growing in some green tea beverages with a neutral pH. In contrast, tea beverages with less bacterial growth contained <em>Streptococcus</em> spp., and the leftovers may be safe to store and drink again.</p></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"66 3","pages":"Pages 628-632"},"PeriodicalIF":2.6,"publicationDate":"2024-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141789435","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
Therapeutic effects of mesenchymal stem cells derived from bone marrow and adipose tissue in a rat model of temporomandibular osteoarthritis 骨髓和脂肪组织间充质干细胞对颞下颌关节炎大鼠模型的治疗效果
IF 2.6 Q1 DENTISTRY, ORAL SURGERY & MEDICINE Pub Date : 2024-07-24 DOI: 10.1016/j.job.2024.07.007
Saba Khazeni , Mohammadali Ghavimi , Mehran Mesgari-Abbasi , Leila Roshangar , Sara Abedi , Tannaz Pourlak

Objectives

To examine the potential of intra-articular administration of mesenchymal stem cells (MSCs) derived from bone marrow or adipose tissue to mitigate synovial inflammation in a rat model of temporomandibular joint (TMJ) osteoarthritis (OA).

Methods

In this experimental study, 40 rats were divided into 4 groups: (1) Control group; (2) Untreated TMJ-OA group; (3) TMJ-OA group treated with bone marrow-derived MSCs; (4) TMJ-OA group treated with adipose tissue-derived MSCs. The TMJ-OA model was established by inducing synovial inflammation through the intra-articular administration of complete Freund's adjuvant (CFA). After 8 weeks of TMJ-OA establishment, the animals were sacrificed and each mandibular condyle was extracted for histological evaluation.

Results

The untreated TMJ-OA group had significantly higher synovial inflammation, as indicated microscopically by higher grades of synovial membrane hyperplasia and adhesion, vascular vasodilation, and fibrin deposition than the control group (p < 0.001). Both TMJ-OA groups treated with MSCs had lower grades of synovial inflammation and less severe synovitis than the untreated TMJ-OA group (p < 0.001). The TMJ-OA group treated with adipose tissue-derived MSCs showed lower grades of synovial membrane hyperplasia and higher grades of fibrin deposition than the that treated with bone marrow-derived MSCs (p < 0.001). Other indicators of synovial inflammation and synovitis severity were comparable between the two treatment groups.

Conclusions

Administration of CFA to the TMJ-OA rat model augmented synovial inflammation. Intra-articular administration of MSCs derived from either bone marrow or adipose tissue attenuated the microscopic manifestations of this inflammation, indicating the therapeutic potential of this treatment for TMJ-OA.
研究目的研究在颞下颌关节(TMJ)骨关节炎(OA)大鼠模型中,通过关节内给予骨髓或脂肪组织间充质干细胞(MSCs)来缓解滑膜炎症的潜力:在这项实验研究中,40 只大鼠被分为 4 组:(1) 对照组;(2) 未经治疗的 TMJ-OA 组;(3) 接受骨髓间充质干细胞治疗的 TMJ-OA 组;(4) 接受脂肪组织间充质干细胞治疗的 TMJ-OA 组。颞下颌关节-OA模型是通过关节内注射完全弗氏佐剂(CFA)诱导滑膜炎症而建立的。颞下颌关节-OA模型建立8周后,动物被处死并提取每个下颌骨髁突进行组织学评估:结果:与对照组相比,未经治疗的 TMJ-OA 组滑膜炎症明显加重,显微镜下可见更高水平的滑膜增生和粘连、血管扩张和纤维蛋白沉积(P < 0.001)。与未经治疗的 TMJ-OA 组相比,接受间充质干细胞治疗的 TMJ-OA 组滑膜炎症程度较低,滑膜炎的严重程度也较轻(P < 0.001)。与骨髓间充质干细胞治疗组相比,接受脂肪组织间充质干细胞治疗的 TMJ-OA 组滑膜增生程度较低,纤维蛋白沉积程度较高(p < 0.001)。两个治疗组的滑膜炎症和滑膜炎严重程度的其他指标相当:结论:对颞下颌关节-OA大鼠模型施用CFA会加重滑膜炎症。结论:对颞下颌关节-OA大鼠模型施用CFA会加重滑膜炎症,而关节内施用骨髓或脂肪组织间充质干细胞会减轻这种炎症的微观表现,这表明这种疗法对颞下颌关节-OA具有治疗潜力。
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引用次数: 0
Cytoarchitecture and intercellular interactions in the trigeminal ganglion: Associations with neuropathic pain in the orofacial region 三叉神经节的细胞结构和细胞间相互作用:与口面部神经性疼痛的关联
IF 2.6 Q1 DENTISTRY, ORAL SURGERY & MEDICINE Pub Date : 2024-07-18 DOI: 10.1016/j.job.2024.07.003
Tetsuya Goto, Eriko Kuramoto, Haruki Iwai, Atsushi Yamanaka

Background

Disorders of the trigeminal nerve, a sensory nerve of the orofacial region, often lead to complications in dental practice, including neuropathic pain, allodynia, and ectopic pain. Management of these complications requires an understanding of the cytoarchitecture of the trigeminal ganglion, where the cell bodies of the trigeminal nerve are located, and the mechanisms of cell-cell interactions.

Highlights

In the trigeminal ganglion, ganglion, satellite, Schwann, and immune cells coexist and interact. Cell-cell interactions are complex and occur through direct contact via gap junctions or through mediators such as adenosine triphosphate, nitric oxide, peptides, and cytokines. Interactions between the nervous and immune systems within the trigeminal ganglion may have neuroprotective effects during nerve injury or may exacerbate inflammation and produce chronic pain. Under pathological conditions of the trigeminal nerve, cell-cell interactions can cause allodynia and ectopic pain. Although cell-cell interactions that occur via mediators can act at some distance, they are more effective when the cells are close together. Therefore, information on the three-dimensional topography of trigeminal ganglion cells is essential for understanding the pathophysiology of ectopic pain.

Conclusions

A three-dimensional map of the somatotopic localization of trigeminal ganglion neurons revealed that ganglion cells innervating distant orofacial regions are often apposed to each other, interacting with and potentially contributing to ectopic pain. Elucidation of the complex network of mediators and their receptors responsible for intercellular communication within the trigeminal ganglion is essential for understanding ectopic pain.

背景:三叉神经是口面部区域的感觉神经,三叉神经失调常常会导致牙科实践中的并发症,包括神经性疼痛、异位性疼痛和异位性疼痛。处理这些并发症需要了解三叉神经节的细胞结构、三叉神经细胞体的位置以及细胞-细胞相互作用的机制:在三叉神经节中,神经节细胞、卫星细胞、许旺细胞和免疫细胞共存并相互作用。细胞与细胞之间的相互作用十分复杂,可通过间隙连接直接接触,也可通过三磷酸腺苷、一氧化氮、肽和细胞因子等介质发生。三叉神经节内的神经系统和免疫系统之间的相互作用可能会在神经损伤时产生神经保护作用,也可能会加剧炎症并产生慢性疼痛。在三叉神经病理情况下,细胞-细胞间的相互作用可导致异感症和异位痛。虽然通过介质发生的细胞-细胞相互作用可以在一定距离内发挥作用,但当细胞靠近时效果更好。因此,有关三叉神经节细胞三维地形图的信息对于了解异位痛的病理生理学至关重要:结论:三叉神经节神经元体位定位的三维地图显示,支配遥远口面部区域的神经节细胞经常相互贴附,与异位痛相互作用并可能导致异位痛。阐明三叉神经节内负责细胞间通信的介质及其受体的复杂网络对于理解异位痛至关重要。
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引用次数: 0
Non-neuronal cells act as crucial players in neuropathic orofacial pain 非神经元细胞是导致神经性口面痛的关键因素。
IF 2.6 Q1 DENTISTRY, ORAL SURGERY & MEDICINE Pub Date : 2024-07-18 DOI: 10.1016/j.job.2024.07.005
Koichi Iwata, Yoshinori Hayashi, Suzuro Hitomi, Yoshiyuki Tsuboi, Masamichi Shinoda

Background

Following peripheral nerve damage, various non-neuronal cells are activated, triggering accumulation in the peripheral and central nervous systems, and communicate with neurons. Evidence suggest that neuronal and non-neuronal cell communication is a critical mechanism of neuropathic pain; however, its detailed mechanisms in contributing to neuropathic orofacial pain development remain unclear.

Highlight

Neuronal and non-neuronal cell communication in the trigeminal ganglion (TG) is believed to cause neuronal hyperactivation following trigeminal nerve damage, resulting in neuropathic orofacial pain. Trigeminal nerve damage activates and accumulates non-neuronal cells, such as satellite cells and macrophages in the TG and microglia, astrocytes, and oligodendrocytes in the trigeminal spinal subnucleus caudalis (Vc) and upper cervical spinal cord (C1–C2). These non-neuronal cells release various molecules, contributing to the hyperactivation of TG, Vc, and C1–C2 nociceptive neurons. These hyperactive nociceptive neurons release molecules that enhance non-neuronal cell activation. This neuron and non-neuronal cell crosstalk causes hyperactivation of nociceptive neurons in the TG, Vc, and C1–C2. Here, we addressed previous and recent data on the contribution of neuronal and non-neuronal cell communication and its involvement in neuropathic orofacial pain development.

Conclusion

Previous and recent data suggest that neuronal and non-neuronal cell communication in the TG, Vc, and C1–C2 is a key mechanism that causes neuropathic orofacial pain associated with trigeminal nerve damage.

背景:外周神经损伤后,各种非神经元细胞被激活,引发外周和中枢神经系统的积聚,并与神经元交流。有证据表明,神经元和非神经元细胞的交流是神经病理性疼痛的一个关键机制;然而,其导致神经病理性口面痛发生的详细机制仍不清楚:三叉神经节(TG)中的神经元和非神经元细胞通讯被认为会在三叉神经损伤后引起神经元过度激活,从而导致神经病理性口面部疼痛。三叉神经损伤会激活和积聚非神经元细胞,如三叉神经节中的卫星细胞和巨噬细胞,以及三叉神经脊髓尾下核(Vc)和上颈脊髓(C1-C2)中的小胶质细胞、星形胶质细胞和少突胶质细胞。这些非神经元细胞释放各种分子,导致 TG、Vc 和 C1-C2 痛觉神经元过度激活。这些痛觉神经元释放的分子会增强非神经元细胞。这种神经元与非神经元细胞之间的串联会导致 TG、Vc 和 C1-C2 中的痛觉神经元过度激活。在此,我们讨论了有关神经元和非神经元细胞通讯的贡献及其参与神经病理性口面痛发展的既往和最新数据:结论:以前和最近的数据表明,TG、Vc 和 C1-C2 中的神经元和非神经元细胞通讯是导致与三叉神经损伤相关的神经性口面痛的关键机制。
{"title":"Non-neuronal cells act as crucial players in neuropathic orofacial pain","authors":"Koichi Iwata,&nbsp;Yoshinori Hayashi,&nbsp;Suzuro Hitomi,&nbsp;Yoshiyuki Tsuboi,&nbsp;Masamichi Shinoda","doi":"10.1016/j.job.2024.07.005","DOIUrl":"10.1016/j.job.2024.07.005","url":null,"abstract":"<div><h3>Background</h3><p><span>Following peripheral nerve damage, various non-neuronal cells are activated, triggering accumulation in the peripheral and </span>central nervous systems<span>, and communicate with neurons. Evidence suggest that neuronal and non-neuronal cell communication is a critical mechanism of neuropathic pain<span>; however, its detailed mechanisms in contributing to neuropathic orofacial pain development remain unclear.</span></span></p></div><div><h3>Highlight</h3><p><span><span><span>Neuronal and non-neuronal cell communication in the trigeminal ganglion (TG) is believed to cause neuronal </span>hyperactivation following </span>trigeminal nerve damage, resulting in neuropathic orofacial pain. Trigeminal nerve damage activates and accumulates non-neuronal cells, such as satellite cells and macrophages in the TG and </span>microglia<span><span>, astrocytes, and oligodendrocytes<span> in the trigeminal spinal subnucleus caudalis (Vc) and upper cervical spinal cord (C1–C2). These non-neuronal cells release various molecules, contributing to the hyperactivation of TG, Vc, and C1–C2 nociceptive neurons. These hyperactive nociceptive neurons release molecules that enhance non-neuronal </span></span>cell activation. This neuron and non-neuronal cell crosstalk causes hyperactivation of nociceptive neurons in the TG, Vc, and C1–C2. Here, we addressed previous and recent data on the contribution of neuronal and non-neuronal cell communication and its involvement in neuropathic orofacial pain development.</span></p></div><div><h3>Conclusion</h3><p>Previous and recent data suggest that neuronal and non-neuronal cell communication in the TG, Vc, and C1–C2 is a key mechanism that causes neuropathic orofacial pain associated with trigeminal nerve damage.</p></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"66 3","pages":"Pages 491-495"},"PeriodicalIF":2.6,"publicationDate":"2024-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141735265","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
Platelet-rich fibrin as an adjunct to scaling and root planing in treatment of shallow periodontal pockets: A randomized clinical trial 富血小板纤维蛋白辅助洗牙和根面平整治疗浅牙周袋:随机临床试验。
IF 2.6 Q1 DENTISTRY, ORAL SURGERY & MEDICINE Pub Date : 2024-07-10 DOI: 10.1016/j.job.2024.07.002

Objectives

To evaluate the efficacy of platelet-rich fibrin (PRF) as an adjunct to scaling and root planing (ScRp) for healing shallow periodontal pockets.

Methods

Twelve patients with periodontitis were enrolled in this split-mouth, randomized clinical trial. A total of 24 shallow periodontal pockets (4–6 mm) were treated by either ScRp alone (control) or PRF (test). Clinical attachment loss (CAL), probing pocket depth (PPD), bleeding on probing (BOP), and plaque index (PLI), as well as platelet-derived growth factor-BB (PDGF-BB) by enzyme-linked immunosorbent assay (ELISA) in gingival crevicular fluid (GCF) were measured at baseline and at 1- and 3-month follow-up visits.

Results

At 1- and 3-month follow-up visits, greater CAL gains (2.6 ± 0.25 mm and 3.26 ± 0.31 mm, respectively) and PPD reductions (2.58 ± 0.38 and 3.31 ± 0.39 mm, respectively) were observed in the test group compared to those in controls (CAL gain of 1.01 ± 0.49 mm and 1.43 ± 0.48 mm; PPD reduction of 1.1 ± 0.55 and 1.37 ± 0.49 mm, respectively). In addition, the increase in PDGF-BB in GCF in the test group (724.5 ± 186.09 pg/μl and 1957.5 ± 472.9 pg/μl) was significantly greater than that in controls (109.3 ± 24.07 and 614.64 ± 209.3 pg/μl) at 1- and 3-month follow-up visits, respectively.

Conclusions

The noninvasive use of PRF as an adjunct to ScRp successfully improved clinical periodontal parameters and might contribute to increased PDGF-BB in GCF.

目的评估富血小板纤维蛋白(PRF)作为洗牙和根面平整术(ScRp)的辅助手段对愈合浅牙周袋的疗效:12名牙周炎患者参加了这项分口随机临床试验。共有 24 个浅牙周袋(4-6 毫米)接受了单纯 ScRp(对照组)或 PRF(试验组)治疗。临床附着丧失(CAL)、探诊袋深度(PPD)、探诊出血(BOP)、牙菌斑指数(PLI)以及龈沟液(GCF)中血小板衍生生长因子-BB(PDGF-BB)的酶联免疫吸附测定(ELISA)均在基线、1个月和3个月随访时进行了测定:在 1 个月和 3 个月的随访中,与对照组相比,试验组观察到更大的 CAL 增加(分别为 2.6 ± 0.25 mm 和 3.26 ± 0.31 mm)和 PPD 减少(分别为 2.58 ± 0.38 mm 和 3.31 ± 0.39 mm)(CAL 增加分别为 1.01 ± 0.49 mm 和 1.43 ± 0.48 mm;PPD 减少分别为 1.1 ± 0.55 mm 和 1.37 ± 0.49 mm)。此外,在1个月和3个月的随访中,试验组GCF中PDGF-BB的增加量(724.5 ± 186.09 pg/μl和1957.5 ± 472.9 pg/μl)分别显著高于对照组(109.3 ± 24.07和614.64 ± 209.3 pg/μl):无创使用 PRF 作为 ScRp 的辅助治疗成功地改善了临床牙周参数,并可能有助于增加 GCF 中的 PDGF-BB。
{"title":"Platelet-rich fibrin as an adjunct to scaling and root planing in treatment of shallow periodontal pockets: A randomized clinical trial","authors":"","doi":"10.1016/j.job.2024.07.002","DOIUrl":"10.1016/j.job.2024.07.002","url":null,"abstract":"<div><h3>Objectives</h3><p>To evaluate the efficacy of platelet-rich fibrin (PRF) as an adjunct to scaling and root planing<span> (ScRp) for healing shallow periodontal pockets.</span></p></div><div><h3>Methods</h3><p>Twelve patients with periodontitis<span><span><span> were enrolled in this split-mouth, randomized clinical trial<span><span><span>. A total of 24 shallow periodontal pockets (4–6 mm) were treated by either ScRp alone (control) or PRF (test). </span>Clinical attachment loss (CAL), probing pocket depth (PPD), </span>bleeding on probing (BOP), and </span></span>plaque index (PLI), as well as platelet-derived growth factor-BB (PDGF-BB) by enzyme-linked immunosorbent assay (ELISA) in </span>gingival crevicular fluid (GCF) were measured at baseline and at 1- and 3-month follow-up visits.</span></p></div><div><h3>Results</h3><p>At 1- and 3-month follow-up visits, greater CAL gains (2.6 ± 0.25 mm and 3.26 ± 0.31 mm, respectively) and PPD reductions (2.58 ± 0.38 and 3.31 ± 0.39 mm, respectively) were observed in the test group compared to those in controls (CAL gain of 1.01 ± 0.49 mm and 1.43 ± 0.48 mm; PPD reduction of 1.1 ± 0.55 and 1.37 ± 0.49 mm, respectively). In addition, the increase in PDGF-BB in GCF in the test group (724.5 ± 186.09 pg/μl and 1957.5 ± 472.9 pg/μl) was significantly greater than that in controls (109.3 ± 24.07 and 614.64 ± 209.3 pg/μl) at 1- and 3-month follow-up visits, respectively.</p></div><div><h3>Conclusions</h3><p>The noninvasive use of PRF as an adjunct to ScRp successfully improved clinical periodontal parameters and might contribute to increased PDGF-BB in GCF.</p></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"66 3","pages":"Pages 612-618"},"PeriodicalIF":2.6,"publicationDate":"2024-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141601885","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
期刊
Journal of Oral Biosciences
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