Journal of dental research最新文献

{"title":"Dynamics of Human Palatal Wound Healing and the Associated Microbiome.","authors":"H Yuan, G E Chlipala, H I Bangash, R Meenakshi, D Chen, H M Trivedi, L A DiPietro, P Gajendrareddy, L Chen","doi":"10.1177/00220345241288761","DOIUrl":"10.1177/00220345241288761","url":null,"abstract":"<p><p>Wound healing in the oral mucosa is superior to that in the skin, with faster wound closure accompanied by reduced inflammation, less angiogenesis, and minimal scar formation. A well-characterized oral wound model is critical to investigating the mechanisms of oral wound closure and the efficacy of various clinical interventions. Currently, there are a few human oral wound models, although none of them are well characterized. In the present study, we describe and characterize a human hard palate wound healing model. A 3.5-mm circular and two 1 × 5-mm rectangular full-thickness wounds were made in the first and second molar region, 5 mm from the gingival margin, on the hard palate of human subjects. The circular wound was used to monitor wound closure and collect swabs for a microbiome analysis via 16s rRNA sequencing. The rectangular wounds were biopsied and the tissue was used to evaluate the gene expression of wound healing-related mediators by real-time polymerase chain reaction. Saliva was also collected to examine the protein levels of similar molecules by enzyme-linked immunosorbent assays. Circular wounds were nearly closed on day 7 after wounding. Significant changes in the gene expression of inflammatory cytokines, growth factors, antimicrobial peptides, and extracellular matrix-related molecules were identified in day 1 and day 3 wound tissue and compared with unwounded tissue on day 0. Changes in the protein levels of various mediators were limited in the saliva. In addition, alpha diversity, beta diversity, and differential microbiome analysis demonstrated significant changes in bacterial colonization of the wound surface over time compared with unwounded mucosa. In summary, we comprehensively characterize a human hard palate wound-healing model that details the dynamic changes of wound closure, levels of wound healing-related mediators in the wound and saliva, and the oral wound microbiome.</p>","PeriodicalId":94075,"journal":{"name":"Journal of dental research","volume":" ","pages":"97-105"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11667194/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142775779","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dynamics of Mucosal Integration of Machined versus Anodized Titanium Implants.","authors":"J Dworan, F Aellos, J A Grauer, G Fabbri, K G Harder, S Boccardo, P L Cuevas, I Dawid, M Vicini, J A Helms","doi":"10.1177/00220345241296506","DOIUrl":"https://doi.org/10.1177/00220345241296506","url":null,"abstract":"<p><p>The long-term success of dental implants depends on the ability of soft tissues to form a protective barrier, limiting pathogen infiltration into peri-implant tissues. Here, we investigated the impact of an anodized surface modification on mucosal integration. Scanning electron microscopy and surface chemistry characterization were carried out on miniaturized implants. Following placement in fresh extraction sockets of mice, peri-implant tissues were examined at 4 time points. Histology along with quantitative immunohistochemistry for Keratin14, Vimentin, Laminin5, and CD68 were carried out on postimplant day (PID) 3 to assess early events in soft-tissue repair; on PID7, when peri-implant epithelialization was complete; at PID14, when osseointegration was complete; and at PID28, when soft-tissue maturation was nearing completion. In all cases, an intact junctional epithelium served as a reference. These analyses supported 3 conclusions: first, maturation of the peri-implant epithelium (PIE) is a protracted process, consistent with clinical observations. Second, maturation of the soft tissue-implant interface is slower than maturation of the bone-implant interface. Third, there is a benefit, albeit transient, to soft-tissue maturation around an anodized implant surface. Given its prolonged time course, strategies to improve and/or accelerate PIE maturation are likely to have significant clinical benefit.</p>","PeriodicalId":94075,"journal":{"name":"Journal of dental research","volume":" ","pages":"220345241296506"},"PeriodicalIF":0.0,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142866325","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting Epigenetic Dysregulations in Head and Neck Squamous Cell Carcinoma.","authors":"Y Li, C Lu","doi":"10.1177/00220345241297122","DOIUrl":"https://doi.org/10.1177/00220345241297122","url":null,"abstract":"<p><p>Head and neck squamous cell carcinoma (HNSCC) is one of the deadliest human cancers, with the overall 5-year survival rate stagnating in recent decades due to the lack of innovative treatment approaches. Apart from the recently Food and Drug Administration-approved epidermal growth factor receptor inhibitor and immune checkpoint inhibitor, alternative therapeutic strategies that target epigenetic abnormalities, an emerging cancer hallmark, remain to be fully explored. A pathological epigenetic landscape, characterized by widespread reprogramming of chromatin modifications such as DNA methylation and histone modifications, which drives transcription deregulation and genome reorganization, has been extensively documented in numerous cancers, including HNSCC. Growing evidence indicates that these frequent epigenomic alterations play pivotal roles in regulating malignant transformation, promoting metastasis and invasion, and reshaping the tumor microenvironment. Furthermore, these epigenetic changes also present unique vulnerabilities that open new avenues for identifying novel prognostic biomarkers and developing targeted antitumor therapies. In this review, we summarize recent discoveries of epigenetic dysregulations in HNSCC, with a focus on deregulated chromatin modifications, which include aberrant DNA methylation, oncohistone H3 lysine 36 to methionine (H3K36M) mutation, as well as recurrent mutations or altered expression of chromatin-modifying enzymes such as NSD1, EZH2, and KMT2C/D. Importantly, we discuss the various molecular mechanisms underlying the contributions of these epigenetic alterations to HNSCC development, particularly their involvement in deregulated cell proliferation and cell death, metabolic reprogramming, tumor immune evasion, and phenotypic plasticity. Finally, we conclude by highlighting the translational and clinical implications of targeting the epigenetic machinery, which offers promising prospects for overcoming resistance to conventional radiotherapy/chemotherapy and enhancing the response to immunotherapy in HNSCC.</p>","PeriodicalId":94075,"journal":{"name":"Journal of dental research","volume":" ","pages":"220345241297122"},"PeriodicalIF":0.0,"publicationDate":"2024-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142857398","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multiancestry Genome-Wide Association Study of Early Childhood Caries.","authors":"P Shrestha, M Graff, Y Gu, Y Wang, C L Avery, J Ginnis, M A Simancas-Pallares, A G Ferreira Zandoná, R N Alotaibi, E Orlova, H S Ahn, K N Nguyen, H M Highland, D Y Lin, J S Preisser, G D Slade, M L Marazita, K E North, K Divaris","doi":"10.1177/00220345241291528","DOIUrl":"10.1177/00220345241291528","url":null,"abstract":"<p><p>Early childhood caries (ECC) is the most common noncommunicable childhood disease-an important health problem with known environmental and social/behavioral influences lacking consensus genetic risk loci. To address this knowledge gap, we conducted a genome-wide association study of ECC in a multiancestry population of U.S. preschool-age children (<i>N</i> = 6,103) ages 3 to 5 y participating in a community-based epidemiologic study of early childhood oral health. Calibrated examiners used International Caries Detection and Assessment System criteria to measure ECC; the primary trait was the number of primary tooth surfaces with caries experience (i.e., dmfs index). We estimated heritability and concordance rates and conducted genome-wide association analyses to estimate overall genetic effects as well as stratified by sex, household water fluoride, and dietary sugar and leveraged combined gene/gene-environment effects using 2-degree-of-freedom joint tests. Common genetic variants explained 24% of ECC phenotypic variance among unrelated individuals, while concordance rates were 0.64 (95% confidence interval [CI] = 0.42-0.79) among monozygotic twins and 0.44 (95% CI = 0.34-0.53) among first-degree relatives. Across all analyses, we identified 21 novel nonoverlapping genome-wide significant loci (<i>P</i> < 5 × 10^-8) and 1 genome-wide significant gene (<i>TAAR6</i>) associated with ECC. The taste receptor activity gene set, with known roles in chemosensing, bacterial recognition, and innate immunity in the oral cavity, was strongly associated with ECC. While no locus remained significant after studywise multiple-testing correction, 3 loci were nominally significant (<i>P</i> < 0.05) and directionally consistent in external cohorts of 285,248 adults (rs1442369, <i>DLGAP1</i> and rs74606067, <i>RP11-856F16.2</i>) and 18,994 children (rs71327750, <i>SLC41A3</i>). Meanwhile, the strongest marker known to be associated with adult caries (rs1122171, tagging the long noncoding RNA <i>PITX1-AS1</i>) was nominally significant (<i>P</i> = 0.01) and directionally consistent with ECC in our study. Taken together, the results of this study add to the genomics knowledge base for early childhood caries, offer several plausible candidates for future mechanistic studies, and underscore the importance of accounting for sex and pertinent environmental exposures in genetic investigations.</p>","PeriodicalId":94075,"journal":{"name":"Journal of dental research","volume":" ","pages":"220345241291528"},"PeriodicalIF":0.0,"publicationDate":"2024-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142857396","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Early Childhood Exposures to Fluorides and Cognitive Neurodevelopment: A Population-Based Longitudinal Study.","authors":"L G Do, A Sawyer, A John Spencer, S Leary, J K Kuring, A L Jones, T Le, C E Reece, D H Ha","doi":"10.1177/00220345241299352","DOIUrl":"https://doi.org/10.1177/00220345241299352","url":null,"abstract":"<p><p>It is important to maintain confidence in the risk and benefit balance of major caries-preventive programs using fluoride. The ongoing debate about potential effects of early-life exposures to fluoride on cognitive neurodevelopment requires high-quality scientific evidence. This study aimed to investigate the potential effects of fluoride exposure on cognitive neurodevelopment assessed with the Wechsler Adult Intelligence Scale 4th edition (WAIS-IV) in an Australian population-based sample. The sample was selected from the National Child Oral Health Study (NCOHS) 2012-2014. NCOHS collected data on socioeconomic factors, oral health behaviors, and residential history to estimate percentage lifetime exposure to fluoridated water during the first 5 y of life (%LEFW). NCOHS children were also examined by trained and calibrated examiners to assess dental fluorosis (a reliable and valid individual biomarker of total fluoride intake during early childhood). The sample was followed up in 2022-2023 to collect data on cognitive neurodevelopment (intelligence quotient [IQ]) using the WAIS-IV, which was administered by trained and calibrated qualified psychologists. Multivariable regression models were generated to investigate associations between the 2 exposure measurements (%LEFW and dental fluorosis) with full-scale IQ (FSIQ) scores, controlling for important confounding effects. Hypotheses of noninferiority were also tested, contrasting different levels of exposure to fluoride. Some 357 participants aged 16 to 26 y completed the WAIS-IV, with a mean FSIQ score of 109.2 (95% confidence interval [CI]: 107.8-110.5). The estimates of the multivariable regression models demonstrated slightly higher FSIQ scores among the exposed than the nonexposed. The adjusted β of 100%LEFW versus 0%LEFW was 1.07 (95% CI: -2.86, 5.01) and of having dental fluorosis versus no fluorosis was 0.28 (95% CI: -3.00, 3.57). The hypothesis of noninferiority tests found that FSIQ scores of those exposed and nonexposed to fluoride were equivalent. The study provided consistent evidence that early childhood exposure to fluoride does not have effects on cognitive neurodevelopment.</p>","PeriodicalId":94075,"journal":{"name":"Journal of dental research","volume":" ","pages":"220345241299352"},"PeriodicalIF":0.0,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142848485","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Detecting Mandible Fractures in CBCT Scans Using a 3-Stage Neural Network.","authors":"N van Nistelrooij, S Schitter, P van Lierop, K El Ghoul, D König, M Hanisch, A Tel, T Xi, D G E Thiem, R Smeets, L Dubois, T Flügge, B van Ginneken, S Bergé, S Vinayahalingam","doi":"10.1177/00220345241256618","DOIUrl":"10.1177/00220345241256618","url":null,"abstract":"<p><p>After nasal bone fractures, fractures of the mandible are the most frequently encountered injuries of the facial skeleton. Accurate identification of fracture locations is critical for effectively managing these injuries. To address this need, JawFracNet, an innovative artificial intelligence method, has been developed to enable automated detection of mandibular fractures in cone-beam computed tomography (CBCT) scans. JawFracNet employs a 3-stage neural network model that processes 3-dimensional patches from a CBCT scan. Stage 1 predicts a segmentation mask of the mandible in a patch, which is subsequently used in stage 2 to predict a segmentation of the fractures and in stage 3 to classify whether the patch contains any fracture. The final output of JawFracNet is the fracture segmentation of the entire scan, obtained by aggregating and unifying voxel-level and patch-level predictions. A total of 164 CBCT scans without mandibular fractures and 171 CBCT scans with mandibular fractures were included in this study. Evaluation of JawFracNet demonstrated a precision of 0.978 and a sensitivity of 0.956 in detecting mandibular fractures. The current study proposes the first benchmark for mandibular fracture detection in CBCT scans. Straightforward replication is promoted by publicly sharing the code and providing access to JawFracNet on grand-challenge.org.</p>","PeriodicalId":94075,"journal":{"name":"Journal of dental research","volume":" ","pages":"1384-1391"},"PeriodicalIF":0.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11633064/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141444001","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advanced Imaging in Dental Research: From Gene Mapping to AI Global Data.","authors":"D T Graves, S E Uribe","doi":"10.1177/00220345241293040","DOIUrl":"10.1177/00220345241293040","url":null,"abstract":"<p><p>Advances in imaging technologies combined with artificial intelligence (AI) are transforming dental, oral, and craniofacial research. This editorial highlights breakthroughs ranging from gene expression mapping to visualizing the availability of global AI data, providing new insights into biological complexity and clinical applications.</p>","PeriodicalId":94075,"journal":{"name":"Journal of dental research","volume":" ","pages":"1329-1330"},"PeriodicalIF":0.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11633075/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142515370","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ultrasonographic Evaluation of Vascular Response to Mechanical Compression during Induced Gingival Inflammation.","authors":"J Woo, O Kripfgans, I-C Wang, A Samal, A R Betancourt, J C Fenno, H-L Chan","doi":"10.1177/00220345241286807","DOIUrl":"10.1177/00220345241286807","url":null,"abstract":"<p><p>The aim of this study was to evaluate the gingival vascular response to mechanical compression during inflammation using ultrasonography. Four female and 4 male Sinclair mini pigs 18 mo of age were included in the study. Pathogenic bacteria-impregnated silk ligatures were placed around the third premolars (PM3), fourth premolars (PM4), and first molars (M1). Ligatures were placed per quadrant at 2-wk intervals in random order. Ultrasonographic study was performed at 2-wk intervals following baseline until the 10th week. Brightness mode (B-mode) images and color flow cine loops were captured at 2 different conditions: 1 with only coupling gel between the ultrasound transducer and the mucosal surface and 1 with the transducer compressing the mucosal surface. The compression was visually adjusted until minimal to no blood flow was detected in color-flow mode. Compression was facilitated using a solid gel pad attached to the transducer. Strain values were obtained from B-mode images of the gel pad and plotted versus study weeks. The <i>t</i> test comparisons were obtained to the baseline (week 0). Data from female and male pigs were plotted and analyzed separately for comparison. Gel pad strain increased with peak around week 4 and gradually decreased in both sexes. In male pigs, the increase in strain was statistically significant in weeks 2, 4, and 6 of all teeth regions and week 8 of PM4 and M1 regions. In female pigs, the increase in strain was significant in only week 4 of PM4. Higher strain required for stoppage of blood flow implies increased gingival blood flow with inflammation, which corresponds with previous studies. Considerably smaller changes in gel pad strain were noted from female pigs, indicating a smaller increase in gingival blood flow compared with males. This study demonstrated a possible application of intraoral ultrasonography for assessment of gingival inflammation.</p>","PeriodicalId":94075,"journal":{"name":"Journal of dental research","volume":" ","pages":"1403-1411"},"PeriodicalIF":0.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11653338/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142712106","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Spatial Transcriptomics Unravel the Tissue Complexity of Oral Pathogenesis.","authors":"J Haller, N Abedi, A Hafedi, O Shehab, M S Wietecha","doi":"10.1177/00220345241271934","DOIUrl":"10.1177/00220345241271934","url":null,"abstract":"<p><p>Spatial transcriptomics (ST) is a cutting-edge methodology that enables the simultaneous profiling of global gene expression and spatial information within histological tissue sections. Traditional transcriptomic methods lack the spatial resolution required to sufficiently examine the complex interrelationships between cellular regions in diseased and healthy tissue states. We review the general workflows for ST, from specimen processing to ST data analysis and interpretations of the ST dataset using visualizations and cell deconvolution approaches. We show how recent studies used ST to explore the development or pathogenesis of specific craniofacial regions, including the cranium, palate, salivary glands, tongue, floor of mouth, oropharynx, and periodontium. Analyses of cranial suture patency and palatal fusion during development using ST identified spatial patterns of bone morphogenetic protein in sutures and osteogenic differentiation pathways in the palate, in addition to the discovery of several genes expressed at critical locations during craniofacial development. ST of salivary glands from patients with Sjögren's disease revealed co-localization of autoimmune antigens with ductal cells and a subpopulation of acinar cells that was specifically depleted by the dysregulated autoimmune response. ST of head and neck lesions, such as premalignant leukoplakia progressing to established oral squamous cell carcinomas, oral cancers with perineural invasions, and oropharyngeal lesions associated with HPV infection spatially profiled the complex tumor microenvironment, showing functionally important gene signatures of tumor cell differentiation, invasion, and nontumor cell dysregulation within patient biopsies. ST also enabled the localization of periodontal disease-associated gene expression signatures within gingival tissues, including genes involved in inflammation, and the discovery of a fibroblast subtype mediating the transition between innate and adaptive immune responses in periodontitis. The increased use of ST, especially in conjunction with single-cell analyses, promises to improve our understandings of craniofacial development and pathogenesis at unprecedented tissue-level resolution in both space and time.</p>","PeriodicalId":94075,"journal":{"name":"Journal of dental research","volume":" ","pages":"1331-1339"},"PeriodicalIF":0.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11653320/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142396341","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Spatial Multi-omics Reveals the Role of the Wnt Modulator, Dkk2, in Palatogenesis'.","authors":"J O Piña, R Raju, D M Roth, E W Winchester, C Padilla, J Iben, F R Faucz, J L Cotney, R N D'Souza","doi":"10.1177/00220345241256600","DOIUrl":"10.1177/00220345241256600","url":null,"abstract":"<p><p>Multiple genetic and environmental etiologies contribute to the pathogenesis of cleft palate, which is the most common of the inherited disorders of the craniofacial complex. Insights into the molecular mechanisms regulating osteogenic differentiation and patterning in the palate during embryogenesis are limited and needed for the development of innovative diagnostics and cures. This study used the <i>Pax9</i>^-/- mouse model with a consistent phenotype of cleft secondary palate to investigate the role of <i>Pax9</i> in the process of palatal osteogenesis. Although prior research has identified the upregulation of Wnt pathway modulators <i>Dkk1</i> and <i>Dkk2</i> in <i>Pax9</i>^-/- palate mesenchyme, limitations of spatial resolution and technology restricted a more robust analysis. Here, data from single-nucleus transcriptomics and chromatin accessibility assays validated by in situ highly multiplex targeted single-cell spatial profiling technology suggest a distinct relationship between <i>Pax9+</i> and osteogenic populations. Loss of <i>Pax9</i> results in spatially restricted osteogenic domains bounded by <i>Dkk2</i>, which normally interfaces with <i>Pax9</i> in the mesenchyme. Moreover, the loss of <i>Pax9</i> leads to a disruption in the normal osteodifferentiaion of palatal osteogenic mesenchymal cells. These results suggest that Pax9-dependent Wnt signaling modulators influence osteogenic programming during palate formation, potentially contributing to the observed cleft palate phenotype.</p>","PeriodicalId":94075,"journal":{"name":"Journal of dental research","volume":" ","pages":"1412-1420"},"PeriodicalIF":0.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11653329/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141444003","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}