Journal of Dental Research最新文献

{"title":"Zinc- and Fluoride-Releasing Bioactive Glass as a Novel Bone Substitute","authors":"T. Kondo, K. Otake, H. Kakinuma, Y. Sato, S. Ambo, H. Egusa","doi":"10.1177/00220345241231772","DOIUrl":"https://doi.org/10.1177/00220345241231772","url":null,"abstract":"Bioglass 45S5, a silica-based glass, has pioneered a new field of biomaterials. Bioglass 45S5 promotes mineralization through calcium ion release and is widely used in the dental field, including toothpaste formulations. However, the use of Bioglass 45S5 for bone grafting is limited owing to the induction of inflammation, as well as reduced degradation and ion release. Phosphate-based glasses exhibit higher solubility and ion release than silica-based glass. Given that these glasses can be synthesized at low temperatures (approximately 1,000°C), they can easily be doped with various metal oxides to confer therapeutic properties. Herein, we fabricated zinc- and fluoride-doped phosphate-based glass (multicomponent phosphate [MP] bioactive glass) and further doped aluminum oxide into the MP glass (4% Al-MP glass) to overcome the striking solubility of phosphate-based glass. Increased amounts of zinc and fluoride ions were detected in water containing the MP glass. Doping of aluminum oxide into the MP glass suppressed the striking dissolution in water, with 4% Al-MP glass exhibiting the highest stability in water. Compared with Bioglass 45S5, 4% Al-MP glass in water had a notably reduced particle size, supporting the abundant ion release of 4% Al-MP glass. Compared with Bioglass 45S5, 4% Al-MP glass enhanced the osteogenesis of mouse bone marrow–derived mesenchymal stem cells. Mouse macrophages cultured with 4% Al-MP glass displayed enhanced induction of anti-inflammatory M2 macrophages and reduced proinflammatory M1 macrophages, indicating M2 polarization. Upon implanting 4% Al-MP glass or Bioglass 45S5 in a mouse calvarial defect, 4% Al-MP glass promoted significant bone regeneration when compared with Bioglass 45S5. Hence, we successfully fabricated zinc- and fluoride-releasing bioactive glasses with improved osteogenic and anti-inflammatory properties, which could serve as a promising biomaterial for bone regeneration.","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":"78 1","pages":""},"PeriodicalIF":7.6,"publicationDate":"2024-04-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140533935","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":"A Remineralizing and Antibacterial Coating for Arresting Caries.","authors":"D Lu,&nbsp;F Li,&nbsp;C Zhao,&nbsp;Y Ye,&nbsp;X Zhang,&nbsp;P Yang,&nbsp;X Zhang","doi":"10.1177/00220345231189992","DOIUrl":"10.1177/00220345231189992","url":null,"abstract":"<p><p>Dental caries is a dynamic disease induced by the unbalance between demineralization of dental hard tissues caused by biofilm and remineralization of them; however, although various effective remineralization methods have been well documented, it is a challenge to reestablish the balance by enhancing remineralization alone while ignoring the antibacterial therapy. Therefore, the integration of remineralizing and antibacterial technologies offers a promising strategy to halt natural caries progression in clinical practice. Here, the conception of interrupting dental caries (IDC) was proposed based on the development of dual-functional coating with remineralizing and antibacterial properties. In this study, bovine serum albumin (BSA) loaded octenidine (OCT) successfully to form a BSA-OCT composite. Subsequently, through fast amyloid-like aggregation, the phase-transited BSA-OCT (PTB-OCT) coating can be covered on teeth, resin composite, or sealant surfaces in 30 min by a simple smearing process. The PTB-OCT coating showed satisfactory effects in promoting the remineralization of demineralized enamel and dentin in vitro. Moreover, this coating also exerted significant acid-resistance stability and anti-biofilm properties. Equally importantly, this coating exhibited promising abilities in reducing the microleakage between the tooth and resin composite in vitro and preventing primary and secondary caries in vivo. In conclusion, this novel dual-functional PTB-OCT coating could reestablish the balance between demineralization and remineralization in the process of caries, thereby potentially preventing or arresting caries.</p>","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":" ","pages":"1315-1325"},"PeriodicalIF":7.6,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10580423","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":"Determinants of Microscale pH in In Situ-Grown Dental Biofilms.","authors":"M F Kristensen,&nbsp;M B Lund,&nbsp;A Schramm,&nbsp;E Frandsen Lau,&nbsp;S Schlafer","doi":"10.1177/00220345231190563","DOIUrl":"10.1177/00220345231190563","url":null,"abstract":"<p><p>Dental biofilm pH is the most important determinant of virulence for the development of caries lesions. Confocal microscopy-based pH ratiometry allows monitoring biofilm pH with high spatial resolution. Experiments performed on simplified biofilm models under static conditions identified steep pH gradients as well as localized acidogenic foci that promote enamel demineralization. The present work used pH ratiometry to perform a comprehensive analysis of the effect of whole saliva flow on the microscale pH in complex, in situ-grown 48-h and 96-h biofilms (<i>n</i> = 54) from 9 healthy participants. pH was monitored in 12 areas at the biofilm bottom and top, and saliva flow with film thicknesses corresponding to those in the oral cavity was provided by an additively manufactured microfluidic flow cell. Biofilm pH was correlated to the bacterial composition, as determined by 16S rRNA gene sequencing. Biofilm acidogenicity varied considerably between participants and individual biofilms but also between different areas inside one biofilm, with pH gradients of up to 2 units. pH drops were more pronounced in 96-h than in 48-h biofilms (<i>P</i> = 0.0121) and virtually unaffected by unstimulated saliva flow (0.8 mm/min). Stimulated flow (8 mm/min) raised average biofilm pH to near-neutral values but it did not equilibrate vertical and horizontal pH gradients in the biofilms. pH was significantly lower at the biofilm base than at the top (<i>P</i> < 0.0001) and lower downstream than upstream (<i>P</i> = 0.0046), due to an accumulation of acids along the flow path. pH drops were positively correlated with biofilm thickness and negatively with the thickness of the saliva film covering the biofilm. Bacterial community composition was significantly different between biofilms with strong and weak pH responses but not their species richness. The present experimental study demonstrates that stimulated saliva flow, saliva film thickness, biofilm age, biofilm thickness, and bacterial composition are important modulators of microscale pH in dental biofilms.</p>","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":" ","pages":"1348-1355"},"PeriodicalIF":7.6,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10580418","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":"Evidence-Informed Oral Health Policy Making: Opportunities and Challenges.","authors":"S Listl, R Baltussen, A Carrasco-Labra, F C Carrer, J N Lavis","doi":"10.1177/00220345231187828","DOIUrl":"10.1177/00220345231187828","url":null,"abstract":"<p><p>Despite a clear need for improvement in oral health systems, progress in oral health systems transformation has been slow. Substantial gaps persist in leveraging evidence and stakeholder values for collective problem solving. To truly enable evidence-informed oral health policy making, substantial \"know-how\" and \"know-do\" gaps still need to be overcome. However, there is a unique opportunity for the oral health community to learn and evolve from previous successes and failures in evidence-informed health policy making. As stated by the Global Commission on Evidence to Address Societal Challenges, COVID-19 has created a once-in-a-generation focus on evidence, which has fast-tracked collaboration among decision makers, researchers, and evidence intermediaries. In addition, this has led to a growing recognition of the need to formalize and strengthen evidence-support systems. This article provides an overview of recent advancements in evidence-informed health policy making, including normative goals and a health systems taxonomy, the role of evidence-support and evidence-implementation systems to improve context-specific decision-making processes, the evolution of learning health systems, and the important role of citizen deliberations. The article also highlights opportunities for evidence-informed policy making to drive change in oral health systems. All in all, strengthening capacities for evidence-informed health policy making is critical to enable and enact improvements in oral health systems.</p>","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":" ","pages":"1293-1302"},"PeriodicalIF":5.7,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/c3/fa/10.1177_00220345231187828.PMC10604434.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10011223","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":"Osteoprotective Role of the <i>Mir338</i> Cluster Ablation during Periodontitis.","authors":"H S Zhang,&nbsp;C X Jiang,&nbsp;Y T Ji,&nbsp;Y F Zhang,&nbsp;Z Chen,&nbsp;Z G Cao,&nbsp;H Liu","doi":"10.1177/00220345231187288","DOIUrl":"10.1177/00220345231187288","url":null,"abstract":"<p><p>Periodontitis is a chronic inflammatory disease that compromises the integrity of the supporting tissues of the teeth and leads to the loss of the alveolar bone. The <i>Mir338</i> cluster has been proven to be a potential target for the treatment of osteoporosis and is also enriched in gingival tissues with periodontitis; however, its role in periodontitis remains unknown. Here, we aimed to use periodontitis as a model to expand our understanding of the <i>Mir338</i> cluster in osteoimmunology and propose a new target to protect against bone loss during periodontitis progression. Significant enrichment of the <i>Mir338</i> cluster was validated in gingival tissues from patients with chronic periodontitis and a ligature-induced periodontitis mouse model. In vivo, attenuation of alveolar bone loss after 7 d of ligature was observed in the <i>Mir338</i> cluster knockout (KO) mice. Interestingly, immunofluorescence and RNA sequencing showed that ablation of the <i>Mir338</i> cluster reduced osteoclast formation and elevated the inflammatory response, with enrichment of IFN-γ and JAK-STAT signaling pathways. Ablation of the <i>Mir338</i> cluster also skewed macrophages toward the M1 phenotype and inhibited osteoclastogenesis via <i>Stat1</i> in vitro and in vivo. Furthermore, the local administration of <i>miR-338-3p</i> antagomir prevented alveolar bone loss from periodontitis. In conclusion, the <i>Mir338</i> cluster balanced M1 macrophage polarization and osteoclastogenesis and could serve as a novel therapeutic target against periodontitis-related alveolar bone loss.</p>","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":" ","pages":"1337-1347"},"PeriodicalIF":7.6,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10540642","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":"Increased STAT3 Activation in Periodontitis Drives Inflammatory Bone Loss.","authors":"M Arce, M Rodriguez-Peña, J Espinoza-Arrue, R A Godoy, M Reyes, T Kajikawa, T Greenwell-Wild, G Hajishengallis, L Abusleme, N Moutsopoulos, N Dutzan","doi":"10.1177/00220345231192381","DOIUrl":"10.1177/00220345231192381","url":null,"abstract":"<p><p>Periodontitis is one of the most prevalent human inflammatory diseases. It is characterized by periodontal tissue destruction, progressively driven by the host response. In this regard, cytokines associated with tissue destruction, such as interleukin (IL)-6 and IL-23, use a common signaling pathway mediated by STAT3. This transcription factor is also needed for IL-17A production, a key mediator in periodontitis pathogenesis. Although several studies have reported increased activation of STAT3 in experimental periodontitis, a detailed characterization of STAT3 activation in human gingival tissues and its involvement in alveolar bone loss has yet to be explored. Using a cross-sectional study design, we detected increased proportions of pSTAT3-positive cells during periodontitis compared with health, particularly in epithelial cells and T cells. Other cell types of hematopoietic and nonhematopoietic origin also display STAT3 activation in gingival tissues. We detected increased STAT3 phosphorylation and expression of STAT3-related genes during experimental periodontitis. Next, we evaluated the role of STAT3 in alveolar bone destruction using a mouse model of STAT3 loss of function (mut-<i>Stat3</i> mice). Compared with controls, mut-<i>Stat3</i> mice had reduced alveolar bone loss following ligature-induced periodontitis. We also evaluated pharmacologic inhibition of STAT3 in ligature-induced periodontitis. Like mut-<i>Stat3</i> mice, mice treated with STAT3 small-molecule inhibitor had reduced bone loss compared with controls. Our results demonstrate that STAT3 activation is increased in epithelial and T cells during periodontitis and indicate a pathogenic role of STAT3 in inflammatory alveolar bone loss.</p>","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":" ","pages":"1366-1375"},"PeriodicalIF":5.7,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10714379/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10213948","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":"Antibacterial Activity of a Lysin LysP53 against <i>Streptococcus mutans</i>.","authors":"X Zhao,&nbsp;C Li,&nbsp;H Yang,&nbsp;H Wei,&nbsp;Y Li","doi":"10.1177/00220345231182675","DOIUrl":"10.1177/00220345231182675","url":null,"abstract":"<p><p>Dental caries is a common disease affecting quality of life globally. In the present study, we found that a bacteriophage lysin LysP53 against <i>Acinetobacter baumannii</i> possesses selective activity on <i>Streptococcus mutans</i>, the main etiological agent of dental caries, even in low pH caries microenvironments, whereas only minor LysP53 activity was detected against <i>Streptococcus sanguinis</i>, <i>Streptococcus oralis</i>, and <i>Streptococcus mitis</i>. Testing activity against <i>S. mutans</i> planktonic cells showed that 4 μM LysP53 could kill more than 84% of <i>S. mutans</i> within 1 min in buffer with optimal pHs ranging from 4.0 to 6.5. Daily application of LysP53 on biofilms formed in BHI medium supplemented or not with sucrose could reduce exopolysaccharides, expression of genes related to acid resistance and adhesion, and the number of live bacteria in the biofilms. LysP53 treatment also showed similar effects as 0.12% chlorhexidine in preventing enamel demineralization due to <i>S. mutans</i> biofilms, as well as effective removal of <i>S. mutans</i> colonization of tooth surfaces in mice without observed toxic effects. Because of its selective activity against main cariogenic bacteria and good activity in low pH caries microenvironments, it is advantageous to use LysP53 as an active agent for preventing caries.</p>","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":" ","pages":"1231-1240"},"PeriodicalIF":7.6,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10564668","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":"MEMO1 Is Required for Ameloblast Maturation and Functional Enamel Formation.","authors":"M Kiel, S Wuebker, M T Remy, K A Riemondy, F Smith, C M Carey, T Williams, E Van Otterloo","doi":"10.1177/00220345231185758","DOIUrl":"10.1177/00220345231185758","url":null,"abstract":"<p><p>Coordinated mineralization of soft tissue is central to organismal form and function, while dysregulated mineralization underlies several human pathologies. Oral epithelial-derived ameloblasts are polarized, secretory cells responsible for generating enamel, the most mineralized substance in the human body. Defects in ameloblast development result in enamel anomalies, including amelogenesis imperfecta. Identifying proteins critical in ameloblast development can provide insight into specific pathologies associated with enamel-related disorders or, more broadly, mechanisms of mineralization. Previous studies identified a role for MEMO1 in bone mineralization; however, whether MEMO1 functions in the generation of additional mineralized structures remains unknown. Here, we identify a critical role for MEMO1 in enamel mineralization. First, we show that <i>Memo1</i> is expressed in ameloblasts and, second, that its conditional deletion from ameloblasts results in enamel defects, characterized by a decline in mineral density and tooth integrity. Histology revealed that the mineralization defects in <i>Memo1</i> mutant ameloblasts correlated with a disruption in ameloblast morphology. Finally, molecular profiling of ameloblasts and their progenitors in <i>Memo1</i> oral epithelial mutants revealed a disruption to cytoskeletal-associated genes and a reduction in late-stage ameloblast markers, relative to controls. Collectively, our findings integrate MEMO1 into an emerging network of molecules important for ameloblast development and provide a system to further interrogate the relationship of cytoskeletal and amelogenesis-related defects.</p>","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":" ","pages":"1261-1271"},"PeriodicalIF":5.7,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11066519/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10204517","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":"Pth1r Signal in Gli1+ Cells Maintains Postnatal Cranial Base Synchondrosis.","authors":"K Amano,&nbsp;Y Kitaoka,&nbsp;S Kato,&nbsp;M Fujiwara,&nbsp;D Okuzaki,&nbsp;T Aikawa,&nbsp;M Kogo,&nbsp;S Iida","doi":"10.1177/00220345231184405","DOIUrl":"10.1177/00220345231184405","url":null,"abstract":"<p><p>Cranial base synchondroses are the endochondral ossification centers for cranial base growth and thus indispensable for proper skull, brain, and midfacial development. The synchondroses are composed of mirror-image growth plates that are continuously maintained from the embryonic to postnatal stage through chondrocyte differentiation. Several factors, including Pth1r signaling, are known to control fetal synchondrosis development. However, there are currently no reports regarding any role for Pth1r signaling in postnatal cranial base and synchondrosis development. Also, the mesenchymal cells that source Pth1r signaling for synchondroses are not known. Here, we employed an inducible mouse model, a hedgehog-responsive <i>Gli1-Cre^ERT2</i> driver, focusing on the postnatal study. We performed 2 inducible protocols using <i>Gli1-Cre^ERT2;Tomato^fl/+</i> mice that uncovered distinct patterning of Gli1-positive and Gli1-negative chondrocytes in the synchondrosis cartilage. Moreover, we generated <i>Gli1-Cre^ERT2;Pth1r^fl/fl;Tomato^fl/+</i> mice to assess their functions in postnatal synchondrosis and found that the mutants had survived postnatally. The mutant skulls morphologically presented unambiguous phenotypes where we noticed the shortened cranial base and premature synchondrosis closure. Histologically, gradual disorganization in mutant synchondroses caused an uncommon remaining central zone between hypertrophic zones on both sides while the successive differentiation of round, flat, and hypertrophic chondrocytes was observed in control sections. These mutant synchondroses disappeared and were finally replaced by bone. Of note, the mutant fusing synchondroses lost their characteristic patterning of Gli1-positive and Gli1-negative chondrocytes, suggesting that loss of Pth1r signaling alters the distribution of hedgehog-responsive chondrocytes. Moreover, we performed laser microdissection and RNA sequencing to characterize the flat proliferative and round resting chondrocytes where we found flat chondrocytes have a characteristic feature of both chondrocyte proliferation and maturation. Taken together, these data demonstrate that Pth1r signaling in Gli1-positive cells is essential for postnatal development and maintenance in cranial base synchondroses. Our findings will elucidate previously unknown aspects of Pth1r functions in cranial biology and development.</p>","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":" ","pages":"1241-1251"},"PeriodicalIF":7.6,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10343638","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":"Analysis of Hepatitis D Virus in Minor Salivary Gland of Sjögren's Disease.","authors":"M C Hesterman, S V Furrer, B S Fallon, M L Weller","doi":"10.1177/00220345231186394","DOIUrl":"10.1177/00220345231186394","url":null,"abstract":"<p><p>Hepatitis delta virus (HDV) has been detected in the minor salivary gland (MSG) tissue of Sjögren's disease (SjD) patients in the absence of a hepatitis B virus (HBV) coinfection. Previous research has shown that HDV antigen (HDAg) expression can trigger an SjD-like phenotype in vivo, demonstrating a potential cause-and-effect relationship. We hypothesize that if HDV plays a role in the development of SjD, then HDV profiles may be correlated with disease manifestations. This retrospective study characterized HDV in a cohort of 48 SjD MSG samples collected between 2014 and 2021. Analyses of HDAg expression, including cell type and subcellular localization, in situ hybridization of HDV RNA, and comparative analyses with associated SjD and viral hepatitis clinical features, were conducted. HDAg was detected in MSG acinar, ductal, myoepithelial, and adipose cells and localized with the nuclei, cytoplasm, and mitochondria. In situ hybridization detected HDV genomic RNA localization in the MSG nuclei. A significant negative correlation was found between HDAg intensity and focal lymphocytic inflammation and in patients with both anti-SSA/Ro-52 and anti-SSA/Ro-60. In analyzing autoimmune disease comorbidities with SjD, it was found that SjD patients diagnosed with autoimmune thyroiditis and/or hypothyroidism were significantly more represented in the high HDAg intensity group compared to the negative and moderate HDAg intensity groups. No significant associations were detected between MSG-localized HDAg and liver enzymes or an evident HBV coinfection. This study has further confirmed that there is a nonhepatic reservoir for chronic HDV persistence in SjD-affected salivary gland tissue in a third independent SjD patient cohort. In addition, this study describes the unique colocalization of HDAg with mitochondria. The detection of HDV antigen and sequence within SjD-affected salivary gland tissue, and in the absence of an evident current or past HBV coinfection, warrants further investigation.</p>","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":" ","pages":"1272-1279"},"PeriodicalIF":5.7,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10626587/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10136434","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}