Journal of Dental Research最新文献

{"title":"Dysbiotic Microbiome–Metabolome Axis in Childhood Obesity and Metabolic Syndrome","authors":"U. Salman, S.M. Dabdoub, A. Reyes, A. Sidahmed, K. Weber-Gasperoni, R. Brown, I.A. Evans, E. Taylor, A. Mangalam, L. Kanner, V. Curtis, S.M. Ganesan","doi":"10.1177/00220345251336129","DOIUrl":"https://doi.org/10.1177/00220345251336129","url":null,"abstract":"The prevalence of childhood metabolic syndrome (MetS) and obesity is rising, with emerging evidence suggesting these conditions negatively affect oral health. However, the underlying molecular determinants are unclear. This study investigated the oral microbiome, inflammatory markers, and metabolites in children with obesity and MetS to explore the interrelationships between systemic disease and oral health. We recruited 76 periodontally healthy, caries-free individuals aged 10 to 17 y into 3 groups: MetS (29), metabolically healthy obesity (MHO) (30), and normal-weight healthy (NWH) controls (17). Unstimulated saliva was collected. Bacterial DNA was isolated, V3–V4 regions amplified, and 16S sequencing performed on the Illumina MiSeq platform. Sequences were annotated against the HOMD database. Multiplex assays quantified adipokines and cytokines, with significance determined by Tukey honestly significant difference. Gas chromatography/mass spectrometry identified metabolite peaks that were annotated against the Small Molecule Pathway Database, with enrichment analysis determining significance. Integrated multiomics analysis was performed using multiblock sparse partial least squares regression discriminant analysis. The MHO and MetS groups demonstrated lower abundances of <jats:italic>Streptococcus</jats:italic> , <jats:italic>Actinomyces</jats:italic> , and <jats:italic>Schaalia</jats:italic> and higher levels of <jats:italic>Aggregatibacter</jats:italic> , <jats:italic>Campylobacter</jats:italic> , <jats:italic>Alloprevotella</jats:italic> , <jats:italic>Prevotella</jats:italic> , <jats:italic>Leptotrichia</jats:italic> , and <jats:italic>Porphyromonas</jats:italic> compared with NWH, despite similar clinical oral status in all cohorts. MetS and MHO also had increased leptin, tumor necrosis factor–α, interleukin (IL)–1β, and IL-15 and decreased adiponectin levels versus NWH. Disease-associated metabolites, including glutamate, cholesterol, isoleucine, tyrosine, phenylalanine, serine, and indoleacetic acid, were significantly enriched in the MetS and MHO groups. Integrated multiomic analysis identified key correlations in the saliva of subjects with metabolic health or disease. Decreases in health-associated species and increases in proinflammatory cytokines and disease-associated metabolites in the saliva of MetS and obese adolescents with clinical oral health indicate an “at-risk” environment, potentially explaining their elevated risk for oral diseases. Increased salivary leptin and decreased adiponectin levels highlight the potential of saliva as a noninvasive biomarker source for childhood MetS.","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":"52 1","pages":""},"PeriodicalIF":7.6,"publicationDate":"2025-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144188836","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}

{"title":"Epithelial YAP1 Regulates Ameloblast Differentiation through SHH/FGF Signaling","authors":"Y. Zheng, Y. Qu, H. Liu, H. Huang, J. Li, M. Qiu, F. Li","doi":"10.1177/00220345251336164","DOIUrl":"https://doi.org/10.1177/00220345251336164","url":null,"abstract":"Enamel produced by ameloblasts derived from the oral epithelium is the hardest and most mineralized tissue. Developmental enamel defects have significant clinical implications, such as enamel hypoplasia or opacities, increased tooth sensitivity, and impaired mastication. <jats:italic>Yap1</jats:italic> is a transcriptional coactivator that has been shown to be involved in regulating cell proliferation and differentiation. Although <jats:italic>Yap1</jats:italic> has been reported to play an important role in tooth development, the mechanism by which <jats:italic>Yap1</jats:italic> regulates enamel formation and ameloblast differentiation remains unclear. In this study, we report that ablation of <jats:italic>Yap1</jats:italic> in the dental epithelium using <jats:italic> Pitx2 <jats:sup>Cre</jats:sup> </jats:italic> leads to the defect of enamel formation. In the <jats:italic> Yap1 <jats:sup>Pitx2Cre</jats:sup> </jats:italic> mutant incisors, the expression of <jats:italic>Amelx</jats:italic> , <jats:italic>Ambn</jats:italic> , and <jats:italic>Mmp20</jats:italic> was greatly reduced in ameloblasts, indicating a defect in ameloblast differentiation. The proliferation of epithelial and mesenchymal cells was significantly reduced in <jats:italic> Yap1 <jats:sup>Pitx2Cre</jats:sup> </jats:italic> mutant incisors; however, there was no significant difference in apoptosis between wild type and mutant. Transcriptome analysis and in situ hybridization identified that <jats:italic>Shh</jats:italic> , <jats:italic>Ptch1</jats:italic> , <jats:italic>Fgf3</jats:italic> , <jats:italic>Fgf10</jats:italic> , <jats:italic>Etv4</jats:italic> , and <jats:italic>Etv5</jats:italic> were significantly downregulated after <jats:italic>Yap1</jats:italic> deletion. In the labial cervical loop of <jats:italic> Yap1 <jats:sup>Pitx2Cre</jats:sup> </jats:italic> mutant incisors, both SHH signaling and FGF signaling were significantly decreased. Furthermore, our results suggest that FGF signaling is regulated by SHH. SHH treatment induces <jats:italic>Fgf3</jats:italic> expression in vitro, and activation of the hedgehog pathway upregulates FGF signaling in vivo. Overexpression of <jats:italic>Ihh</jats:italic> attenuates enamel formation and cell proliferation defects caused by <jats:italic>Yap1</jats:italic> deletion, confirming the genetic integration of Hedgehog signaling. In summary, our study shows that epithelial <jats:italic>Yap1</jats:italic> may regulate ameloblast differentiation by modulating SHH/FGF signaling.","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":"9 1","pages":""},"PeriodicalIF":7.6,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144183854","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}

{"title":"The IADR and AADOCR Policy Statement on Tobacco Industry-Funded Research.","authors":"P Arany,M Charles-Ayinde,F Cieplik,N Damé-Teixeira,T Do,X Li,H Priya,B Wu,Y-H Yu,C Fox","doi":"10.1177/00220345251326085","DOIUrl":"https://doi.org/10.1177/00220345251326085","url":null,"abstract":"","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":"30 1","pages":"220345251326085"},"PeriodicalIF":7.6,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144087770","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}

{"title":"Practice-Based Study on CAD/CAM Inlays, Onlays, and Crowns: Longevity and Risks.","authors":"R J Wierichs,E J Kramer,B Reiss,M M Laske,N Opdam,S Abou-Ayash","doi":"10.1177/00220345251332882","DOIUrl":"https://doi.org/10.1177/00220345251332882","url":null,"abstract":"This prospective, multicenter, practice-based cohort study aimed to analyze factors associated with the success of all-ceramic inlays, onlays, and crowns. All-ceramic indirect restorations placed in a practice-based research network (Ceramic Success Analysis) were analyzed. Data were evaluated from 12,468 patients with restorations manufactured by CAD/CAM (computer-aided design/computer-aided manufacturing) and placed between 1994 and 2023 by 303 dentists. Restorations with at least 1 follow-up visit were included (n = 17,725). Additionally, restorations were followed for ≥5 y, and all failures were included (n = 4,635). At the last follow-up visit, crown restorations were classified as successful if no intervention was required (e.g., no renewal, repair, or recementation). Failure included lost restorations and those needing any reintervention. Multilevel Cox proportional hazards models were used to evaluate the association between a range of predictors and time of success or survival. Within a mean (SD) follow-up of 3.3 y (3.5; all-years scenario) and 8.6 y (3.7; 5-y scenario; maximum, 25 y), 940 restorations failed (annual failure rate: 5 y, 2.7%). The main failure types were fracture of the ceramic (n = 151), endodontic complications (n = 87), and fracture of the tooth (n = 77). In both scenarios, endodontic treatment (hazard ratio [95% CI]: 5 y, 1.6 [1.4 to 1.9]), a positive papilla bleeding index (1.2 [1.1 to 1.4]), and use of an EVA instrument (1.8 [1.4 to 2.0]) significantly increased the failure rate as compared with nonpresence/nonuse (P ≤ 0.043). Furthermore, ZrO2 (0.6 [0.4 to 0.9]) significantly increased the time until any failure (P = 0.027). For CAD/CAM-manufactured all-ceramic restorations, high success rates could be found up to 25 y. Furthermore, after 8 y, tooth-, technique-, and material-level factors were significantly associated with failure (German Clinical Trials Register DRKS00020271).","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":"36 1","pages":"220345251332882"},"PeriodicalIF":7.6,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144065922","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}

{"title":"PTX3 Deficiency Aggravates Periodontitis by the Complement C5a-C5aR1 Axis.","authors":"W Dong,D Guo,C Yang,Q Xu,J Wang","doi":"10.1177/00220345251329027","DOIUrl":"https://doi.org/10.1177/00220345251329027","url":null,"abstract":"Dysregulation of the complement system plays a critical role in periodontitis progression. In addition to the harmful effects of biofilm, aberrant expression of complement regulatory proteins is also a potential cause of periodontitis. Pentraxin 3 (PTX3) is involved in complement activation and regulation, seeking a balance between amplifying complement-mediated immune responses and avoiding complement-mediated tissue damage. However, its role in periodontitis remains unexplored. This study aimed to investigate the effects of PTX3 on inflammation onset and resolution, with a particular emphasis on its complement regulatory function. We found that PTX3 is predominantly expressed in human and mouse inflammatory monocytes and is significantly upregulated during periodontitis. In vivo experiments showed that PTX3 deficiency led to the accumulation of complement C5a, massive infiltration of inflammatory monocytes, and alveolar bone loss in a ligation-induced mouse periodontitis model. Inhibition of C5a signaling with PMX53 or NLRP3 inflammasome with MCC950 significantly alleviated these adverse effects. In addition, PTX3 deficiency delayed the resolution of inflammation and alveolar bone repair during the recovery phase of periodontitis. In vitro studies showed that PTX3 deficiency promoted C5a conversion and release in monocytes, thereby activating the NLRP3 inflammasome via the C5a-C5aR1 axis-mediated mitogen-activated protein kinase and nuclear factor κB signaling in an inflammatory environment. In conclusion, these data elucidate the link between PTX3 in regulating complement activation and periodontitis progression, providing a potential target for innate immune-based therapy of periodontitis.","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":"28 1","pages":"220345251329027"},"PeriodicalIF":7.6,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144065920","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}

{"title":"Richard Ranney, a Visionary Academician","authors":"J.C. Gunsolley, P. Ranney, K.G. Palcanis, B.J. Sessle","doi":"10.1177/00220345251329327","DOIUrl":"https://doi.org/10.1177/00220345251329327","url":null,"abstract":"It is with sadness that we report the passing of Richard (Dick) R. Ranney, DDS, MS, on November 13, 2024, at the age of 85. Dick conducted significant and unique research on early-onset periodontitis, focusing on the clinical, microbiological, and immunological aspects of the disease. He was a dean of 2 dental schools, University of Alabama at Birmingham School of Dentistry and University of Maryland Baltimore School of Dentistry. He served as the president of the American Association for Dental, Oral, and Craniofacial Research from 1990–1991 and president of the International Association for Dental, Oral, and Craniofacial Research from 1995–1996.","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":"4 1","pages":""},"PeriodicalIF":7.6,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144067155","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}

{"title":"The Functional Impact of the Noncoding SNP rs3741442 on Orofacial Clefting.","authors":"N Funato,S R F Twigg","doi":"10.1177/00220345251334385","DOIUrl":"https://doi.org/10.1177/00220345251334385","url":null,"abstract":"Orofacial cleft (OFC) is a common congenital anomaly in humans with variable birth prevalence in different ethnic groups. Although genome-wide association studies (GWAS) have identified single nucleotide polymorphisms (SNPs) associated with nonsyndromic OFC (nsOFC), understanding of the underlying biological mechanisms of causative SNPs and genes in nsOFC remains limited. Here, we report that the noncoding SNP, rs3741442, has an expression quantitative trait locus (eQTL) effect on epithelial genes associated with periderm differentiation. Using a combination of epigenetic markers and in silico analysis, we prioritized the intergenic SNP rs3741442 as a potential causal factor in nsOFC. The risk allele of rs3741442 is prevalent in East Asian populations, and its presence in CRISPR-edited cells leads to reduced expression of neighboring KRT18 and EIF4B. The transcription factor SP1 differentially binds the risk versus nonrisk alleles of rs3741442. Alongside this cis-eQTL impact, rs3741442 has a trans-eQTL effect on the epithelial gene TP63 that is associated with syndromic forms of OFC and psoriasis. These findings provide insights into the mechanism by which an intergenic SNP can affect palatogenesis through the modulation of gene expression.","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":"13 1","pages":"220345251334385"},"PeriodicalIF":7.6,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143932902","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}

{"title":"Oral Health Characteristics 2 Years following Allogeneic Cell Transplant.","authors":"L I Leinbach,S Boroumand,L R Masuch,J T Nguyen,S M Ganesan,J W Mays","doi":"10.1177/00220345251329351","DOIUrl":"https://doi.org/10.1177/00220345251329351","url":null,"abstract":"Allogeneic hematopoietic cell transplantation (allo-HCT) is a treatment modality for cancers and hematopoietic disorders. The number of allo-HCT survivors is increasing in the United States. Allo-HCT is associated with oral health problems that can affect the quality of posttransplantation life. We characterize clinical and patient-reported oral health outcomes from the time of allo-HCT through 2 y following transplantation among a contemporary cohort of patients transplanted between 2019 and 2022. This prospective cohort study analyzed data from participants enrolled in a contemporary allo-HCT natural history study (ClinicalTrials.gov ID: NCT03602599). Clinical characteristics and patient-reported outcomes were captured at 3, 6, 12, 18, and 24 mo post-HCT. Descriptive and bivariable statistics were calculated. Sixty HCT participants were included in the final analysis. Differences were observed in oral pain, oral dryness, diet quality, difficulty swallowing, taste disturbances, and feelings of embarrassment from time of transplantation through the follow-up period. At 2 y, 47.5% of participants reported oral pain, and 44.1% reported xerostomia. Quality-of-life reductions related to taste, pain, and uncomfortable chewing were also observed after 2 y. Oral health problems and reductions in oral health-related quality of life were reported 2 y after allo-HCT. These findings support a tailored approach to oral health care among recipients of allo-HCT. Providing comprehensive and sustained oral health care for this patient population is essential.Knowledge Transfer StatementThis study found time-specific changes in patient-reported symptoms, oral health status, and quality of life that persisted 2 y after allo-HCT. It also suggests that specific attention to long-term oral health care among this patient population remains warranted.","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":"2 1","pages":"220345251329351"},"PeriodicalIF":7.6,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143932879","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}

{"title":"Durable Dentin Bonding with Multifunctional Methacrylated Proanthocyanidins.","authors":"V Hass,N Wickerhauser,N Desch,Y Li,R Wang,Z Peng,Y Wang","doi":"10.1177/00220345251332271","DOIUrl":"https://doi.org/10.1177/00220345251332271","url":null,"abstract":"The degradation of dentin bonding interfaces by enzymes, either originating from the dentin matrix or produced by oral biofilms, contributes to the failure of composite restorations. Proanthocyanidins (PAs) are effective collagen crosslinkers that help preserve collagen, but their interference with adhesive polymerization impairs clinical applications. Methacrylate-functionalized PA (MAPA) was developed as a polymerizable collagen crosslinker, designed to strengthen collagen while copolymerizing with adhesives. This study evaluated the effects of MAPA-containing adhesives on dentin-bonding properties, including collagen crosslinking within bonding interfaces (via sodium dodecyl sulfate-collagen hybridizing peptide assay), microtensile bond strength (µTBS), and collagenolytic activity (in situ zymography) at 24 h and after 2 y (2Y), as well as on biofilm inhibition. Two adhesives, Scotchbond Universal and Prime&Bond Elect, were modified with MAPA or PA at 0%, 5%, and 10% concentrations. Human molar dentin surfaces were bonded and restored using composite resin, then sectioned into sticks or slabs for µTBS and in situ zymography at 24 h or 2Y. Additional specimens were evaluated for biofilm formation (Streptococcus mutans) using live/dead staining, MTT assay, and colony-forming unit counts. Data were analyzed using 2-way analysis of variance and Games-Howell set at 5%. Results showed that MAPA effectively enhanced chemical crosslinking within bonding interfaces without affecting µTBS at 24 h (P > 0.05). Notably, 5%MAPA significantly stabilized bonding interfaces over 2Y (P > 0.05) compared with other groups. All MAPA groups demonstrated a significant reduction in collagenolytic activity (P < 0.05), with 5%MAPA maintaining this effect after 2Y (P > 0.05). In addition, MAPA reduced biofilm formation. MAPA's capacity to copolymerize with adhesives while forming strong chemical interactions with collagen creates a durable, chemically integrated polymer-collagen complex that resists enzymatic degradation and inhibits cariogenic bacterial activity. Incorporating MAPA into adhesives stabilizes bonding interfaces and provides antibiofilm benefits, offering a promising approach to extending the longevity of composite restorations.","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":"3 1","pages":"220345251332271"},"PeriodicalIF":7.6,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143932878","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}

{"title":"The Role of Gut Microbiome in Temporomandibular Joint Disorder Pathogenesis.","authors":"Y Jiang,J Zhou,L Huang,Y Bai,Z Zhang","doi":"10.1177/00220345251332885","DOIUrl":"https://doi.org/10.1177/00220345251332885","url":null,"abstract":"Due to the unclear etiology and pathogenesis of temporomandibular joint disorders (TMDs), current treatments often fail to provide long-term relief or halt disease progression. Therefore, this study aims to explore the underlying etiologic mechanisms by focusing on the causal relationship between the gut microbiome (GM) and TMD through a multi-omics approach. This includes mendelian randomization (MR) analysis of GM, metabolomics, and TMD data, as well as transcriptomic analysis. In accordance with MR guidelines, we utilized summary-level genome-wide association study data to perform bidirectional MR, identifying 28 gut microbial taxa with causal effects on TMD. The following species had the strongest associations with TMD incidence: RUG147 sp900315495 (odds ratio [OR], 2.016; 95% CI, 1.219 to 3.333; P = 0.006), CAG-194 sp002441865 (OR, 0.713; 95% CI, 0.555 to 0.916; P = 0.008), CAG-145 sp000435615 (OR, 1.166; 95% CI, 1.040 to 1.308; P = 0.009), and CAG-81 sp000435795 (OR, 1.150; 95% CI, 1.036 to 1.276; P = 0.009). To explore the mediating role of metabolites, a 2-step mediation MR approach was employed, revealing that lipid-related metabolites serve as key mediators in the GM-TMD interaction. Specifically, total cholesterol in high-density lipoprotein 3 was identified as a mediator of CAG-145 sp000435615 on TMD (-4.13%). Further analysis based on transcriptomic data identified differentially expressed and shared genes between GM and TMD, with the AGE-RAGE (advanced glycation end products-receptor for advanced glycation end products) and processes related to cell adhesion and inflammation emerging as significant pathways. These findings highlight the role of GM dysbiosis in TMD pathogenesis, potentially through disruptions in lipid metabolism and inflammatory processes, suggesting new therapeutic strategies targeting GM and its associated pathways.","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":"26 1","pages":"220345251332885"},"PeriodicalIF":7.6,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143932877","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}