International Journal of Oral Science最新文献

Community dynamics during de novo colonization of the nascent peri-implant sulcus 新生种植体周围沟重新定植期间的群落动态

IF 14.9 1区医学

International Journal of Oral Science Pub Date : 2025-04-29 DOI: 10.1038/s41368-025-00367-7

Tamires Pereira Dutra, Nicolas Robitaille, Khaled Altabtbaei, Shareef M. Dabdoub, Purnima S. Kumar

{"title":"Community dynamics during de novo colonization of the nascent peri-implant sulcus","authors":"Tamires Pereira Dutra, Nicolas Robitaille, Khaled Altabtbaei, Shareef M. Dabdoub, Purnima S. Kumar","doi":"10.1038/s41368-025-00367-7","DOIUrl":"https://doi.org/10.1038/s41368-025-00367-7","url":null,"abstract":"Dental implants have restored masticatory function to over 100 000 000 individuals, yet almost 1 000 000 implants fail each year due to peri-implantitis, a disease triggered by peri-implant microbial dysbiosis. Our ability to prevent and treat peri-implantitis is hampered by a paucity of knowledge of how these biomes are acquired and the factors that engender normobiosis. Therefore, we combined a 3-month interventional study of 15 systemically and periodontally healthy adults with whole genome sequencing, fine-scale enumeration and graph theoretics to interrogate colonization dynamics in the pristine peri-implant sulcus. We discovered that colonization trajectories of implants differ substantially from adjoining teeth in acquisition of new members and development of functional synergies. Source-tracking algorithms revealed that this niche is initially seeded by bacteria trapped within the coverscrew chamber during implant placement. These pioneer species stably colonize the microbiome and exert a sustained influence on the ecosystem by serving as anchors of influential hubs and by providing functions that enable cell replication and biofilm maturation. Unlike the periodontal microbiome, recruitment of new members to the peri-implant community occurs on nepotistic principles. Maturation is accompanied by a progressive increase in anaerobiosis, however, the predominant functionalities are oxygen-dependent over the 12-weeks. The peri-implant community is easily perturbed following crown placement, but demonstrates remarkable resilience; returning to pre-perturbation states within three weeks. This study highlights important differences in the development of the periodontal and peri-implant ecosystems, and signposts the importance of placing implants in periodontally healthy individuals or following the successful resolution of periodontal disease.","PeriodicalId":14191,"journal":{"name":"International Journal of Oral Science","volume":"35 1","pages":""},"PeriodicalIF":14.9,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143884708","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

Mandible-derived extracellular vesicles regulate early tooth development in miniature swine via targeting KDM2B 下颌骨来源的细胞外囊泡通过靶向KDM2B调控小型猪早期牙齿发育

IF 14.9 1区医学

International Journal of Oral Science Pub Date : 2025-04-27 DOI: 10.1038/s41368-025-00348-w

Ye Li, Meng Sun, Yi Ding, Ang Li

引用次数: 0

Single-cell sequencing systematically analyzed the mechanism of Emdogain on the restoration of delayed replantation periodontal membrane 单细胞测序系统分析 Emdogain 对延迟再植牙周膜修复的作用机制

IF 14.9 1区医学

International Journal of Oral Science Pub Date : 2025-04-17 DOI: 10.1038/s41368-024-00345-5

Yanyi Liu, Yuhao Peng, Lanhui Chen, Yangfan Xiang, Ximu Zhang, Jinlin Song

{"title":"Single-cell sequencing systematically analyzed the mechanism of Emdogain on the restoration of delayed replantation periodontal membrane","authors":"Yanyi Liu, Yuhao Peng, Lanhui Chen, Yangfan Xiang, Ximu Zhang, Jinlin Song","doi":"10.1038/s41368-024-00345-5","DOIUrl":"https://doi.org/10.1038/s41368-024-00345-5","url":null,"abstract":"The repair of the periodontal membrane is essential for the successful management of periodontal disease and dental trauma. Emdogain® (EMD) is widely used in periodontal therapy due to its ability to promote repair. Despite substantial research, the cellular and molecular mechanisms underlying EMD’s effects, particularly at the single-cell resolution, remain incompletely understood. This study established a delayed tooth replantation model in rats to investigate these aspects. Tooth loss rate and degree of loosening were evaluated at 4 and 8 weeks. Micro-CT, HE staining, TRAP staining, and immunofluorescence staining were evaluated to assess EMD’s efficacy. Single-cell sequencing analyses generated single-cell maps that explored enrichment pathways, cell communication, and potential repair mechanisms. Findings indicated that EMD could reduce the rate of tooth loss, promote periodontal membrane repair, and reduce root and bone resorption. Single-cell analysis revealed that EMD promotes the importance of Vtn+ fibroblasts, enhancing matrix and tissue regeneration functions. Additionally, EMD stimulated osteogenic pathways, reduced osteoclastic activity, and promoted angiogenesis-related pathways, particularly bone-related H-type vessel expression in endothelial cells. Gene modules associated with angiogenesis, osteogenesis, and odontoblast differentiation were identified, suggesting EMD might facilitate osteogenesis and odontoblast differentiation by upregulating endothelium-related genes. Immune cell analysis indicated that EMD did not elicit a significant immune response. Cell communication analysis suggested that EMD fostered pro-regenerative networks driven by interactions between mesenchymal stem cells, fibroblasts, and endothelial cells. In conclusion, EMD proves to be an effective root surface therapy agent that supports the restoration of delayed replantation teeth.","PeriodicalId":14191,"journal":{"name":"International Journal of Oral Science","volume":"5 1","pages":""},"PeriodicalIF":14.9,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143841306","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

Lysine-specific demethylase 1 controls key OSCC preneoplasia inducer STAT3 through CDK7 phosphorylation during oncogenic progression and immunosuppression 赖氨酸特异性去甲基化酶1通过CDK7磷酸化在肿瘤进展和免疫抑制过程中控制关键的OSCC瘤前病变诱导因子STAT3

IF 14.9 1区医学

International Journal of Oral Science Pub Date : 2025-04-17 DOI: 10.1038/s41368-025-00363-x

Amit Kumar Chakraborty, Rajnikant Dilip Raut, Kisa Iqbal, Chumki Choudhury, Thabet Alhousami, Sami Chogle, Alexa S. Acosta, Lana Fagman, Kelly Deabold, Marilia Takada, Bikash Sahay, Vikas Kumar, Manish V. Bais

{"title":"Lysine-specific demethylase 1 controls key OSCC preneoplasia inducer STAT3 through CDK7 phosphorylation during oncogenic progression and immunosuppression","authors":"Amit Kumar Chakraborty, Rajnikant Dilip Raut, Kisa Iqbal, Chumki Choudhury, Thabet Alhousami, Sami Chogle, Alexa S. Acosta, Lana Fagman, Kelly Deabold, Marilia Takada, Bikash Sahay, Vikas Kumar, Manish V. Bais","doi":"10.1038/s41368-025-00363-x","DOIUrl":"https://doi.org/10.1038/s41368-025-00363-x","url":null,"abstract":"Oral squamous cell carcinoma (OSCC) progresses from preneoplastic precursors via genetic and epigenetic alterations. Previous studies have focused on the treatment of terminally developed OSCC. However, the role of epigenetic regulators as therapeutic targets during the transition from preneoplastic precursors to OSCC has not been well studied. Our study identified lysine-specific demethylase 1 (LSD1) as a crucial promoter of OSCC, demonstrating that its knockout or pharmacological inhibition in mice reversed OSCC preneoplasia. LSD1 inhibition by SP2509 disrupted cell cycle, reduced immunosuppression, and enhanced CD4+ and CD8+ T-cell infiltration. In a feline model of spontaneous OSCC, a clinical LSD1 inhibitor (Seclidemstat or SP2577) was found to be safe and effectively inhibit the STAT3 network. Mechanistic studies revealed that LSD1 drives OSCC progression through STAT3 signaling, which is regulated by phosphorylation of the cell cycle mediator CDK7 and immunosuppressive CTLA4. Notably, LSD1 inhibition reduced the phosphorylation of CDK7 at Tyr170 and eIF4B at Ser422, offering insights into a novel mechanism by which LSD1 regulates the preneoplastic-to-OSCC transition. This study provides a deeper understanding of OSCC progression and highlights LSD1 as a potential therapeutic target for controlling OSCC progression from preneoplastic lesions.","PeriodicalId":14191,"journal":{"name":"International Journal of Oral Science","volume":"13 1","pages":""},"PeriodicalIF":14.9,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143841299","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

Dimethyl fumarate modulates M1/M2 macrophage polarization to ameliorate periodontal destruction by increasing TUFM-mediated mitophagy 富马酸二甲酯调节M1/M2巨噬细胞极化，通过增加tufm介导的线粒体自噬来改善牙周破坏

IF 14.9 1区医学

International Journal of Oral Science Pub Date : 2025-04-17 DOI: 10.1038/s41368-025-00360-0

Liang Chen, Pengxiao Hu, Xinhua Hong, Bin Li, Yifan Ping, ShuoMin Chen, Tianle Jiang, Haofu Jiang, Yixin Mao, Yang Chen, Zhongchen Song, Zhou Ye, Xiaoyu Sun, Shufan Zhao, Shengbin Huang

{"title":"Dimethyl fumarate modulates M1/M2 macrophage polarization to ameliorate periodontal destruction by increasing TUFM-mediated mitophagy","authors":"Liang Chen, Pengxiao Hu, Xinhua Hong, Bin Li, Yifan Ping, ShuoMin Chen, Tianle Jiang, Haofu Jiang, Yixin Mao, Yang Chen, Zhongchen Song, Zhou Ye, Xiaoyu Sun, Shufan Zhao, Shengbin Huang","doi":"10.1038/s41368-025-00360-0","DOIUrl":"https://doi.org/10.1038/s41368-025-00360-0","url":null,"abstract":"Periodontitis is a common oral disease characterized by progressive alveolar bone resorption and inflammation of the periodontal tissues. Dimethyl fumarate (DMF) has been used in the treatment of various immune-inflammatory diseases due to its excellent anti-inflammatory and antioxidant functions. Here, we investigated for the first time the therapeutic effect of DMF on periodontitis. In vivo studies showed that DMF significantly inhibited periodontal destruction, enhanced mitophagy, and decreased the M1/M2 macrophage ratio. In vitro studies showed that DMF inhibited macrophage polarization toward M1 macrophages and promoted polarization toward M2 macrophages, with improved mitochondrial function, inhibited oxidative stress, and increased mitophagy in RAW 264.7 cells. Furthermore, DMF increased intracellular mitochondrial Tu translation elongation factor (TUFM) levels to maintain mitochondrial homeostasis, promoted mitophagy, and modulated macrophage polarization, whereas TUFM knockdown decreased the protective effect of DMF. Finally, mechanistic studies showed that DMF increased intracellular TUFM levels by protecting TUFM from degradation via the ubiquitin-proteasomal degradation pathway. Our results demonstrate for the first time that DMF protects mitochondrial function and inhibits oxidative stress through TUFM-mediated mitophagy in macrophages, resulting in a shift in the balance of macrophage polarization, thereby attenuating periodontitis. Importantly, this study provides new insights into the prevention of periodontitis.","PeriodicalId":14191,"journal":{"name":"International Journal of Oral Science","volume":"22 1","pages":""},"PeriodicalIF":14.9,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143841302","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

Fibroblast derived C3 promotes the progression of experimental periodontitis through macrophage M1 polarization and osteoclast differentiation 成纤维细胞来源的C3通过巨噬细胞M1极化和破骨细胞分化促进实验性牙周炎的进展

IF 14.9 1区医学

International Journal of Oral Science Pub Date : 2025-04-17 DOI: 10.1038/s41368-025-00361-z

Feilong Ren, Shize Zheng, Huanyu Luo, Xiaoyi Yu, Xianjing Li, Shaoyi Song, Wenhuan Bu, Hongchen Sun

{"title":"Fibroblast derived C3 promotes the progression of experimental periodontitis through macrophage M1 polarization and osteoclast differentiation","authors":"Feilong Ren, Shize Zheng, Huanyu Luo, Xiaoyi Yu, Xianjing Li, Shaoyi Song, Wenhuan Bu, Hongchen Sun","doi":"10.1038/s41368-025-00361-z","DOIUrl":"https://doi.org/10.1038/s41368-025-00361-z","url":null,"abstract":"Complement C3 plays a critical role in periodontitis. However, its source, role and underlying mechanisms remain unclear. In our study, by analyzing single-cell sequencing data from mouse model of periodontitis, we identified that C3 is primarily derived from periodontal fibroblasts. Subsequently, we demonstrated that C3a has a detrimental effect in ligature-induced periodontitis. C3ar−/− mice exhibited significantly less destruction of periodontal support tissues compared to wild-type mice, characterized by mild gingival tissue damage and reduced alveolar bone loss. This reduction was associated with decreased production of pro-inflammatory mediators and reduced osteoclast infiltration in the periodontal tissues. Mechanistic studies suggested that C3a could promote macrophage polarization and osteoclast differentiation. Finally, by analyzing single-cell sequencing data from the periodontal tissues of patients with periodontitis, we found that the results observed in mice were consistent with human data. Therefore, our findings clearly demonstrate the destructive role of fibroblast-derived C3 in ligature-induced periodontitis, driven by macrophage M1 polarization and osteoclast differentiation. These data strongly support the feasibility of C3a-targeted interventions for the treatment of human periodontitis.","PeriodicalId":14191,"journal":{"name":"International Journal of Oral Science","volume":"2 1","pages":""},"PeriodicalIF":14.9,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143841300","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

NUP62 alleviates senescence and promotes the stemness of human dental pulp stem cells via NSD2-dependent epigenetic reprogramming NUP62通过依赖nsd2的表观遗传重编程，减轻人牙髓干细胞的衰老并促进其干性

IF 14.9 1区医学

International Journal of Oral Science Pub Date : 2025-04-17 DOI: 10.1038/s41368-025-00362-y

Xiping Wang, Li Wang, Linxi Zhou, Lu Chen, Jiayi Shi, Jing Ge, Sha Tian, Zihan Yang, Yuqiong Zhou, Qihao Yu, Jiacheng Jin, Chen Ding, Yihuai Pan, Duohong Zou

{"title":"NUP62 alleviates senescence and promotes the stemness of human dental pulp stem cells via NSD2-dependent epigenetic reprogramming","authors":"Xiping Wang, Li Wang, Linxi Zhou, Lu Chen, Jiayi Shi, Jing Ge, Sha Tian, Zihan Yang, Yuqiong Zhou, Qihao Yu, Jiacheng Jin, Chen Ding, Yihuai Pan, Duohong Zou","doi":"10.1038/s41368-025-00362-y","DOIUrl":"https://doi.org/10.1038/s41368-025-00362-y","url":null,"abstract":"Stem cells play a crucial role in maintaining tissue regenerative capacity and homeostasis. However, mechanisms associated with stem cell senescence require further investigation. In this study, we conducted a proteomic analysis of human dental pulp stem cells (HDPSCs) obtained from individuals of various ages. Our findings showed that the expression of NUP62 was decreased in aged HDPSCs. We discovered that NUP62 alleviated senescence-associated phenotypes and enhanced differentiation potential both in vitro and in vivo. Conversely, the knocking down of NUP62 expression aggravated the senescence-associated phenotypes and impaired the proliferation and migration capacity of HDPSCs. Through RNA-sequence and decoding the epigenomic landscapes remodeled induced by NUP62 overexpression, we found that NUP62 helps alleviate senescence in HDPSCs by enhancing the nuclear transport of the transcription factor E2F1. This, in turn, stimulates the transcription of the epigenetic enzyme NSD2. Finally, the overexpression of NUP62 influences the H3K36me2 and H3K36me3 modifications of anti-aging genes (HMGA1, HMGA2, and SIRT6). Our results demonstrated that NUP62 regulates the fate of HDPSCs via NSD2-dependent epigenetic reprogramming.","PeriodicalId":14191,"journal":{"name":"International Journal of Oral Science","volume":"4 1","pages":""},"PeriodicalIF":14.9,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143841303","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

IF 14.9 1区医学

International Journal of Oral Science Pub Date : 2025-04-17 DOI: 10.1038/s41368-025-00352-0

Shengjie Cui, Yanning Guo, Yu Fu, Ting Zhang, Jieni Zhang, Yehua Gan, Yanheng Zhou, Yan Gu, Eileen Gentleman, Yan Liu, Xuedong Wang

{"title":"Inflammation-related collagen fibril destruction contributes to temporomandibular joint disc displacement via NF-κB activation","authors":"Shengjie Cui, Yanning Guo, Yu Fu, Ting Zhang, Jieni Zhang, Yehua Gan, Yanheng Zhou, Yan Gu, Eileen Gentleman, Yan Liu, Xuedong Wang","doi":"10.1038/s41368-025-00352-0","DOIUrl":"https://doi.org/10.1038/s41368-025-00352-0","url":null,"abstract":"Temporomandibular joint (TMJ) disc displacement is one of the most significant subtypes of temporomandibular joint disorders, but its etiology and mechanism are poorly understood. In this study, we elucidated the mechanisms by which destruction of inflamed collagen fibrils induces alterations in the mechanical properties and positioning of the TMJ disc. By constructing a rat model of TMJ arthritis, we observed anteriorly dislocated TMJ discs with aggravated deformity in vivo from five weeks to six months after a local injection of Freund’s complete adjuvant. By mimicking inflammatory conditions with interleukin-1 beta in vitro, we observed enhanced expression of collagen-synthesis markers in primary TMJ disc cells cultured in a conventional two-dimensional environment. In contrast, three-dimensional (3D)-cultivated disc cell sheets demonstrated the disordered assembly of inflamed collagen fibrils, inappropriate arrangement, and decreased Young’s modulus. Mechanistically, inflammation-related activation of the nuclear factor kappa-B (NF-κB) pathway occurs during the progression of TMJ arthritis. NF-κB inhibition reduced the collagen fibril destruction in the inflamed disc cell sheets in vitro, and early NF-κB blockade alleviated collagen degeneration and dislocation of the TMJ discs in vivo. Therefore, the NF-κB pathway participates in the collagen remodeling in inflamed TMJ discs, offering a potential therapeutic target for disc displacement.","PeriodicalId":14191,"journal":{"name":"International Journal of Oral Science","volume":"263 1","pages":""},"PeriodicalIF":14.9,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143841301","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

Programmed death-ligand 1 regulates ameloblastoma growth and recurrence 程序性死亡配体1调节成釉细胞瘤的生长和复发

IF 14.9 1区医学

International Journal of Oral Science Pub Date : 2025-04-16 DOI: 10.1038/s41368-025-00364-w

Linzhou Zhang, Hao Lin, Jiajie Liang, Xuanhao Liu, Chenxi Zhang, Qiwen Man, Ruifang Li, Yi Zhao, Bing Liu

{"title":"Programmed death-ligand 1 regulates ameloblastoma growth and recurrence","authors":"Linzhou Zhang, Hao Lin, Jiajie Liang, Xuanhao Liu, Chenxi Zhang, Qiwen Man, Ruifang Li, Yi Zhao, Bing Liu","doi":"10.1038/s41368-025-00364-w","DOIUrl":"https://doi.org/10.1038/s41368-025-00364-w","url":null,"abstract":"Tumor cell-intrinsic programmed death-ligand 1 (PD-L1) signals mediate tumor initiation, progression and metastasis, but their effects in ameloblastoma (AM) have not been reported. In this comprehensive study, we observed marked upregulation of PD-L1 in AM tissues and revealed the robust correlation between elevated PD-L1 expression and increased tumor growth and recurrence rates. Notably, we found that PD-L1 overexpression markedly increased self-renewal capacity and promoted tumorigenic processes and invasion in hTERT+-AM cells, whereas genetic ablation of PD-L1 exerted opposing inhibitory effects. By performing high-resolution single-cell profiling and thorough immunohistochemical analyses in AM patients, we delineated the intricate cellular landscape and elucidated the mechanisms underlying the aggressive phenotype and unfavorable prognosis of these tumors. Our findings revealed that hTERT+-AM cells with upregulated PD-L1 expression exhibit increased proliferative potential and stem-like attributes and undergo partial epithelial‒mesenchymal transition. This phenotypic shift is induced by the activation of the PI3K-AKT-mTOR signaling axis; thus, this study revealed a crucial regulatory mechanism that fuels tumor growth and recurrence. Importantly, targeted inhibition of the PD-L1-PI3K-AKT-mTOR signaling axis significantly suppressed the growth of AM patient-derived tumor organoids, highlighting the potential of PD-L1 blockade as a promising therapeutic approach for AM.","PeriodicalId":14191,"journal":{"name":"International Journal of Oral Science","volume":"6 1","pages":""},"PeriodicalIF":14.9,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143836978","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

Expert consensus on orthodontic treatment of patients with periodontal disease 牙周病患者正畸治疗的专家共识

IF 14.9 1区医学

International Journal of Oral Science Pub Date : 2025-04-03 DOI: 10.1038/s41368-025-00356-w

Wenjie Zhong, Chenchen Zhou, Yuanyuan Yin, Ge Feng, Zhihe Zhao, Yaping Pan, Yuxing Bai, Zuolin Jin, Yan Xu, Bing Fang, Yi Liu, Hong He, Faming Chen, Weiran Li, Shaohua Ge, Ang Li, Yi Ding, Lili Chen, Fuhua Yan, Jinlin Song

{"title":"Expert consensus on orthodontic treatment of patients with periodontal disease","authors":"Wenjie Zhong, Chenchen Zhou, Yuanyuan Yin, Ge Feng, Zhihe Zhao, Yaping Pan, Yuxing Bai, Zuolin Jin, Yan Xu, Bing Fang, Yi Liu, Hong He, Faming Chen, Weiran Li, Shaohua Ge, Ang Li, Yi Ding, Lili Chen, Fuhua Yan, Jinlin Song","doi":"10.1038/s41368-025-00356-w","DOIUrl":"https://doi.org/10.1038/s41368-025-00356-w","url":null,"abstract":"Patients with periodontal disease often require combined periodontal-orthodontic interventions to restore periodontal health, function, and aesthetics, ensuring both patient satisfaction and long-term stability. Managing these patients involving orthodontic tooth movement can be particularly challenging due to compromised periodontal soft and hard tissues, especially in severe cases. Therefore, close collaboration between orthodontists and periodontists for comprehensive diagnosis and sequential treatment, along with diligent patient compliance throughout the entire process, is crucial for achieving favorable treatment outcomes. Moreover, long-term orthodontic retention and periodontal follow-up are essential to sustain treatment success. This expert consensus, informed by the latest clinical research and practical experience, addresses clinical considerations for orthodontic treatment of periodontal patients, delineating indications, objectives, procedures, and principles with the aim of providing clear and practical guidance for clinical practitioners.","PeriodicalId":14191,"journal":{"name":"International Journal of Oral Science","volume":"32 1","pages":""},"PeriodicalIF":14.9,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143766627","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