Journal of periodontal research最新文献

{"title":"Treatment Options for the Management of the Postextraction Socket: Report From the First Giuseppe Cardaropoli Foundation Consensus Conference.","authors":"Daniele Cardaropoli, Mauricio Araujo, Daniel Buser, Ueli Grunder, Joseph Kan, Robert A Levine, Mariano Sanz, Giovanni Zucchelli, Otto Zuhr, Søren Jepsen","doi":"10.1111/jre.13385","DOIUrl":"https://doi.org/10.1111/jre.13385","url":null,"abstract":"<p><strong>Aim: </strong>Different approaches have been proposed for implant placement following tooth extraction. A Consensus conference was organised to provide expert-based recommendations for the treatment of the postextraction site in the aesthetic zone in conjunction with implant therapy.</p><p><strong>Methods: </strong>A panel of eight experts with a documented longstanding clinical and research experience in the field of implant therapy in the aesthetic zone were invited to participate in a structured survey. Participants were asked to select their preferred treatment approach for different clinical scenarios of the postextraction site from a list of different treatment options. Results were summarised and discussed in person at a 2 day consensus conference. Based on the outcome, treatment recommendations were phrased and are reported here.</p><p><strong>Results: </strong>The group agreed that in case of an intact alveolus, immediate implant placement with immediate prosthetics represents the reference choice if proper primary stability can be achieved and the buccal bone plate is present. A bone-to-implant gap more than 2 mm should be seeked and grafted. Alveolar ridge preservation and early placement with contour augmentation may represent an alternative. If the alveolus is compromised, a staged approach (early or delayed placement) with bone augmentation may be preferred.</p><p><strong>Conclusions: </strong>The characteristics of the site, in terms of the available bone volume, the integrity of the buccal bone plate and the periodontal phenotype are determining factors in the therapeutic choice. Therefore, case selection based on well-defined selection criteria is extremely important and is the adequate way to guide the clinician in choosing the most appropriate approach to postextraction site management and timing for implant placement.</p>","PeriodicalId":16715,"journal":{"name":"Journal of periodontal research","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143501998","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Xanthine Derivative KMUP-3 Alleviates Periodontal Bone Resorption by Inhibiting Osteoclastogenesis and Macrophage Pyroptosis.","authors":"Shang-En Huang, Kai-Fang Hu, Meng-Xuan Lin, Ching-Jiunn Tseng, Bin-Nan Wu, Zen-Kong Dai, Jong-Hau Hsu, Jwu-Lai Yeh","doi":"10.1111/jre.13393","DOIUrl":"https://doi.org/10.1111/jre.13393","url":null,"abstract":"<p><strong>Aim: </strong>This study investigated the function effects of KMUP-3, a self-developed synthetic xanthine-based derivative, in suppressing Porphyromonas gingivalis (Pg-LPS)-aggravated osteoclastogenesis and pyroptosis as a potential treatment for periodontitis.</p><p><strong>Methods: </strong>In vitro, the effects of Pg-LPS and KMUP-3 on osteoclast formation and macrophage pyroptosis were investigated using the receptor activator of nuclear factor-κB ligand (RANKL)-primed RAW264.7 macrophages. In vivo, the therapeutic effects of KMUP-3 were evaluated in a model of experimental periodontitis induced by gingival ligature placement.</p><p><strong>Results: </strong>We reveal that KMUP-3 suppressed osteoclastogenesis, inducible nitric oxide synthase activation, and reduced nitric oxide production enhanced by Pg-LPS in RANKL-primed RAW264.7 cells while also decreasing TLR4/NF-κB p65 pathway activation and decreased pro-inflammatory cytokine production; moreover, Pg-LPS promoted NLRP3 activation and exacerbated pyroptosis induction effects that were abolished by KMUP-3. Finally, KMUP-3 ameliorated alveolar bone loss and IL-1β levels in the gingival crevicular fluid in the rat ligature periodontitis model.</p><p><strong>Conclusions: </strong>Our study demonstrated that KMUP-3 attenuates Pg-LPS-enhanced osteoclastogenesis and macrophage pyroptosis. Notably, KMUP-3 alleviates alveolar bone loss in experimental periodontitis rats and thus suggests its certain role in safeguarding against periodontal bone resorption.</p>","PeriodicalId":16715,"journal":{"name":"Journal of periodontal research","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143502020","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Toll-Like Receptor 7 Promotes Periodontal Inflammation and Alveolar Bone Resorption Through the NF-κB Signaling Pathway.","authors":"Rui Jing, Jiawei Lu, Ruiling Wang, Zehui Xiong, Yanan Yang, Lijun Luo","doi":"10.1111/jre.13394","DOIUrl":"https://doi.org/10.1111/jre.13394","url":null,"abstract":"<p><strong>Aim: </strong>To investigate the role of Toll-like receptor 7 (TLR7) in periodontitis and its potential mechanisms.</p><p><strong>Methods: </strong>TLR7 expression in periodontal tissues was analyzed using GEO database single-cell sequencing data and confirmed with gingival samples from healthy individuals and periodontitis patients. In vivo, a mouse model of periodontitis was used to assess the effect of M5049, the TLR7's inhibitor, on alveolar bone loss and inflammation. In vitro, mouse bone marrow-derived macrophages (BMDMs) were treated with Imiquimod to activate TLR7. The inflammatory response was further evaluated using Pg-LPS-stimulated BMDMs, with TLR7 knockdown and NF-κB inhibition by PDTC.</p><p><strong>Results: </strong>TLR7 expression in the gingival tissues of periodontitis patients was significantly elevated compared to healthy gingival tissues. In vivo, TLR7 inhibition reduced bone loss and inflammation, with decreased osteoclast formation and cytokine expression. In vitro, activation of TLR7 heightened inflammation; conversely, TLR7 knockdown and NF-κB inhibition diminished cytokine expression, suggesting a role for NF-κB in TLR7-mediated inflammatory responses.</p><p><strong>Conclusion: </strong>TLR7 is upregulated in periodontitis and may promote the progression of the disease by activating the NF-κB signaling pathway, potentially serving as a therapeutic target. The findings reveal a novel role for TLR7 in periodontitis and highlight the TLR7-NF-κB axis as a key pathway in disease pathogenesis, with broader implications for understanding and treating inflammatory conditions.</p>","PeriodicalId":16715,"journal":{"name":"Journal of periodontal research","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143501992","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Association of Intake of Vitamin Mixtures With Periodontitis: A Machine Learning Approach on NHANES.","authors":"Qinglian Zhang, Hanxin Que, Shengming Xu, Leyan Xu, Jian Lin, Hui Deng, Ke Deng, Yi Wang","doi":"10.1111/jre.13387","DOIUrl":"https://doi.org/10.1111/jre.13387","url":null,"abstract":"<p><strong>Aims: </strong>Previous studies have focused on the association of single vitamin intake with periodontitis. However, the consumption of vitamins is commonly in the form of mixtures. The relationship between the consumption of multiple vitamins and the prevalence of periodontitis needs to be investigated.</p><p><strong>Methods: </strong>In this cross-sectional study, 8512 participants with full-mouth periodontal examination records and vitamin intake (vitamins A, B₁, B₂, B₆, B₁₂, C, D, E, and K) data from the US National Health and Nutrition Examination Survey (NHANES, 2009-2014) datasets were included. GLM and Bayesian kernel machine regression (BKMR) were used to estimate the association of individual and mixed vitamins with periodontitis, respectively. Sensitivity analyses were performed using mean probing depth and mean clinical attachment loss as continuous indicators of periodontitis severity.</p><p><strong>Results: </strong>Vitamins A (OR = 0.90, 95% CI: 0.95-0.99) and E (OR = 0.95, 95% CI: 0.93-0.97) were both negatively associated with periodontitis in GLM estimates and BKMR modeling in the context of vitamin mixtures. Moreover, the intake of vitamin mixtures within a certain range (< 75% percentile) was negatively associated with the estimated risk of periodontitis, which was predominantly driven by vitamins A and E. A potential interaction between vitamins A and E in their association with periodontitis was observed. Similar findings were found in sensitive analyses.</p><p><strong>Conclusions: </strong>BKMR estimates suggested that higher intake of vitamin mixtures might account for decreased odds of periodontitis, with vitamins A and E identified as the most influential factors. Future studies are highly warranted to clarify the underlying mechanisms.</p>","PeriodicalId":16715,"journal":{"name":"Journal of periodontal research","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143483562","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Implant Dentistry: The Past, the Present, the Future","authors":"Niklaus P. Lang","doi":"10.1111/jre.13388","DOIUrl":"10.1111/jre.13388","url":null,"abstract":"","PeriodicalId":16715,"journal":{"name":"Journal of periodontal research","volume":"60 2","pages":"97-100"},"PeriodicalIF":3.4,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143468331","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Amyloid-β and Bacterial Lipopolysaccharide at Implants With Peri-Implantitis: Ex Vivo Colocalization and Decontamination Protocol.","authors":"Manuel Toledano-Osorio, Carolina Cifuentes-Jiménez, Manuel Toledano, Mariano Sanz, Osorio Raquel","doi":"10.1111/jre.13386","DOIUrl":"https://doi.org/10.1111/jre.13386","url":null,"abstract":"<p><strong>Aim: </strong>To study the differential presence of amyloid-β and bacterial lipopolysaccharide (LPS) in freshly extracted titanium implants, either affected by peri-implantitis (PI) or explanted by other causes, and to address a method for removal LPS and amyloid-β from contaminated surfaces.</p><p><strong>Methods: </strong>Twenty-four explanted implants were harvested from patients with (n = 12) or without (n = 12) peri-implantitis, and their surfaces were analyzed by attenuated total reflectance (ATR) and Fourier transform infrared spectroscopy (FTIR) to localize amyloid-β and LPS. Presence of amyloid-β on the implants surfaces was further analyzed by light microscopy after specific amyloid staining with Congo red. Titanium discs were contaminated with LPS and amyloid-β, these discs as well as six contaminated implants were treated with 0.25% NaOCl to assess its decontamination ability.</p><p><strong>Results: </strong>LPS and amyloid-β were observed at PI affected implant surfaces, but not in implants extracted by other causes. 0.25% NaOCl application was an efficient method for removing LPS and amyloid-β from titanium surfaces.</p><p><strong>Conclusions: </strong>The concurrent presence of LPS and amyloid-β on the surface of implants affected by PI was demonstrated and it may act as potential comediators of PI inflammatory process. Eliminating these products from implants surfaces is possible after a proteolytic agent (0.25% NaOCl) application.</p>","PeriodicalId":16715,"journal":{"name":"Journal of periodontal research","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143440468","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Extracellular Vesicles From Dental Pulp Cells Promote Osteogenic Differentiation in Periodontal Ligament Cells.","authors":"Yuwang Li, Fenglan Li, Haitao Liu, Limei Li, Jie Hao","doi":"10.1111/jre.13390","DOIUrl":"https://doi.org/10.1111/jre.13390","url":null,"abstract":"<p><strong>Aim: </strong>Periodontal osseous defects are mainly caused by periodontitis, which seriously affects the quality of patient life. Dental pulp cells (DpCs)-derived extracellular vesicles (EVs) can effectively promote tissue regeneration. Homeobox A9 (HOXA9) mRNA is abundant in EVs derived from DSCs, which may be related to promoting alveolar bone regeneration, but the specific mechanism is unclear. We aimed to elucidate the mechanism through which HOXA9 from DPCs-derived EVs can impact the osteogenic differentiation of periodontal ligament cells (PDLCs).</p><p><strong>Methods: </strong>DPCs-derived EVs were isolated and characterized by transmission electron microscopy (TEM), nanoparticle tracking analysis (NTA), and western blot. Lipopolysaccharide (LPS) was employed to induce the inflammatory environment. Cell viability was assessed by CCK8 assay. Calcium deposition was determined by Alizarin red staining. H3K27ac enrichment in the FLI1 enhancer region and the interaction between C/EBPα, HOXA9, and FLI1 were analyzed by ChIP assay. The interaction between HOXA9 and FLI1 enhancer in 293T cells was analyzed by dual luciferase reporter gene assay.</p><p><strong>Results: </strong>DPCs-derived EVs promoted PDLC osteogenesis under LPS treatment and increased HOXA9 expression in PDLCs. HOXA9 knockdown in DPCs reversed the promoting effect of DPCs-derived EVs on PDLC osteogenic differentiation. HOXA9 from DPCs-derived EVs promoted H3K27ac enrichment in the FLI1 enhancer region by facilitating HOXA9 competitively binding FLI1 enhancer region with C/EBPα. Moreover, HOXA9 from DPCs-derived EVs promoted PDLC osteogenesis by activating the PI3K/AKT pathway through upregulating FLI1.</p><p><strong>Conclusion: </strong>HOXA9 from DPCs-derived EVs promoted PDLC osteogenic differentiation by activating the PI3K/AKT pathway through promoting H3K27ac enrichment in the FLI1 enhancer region and upregulating FLI1. Our study identified a previously unknown mechanism that HOXA9/FLI1 signaling axis participates in the processes of EVs derived from DPCs to treat bone tissue injury. Our research presents a theoretical basis for using EVs derived from DPCs to treat bone tissue injury.</p>","PeriodicalId":16715,"journal":{"name":"Journal of periodontal research","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143365215","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Novel Gene DUSP8 Missense Mutation Causes Nonsyndromic Hereditary Gingival Fibromatosis by Dysregulating Lysine Lactylation.","authors":"Xiu Liu, Chao Liang, Shengnan Wang, Xuejiu Wang, Xiaobing Guan, Ying Hu","doi":"10.1111/jre.13391","DOIUrl":"https://doi.org/10.1111/jre.13391","url":null,"abstract":"<p><strong>Aims: </strong>The goal of this study was to explore new candidate genes and pathogenesis mechanisms of nonsyndromic hereditary gingival fibromatosis (nsHGF) and to provide an experimental basis for the diagnosis of nsHGF.</p><p><strong>Methods: </strong>Whole-exome sequencing (WES) was performed on peripheral blood DNA from three nsHGF family members to screen for new candidate genes, and Sanger sequencing and related databases were used to verify the pathogenicity of this gene deficiency. Moreover, the effects of gene deficiency on the biological characteristics of human gingival fibroblasts (HGFs) were evaluated via cell proliferation assays, extracellular matrix (ECM) deposition detection, cell apoptosis and cell cycle assessment, cell migration and gene expression analyses.</p><p><strong>Results: </strong>A novel missense mutation in dual-specificity phosphatase 8 (DUSP8, c.1348C>T, p.R450C), which is in the nsHGF-related GINGF4 locus, was identified via WES analysis. A functional study revealed that knocking down DUSP8 expression increased cell proliferation, cell migration and the expression of profibrotic factors (particularly COL1A1), inhibited cell apoptosis, and ultimately resulted in nsHGF. Similarly, this DUSP8 mutation inhibited the expression of the encoded protein and promoted cell proliferation and the expression of profibrotic factors. In addition, both DUSP8 knockdown and DUSP8 mutation induced nsHGF by accelerating glycolysis and panlysine lactylation (Kla) to promote cell proliferation and the expression of ECM-related factors.</p><p><strong>Conclusion: </strong>DUSP8 deficiency might be a novel pathogenic factor that contributes to nsHGF.</p>","PeriodicalId":16715,"journal":{"name":"Journal of periodontal research","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143066337","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A BiO-Optimizing Site Targeted (BOOST) Approach to Periodontal Regeneration Through Local Doxycycline Prior to Surgery: A Randomized Clinical Trial.","authors":"Mario Aimetti, Giacomo Baima, Virginia Lorenzetti, Nargiz Aliyeva, Mario Bottone, Giulia Maria Mariani, Federica Romano","doi":"10.1111/jre.13389","DOIUrl":"https://doi.org/10.1111/jre.13389","url":null,"abstract":"<p><strong>Aim: </strong>To test a BiO-Optimizing Site Targeted (BOOST) approach to periodontal regeneration by the adjunctive use of locally delivered doxycycline (DOX) 2 weeks prior to minimally invasive surgery in terms of clinical and radiographic outcomes at 1 year.</p><p><strong>Methods: </strong>For this randomized clinical trial, stage III/IV periodontitis patients presenting sites with intrabony defects and bleeding on probing (BoP+) after steps 1-2 of periodontal treatment were included. Sites were treated via subgingival instrumentation with or without a BOOST approach by local DOX. After 2 weeks, defects were accessed by minimally invasive surgical technique with xenograft and amelogenins. Primary (clinical attachment level [CAL] gain) and secondary (probing pocket depth [PPD] reduction, composite outcomes, radiographic bone defect fill) outcomes were assessed at 12 months.</p><p><strong>Results: </strong>Sixty patients completed the study (30 on each group). BOOST led to lower preoperative BoP (p < 0.001) and better wound healing after surgery (p = 0.027). Both groups showed clinical and radiographic improvements at 1 year, with significant differences in mean CAL gain (4.1 ± 1.9 vs. 3.2 ± 2.0 mm; p = 0.019) and PPD reduction (4.4 ± 1.8 vs. 3.6 ± 1.9 mm; p = 0.040) favoring the test group. BOOST group also achieved higher composite outcome measure (PPD ≤ 4 mm and CAL gain ≥ 3; 83.3% vs. 46.7%; p = 0.006), pocket closure (PPD ≤ 3 mm or 4 mm BoP-; 83.3% vs. 60.0%; p = 0.045), and defect fill (3.5 ± 1.2 vs. 2.7 ± 1.3 mm; p < 0.001) compared to the control group.</p><p><strong>Conclusion: </strong>A BOOST approach by local doxycycline 2 weeks before surgery enhanced the local inflammatory control prior to periodontal regeneration and post-operative early wound healing, yielding to improved clinical and radiographic outcomes at 1 year.</p><p><strong>Trial registration: </strong>ClinicalTrials.gov identifier: NCT05878353.</p>","PeriodicalId":16715,"journal":{"name":"Journal of periodontal research","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143046979","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Periodontitis Exacerbates Colorectal Cancer by Altering Gut Microbiota-Derived Metabolomics in Mice.","authors":"Xiaoxue Wang, Zhichao Li, Haiquan Zhou, Qianyi Liu, Xueyang Zhang, Fei Hu","doi":"10.1111/jre.13380","DOIUrl":"https://doi.org/10.1111/jre.13380","url":null,"abstract":"<p><strong>Aim: </strong>The correlation between periodontitis and colorectal cancer (CRC) has drawn widespread attention. However, how periodontitis affects CRC progression remains unclear.</p><p><strong>Methods: </strong>C57BL/6 mice were used to establish experimental periodontitis and CRC model. Histological alterations of periodontium and colon were observed by hematoxylin and eosin staining. Micro-computed tomography (micro-CT) was applied to evaluate alveolar bone loss (ABL). Tumor growth was detected by immunofluorescence. Gut bacteria were analyzed using 16S rRNA sequencing. Gas chromatography-mass spectrometry (GC-MS) was performed to observe the alterations of gut microbial metabolites. The detection of associated pathways was carried out using quantitative real-time PCR (qRT-PCR).</p><p><strong>Results: </strong>Experimental periodontitis significantly induced increases in tumor number in mice with CRC. Double immunofluorescence for Ki67 and β-catenin, as well as Cyclin D1 and β-catenin, indicated that experimental periodontitis observably promoted tumor growth. 16S rRNA sequencing and untargeted metabolomics analysis displayed that experimental periodontitis altered gut microbial community and metabolite profiles in CRC mice. Notably, we found that experimental periodontitis dramatically increased the level of three oncometabolites (serotonin, adenosine, and spermine) in mice with CRC.</p><p><strong>Conclusion: </strong>Alterations of gut microbial community and metabolites might be relevant in experimental periodontitis deteriorating CRC.</p>","PeriodicalId":16715,"journal":{"name":"Journal of periodontal research","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143023566","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}