Archives of oral biology最新文献_第7页

NFIC activates DEPTOR and blocks mTOR signaling to inhibit glycolysis and immune escape in oral squamous cell carcinoma NFIC激活DEPTOR并阻断mTOR信号，抑制口腔鳞状细胞癌的糖酵解和免疫逃逸

IF 2.1 4区医学 Q2 DENTISTRY, ORAL SURGERY & MEDICINE

Archives of oral biology

Pub Date : 2026-01-01 Epub Date: 2025-10-26 DOI: 10.1016/j.archoralbio.2025.106442

Jian Xu , Mohang Sun , Xin Wang , Yuxin Zou , Lina Wang

Objective

Oral squamous cell carcinoma (OSCC) has a poor prognosis and high mortality. This study aims to investigate the potential molecular mechanisms of NFIC/DEPTOR/mTOR signaling in glycolysis and tumor immune escape in OSCC.

Design

In vitro, the effects of the NFIC/DEPTOR/mTOR axis on the proliferative capacity and apoptosis of HN30 and SCC-25 cells were investigated using colony formation assays, EdU staining, and TUNEL after lentiviral gene interference. The glycolytic activity of OSCC cells was analyzed through glucose uptake, ECAR, and lactate production. CD8⁺ T cells were co-cultured with OSCC cells to analyze the cytotoxic activity of CD8⁺ T cells. SCC-25 cells with different genetic interventions were injected subcutaneously into NOG mice to investigate the effects of NFIC/DEPTOR/mTOR on subcutaneous tumor growth, tumor microenvironment (TME) acidity, and CD8⁺ T cell infiltration and activity. ChIP-qPCR and dual-luciferase assays were used to investigate the regulatory relationship between NFIC and the DEPTOR promoter in OSCC cells.

Results

NFIC and DEPTOR were significantly downregulated in OSCC cells and tissues, accompanied by enhanced mTOR signaling. NFIC activated DEPTOR by binding to its promoter. Overexpression of either NFIC or DEPTOR significantly inhibited OSCC cell proliferation, glycolytic activity, and enhanced CD8⁺ T cell killing capacity. Similarly, they inhibited tumor growth in vivo, blocked TME acidification, and weakened tumor immune escape. Combined DEPTOR knockdown rescued the malignant progression of OSCC inhibited by NFIC overexpression.

Conclusion

NFIC mediates DEPTOR transcription to repress mTOR signaling, thereby hindering OSCC progression by suppressing cell proliferation, glycolytic activity, and CD8⁺ T cell-related immune escape.

目的口腔鳞状细胞癌（OSCC）预后差，死亡率高。本研究旨在探讨NFIC/DEPTOR/mTOR信号在OSCC糖酵解和肿瘤免疫逃逸中的潜在分子机制。在体外实验中，采用集落形成法、EdU染色法和TUNEL法研究NFIC/DEPTOR/mTOR轴对HN30和SCC-25细胞增殖能力和凋亡的影响。通过葡萄糖摄取、ECAR和乳酸生成来分析OSCC细胞的糖酵解活性。将CD8+ T细胞与OSCC细胞共培养，分析CD8+ T细胞的细胞毒活性。将不同基因干预的SCC-25细胞皮下注射到NOG小鼠体内，研究NFIC/DEPTOR/mTOR对皮下肿瘤生长、肿瘤微环境（TME）酸度、CD8+ T细胞浸润和活性的影响。采用ChIP-qPCR和双荧光素酶法研究了OSCC细胞中NFIC与DEPTOR启动子之间的调控关系。结果snfic和DEPTOR在OSCC细胞和组织中显著下调，并伴有mTOR信号增强。NFIC通过结合其启动子激活DEPTOR。过表达NFIC或DEPTOR均可显著抑制OSCC细胞增殖、糖酵解活性和增强CD8+ T细胞杀伤能力。同样，它们在体内抑制肿瘤生长，阻断TME酸化，减弱肿瘤免疫逃逸。联合敲除detor可挽救被NFIC过表达抑制的OSCC的恶性进展。结论nfic介导DEPTOR转录抑制mTOR信号，通过抑制细胞增殖、糖酵解活性和CD8+ T细胞相关免疫逃逸，从而阻碍OSCC进展。

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引用次数: 0

TWF1 promotes tumor progression in head and neck squamous cell carcinoma via AKT phosphorylation TWF1通过AKT磷酸化促进头颈部鳞状细胞癌的肿瘤进展。

IF 2.1 4区医学 Q2 DENTISTRY, ORAL SURGERY & MEDICINE

Archives of oral biology

Pub Date : 2026-01-01 Epub Date: 2025-10-14 DOI: 10.1016/j.archoralbio.2025.106425

Yingshun Yang , Kaicheng Yang , Shixiong Peng , Shasha Man , He Chen

Objective

To investigate the molecular mechanisms underlying how Twinfilin actin-binding protein 1 (TWF1) drives the malignant progression of head and neck squamous cell carcinoma (HNSCC).

Design

A pan-cancer analysis of TCGA datasets was performed to evaluate TWF1 expression and prognostic significance, followed by validation using quantitative real-time PCR (qPCR) and immunohistochemistry (IHC) in clinical HNSCC specimens. Functional assays (CCK-8, colony formation, wound healing, and Transwell invasion) were conducted following siRNA-mediated TWF1 knockdown in SCC9 cells. Additionally, the same functional assays were conducted in an HSC3 cell model overexpressing TWF1 to further evaluate its oncogenic function. The involvement of the AKT signaling pathway was examined by Western blot and validated through rescue experiments with the AKT activator SC79.

Results

TWF1 was found to be upregulated in 13 cancer types, including HNSCC. Elevated TWF1 expression, advanced T stage, and lymph node metastasis were identified as independent prognostic indicators in HNSCC. qPCR confirmed increased TWF1 expression, and IHC showed higher TWF1 protein levels in HNSCC tissues. TWF1 knockdown suppressed SCC9 cell proliferation, migration, and invasion, and reduced phosphorylated AKT levels. Conversely, TWF1 overexpression in HSC3 cells promoted proliferation, migration, and invasion while enhancing AKT phosphorylation. SC79 treatment partially reversed the malignant phenotypes suppressed by TWF1 knockdown, supporting TWF1’s regulatory role through AKT phosphorylation.

Conclusion

TWF1 acts as an oncogenic driver in HNSCC, promoting tumor progression through the AKT signaling pathway. It may serve as a potential therapeutic target in precision medicine for HNSCC.

目的：探讨Twinfilin actin-binding protein 1 （TWF1）驱动头颈部鳞状细胞癌（HNSCC）恶性进展的分子机制。设计：对TCGA数据集进行泛癌分析，评估TWF1的表达和预后意义，随后使用定量实时PCR （qPCR）和免疫组织化学（IHC）对临床HNSCC标本进行验证。在SCC9细胞中sirna介导的TWF1敲除后进行功能测定（CCK-8、菌落形成、伤口愈合和Transwell侵袭）。此外，在过表达TWF1的HSC3细胞模型中进行了相同的功能测定，以进一步评估其致癌功能。通过Western blot检测AKT信号通路的参与情况，并通过AKT激活剂SC79的拯救实验进行验证。结果：在包括HNSCC在内的13种癌症类型中发现TWF1表达上调。TWF1表达升高、T分期晚期和淋巴结转移被确定为HNSCC的独立预后指标。qPCR证实TWF1表达升高，IHC显示HNSCC组织中TWF1蛋白水平升高。TWF1敲除抑制SCC9细胞增殖、迁移和侵袭，降低磷酸化AKT水平。相反，在HSC3细胞中，TWF1过表达促进增殖、迁移和侵袭，同时增强AKT磷酸化。SC79治疗部分逆转了TWF1敲低抑制的恶性表型，支持了TWF1通过AKT磷酸化的调节作用。结论：TWF1在HNSCC中发挥致癌驱动作用，通过AKT信号通路促进肿瘤进展。它可能成为HNSCC精准医学的潜在治疗靶点。

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引用次数: 0

Extracellular vesicles derived from Filifactor alocis induce interleukin-6 production in osteoblasts via Toll-like receptor 2 signaling 细胞外囊泡来源于细丝因子alocis通过toll样受体2信号传导诱导成骨细胞产生白细胞介素-6。

IF 2.1 4区医学 Q2 DENTISTRY, ORAL SURGERY & MEDICINE

Archives of oral biology

Pub Date : 2026-01-01 Epub Date: 2025-10-28 DOI: 10.1016/j.archoralbio.2025.106443

Yuma Tsuruta , Tongxin Liu , Haruna Yokoi , Kentaro Maruyama , Eiji Nemoto , Takashi Nishioka , Kenji Matsushita , Hiroyuki Tada

Objective

This study aimed to investigate the effect of the periodontal bacterium Filifactor alocis on proinflammatory cytokine production by osteoblasts. Specifically, we examined the mechanisms underlying interleukin (IL)-6 production by osteoblasts stimulated with live and lyophilized F. alocis, and F. alocis-derived extracellular vesicles (EVs).

Design

MC3T3-E1 mouse osteoblasts were stimulated with live bacteria of F. alocis and, as a comparative control, P. gingivalis. Furthermore, cells were treated with F. alocis lyophilized whole cells or EVs, and IL-6 production was quantified by ELISA; cytokine expression profiled using membrane-based array; and mRNA expression analyzed by RT-qPCR. Signaling pathways were analyzed using specific inhibitors. Statistical analyses were performed using non-parametric tests with significance set at p < 0.05.

Results

F. alocis live bacteria, lyophilized whole cells, and F. alocis-derived EVs induced IL-6, leukemia inhibitory factor, and chemokines in MC3T3-E1 cells. Mechanistically, IL-6 production by F. alocis involved osteoblast activation via Toll-like receptor (TLR) 2 on the bacterial surface or released EVs. Lyophilized F. alocis induced IκB-ζ mRNA expression in osteoblasts. Moreover, F. alocis-derived EVs induced IL-6 production in osteoblasts via protein kinase C (PKC).

Conclusions

Live and lyophilized F. alocis and F. alocis-derived EVs induce the production of proinflammatory cytokines by osteoblasts, including IL-6. Additionally, the induction of IL-6 by F. alocis-derived EVs involves the activation of TLR2 and PKC. Conclusively, these findings suggest that F. alocis-induced cytokine production by osteoblasts may induce osteoclast differentiation, highlighting its role in the pathogenesis of periodontitis.

目的：探讨牙周细菌嗜酸丝状因子对成骨细胞产生促炎细胞因子的影响。具体来说，我们研究了活的和冻干的F. alocis以及F. alocis衍生的细胞外囊泡（EVs）刺激成骨细胞产生白细胞介素(IL)-6的机制。设计：用alocis活菌刺激MC3T3-E1小鼠成骨细胞，并以牙龈假单胞菌作为对照。用冻干的alocis全细胞或ev处理细胞，ELISA法测定IL-6的产量；基于膜的细胞因子表达谱分析RT-qPCR分析mRNA表达情况。使用特定抑制剂分析信号通路。结果：F. alocis活菌、冻干全细胞和F. alocis衍生的ev可诱导MC3T3-E1细胞中的IL-6、白血病抑制因子和趋化因子。从机制上讲，F. alocis产生IL-6涉及通过细菌表面的toll样受体（TLR） 2激活成骨细胞或释放ev。冻干F. alocis诱导成骨细胞i - κ b -ζ mRNA表达。此外，F. alocis衍生的ev通过蛋白激酶C （PKC）诱导成骨细胞产生IL-6。结论：活的和冻干的F. alocis和F. alocis衍生的EVs诱导成骨细胞产生促炎细胞因子，包括IL-6。此外，F. alocis衍生的ev诱导IL-6涉及TLR2和PKC的激活。总之，这些发现表明，F. alocis诱导的成骨细胞产生的细胞因子可能诱导破骨细胞分化，突出了其在牙周炎发病机制中的作用。

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引用次数: 0

Biomechanical impact of tooth root morphology to inform dental implant design 牙根形态对种植体设计的生物力学影响。

IF 2.1 4区医学 Q2 DENTISTRY, ORAL SURGERY & MEDICINE

Archives of oral biology

Pub Date : 2026-01-01 Epub Date: 2025-11-09 DOI: 10.1016/j.archoralbio.2025.106455

Amber P. Wood-Bailey , Chris Smith , Laura C. Fitton , Alana C. Sharp

Objective

Using finite element analysis (FEA), this study aims to investigate the impact of different tooth root morphologies and implant designs, including a standard implant and a custom root-analogue implant on stress and strain distribution across the mandible.

Design

Six models were created by varying the root morphology of one tooth (the mandibular first molar) under identical loading scenarios: an original molar root, an incisor root, a canine root, a taurodont root, a standard implant, and a custom root-analogue implant replicating the original root morphology.

Results

Models with the original molar and custom implant exhibited similar stress and strain distributions over the mandible and had higher principal strains (tensile and compressive) compared to the single-rooted and standard implant models. Specifically, the maximum tensile and compressive strain values in the mandible of the custom implant model reach 94.89 % and 99.15 % of those in the original tooth root model. In contrast, the other models show less than 55.68 % similarity.

Conclusions

Custom root-analogue implants, which mimic natural root morphology, demonstrated more favourable stress distribution patterns, similar to those of the natural molar, compared to single-root implants. Our findings suggest that multi-rooted teeth are biomechanically optimized for dissipating masticatory loads, and standard single-root implants may not adequately replicate these properties, leading to poor load distribution and increased failure risk in posterior locations. Further research is needed to refine custom root-analogue implant designs and optimize their clinical application to better match the natural biomechanical environment of the maxilla and mandible.

目的：采用有限元分析（FEA），研究不同牙根形态和种植体设计对下颌骨应力应变分布的影响，包括标准种植体和定制模拟牙根种植体。设计：通过改变一颗牙齿（下颌第一磨牙）在相同加载情景下的牙根形态，创建了6个模型：原始磨牙根、门牙根、犬牙根、牛头齿根、标准种植体和复制原始牙根形态的定制牙根模拟种植体。结果：与单根和标准种植体模型相比，原始磨牙和定制种植体模型在下颌骨上表现出相似的应力和应变分布，并且具有更高的主应变（拉伸和压缩）。其中，定制种植体模型下颌骨的最大拉伸应变和最大压缩应变分别达到原牙根模型的94.89 %和99.15 %。相比之下，其他模型的相似度小于55.68 %。结论：与单根种植体相比，模拟天然根形态的定制根模拟种植体表现出与天然磨牙相似的更有利的应力分布模式。我们的研究结果表明，多根牙在生物力学上优化了咀嚼负荷的消散，而标准的单根种植体可能无法充分复制这些特性，导致负荷分布不佳，增加了后牙位置失败的风险。需要进一步的研究来完善定制的根模拟种植体设计并优化其临床应用，以更好地匹配上下颌骨的自然生物力学环境。

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引用次数: 0

The microRNA-34b-3p/SOX5 axis regulates cellular activities and tumor angiogenesis in oral squamous cell carcinoma microRNA-34b-3p/SOX5轴调控口腔鳞状细胞癌的细胞活性和肿瘤血管生成

IF 2.1 4区医学 Q2 DENTISTRY, ORAL SURGERY & MEDICINE

Archives of oral biology

Pub Date : 2026-01-01 Epub Date: 2025-10-22 DOI: 10.1016/j.archoralbio.2025.106438

Mingke Huang , Yu Ren , Jiwen Zheng , Yang Cao , Yu Zhu , Jun Zhou , Zhuo Ling , Guoyu Xiong , Hangyu Zhou

Objective

This study aimed to ascertain the significance of microRNA-34b-3p (miR-34b-3p) in the prognosis and tumor angiogenesis associated with the development of oral squamous cell carcinoma (OSCC).

Design

The relative abundances of miR-34b-3p and tumor angiogenesis-associated genes were quantified using quantitative real-time polymerase chain reaction. Cellular events were monitored using the Cell Counting Kit-8 and Transwell assays. Additionally, a luciferase reporter assay was carried out to verify the interaction between miR-34b-3p and Sex Determining Region Y-box Protein 5 (SOX5).

Results

MiR-34b-3p was significantly decreased in tissue samples from OSCC patients in comparison to healthy individuals (P < 0.001) and displayed a robust diagnostic accuracy in distinguishing OSCC patients from healthy controls. Moreover, OSCC patients expressing low miR-34b-3p levels displayed a short overall survival time (P = 0.002). Additionally, low miR-34b-3p expression was an independent predictor for the clinical outcome of OSCC patients (P = 0.011, HR=0.447, 95 %CI=0.239–0.834). Through biological experiments, downregulation of miR-34b-3p could promote cell proliferation, migration and invasion of OSCC cells. Notably, following transfection miR-34b-3p inhibitor, VEGFA and MMP9 mRNA expressions were dramatically enhanced (P < 0.001). SOX5 was identified as a potential target of miR-34b-3p. Recovery experiments verified that the knockdown of SOX5 counteracted the impacts of miR-34b-3p on cellular activities and angiogenesis.

Conclusions

Downregulated miR-34b-3p expression promoted OSCC progression by enhancing cellular activities and upregulating the expression of pro-angiogenic factors via targeting SOX5.

目的探讨microRNA-34b-3p （miR-34b-3p）在口腔鳞状细胞癌（OSCC）预后及肿瘤血管生成中的意义。设计采用实时定量聚合酶链反应定量检测miR-34b-3p和肿瘤血管生成相关基因的相对丰度。使用细胞计数试剂盒-8和Transwell法监测细胞事件。此外，我们还进行了荧光素酶报告试验，以验证miR-34b-3p与性别决定区Y-box蛋白5 （SOX5）之间的相互作用。结果与健康人群相比，OSCC患者组织样本中的smir -34b-3p显著降低（P <； 0.001），并且在区分OSCC患者和健康对照组方面显示出强大的诊断准确性。此外，表达低miR-34b-3p水平的OSCC患者总体生存时间较短（P = 0.002）。此外，miR-34b-3p低表达是OSCC患者临床结局的独立预测因子（P = 0.011，HR=0.447, 95 %CI= 0.239-0.834）。生物学实验表明，下调miR-34b-3p可促进OSCC细胞的增殖、迁移和侵袭。值得注意的是，转染miR-34b-3p抑制剂后，VEGFA和MMP9 mRNA的表达显著增强（P <； 0.001）。SOX5被确定为miR-34b-3p的潜在靶标。恢复实验证实，SOX5的敲低抵消了miR-34b-3p对细胞活性和血管生成的影响。结论miR-34b-3p表达下调可通过靶向SOX5增强细胞活性，上调促血管生成因子的表达，从而促进OSCC的进展。

{"title":"The microRNA-34b-3p/SOX5 axis regulates cellular activities and tumor angiogenesis in oral squamous cell carcinoma","authors":"Mingke Huang , Yu Ren , Jiwen Zheng , Yang Cao , Yu Zhu , Jun Zhou , Zhuo Ling , Guoyu Xiong , Hangyu Zhou","doi":"10.1016/j.archoralbio.2025.106438","DOIUrl":"10.1016/j.archoralbio.2025.106438","url":null,"abstract":"<div><h3>Objective</h3><div>This study aimed to ascertain the significance of microRNA-34b-3p (miR-34b-3p) in the prognosis and tumor angiogenesis associated with the development of oral squamous cell carcinoma (OSCC).</div></div><div><h3>Design</h3><div>The relative abundances of miR-34b-3p and tumor angiogenesis-associated genes were quantified using quantitative real-time polymerase chain reaction. Cellular events were monitored using the Cell Counting Kit-8 and Transwell assays. Additionally, a luciferase reporter assay was carried out to verify the interaction between miR-34b-3p and Sex Determining Region Y-box Protein 5 (SOX5).</div></div><div><h3>Results</h3><div>MiR-34b-3p was significantly decreased in tissue samples from OSCC patients in comparison to healthy individuals (<em>P</em> < 0.001) and displayed a robust diagnostic accuracy in distinguishing OSCC patients from healthy controls. Moreover, OSCC patients expressing low miR-34b-3p levels displayed a short overall survival time (<em>P</em> = 0.002). Additionally, low miR-34b-3p expression was an independent predictor for the clinical outcome of OSCC patients (<em>P</em> = 0.011, HR=0.447, 95 %CI=0.239–0.834). Through biological experiments, downregulation of miR-34b-3p could promote cell proliferation, migration and invasion of OSCC cells. Notably, following transfection miR-34b-3p inhibitor, VEGFA and MMP9 mRNA expressions were dramatically enhanced (<em>P</em> < 0.001). SOX5 was identified as a potential target of miR-34b-3p. Recovery experiments verified that the knockdown of SOX5 counteracted the impacts of miR-34b-3p on cellular activities and angiogenesis.</div></div><div><h3>Conclusions</h3><div>Downregulated miR-34b-3p expression promoted OSCC progression by enhancing cellular activities and upregulating the expression of pro-angiogenic factors via targeting SOX5.</div></div>","PeriodicalId":8288,"journal":{"name":"Archives of oral biology","volume":"181 ","pages":"Article 106438"},"PeriodicalIF":2.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145474891","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Action mechanisms of progesterone in managing bone loss in periodontitis: An in vitro study 黄体酮在牙周炎骨质流失中的作用机制：一项体外研究

IF 2.1 4区医学 Q2 DENTISTRY, ORAL SURGERY & MEDICINE

Archives of oral biology

Pub Date : 2026-01-01 Epub Date: 2025-10-21 DOI: 10.1016/j.archoralbio.2025.106436

Ying Man , Shengjie Yan , Jianyong Qin, Xiaofei Li, Hongliang Qiu, Xinyue Zhang

Objective

Progesterone (PG) is a sex steroid hormone that has the potential to control bone loss in periodontitis. This study aimed to reveal the underlying mechanisms of action of PG on osteogenesis in periodontitis and to identify key target genes in vitro.

Design

Primary human periodontal mesenchymal stem cells (hPDLSCs) were isolated and treated with lipopolysaccharide (LPS) in combination with or without PG. Subsequently, RNA sequencing was performed after osteogenic induction, and the differential expressed genes (DEGs), functional enrichment (GO and KEGG), and protein-protein interaction (PPI) were bioinformatically analysed. The expression of two key DEGs, BUB1 and UBE2C, were verified by qRT-PCR. Relevant regulatory mechanisms involving osteogenesis were verified by detecting the levels of osteogenesis-related proteins, Runx2 and ALP (Western blot) after silencing.

Results

A total of 212 DEGs (104 up-regulated and 108 down-regulated genes) were identified between the LPS and LPS + PG groups. These DEGs were mainly enriched in the GO terms of cell division, adhesion, sodium/potassium channel, etc., and in the KEGG terms of oocyte meiosis, estrogen signalling, cell apoptosis, and adhesion. In the PPI networks, most of the hub proteins are related to cell cycle and division. Of note, BUB1 and UBE2C, two node genes, were down-regulated in LPS-treated hPDLSCs. The intervention of PG significantly eliminated the effects of LPS on the down-regulation of BUB1 and UBE2C. Upon LPS treatment, silencing of BUB1 and UBE2C both reversed the PG-induced osteogenesis in hPDLSCs.

Conclusions

BUB1 and UBE2C, two important mediators of osteogenesis, are potential molecular targets of PG. PG may promote the osteogenesis of hPDLSCs under inflammatory conditions through the up-regulation of BUB1 and UBE2C, suggesting a potential mechanism that may contribute to the remission of periodontitis.

目的黄体酮（PG）是一种具有控制牙周炎骨质流失潜力的性类固醇激素。本研究旨在揭示PG对牙周炎成骨作用的潜在机制，并在体外鉴定关键靶基因。设计分离原代人牙周间充质干细胞（hPDLSCs），用脂多糖（LPS）联合或不联合PG处理，随后在成骨诱导后进行RNA测序，并对差异表达基因（DEGs）、功能富集（GO和KEGG）和蛋白-蛋白相互作用（PPI）进行生物信息学分析。通过qRT-PCR验证了两个关键deg BUB1和UBE2C的表达。通过检测沉默后成骨相关蛋白、Runx2和ALP的水平（Western blot），验证了与成骨相关的相关调控机制。结果LPS组和LPS + PG组共鉴定出212个deg，其中上调104个，下调108个。这些deg主要富集于细胞分裂、粘附、钠钾通道等方面的GO，以及卵母细胞减数分裂、雌激素信号、细胞凋亡和粘附等方面的KEGG。在PPI网络中，大多数枢纽蛋白与细胞周期和分裂有关。值得注意的是，在lps处理的hPDLSCs中，两个节点基因BUB1和UBE2C下调。PG的干预显著消除了LPS对BUB1和UBE2C下调的影响。在LPS处理后，沉默BUB1和UBE2C均逆转了pg诱导的hPDLSCs成骨。结论BUB1和UBE2C是两种重要的成骨介质，是PG的潜在分子靶点，PG可能通过上调BUB1和UBE2C促进炎症条件下hPDLSCs的成骨，提示其参与牙周炎缓解的潜在机制。

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引用次数: 0

Influence of head and neck radiotherapy doses on apical periodontitis progression: An animal-based study 头颈部放疗剂量对根尖牙周炎进展的影响：一项基于动物的研究。

IF 2.1 4区医学 Q2 DENTISTRY, ORAL SURGERY & MEDICINE

Archives of oral biology

Pub Date : 2026-01-01 Epub Date: 2025-10-24 DOI: 10.1016/j.archoralbio.2025.106422

Gustavo Guimarães Guerrero , Giovanna B. Minhoto , Camilla dos S. Tibúrcio-Machado , Rayana D. Khoury , Carolina O. Lima , Emmanuel J.N.L. Silva , Claudio A. Federico , Marcia C. Valera

Aim

The aim of this study was to assess the dose-dependent effects of radiotherapy on the progression of apical periodontitis (AP) in rats.

Methods

Forty-five animals were divided into five groups based on radiation dose and apical periodontitis induction (n = 9): AP-RT7 (irradiated with a dose of 7.5 Gy + AP); AP-RT10 (10 Gy dose + AP); AP-RT15 (15 Gy dose + AP); AP (AP without radiation), and Control (no intervention). Radiation therapy was administered on the first day of the experiment. After seven days, the apical periodontitis induction was carried out in all groups except Control. All animals were euthanized after 21 days of AP progression (day 28), and the area and volume of AP were analyzed using radiography, micro-CT, and histological analyses. Inflammation intensity and extent were assessed histologically. Statistical analysis was performed using ANOVA and Student's t test for quantitative data, and Kruskal-Wallis for ordinal data (P < 0.05).

Results

The AP-RT15 group exhibited significantly larger apical periodontitis lesions compared to the AP-RT7.5, AP-RT10, and AP groups, as demonstrated by radiographic (p < 0.05), micro-CT (p < 0.0001), and histological analyses (p < 0.0001). Histological examination further revealed a more extensive and intense inflammatory response in the AP-RT15 group (p < 0.01). Overall, radiotherapy contributed to increased apical bone resorption and exacerbated inflammation in a dose-dependent manner.

Conclusions

The progression of apical periodontitis in irradiated animals follows a dose-dependent pattern, with higher radiation doses markedly amplifying the lesion's area, volume, and inflammatory severity.

目的：本研究的目的是评估放射治疗对大鼠根尖牙周炎（AP）进展的剂量依赖性。方法：45只动物根据辐照剂量和对根尖牙周炎的诱导程度分为5组（n = 9）：AP- rt7（辐照剂量为7.5 Gy + AP）；AP- rt10(10 Gy剂量+ AP)；AP- rt15(15 Gy剂量+ AP)；AP（无放疗）和Control（无干预）。在实验的第一天进行放射治疗。7 d后，除对照组外，其余各组均行根尖牙周炎诱导。所有动物在AP进展21天后（第28天）被安乐死，并通过x线摄影、显微ct和组织学分析AP的面积和体积。用组织学方法评估炎症强度和程度。对定量数据采用方差分析和学生t检验，对有序数据采用Kruskal-Wallis检验（P ）结果：AP- rt15组与AP- rt7.5、AP- rt10和AP组相比，显示出明显更大的根尖牙周炎病变，x线摄影证实（P ）。受辐射动物的根尖牙周炎的进展遵循剂量依赖模式，较高的辐射剂量显著放大病变的面积、体积和炎症严重程度。

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引用次数: 0

Elaeodendron buchananii (Loes.) Loes. stem bark: Unveiling the phytochemical profiles and selective bioactivity to combat tongue cancer 白桦（Elaeodendron buchananii）卫矛。茎皮：揭示对抗舌癌的植物化学特征和选择性生物活性

IF 2.1 4区医学 Q2 DENTISTRY, ORAL SURGERY & MEDICINE

Archives of oral biology

Pub Date : 2026-01-01 Epub Date: 2025-10-20 DOI: 10.1016/j.archoralbio.2025.106434

Abhay Prakash Mishra , Anyapat Atipimonpat , Manisha Nigam , Masande Yalo , Sudarshan Singh , Chuda Chittasupho , Jennifer Nambooze , Jarunya Ngamkham , Neti Waranuch

Objective

The study aimed to investigate the cytotoxic and anti-inflammatory potential of the methanolic stem bark extract of Elaeodendron buchananii (EB) through in vitro assays and LC-MS based phytochemical profiling.

Design

The cytotoxicity of EB was evaluated using the MTT assay on cell lines: RAW 264.7 (murine macrophages), HGF-1 (human gingival fibroblasts), and SCC-25 (human tongue squamous carcinoma cells). Oxidative stress and membrane damage were evaluated using reactive oxygen species (ROS) and lactate dehydrogenase (LDH) assays, respectively, while susceptibility to oxidative stress was examined through H₂O₂ challenge. A Griess reagent assay was used to determine EB's anti-inflammatory properties in LPS-stimulated RAW 264.7 cells.

Results

EB exhibited no toxicity to HGF-1 across a concentration range of 50–800 µg/mL, while showing moderate cytotoxicity against RAW 264.7 cells, at 1000 µg/mL (cell viability 67.63 ± 2.81 %). Notably, EB demonstrated selective cytotoxicity against SCC-25 cells (IC₅₀ = 581.9 µg/mL). Additionally, a significant reduction in nitric oxide (NO) production by EB was observed against RAW 264.7 cells when stimulated with LPS, indicating anti-inflammatory (IC₅₀ = 401.40 µg/mL) properties. LC-MS analysis identified 16 phytochemicals, including various secondary metabolites (such as ursolic acid, elaeodendroside F, and oleandrin), each recognized for their pharmacological relevance.

Conclusion

The findings demonstrate that EB possesses selective cytotoxicity toward tongue carcinoma cells and exhibits significant anti-inflammatory effects. These findings support its traditional medical application and point to its potential for additional phytopharmaceutical development. This report is the first to explore the in vitro cytotoxic effects of E. buchananii on tongue cancer cells.

目的通过体外实验和基于LC-MS的植物化学谱分析，研究北棘（Elaeodendron buchananii， EB）茎皮甲醇提取物的细胞毒和抗炎作用。设计采用MTT法对RAW 264.7（小鼠巨噬细胞）、HGF-1（人牙龈成纤维细胞）和SCC-25（人舌鳞癌细胞）细胞系进行细胞毒性评价。氧化应激和膜损伤分别采用活性氧（ROS）和乳酸脱氢酶（LDH）测定，氧化应激的易感性则通过H₂O₂挑战检测。采用Griess试剂法测定EB对lps刺激的RAW 264.7细胞的抗炎特性。结果tsb在50-800 µg/mL浓度范围内对HGF-1无毒性，在1000 µg/mL浓度范围内对RAW 264.7细胞有中等毒性（细胞活力67.63 ± 2.81 %）。值得注意的是，EB显示出对SCC-25细胞的选择性细胞毒性（IC₅₀= 581.9 µg/mL）。此外，当用LPS刺激RAW 264.7细胞时，观察到EB对一氧化氮（NO）产生的显着减少，表明抗炎（IC₅₀= 401.40 µg/mL）特性。LC-MS分析鉴定出16种植物化学物质，包括各种次生代谢物（如熊果酸、elaeodendro苷F和夹竹桃素），每种化学物质都具有药理相关性。结论EB对舌癌细胞具有选择性杀伤作用，具有明显的抗炎作用。这些发现支持了它的传统医学应用，并指出了它在其他植物药物开发方面的潜力。本报告首次探讨了布chananii对舌癌细胞的体外细胞毒作用。

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引用次数: 0

Exercise modulates local inflammation and tissue loss in experimental periodontitis: A histomorphometric and immunohistochemical study in ra 运动调节实验性牙周炎的局部炎症和组织损失：ra的组织形态学和免疫组织化学研究

IF 2.1 4区医学 Q2 DENTISTRY, ORAL SURGERY & MEDICINE

Archives of oral biology

Pub Date : 2026-01-01 Epub Date: 2025-10-18 DOI: 10.1016/j.archoralbio.2025.106435

Gümrükçüoğlu Zehra , Burcu Özkan Çetinkaya , Ferda Pamuk Özer , Sinem İnal , Sevda Kurt Bayrakdar , Muhammed Taha Kaya

Objective

This study aimed to investigate the effects of resistance exercise on the progression of periodontal disease in rats, focusing on alveolar bone loss, attachment loss, and local inflammatory and bone metabolic markers.

Materials and methods

Forty male Wistar albino rats were allocated into four experimental groups in a 2 × 2 factorial design: G1 or G2 and G3 or G4. The exercise protocol consisted of progressive swimming sessions over eight weeks, with resistance provided by weights tied to the animals. In the final week, MBT was performed, and rats were sacrificed for histomorphometric and immunohistochemical analysis.

Results

The values for alveolar bone loss and attachment loss were significantly lower in the exercised groups compared to both the G1 and G2 groups (p < 0.001). Among the rats with periodontitis, TNF-α expression was significantly lower in the exercised group (p = 0.002), whereas IL-10 levels showed no significant differences (p > 0.005). RANKL expression was elevated in G2 (p = 0.039), with no significant variation in OPG among groups. In MBT, G2 showed significantly higher values compared to G1 and G3 (p = 0.004). G4 displayed intermediate values, higher than G3 but lower than G2, without statistical significance (p > 0.005).

Conclusion

Physical exercise reduced TNF-α levels in the presence of periodontitis and increased IL-10, although the latter change was not statistically significant. Exercise also contributed to a decrease in RANKL/OPG expression, suggesting a protective effect on alveolar bone resorption. MBT findings further indicate that exercise may alleviate periodontitis-associated behavioral alterations, supporting its potential role as an adjunctive therapy in managing periodontitis.

目的探讨阻力运动对大鼠牙周病进展的影响，重点关注牙槽骨丢失、附着丧失以及局部炎症和骨代谢标志物。材料与方法40只雄性Wistar白化大鼠按2 × 2因子设计分为4个实验组：G1或G2和G3或G4。锻炼方案包括在八周内进行渐进式游泳，并通过拴在动物身上的重物提供阻力。最后一周进行MBT，处死大鼠进行组织形态学和免疫组化分析。结果运动组的牙槽骨丢失和附着体丢失值明显低于G1和G2组（p <； 0.001）。在牙周炎大鼠中，运动组TNF-α表达明显降低（p = 0.002），而IL-10水平无显著差异（p >； 0.005）。RANKL在G2组表达升高（p = 0.039），OPG组间差异无统计学意义。在MBT中，G2的数值明显高于G1和G3 （p = 0.004）。G4为中间值，高于G3，低于G2，差异无统计学意义（p >； 0.005）。结论体育锻炼可降低牙周炎患者TNF-α水平，升高IL-10水平，但后者的变化无统计学意义。运动还导致RANKL/OPG表达降低，提示运动对牙槽骨吸收有保护作用。MBT研究结果进一步表明，运动可以减轻牙周炎相关的行为改变，支持其作为治疗牙周炎的辅助治疗的潜在作用。

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引用次数: 0

DPM1 expression as a potential prognostic tumor marker in oral squamous cell carcinoma DPM1表达作为口腔鳞状细胞癌的潜在预后肿瘤标志物。

IF 2.1 4区医学 Q2 DENTISTRY, ORAL SURGERY & MEDICINE

Archives of oral biology

Pub Date : 2026-01-01 Epub Date: 2025-10-17 DOI: 10.1016/j.archoralbio.2025.106432

Hongyu Liu , Buling Wu

Objective

This study investigates how dolichol phosphate mannose synthase (DPMS) subunits DPM1/2/3 affect oral squamous cell carcinoma (OSCC) prognosis and their associations with OSCC.

Design

To evaluate the connections between DPMS subunits DPM1/2/3 and OSCC, we utilized a wide array of databases and analytical resources, including The Cancer Genome Atlas (TCGA), Metascape, and MethSurv. For initial verification, we applied real-time quantitative polymerase chain reaction (RT-qPCR) to OSCC cell lines and tissues.

Results

DPM1 and DPM2 expression was higher in OSCC tissues than normal ones. Univariate and multivariate COX analyses showed high DPM1 expression independently correlated with poorer OSCC overall survival. Gene ontology (GO) analysis via Metascape revealed DPM1/2/3 and co-expressed genes enriched in cell cycle, nucleic acid metabolism, and translation. Gene set enrichment analysis (GSEA) linked them to pathways like complement activation, BCR signaling, and immune systems. Besides, high DPMS expression was tied to a more unfavorable prognosis in OSCC patients, and DPM1/2/3 was associated with the infiltration of tumor immune cells in OSCC patients. We found that methylation levels might be related to the prognosis of OSCC patients. By means of RT-qPCR, we ascertained the differential expression levels of DPM1 in human normal oral keratinocytes (HOK) and human tongue squamous cell carcinoma cells (Cal27, SCC9), cancer and paracancerous tissues of OSCC.

Conclusion

Our findings imply that DPM1, a subunit of DPMS, can serve as a potential molecular indicator for poor prognosis in OSCC and may act as a novel target in OSCC treatment strategies.

目的：探讨磷酸膦醇甘露糖合成酶（DPMS）亚基DPM1/2/3对口腔鳞状细胞癌（OSCC）预后的影响及其与OSCC的关系。设计：为了评估DPMS亚基DPM1/2/3和OSCC之间的联系，我们利用了广泛的数据库和分析资源，包括the Cancer Genome Atlas （TCGA）、metscape和MethSurv。为了初步验证，我们对OSCC细胞系和组织进行了实时定量聚合酶链反应（RT-qPCR）。结果：DPM1、DPM2在OSCC组织中的表达高于正常组织。单因素和多因素COX分析显示，高DPM1表达与较差的OSCC总生存率独立相关。通过Metascape进行基因本体（GO）分析，发现DPM1/2/3和共表达基因富集于细胞周期、核酸代谢和翻译中。基因集富集分析（GSEA）将它们与补体激活、BCR信号和免疫系统等途径联系起来。此外，DPMS高表达与OSCC患者预后不良相关，DPM1/2/3与OSCC患者肿瘤免疫细胞浸润相关。我们发现甲基化水平可能与OSCC患者的预后有关。通过RT-qPCR，我们确定了DPM1在人正常口腔角质形成细胞（HOK）和人舌鳞癌细胞（Cal27、SCC9）、OSCC癌及癌旁组织中的差异表达水平。结论：DPMS亚基DPM1可作为OSCC不良预后的潜在分子指标，并可能作为OSCC治疗策略的新靶点。

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引用次数: 0