International Journal of Oral Science最新文献_第6页

Engineered Lactobacillus reuteri for scavenging reactive oxygen species and modulating oral microflora in periodontitis therapy. 在牙周炎治疗中清除活性氧和调节口腔微生物群的工程罗伊氏乳杆菌。

IF 17.6 1区医学

International Journal of Oral Science Pub Date : 2026-02-10 DOI: 10.1038/s41368-025-00418-z

Yuqiang Wang, Ying Tang, Qianxiao Huang, Jiaxin An, Yueli Zhou, Hongye Yang, Fangfang Song, Xianzheng Zhang, Cui Huang

{"title":"Engineered Lactobacillus reuteri for scavenging reactive oxygen species and modulating oral microflora in periodontitis therapy.","authors":"Yuqiang Wang, Ying Tang, Qianxiao Huang, Jiaxin An, Yueli Zhou, Hongye Yang, Fangfang Song, Xianzheng Zhang, Cui Huang","doi":"10.1038/s41368-025-00418-z","DOIUrl":"10.1038/s41368-025-00418-z","url":null,"abstract":"The onset and progression of periodontitis are closely associated with subgingival dysbiosis and excessive localized oxidative stress. While some oral probiotics exhibit certain inhibitory effects on periodontitis-related pathogens, they often struggle to effectively colonize and antagonize these pathogens due to the complex oxidative stress at the site of periodontitis. In this study, we engineer Lactobacillus reuteri with a reactive oxygen species (ROS)-responsive adhesive polymer (phenylboric acid-dopamine-hyaluronic acid) (LR@PDH). In the periodontitis microenvironment, this polymer can consume ROS and then expose the phenolic hydroxyl group of dopamine, promoting the selective adhesion and colonization of Lactobacillus reuteri at the site of inflammation to antagonize pathogens. The results show that, compared to conventional probiotic therapy, inflammation-responsive adhesive Lactobacillus reuteri effectively alleviates local oxidative stress, reduces the abundance of pathogenic bacteria in the subgingival microbiome, and inhibits the progression of periodontitis. Additionally, its good biocompatibility and safety highlight its potential as a therapeutic approach for clinical treatment of periodontitis.","PeriodicalId":14191,"journal":{"name":"International Journal of Oral Science","volume":"18 1","pages":"16"},"PeriodicalIF":17.6,"publicationDate":"2026-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12887038/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146149689","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Stimuli-responsive, antimicrobial-loaded nanocarriers for oral biofilm control and microbiome restoration. 刺激反应，抗菌剂负载纳米载体口腔生物膜控制和微生物群恢复。

IF 17.6 1区医学

International Journal of Oral Science Pub Date : 2026-02-10 DOI: 10.1038/s41368-025-00422-3

Ding Chen, Dize Li, Linzhu Su, Da-Yuan Wang, Yijin Ren, Henny C van der Mei, Linqi Shi, Tao Chen, Henk J Busscher

{"title":"Stimuli-responsive, antimicrobial-loaded nanocarriers for oral biofilm control and microbiome restoration.","authors":"Ding Chen, Dize Li, Linzhu Su, Da-Yuan Wang, Yijin Ren, Henny C van der Mei, Linqi Shi, Tao Chen, Henk J Busscher","doi":"10.1038/s41368-025-00422-3","DOIUrl":"10.1038/s41368-025-00422-3","url":null,"abstract":"Nanotechnology has provided thousands of novel nano-antimicrobials possessing features uncommon in clinically available antimicrobials. Here, nanocarriers loaded with conventional antimicrobials and responding to environmental changes upon entry into oral biofilms are reviewed. Supra-gingival biofilms are characterized by acidic pH, the presence of bacterial enzymes, and the development of hypoxia in deeper layers. Sub-gingival biofilms are slightly alkaline, with hypoxia occurring over their entire depth. Upon entering biofilms, negatively charged, pH- and/or hypoxia-responsive nanocarriers become positively charged. This charge reversal leads to electrostatic double-layer attraction between positively charged nanocarriers towards negatively charged, water-filled channel walls in biofilms, enhancing their accumulation in a biofilm. Degradation of bacterial enzyme-responsive nanocarriers causes in-biofilm release of antimicrobial cargo, yielding higher local antimicrobial concentrations than can be achieved through their direct, oral administration without harming soft tissues. Enhanced antibiofilm activity after in-biofilm antimicrobial release from biofilm-responsive micelles and liposomes has been demonstrated in vitro towards single-species Streptococcus mutans and Staphylococcus aureus biofilms or in vivo using specific-pathogen-free rodents inoculated with selected pathogens. This preferential antibacterial activity regulated the microbial composition of ex vivo human oral biofilm towards a more healthy microbiome composition. Although clinical confirmation is limited, the potential benefits of stimuli-responsive, antimicrobial-loaded nanocarriers for oral biofilm control and microbiome restoration are worth further investigation towards clinical translation.","PeriodicalId":14191,"journal":{"name":"International Journal of Oral Science","volume":"18 1","pages":"17"},"PeriodicalIF":17.6,"publicationDate":"2026-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12891596/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146157059","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Porphyromonas gingivalis-derived extracellular vesicles aggravate bone destruction in rheumatoid arthritis by promoting Syk-dependent osteoclastogenesis. 牙龈卟啉单胞菌衍生的细胞外囊泡通过促进syk依赖性破骨细胞生成加重类风湿关节炎的骨破坏。

IF 17.6 1区医学

International Journal of Oral Science Pub Date : 2026-02-05 DOI: 10.1038/s41368-025-00416-1

Jiajie Guo, Qiujing Qiu, Xiaoyuan Yan, Zeying Zhang, Xiyue Zhang, Na An, Chengcheng Yin, Di Yang, Hirohiko Okamura, Kaya Yoshida, Hongchen Sun, Lihong Qiu

{"title":"Porphyromonas gingivalis-derived extracellular vesicles aggravate bone destruction in rheumatoid arthritis by promoting Syk-dependent osteoclastogenesis.","authors":"Jiajie Guo, Qiujing Qiu, Xiaoyuan Yan, Zeying Zhang, Xiyue Zhang, Na An, Chengcheng Yin, Di Yang, Hirohiko Okamura, Kaya Yoshida, Hongchen Sun, Lihong Qiu","doi":"10.1038/s41368-025-00416-1","DOIUrl":"10.1038/s41368-025-00416-1","url":null,"abstract":"Rheumatoid arthritis (RA) is an autoimmune disorder that triggers progressive joint destruction by inducing excessive osteoclastogenesis. Porphyromonas gingivalis (Pg), the main pathogenic bacterium involved in periodontitis (PD), is closely related to RA. Pg can secrete extracellular vesicles (EVs), which carry numerous virulence factors. The aim of this study was to investigate whether Pg-derived EVs can be transported and exacerbate bone destruction in RA by promoting osteoclastogenesis and to elucidate the underlying mechanisms involved. EVs derived from Porphyromonas endodontalis (Pe), which is weakly associated with PD or RA, were used as controls. Pg and Pe EVs interact with osteoclasts after translocating into the marrow and metacarpal joints of mice. In vitro, Pg EVs induce osteoclastogenesis via various components, such as lipopolysaccharide, proteins, lipoproteins, and proteases. TNF-α, IL-1β, and IL-6 promote but cannot independently control Pg EV-induced osteoclastogenesis. RNA sequencing and verification experiments further demonstrated that Pg EVs induced osteoclastogenesis by promoting the phosphorylation of spleen tyrosine kinase (Syk). In vivo, Pg EVs exacerbated RA-induced bone destruction by activating Syk-dependent osteoclastogenesis. R406, a Syk inhibitor, significantly attenuated Pg EV-induced RA osteoclastogenesis and bone destruction. However, Pe-derived EVs presented an extremely weak ability to promote osteoclastogenesis and RA. Our findings reveal a new mechanism by which Pg EVs can exacerbate RA via transport through the circulation and the promote Syk-dependent osteoclastogenesis. This study deepens our understanding of the significant pathogenic role of EVs derived from oral bacterial in RA and explores targeted therapeutic strategies by inhibiting the activation of Syk.","PeriodicalId":14191,"journal":{"name":"International Journal of Oral Science","volume":"18 1","pages":"6"},"PeriodicalIF":17.6,"publicationDate":"2026-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12873129/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146119084","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

LOXL2 deletion triggers TMJ osteoarthritis, while overexpression protects it from NF-κB-induced chondrocyte apoptosis. LOXL2缺失触发TMJ骨关节炎，而过表达则保护其免受NF-κ b诱导的软骨细胞凋亡。

IF 17.6 1区医学

International Journal of Oral Science Pub Date : 2026-02-04 DOI: 10.1038/s41368-025-00409-0

Rajnikant Dilip Raut, Chumki Choudhury, Faiza Ali, Amit Kumar Chakraborty, Mohammed Moeeduddin Ahmed, Cheyleann Del Valle Ponce De Leon, Harshal V Modh, Pushkar Mehra, Yuwei Fan, Alejandro Almarza, Manish V Bais

{"title":"LOXL2 deletion triggers TMJ osteoarthritis, while overexpression protects it from NF-κB-induced chondrocyte apoptosis.","authors":"Rajnikant Dilip Raut, Chumki Choudhury, Faiza Ali, Amit Kumar Chakraborty, Mohammed Moeeduddin Ahmed, Cheyleann Del Valle Ponce De Leon, Harshal V Modh, Pushkar Mehra, Yuwei Fan, Alejandro Almarza, Manish V Bais","doi":"10.1038/s41368-025-00409-0","DOIUrl":"10.1038/s41368-025-00409-0","url":null,"abstract":"Temporomandibular joint osteoarthritis (TMJ-OA) affects a significant proportion of the population worldwide. However, there has been no substantial progress in the development of FDA-approved drugs for treatment due to a lack of understanding of the specific factors regulating key TMJ-OA molecular mechanisms. Lysyl Oxidase-Like-2 (LOXL2) promotes knee joint cartilage protection and is downregulated in a TMJ-OA animal model. We evaluated the role of LOXL2 in TMJ cartilage, its molecular mechanism, and gene networks using in vivo Loxl2 knockout mice (Acan-Cre; Loxl2flox/flox) and ex vivo goat TMJ cartilage. Our results show that Loxl2 knockout in mouse cartilage upregulates Il1b, Mmp9, Mmp13, Adamts4, and Adamts5, but reduces the levels of aggrecan and proteoglycan. Loxl2 deleted TMJ cartilage show a higher enrichment of inflammatory response, TNFA signaling via NF-κB, extracellular matrix (ECM), and collagen degradation pathway network. Conversely, LOXL2 treatment reduces interleukin-1 beta (IL-1β)-induced expression of Mmp13, protects mitochondrial function, and ECM from degeneration. Importantly, LOXL2 attenuates IL-1β-induced chondrocyte apoptosis via the phosphorylation of NF-κB and expression of the pain-related gene PTGS2 (encodes COX2). Taken together, Loxl2 knockout mice exacerbate TMJ-OA through cartilage/ECM degradation, mitochondrial dysfunction, chondrocyte apoptosis, and inflammatory gene expression, whereas LOXL2 treatment mitigate these effects.","PeriodicalId":14191,"journal":{"name":"International Journal of Oral Science","volume":"18 1","pages":"8"},"PeriodicalIF":17.6,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12868859/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146112772","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Enamel decussation pattern originates from directional sliding of ameloblasts. 釉质讨论纹起源于成釉细胞的定向滑动。

IF 17.6 1区医学

International Journal of Oral Science Pub Date : 2026-02-03 DOI: 10.1038/s41368-025-00412-5

Vladislav Rakultsev, Josef Lavicky, Marcos Gonzalez Lopez, Klara Cigosova, Igor Adameyko, Jan Krivanek

{"title":"Enamel decussation pattern originates from directional sliding of ameloblasts.","authors":"Vladislav Rakultsev, Josef Lavicky, Marcos Gonzalez Lopez, Klara Cigosova, Igor Adameyko, Jan Krivanek","doi":"10.1038/s41368-025-00412-5","DOIUrl":"10.1038/s41368-025-00412-5","url":null,"abstract":"Enamel, the inorganic tissue covering the crowns of teeth, is known for its remarkable resilience and hardness. These properties originate from its high proportion of mineralized matrix and complex internal microarchitecture. On an ultrastructural level, it consists of directionally arranged enamel prisms. Continuously growing rodent incisors are an exemplary case of this phenomenon. Their enamel has a consistent decussation pattern, providing teeth with extremely high resistance and ensuring they remain constantly sharp. While the decussation pattern has been described in detail, mechanisms behind its formation have not been experimentally proven. Here, we show that the highly organized enamel micropattern is generated by directional epithelial sliding of enamel-forming ameloblasts in vivo. Our results detail how enamel micropatterning stems from individual cell cluster segregation and subsequent reciprocal interweaving. Based on this determination, we introduce and experimentally demonstrate a new model of enamel decussation pattern formation.","PeriodicalId":14191,"journal":{"name":"International Journal of Oral Science","volume":"18 1","pages":"7"},"PeriodicalIF":17.6,"publicationDate":"2026-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12864829/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146105281","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Cuproptosis promotes inflammatory osteolysis via GYS1-mediated glycogen metabolism. 铜质增生通过gys1介导的糖原代谢促进炎性溶骨。

IF 17.6 1区医学

International Journal of Oral Science Pub Date : 2026-02-03 DOI: 10.1038/s41368-025-00408-1

Lu Zhou, Hanqing Mao, Yuanhao Wen, Zhi Chen, Lu Zhang

{"title":"Cuproptosis promotes inflammatory osteolysis via GYS1-mediated glycogen metabolism.","authors":"Lu Zhou, Hanqing Mao, Yuanhao Wen, Zhi Chen, Lu Zhang","doi":"10.1038/s41368-025-00408-1","DOIUrl":"10.1038/s41368-025-00408-1","url":null,"abstract":"Copper, predominantly present in bones, plays a crucial role in bone formation. However, when copper homeostasis is disrupted, excessive copper can trigger harmful inflammation and a novel form of cell death known as cuproptosis. The impact of cuproptosis on bone metabolism remains unclear. In this study, we demonstrated that excessive copper acts as an aggravator in osteoclastogenesis and bone resorption. We observed that the expression levels of the copper importer SLC31A1 and dihydrolipoamide S-acetyltransferase (DLAT) were positively correlated with bone loss in both human chronic apical periodontitis (CAP) tissues and mouse CAP models. Untargeted metabolomics analysis and screening of glucose metabolism enzymes revealed that glycogen synthesis was inhibited during cuproptosis. Mechanistically, excessive copper hindered glycogen synthesis via glycogen synthase 1 (GYS1), which limited the availability of glycogenolysis-derived glucose-6-phosphate (G6P) flux into pentose phosphate pathway (PPP), and was unable to yield abundant NADPH to ensure high demand of glutathione (GSH) for macrophage survival. The inhibition of glycogen synthesis intensified cuproptosis and bone-resorption activity. Moreover, excessive copper bound to H3K27me3, which further epigenetically inhibited the gene transcription of GYS1, thereby affecting glycogen synthesis and exacerbating cuproptosis and bone resorption. Furthermore, the disruption of glycogen metabolism intensified cuproptosis and promoted inflammatory bone loss in vivo. Our finding highlighted the complex interplay among copper homeostasis, glycogen metabolism, and the osteo-immune system, suggesting new therapeutic strategies for managing inflammatory bone diseases and other copper accumulation-related conditions through the metabolic reprogramming of cells.","PeriodicalId":14191,"journal":{"name":"International Journal of Oral Science","volume":"18 1","pages":"13"},"PeriodicalIF":17.6,"publicationDate":"2026-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12864900/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146105013","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Partial-EMT in oral squamous cell carcinoma: molecular circuitry and clinical translation. 口腔鳞状细胞癌的部分emt：分子电路和临床翻译。

IF 14.9 1区医学

International Journal of Oral Science Pub Date : 2026-01-30 DOI: 10.1038/s41368-025-00417-0

Chunhua Wang,Motoharu Sarubo,Siqi Chen,Yasusei Kudo

{"title":"Partial-EMT in oral squamous cell carcinoma: molecular circuitry and clinical translation.","authors":"Chunhua Wang,Motoharu Sarubo,Siqi Chen,Yasusei Kudo","doi":"10.1038/s41368-025-00417-0","DOIUrl":"https://doi.org/10.1038/s41368-025-00417-0","url":null,"abstract":"Oral squamous cell carcinoma (OSCC) is a prevalent malignancy with high morbidity and mortality. Globally, about 400 000 people are affected, often with a poor quality of life. Its high mortality is mainly due to its aggressive growth and tendency to spread. Epithelial-mesenchymal transition (EMT) is a central regulatory hub driving tumor cell migration and invasion by enabling changes in cell characteristics. During EMT, epithelial cells gradually take on mesenchymal traits, gaining mobility and spreading more easily. Recent multi-omics studies show that many cancer cells exist in a hybrid or partial-EMT state, which lies between the full epithelial and mesenchymal forms. Cells in this state are especially invasive and metastatic, with high plasticity that promotes tumor progression. This review summarizes the role of partial-EMT in OSCC, with a focus on how it alters the tumor microenvironment (TME), promotes invasion and metastasis, and influences cancer stem cells (CSCs). We also highlight the link between partial-EMT and treatment resistance in OSCC. Based on these insights, we discuss therapeutic strategies targeting partial-EMT to improve outcomes. Targeting partial-EMT may offer promising strategies to enhance treatment effectiveness and improve patient survival and quality of life.","PeriodicalId":14191,"journal":{"name":"International Journal of Oral Science","volume":"281 1","pages":"15"},"PeriodicalIF":14.9,"publicationDate":"2026-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146073325","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Periodontitis-associated salivary microbiota exacerbates systemic osteoclastogenesis via gut modulation and tryptophan metabolism suppression in ovariectomized mice. 在去卵巢小鼠中，牙周炎相关的唾液微生物群通过肠道调节和色氨酸代谢抑制加剧了系统性破骨细胞的形成。

IF 17.6 1区医学

International Journal of Oral Science Pub Date : 2026-01-27 DOI: 10.1038/s41368-025-00415-2

Nannan Wang, Jun Qian, Min Wang, Lili Li, Wenzheng Liao, Rixin Chen, Hua Nie, Ruiyang Ge, Fangfang Sun, Fuhua Yan

{"title":"Periodontitis-associated salivary microbiota exacerbates systemic osteoclastogenesis via gut modulation and tryptophan metabolism suppression in ovariectomized mice.","authors":"Nannan Wang, Jun Qian, Min Wang, Lili Li, Wenzheng Liao, Rixin Chen, Hua Nie, Ruiyang Ge, Fangfang Sun, Fuhua Yan","doi":"10.1038/s41368-025-00415-2","DOIUrl":"10.1038/s41368-025-00415-2","url":null,"abstract":"Epidemiological studies have highlighted an association between periodontitis and osteoporosis. However, the mechanism underlining this association remains unclear. Here, we revealed significant differences in the salivary microbiota between periodontally healthy individuals and periodontitis patients, with periodontitis patients exhibiting increased salivary microbiota diversity and an elevated abundance of pathogenic bacteria. Using an ovariectomized (OVX) mouse model, we demonstrated that the salivary microbiota from periodontitis patients exacerbated bone destruction by modulating the gut microbiota. Metabolomic analysis revealed that the periodontitis-associated salivary microbiota suppressed tryptophan metabolism. The tryptophan metabolite indole-3-lactic acid (ILA) directly inhibited osteoclast formation and differentiation. In OVX mice treated with periodontitis salivary microbiota, supplementation with ILA effectively suppressed osteoclastogenesis and alleviated the detrimental effects of periodontitis-associated salivary microbiota on systemic bones. In summary, our data demonstrate that periodontitis can affect systemic bone metabolism via the oral-gut axis and that ILA supplementation serves as a potential therapeutic option to mitigate these adverse effects.","PeriodicalId":14191,"journal":{"name":"International Journal of Oral Science","volume":"18 1","pages":"14"},"PeriodicalIF":17.6,"publicationDate":"2026-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12834969/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146052024","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Expert consensus on the diagnosis and management of tooth developmental anomalies. 专家对牙齿发育异常的诊断和处理的共识。

IF 17.6 1区医学

International Journal of Oral Science Pub Date : 2026-01-20 DOI: 10.1038/s41368-025-00401-8

Jingxian Zhu, Mian Wan, Xiaohong Duan, Zhipeng Fan, Yao Sun, Xudong Wang, Shuguo Zheng, Liwei Zheng, Qinglin Zhu, Dong Chen, Jiewen Dai, Dong Han, Miao He, Cui Huang, Yuegui Jiang, Zhonglin Jia, Yihuai Pan, Yongchu Pan, Tiemei Wang, Wenmei Wang, Baoshan Xu, Wei Yin, Tingting Zhang, Yanli Zhang, Zhenjin Zhao, Zhuan Bian, Yaling Song

{"title":"Expert consensus on the diagnosis and management of tooth developmental anomalies.","authors":"Jingxian Zhu, Mian Wan, Xiaohong Duan, Zhipeng Fan, Yao Sun, Xudong Wang, Shuguo Zheng, Liwei Zheng, Qinglin Zhu, Dong Chen, Jiewen Dai, Dong Han, Miao He, Cui Huang, Yuegui Jiang, Zhonglin Jia, Yihuai Pan, Yongchu Pan, Tiemei Wang, Wenmei Wang, Baoshan Xu, Wei Yin, Tingting Zhang, Yanli Zhang, Zhenjin Zhao, Zhuan Bian, Yaling Song","doi":"10.1038/s41368-025-00401-8","DOIUrl":"10.1038/s41368-025-00401-8","url":null,"abstract":"Tooth developmental anomalies are a group of disorders caused by unfavorable factors affecting the tooth development process, resulting in abnormalities in tooth number, structure, and morphology. These anomalies typically manifest during childhood, impairing dental function, maxillofacial development, and facial aesthetics, while also potentially impacting overall physical and mental health. The complex etiology and diverse clinical phenotypes of these anomalies pose significant challenges for prevention, early diagnosis, and treatment. As they usually emerge early in life, long-term management and multidisciplinary collaboration in dental care are essential. However, there is currently a lack of systematic clinical guidelines for the diagnosis and treatment of these conditions, adding to the difficulties in clinical practice. In response to this need, this expert consensus summarizes the classifications, etiology, typical clinical manifestations, and diagnostic criteria of tooth developmental anomalies based on current clinical evidence. It also provides prevention strategies and stage-specific clinical management recommendations to guide clinicians in diagnosis and treatment, promoting early intervention and standardized care for these anomalies.","PeriodicalId":14191,"journal":{"name":"International Journal of Oral Science","volume":"18 1","pages":"12"},"PeriodicalIF":17.6,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12816143/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146002906","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Antisense oligonucleotide targeting TARDBP-EGFR splicing axis inhibits progression of oral squamous cell carcinoma through ABCA1-regulated cholesterol efflux. 靶向TARDBP-EGFR剪接轴的反义寡核苷酸通过abca1调节的胆固醇外排抑制口腔鳞状细胞癌的进展。

IF 14.9 1区医学

International Journal of Oral Science Pub Date : 2026-01-16 DOI: 10.1038/s41368-025-00402-7

Nan Ni,Moxu Wang,Zhiran Yuan,Leqi Zhang,Jilin Cai,Qingqing Du,Pengcheng Li,Chang Gao,Hanwen Zhang,Yuancheng Li,Hua Yuan

{"title":"Antisense oligonucleotide targeting TARDBP-EGFR splicing axis inhibits progression of oral squamous cell carcinoma through ABCA1-regulated cholesterol efflux.","authors":"Nan Ni,Moxu Wang,Zhiran Yuan,Leqi Zhang,Jilin Cai,Qingqing Du,Pengcheng Li,Chang Gao,Hanwen Zhang,Yuancheng Li,Hua Yuan","doi":"10.1038/s41368-025-00402-7","DOIUrl":"https://doi.org/10.1038/s41368-025-00402-7","url":null,"abstract":"Splice quantitative trait loci (sQTL) serve as another critical link between genetic variations and human diseases, besides expression quantitative trait loci (eQTL). Their role in oral squamous cell carcinoma (OSCC) development remains unexplored. We collected surgically resected cancer and adjacent normal epithelial tissue samples from 67 OSCC cases, and extracted RNA for sequencing after quality control. A genome-wide sQTL analysis was performed using the RNA sequencing data from 67 normal oral epithelial tissue samples. We included peripheral blood DNA samples from 1044 patients with OSCC and 3199 healthy controls to conduct a genome-wide association study. Systematic screening of sQTLs associated with OSCC risk identified a sQTL variant-the rs737540-T allele-independent of eQTLs, significantly associated with an increased risk of OSCC (OR = 1.2, P = 6.84 × 10-4). The rs737540-T allele reduced skipping of EGFR alternative exon 4 by enhancing TAR DNA binding protein (TARDBP) binding to the RNA sequence, leading to increased expression of the longer isoform (EGFR-001) and reduced expression of the truncated isoform (EGFR-004). Compared with EGFR-004, EGFR-001 promoted OSCC cell proliferation by reducing ATP-binding cassette subfamily A member 1 (ABCA1) ubiquitination through lower EGFR phosphorylation. ABCA1 was demonstrated to increase the cholesterol content of the plasma membrane via cholesterol efflux, thus affecting membrane fluidity and vimentin-mediated epithelial-mesenchymal transition. An antisense oligonucleotide targeting rs737540 significantly inhibited OSCC proliferation and reversed membrane cholesterol-induced resistance. This study provides novel insights into how genetic variants regulating alternative splicing contribute to OSCC risk and identifies potential therapeutic targets.","PeriodicalId":14191,"journal":{"name":"International Journal of Oral Science","volume":"34 1","pages":"10"},"PeriodicalIF":14.9,"publicationDate":"2026-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145971847","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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