Journal of Dental Research最新文献

{"title":"Developing Bioactive Dental Resins for Restorative Dentistry.","authors":"M A S Melo, I M Garcia, L Mokeem, M D Weir, H H K Xu, C Montoya, S Orrego","doi":"10.1177/00220345231182357","DOIUrl":"10.1177/00220345231182357","url":null,"abstract":"<p><p>Despite its reputation as the most widely used restorative dental material currently, resin-based materials have acknowledged shortcomings. As most systematic survival studies of resin composites and dental adhesives indicate, secondary caries is the foremost reason for resin-based restoration failure and life span reduction. In subjects with high caries risk, the microbial community dominated by acidogenic and acid-tolerant bacteria triggers acid-induced deterioration of the bonding interface and/or bulk material and mineral loss around the restorations. In addition, resin-based materials undergo biodegradation in the oral cavity. As a result, the past decades have seen exponential growth in developing restorative dental materials for antimicrobial applications addressing secondary caries prevention and progression. Currently, the main challenge of bioactive resin development is the identification of efficient and safe anticaries agents that are detrimental free to final material properties and show satisfactory long-term performance and favorable clinical translation. This review centers on the continuous efforts to formulate novel bioactive resins employing 1 or multiple agents to enhance the antibiofilm efficacy or achieve multiple functionalities, such as remineralization and antimicrobial activity antidegradation. We present a comprehensive synthesis of the constraints and challenges encountered in the formulation process, the clinical performance-related prerequisites, the materials' intended applicability, and the current advancements in clinical implementation. Moreover, we identify crucial vulnerabilities that arise during the development of dental materials, including particle aggregation, alterations in color, susceptibility to hydrolysis, and loss of physicomechanical core properties of the targeted materials.</p>","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":" ","pages":"1180-1190"},"PeriodicalIF":5.7,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11066520/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9960704","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dental Medicine and Engineering Unite to Transform Oral Health Innovations.","authors":"H Koo, K Stebe","doi":"10.1177/00220345231183339","DOIUrl":"10.1177/00220345231183339","url":null,"abstract":"<p><p>This perspective article urges the academic community to adopt a coordinated approach uniting dental medicine and engineering to support research, training, and entrepreneurship to address the unmet needs and spur oral health care innovations. We describe a new interschool institute that brings together dentists, scientists and engineers, resources, and a training program dedicated for affordable oral health care innovations, which may serve as a template for dental medicine-engineering integration.</p>","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":" ","pages":"1177-1179"},"PeriodicalIF":7.6,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/76/2a/10.1177_00220345231183339.PMC10548769.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9947572","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fibulin-1 Regulates Initiation of Successional Dental Lamina.","authors":"G Li,&nbsp;Q Li,&nbsp;Z Shen,&nbsp;X Lin,&nbsp;X Li,&nbsp;J Wang,&nbsp;B Zhao,&nbsp;Y Feng,&nbsp;L Feng,&nbsp;W Guo,&nbsp;L Hu,&nbsp;J Wang,&nbsp;C Zhang,&nbsp;Z Fan,&nbsp;S Wang,&nbsp;X Wu","doi":"10.1177/00220345231182052","DOIUrl":"10.1177/00220345231182052","url":null,"abstract":"<p><p>In humans, teeth are replaced only once, and the successional dental lamina (SDL) of the permanent tooth is maintained in a quiescent state until adolescence. Recently, we showed that biomechanical stress generated by the rapid growth of the deciduous tooth inhibits SDL development via integrin β1-RUNX2 signaling at embryonic day 60 (E60) in miniature pigs. However, the mechanism by which RUNX2 regulates SDL initiation within the SDL stem cell niche remains unclear. In the current study, we transcriptionally profiled single cells from SDL and surrounding mesenchyme at E60 and identified the landscape of cellular heterogeneity. We then identified a specific fibroblast subtype in the dental follicle mesenchyme between the deciduous tooth and the SDL of the permanent tooth (DFDP), which constitutes the inner part of the niche (deciduous tooth side). Compared with traditional dental follicle cells, the specific expression profile of DFDP was identified and found to be related to biomechanical stress. Subsequently, we found that RUNX2 could bind to the enhancer regions of <i>Fbln1</i> (gene of fibulin-1), one of the marker genes for DFDP. Through gain- and loss-of-function experiments, we proved that the biomechanical stress-mediated RUNX2-fibulin-1 axis inhibits the initiation of SDL by maintaining SDL niche homeostasis.</p>","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":" ","pages":"1220-1230"},"PeriodicalIF":7.6,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9832284","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":"CREB3L2 Regulates Hemidesmosome Formation during Epithelial Sealing.","authors":"Y Li,&nbsp;J Zhang,&nbsp;W Cai,&nbsp;C Wang,&nbsp;Z Yu,&nbsp;Z Jiang,&nbsp;K Lai,&nbsp;Y Wang,&nbsp;G Yang","doi":"10.1177/00220345231176520","DOIUrl":"10.1177/00220345231176520","url":null,"abstract":"<p><p>The long-term success rate of dental implants can be improved by establishing a favorable biological sealing with a high-quality epithelial attachment. The application of mesenchymal stem cells (MSCs) holds promise for facilitating the soft tissue integration around implants, but the molecular mechanism is still unclear and the general application of MSC sheet for soft tissue integration is also relatively unexplored. We found that gingival tissue-derived MSC (GMSC) sheet treatment significantly promoted the expression of hemidesmosome (HD)-related genes and proteins in gingival epithelial cells (GECs). The formation of HDs played a key role in strengthening peri-implant epithelium (PIE) sealing. Further, high-throughput transcriptome sequencing showed that GMSC sheet significantly upregulated the PI3K/AKT pathway, confirming that cell adhesion and HD expression in GECs were regulated by GMSC sheet. We observed that the expression of transcription factor CREB3L2 in GECs was downregulated. After treatment with PI3K pathway inhibitor LY294002, CREB3L2 messenger RNA and protein expression levels were upregulated. Further experiments showed that overexpression or knockdown of CREB3L2 could significantly inhibit or promote HD-related genes and proteins, respectively. We confirmed that CREB3L2 was a transcription factor downstream of the PI3K/AKT pathway and participated in the formation of HDs regulated by GMSC sheet. Finally, through the establishment of early implant placement model in rats, we clarified the molecular function of CREB3L2 in PIE sealing as a mechanical transmission molecule in GECs. The application of GMSC sheet-implant complex could enhance the formation of HDs at the implant-PIE interface and decrease the penetration distance of horseradish peroxidase between the implant and PIE. Meanwhile, GMSC sheet reduced the length of CREB3L2 protein expression on PIE. These findings elucidate the potential function and molecular mechanism of MSC sheet regulating the epithelial sealing around implants, providing new insights and ideas for the application of stem cell therapy in regenerative medicine.</p>","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":" ","pages":"1199-1209"},"PeriodicalIF":7.6,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9957927","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":"Linking the Mechanics of Chewing to Biology of the Junctional Epithelium.","authors":"X Yuan, B Liu, P Cuevas, J Brunski, F Aellos, J Petersen, T Koehne, S Bröer, R Grüber, A LeBlanc, X Zhang, Q Xu, J A Helms","doi":"10.1177/00220345231185288","DOIUrl":"10.1177/00220345231185288","url":null,"abstract":"<p><p>The capacity of a tissue to continuously alter its phenotype lies at the heart of how an animal is able to quickly adapt to changes in environmental stimuli. Within tissues, differentiated cells are rigid and play a limited role in adapting to new environments; however, differentiated cells are replenished by stem cells that are defined by their phenotypic plasticity. Here we demonstrate that a Wnt-responsive stem cell niche in the junctional epithelium is responsible for the capability of this tissue to quickly adapt to changes in the physical consistency of a diet. Mechanical input from chewing is required to both establish and maintain this niche. Since the junctional epithelium directly attaches to the tooth surface via hemidesmosomes, a soft diet requires minimal mastication, and consequently, lower distortional strains are produced in the tissue. This reduced strain state is accompanied by reduced mitotic activity in both stem cells and their progeny, leading to tissue atrophy. The atrophied junctional epithelium exhibits suboptimal barrier functions, allowing the ingression of bacteria into the underlying connective tissues, which in turn trigger inflammation and mild alveolar bone loss. These data link the mechanics of chewing to the biology of tooth-supporting tissues, revealing how a stem cell niche is responsible for the remarkable adaptability of the junctional epithelium to different diets.</p>","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":" ","pages":"1252-1260"},"PeriodicalIF":5.7,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10626588/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10014117","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An Appreciation of a Giant in Orofacial Sciences Research-John Greenspan.","authors":"S J Challacombe,&nbsp;O D Klein","doi":"10.1177/00220345231181536","DOIUrl":"https://doi.org/10.1177/00220345231181536","url":null,"abstract":"<p><p>Professor John S. Greenspan died on March 31, 2023. He was a renowned and accomplished academic, dentist/scientist, pathologist, and administrator who made sustained and significant international impacts on numerous fields over half a century. John was arguably best known for his work with his wife, Dr. Deborah Greenspan, on the oral aspects of AIDS and the role of viruses in oral epithelial and salivary gland lesions. He had a lifelong interest in Sjögren's syndrome, culminating in the leadership of the Sjögren's International Collaborative Clinical Alliance. He was also widely recognized as one of the leading investigators into the understanding of oral mucosal diseases, including recurrent aphthous stomatitis. He and his colleagues' major contributions to HIV research and care included the discovery of the oral lesion \"hairy leukoplakia,\" its etiological association with Epstein-Barr virus, and other oral lesions in the natural history of HIV disease. In recent years, John turned his attention to global oral health inequalities, helping to establish the International Association for Dental Research's Global Oral Health Inequalities Research Network and serving as its first president. He led many organizations with humble authority, knowledge, wit, and wisdom and mentored colleagues from all over the world, especially from lower- and middle-income countries. John leaves a very special legacy based on example and scientific curiosity, and his work has not only made a lasting impact on his colleagues but also translated to abiding benefit for patients.</p>","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":"102 10","pages":"1073-1077"},"PeriodicalIF":7.6,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10039941","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":"Tmem2 Deficiency Leads to Enamel Hypoplasia and Soft Enamel in Mouse.","authors":"P Nag,&nbsp;T Inubushi,&nbsp;J I Sasaki,&nbsp;T Murotani,&nbsp;S Kusano,&nbsp;Y Nakanishi,&nbsp;Y Shiraishi,&nbsp;H Kurosaka,&nbsp;S Imazato,&nbsp;Y Yamaguchi,&nbsp;T Yamashiro","doi":"10.1177/00220345231182355","DOIUrl":"https://doi.org/10.1177/00220345231182355","url":null,"abstract":"<p><p>Teeth consist of 3 mineralized tissues: enamel, dentin, and cementum. Tooth malformation, the most common craniofacial anomaly, arises from complex genetic and environmental factors affecting enamel structure, size, shape, and tooth eruption. Hyaluronic acid (HA), a primary extracellular matrix component, contributes to structural and physiological functions in periodontal tissue. Transmembrane protein 2 (TMEM2), a novel cell surface hyaluronidase, has been shown to play a critical role during embryogenesis. In this study, we demonstrate <i>Tmem2</i> messenger RNA expression in inner enamel epithelium and presecretory, secretory, and mature ameloblasts. <i>Tmem2</i> knock-in reporter mice reveal TMEM2 protein localization at the apical and basal ends of secretory ameloblasts. Micro-computed tomography analysis of epithelial-specific <i>Tmem2</i> conditional knockout (<i>Tmem2</i>-<i>CKO</i>) mice shows a significant reduction in enamel layer thickness and severe enamel deficiency. Enamel matrix protein expression was remarkably downregulated in <i>Tmem2</i>-<i>CKO</i> mice. Scanning electron microscopy of enamel from <i>Tmem2</i>-<i>CKO</i> mice revealed an irregular enamel prism structure, while the microhardness and density of enamel were significantly reduced, indicating impaired ameloblast differentiation and enamel matrix mineralization. Histological evaluation indicated weak adhesion between cells and the basement membrane in <i>Tmem2</i>-<i>CKO</i> mice. The reduced and irregular expressions of vinculin and integrin β1 suggest that <i>Tmem2</i> deficiency attenuated focal adhesion formation. In addition, abnormal HA accumulation in the ameloblast layer and weak claudin 1 immunoreactivity in <i>Tmem2</i>-<i>CKO</i> mice indicate impaired tight junction gate function. Irregular actin filament assembly was also observed at the apical and basal ends of secretory ameloblasts. Last, we demonstrated that <i>Tmem2</i>-deficient mHAT9d mouse ameloblasts exhibit defective adhesion to HA-containing substrates in vitro. Collectively, our data highlight the importance of TMEM2 in adhesion to HA-rich extracellular matrix, cell-to-cell adhesion, ameloblast differentiation, and enamel matrix mineralization.</p>","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":"102 10","pages":"1162-1171"},"PeriodicalIF":7.6,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10044514","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":"Endothelial Insulin Resistance Exacerbates Experimental Periodontitis.","authors":"T Zeze,&nbsp;T Shinjo,&nbsp;K Sato,&nbsp;Y Nishimura,&nbsp;M Imagawa,&nbsp;S Chen,&nbsp;A-K Ahmed,&nbsp;M Iwashita,&nbsp;A Yamashita,&nbsp;T Fukuda,&nbsp;T Sanui,&nbsp;K Park,&nbsp;G L King,&nbsp;F Nishimura","doi":"10.1177/00220345231181539","DOIUrl":"https://doi.org/10.1177/00220345231181539","url":null,"abstract":"<p><p>Epidemiological studies suggest that the severity of periodontitis is higher in people with diabetes than in healthy individuals. Insulin resistance might play a crucial role in the pathogenesis of multiple diabetic complications and is reportedly induced in the gingiva of rodents with type 2 diabetes; however, the molecular mechanisms underlying the pathogenesis of diabetes-related periodontitis remain unclear. Therefore, we aimed to investigate whether endothelial insulin resistance in the gingiva may contribute to the pathogenesis of periodontitis as well as elucidate its underlying molecular mechanisms. We demonstrated that insulin treatment downregulated lipopolysaccharide (LPS)-induced or tumor necrosis factor α (TNFα)-induced VCAM1 expression in endothelial cells (ECs) via the PI3K/Akt activating pathway, resulting in reduced cellular adhesion between ECs and leukocytes. Hyperglycemia-induced selective insulin resistance in ECs diminished the effect of insulin on LPS- or TNFα-stimulated VCAM1 expression. Vascular endothelial cell-specific insulin receptor knockout (VEIRKO) mice exhibited selective inhibition of the PI3K/Akt pathway in the gingiva and advanced experimental periodontitis-induced alveolar bone loss via upregulation of <i>Vcam1</i>, <i>Tnf</i>α, <i>Mcp-1</i>, <i>Rankl</i>, and neutrophil migration into the gingiva compared with that in the wild-type (WT) mice despite being free from diabetes. We also observed that insulin-mediated activation of FoxO1, a downstream target of Akt, was suppressed in the gingiva of VEIRKO and high-fat diet (HFD)-fed mice, hyperglycemia-treated ECs, and primary ECs from VEIRKO. Further analysis using ECs transfected with intact and mutated FoxO1, with mutations at 3 insulin-mediated phosphorylation sites (T24A, S256D, S316A), suggested that insulin-mediated regulation of VCAM1 expression and cellular adhesion of ECs with leukocytes was attenuated by mutated FoxO1 overexpression. These results suggest that insulin resistance in ECs may contribute to the progression of periodontitis via dysregulated VCAM1 expression and cellular adhesion with leukocytes, resulting from reduced activation of the PI3K/Akt/FoxO1 axis.</p>","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":"102 10","pages":"1152-1161"},"PeriodicalIF":7.6,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10055656","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":"Inhibition of Mertk Signaling Enhances Bone Healing after Tooth Extraction.","authors":"A M Decker, M Matsumoto, J T Decker, A Roh, N Inohara, J Sugai, K Martin, R Taichman, D Kaigler, L D Shea, G Núñez","doi":"10.1177/00220345231177996","DOIUrl":"10.1177/00220345231177996","url":null,"abstract":"<p><p>Regeneration of alveolar bone is an essential step in restoring healthy function following tooth extraction. Growth of new bone in the healing extraction socket can be variable and often unpredictable when systemic comorbidities are present, leading to the need for additional therapeutic targets to accelerate the regenerative process. One such target is the TAM family (Tyro3, Axl, Mertk) of receptor tyrosine kinases. These proteins have been shown to help resolve inflammation and maintain bone homeostasis and thus may have therapeutic benefits in bone regeneration following extraction. Treatment of mice with a pan-TAM inhibitor (RXDX-106) led to accelerated alveolar bone fill following first molar extraction in a mouse model without changing immune infiltrate. Treatment of human alveolar bone mesenchymal stem cells with RXDX-106 upregulated Wnt signaling and primed the cells for osteogenic differentiation. Differentiation of human alveolar bone mesenchymal stem cells with osteogenic media and TAM-targeted inhibitor RXDX-106 (pan-TAM), ASP-2215 (Axl specific), or MRX-2843 (Mertk specific) showed enhanced mineralization with pan-TAM or Mertk-specific inhibitors and no change with Axl-specific inhibitor. First molar extractions in Mertk^-/- mice had increased alveolar bone regeneration in the extraction socket relative to wild type controls 7 d postextraction. Flow cytometry of 7-d extraction sockets showed no difference in immune cell numbers between Mertk<i>^-/-</i> and wild type mice. RNAseq of day 7 extraction sockets showed increased innate immune-related pathways and genes associated with bone differentiation in Mertk<i>^-/-</i> mice. Together, these results indicate that TAM receptor signaling, specifically through Mertk, can be targeted to enhance bone regeneration after injury.</p>","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":"102 10","pages":"1131-1140"},"PeriodicalIF":5.7,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10552464/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10044805","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Relations between Systems of Oppression and Oral Care Access in the United States.","authors":"J L Bastos,&nbsp;E Fleming,&nbsp;D G Haag,&nbsp;H S Schuch,&nbsp;L M Jamieson,&nbsp;H M Constante","doi":"10.1177/00220345231184181","DOIUrl":"https://doi.org/10.1177/00220345231184181","url":null,"abstract":"We applied a structural intersectionality approach to cross-sectionally examine the relationships between macro-level systems of oppression, their intersections, and access to oral care in the United States. Whether and the extent to which the provision of government-funded dental services attenuates the emerging patterns of associations was also assessed in the study. To accomplish these objectives, individual-level information from over 300,000 respondents of the 2010 US Behavioral Risk Factor Surveillance System was linked with state-level data for 2000 and 2010 on structural racism, structural sexism, and income inequality, as provided by Homan et al. Using multilevel models, we investigated the relationships between systems of oppression and restricted access to oral health services among respondents at the intersections of race, gender, and poverty. The degree to which extended provision of government-funded dental services weakens the observed associations was determined in models stratified by state-level coverage of oral care. Our analyses bring to the fore intersectional groups (e.g., non-Hispanic Black women and men below the poverty line) with the highest odds of not seeing a dentist in the previous year. We also show that residing in states where high levels of structural sexism and income inequality intersect was associated with 1.3 greater odds (95% confidence interval, 1.1–1.5) of not accessing dental services in the 12 mo preceding the survey. Stratified analyses demonstrated that a more extensive provision of government-funded dental services attenuates associations between structural oppressions and restricted access to oral health care. On the basis of these and other findings, we urge researchers and health care planners to increase access to dental services in more effective and inclusive ways. Most important, we show that counteracting structural drivers of inequities in dental services access entails providing dental care for all.","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":"102 10","pages":"1080-1087"},"PeriodicalIF":7.6,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10047272","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}