Journal of dental research最新文献

{"title":"Factors Involved in Enamel Knot Establishment and Cap Formation.","authors":"K Steklikova, L Dalecka, J Kubovciak, C Corneloup, S Pantalacci, M Hovorakova","doi":"10.1177/00220345251316834","DOIUrl":"10.1177/00220345251316834","url":null,"abstract":"<p><p>Development of dentition is a commonly studied process as a representative of the development of ectodermal derivates. A key step is the formation of a signaling center called the enamel knot (EK), which organizes tooth crown formation. In the mouse lower jaw, the anterior part of the tooth-forming region undergoes a series of complex events before the first molar primary EK can form more posteriorly and the tooth can progress through the cap stage. Although much is known about the molecular factors involved in tooth development, disentangling their specific roles is difficult. In this study, we circumvented this problem by isolating the posterior part of the tooth-forming region at embryonic day 13.5 and cultivating it in vitro. By treating them with molecules activating or inhibiting Sonic hedgehog (Shh) and fibroblast growth factor (Fgf) pathways, we demonstrate that Shh plays the role of an inhibitor of EK formation, and we suggest that the FGF pathways may have both positive and negative roles, as seen in hair. By RNA-sequencing of the cultivated isolates after 0, 16, or 24 h in vitro, respectively, we screened for genes whose expression varies with EK and cap formation and pointed to <i>Cdkn2b</i> and <i>Sema3b</i> as 2 promising candidates in this process.</p>","PeriodicalId":94075,"journal":{"name":"Journal of dental research","volume":" ","pages":"784-794"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143660144","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":"IL6-Dependent PIEZO1 Activation Promotes M1-Mediated Orthodontic Root Resorption via CXCL12/CXCR4.","authors":"Z H Zhang, R Zhu, Y Liu, F F Wang, A Y Jiang, R C Dan, Y H Liu, Y X Tang, J Liu, J Wang","doi":"10.1177/00220345251316472","DOIUrl":"10.1177/00220345251316472","url":null,"abstract":"<p><p>Orthodontic root resorption (ORR) is a common yet significant complication of orthodontic treatment, largely driven by interactions between periodontal ligament cells (PDLCs) and M1 macrophages. Despite the clinical relevance of ORR, the role of mechanosensitive ion channels in PDLC-mediated ORR and the underlying mechanisms regulating inflammatory cell recruitment remain poorly understood. Here, we identified PIEZO1 as a critical mechanosensitive ion channel that modulates monocyte recruitment and ORR. Using in vivo models treated with the PIEZO1 activator Yoda1 and inhibitor AAV-sh<i>Piezo1</i>, we demonstrated that PIEZO1 activation promoted the recruitment of Ly6C^hi inflammatory monocytes and exacerbated ORR. In contrast, PIEZO1 inhibition attenuated ORR and the accumulation of M1 macrophages. Mechanistically, PIEZO1 positively regulated the C-X-C motif chemokine 12 (CXCL12) and its receptor, C-X-C chemokine receptor type 4 (CXCR4). Blocking the CXCL12/CXCR4 axis using the CXCR4 antagonist AMD3100 significantly alleviated ORR, reversed M1 macrophage accumulation, and mitigated the recruitment of CD11b⁺Ly6C^hi monocytes. Transwell migration assays with application of the PIEZO1 activator Yoda1 and PIEZO1 inhibitor GsMTX4 consistently confirmed the PIEZO1/CXCL12/CXCR4 axis as a key driver of PDLC-monocyte interactions. Notably, PIEZO1 overactivation was linked to excessive IL-6 production, and IL-6 deficiency inhibited the activation of PIEZO1 induced by Yoda1, leading to attenuation of ORR, M1 macrophage accumulation, and CXCL12/CXCR4 axis activation. Collectively, these findings reveal PIEZO1 in PDLCs as a pivotal modulator of inflammatory monocyte recruitment via the CXCL12/CXCR4 axis in ORR, with IL-6 playing an essential role in PIEZO1 activation. This study provides new insights into the molecular crosstalk between PDLCs and macrophages, offering potential therapeutic targets for mitigating ORR in orthodontic patients.</p>","PeriodicalId":94075,"journal":{"name":"Journal of dental research","volume":" ","pages":"763-773"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143617996","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":"Extracellular Z-DNA Enhances Cariogenicity of Biofilm.","authors":"S L Han, J Wang, H S Wang, P Yu, L Y Wang, Y L Ou, L J Ding, J Washio, N Takahashi, L L Zhang","doi":"10.1177/00220345251316822","DOIUrl":"10.1177/00220345251316822","url":null,"abstract":"<p><p>Extracellular DNA (eDNA) is one of the core components of the extracellular matrix (ECM) in biofilms and provides attachment sites for microbes and other ECM components. However, little is known about the functions and underlying mechanisms of eDNA in the cariogenicity of dental plaque biofilms. A recent study demonstrated that conformational diversity of eDNA exists in biofilms, and the transition of eDNA from right-handed (B-DNA) to left-handed (Z-DNA) is associated with the structural stability and pathogenicity of biofilms. Caries-related biofilm is a complex multispecies microenvironment. The presence and biological function of the conformational transition of eDNA within this biofilm have not been previously reported. In this study, we found that extracellular Z-DNA is widely present in carious tissues and cariogenic biofilm, especially <i>Streptococcus mutans</i>, indicating its possible role in the occurrence and activity of dental caries. The content of extracellular Z-DNA showed species heterogeneity. The modulation of Z-DNA formation affected the level of extracellular polysaccharide. Increased formation of Z-DNA substantially strengthened the cariogenicity of the biofilm by increasing DNase resistance, structural density, and acid production. These insights provide a new perspective to understand the underlying function of the conformation transition of eDNA in promoting carious lesions, as well as a possible anti-biofilm strategy targeting extracellular Z-DNA.</p>","PeriodicalId":94075,"journal":{"name":"Journal of dental research","volume":" ","pages":"774-783"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143618062","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":"Mechanisms Tackling Salivary Gland Diseases with Extracellular Vesicle Therapies.","authors":"P Sawutdeechaikul, S Hwang, J Klangprapan, T V Phan, C Buu Lam, Y-J Yoon, S Seo, S Hong, J-Y Lim, J N Ferreira","doi":"10.1177/00220345251319295","DOIUrl":"10.1177/00220345251319295","url":null,"abstract":"<p><p>Extracellular vesicles (EVs) are lipid-enclosed particles released from cells, containing lipids, DNA, RNA, metabolites, and cytosolic and cell surface proteins. EVs support intercellular communication and orchestrate organogenesis by transferring bioactive molecules in between cells. Mesenchymal stem cells are known to produce EVs, which exhibit immunomodulatory and regenerative capabilities in many target organs, including the salivary glands (SGs). Since cell-based therapies still pose challenges (e.g., donor variability, limited hemocompatibility, and safety), specific EVs may constitute a therapeutic alternative for SG diseases. New EV guidelines (MISEV2023) have recently been updated and reported by our consortium to consolidate the principles of EV biology and expand the boundaries toward innovative therapies. These guidelines provide valuable guidance for researchers to consistently assess the effectiveness of mesenchymal stem cell-derived EV cargo cues, such as microRNA, proteins, and other molecules, to target SG diseases. This review provides a narrative synthesis of preclinical studies on EVs by highlighting EV mechanisms and their potential therapeutic applications for SG diseases, such as radiotherapy-induced SG hypofunction and Sjögren's syndrome, as well as inflammatory and aging-related SG conditions. Additionally, we highlight key areas of the MISEV2023 guidelines that will support future EV-based therapies in SG research. This review adhered to PRESS guidelines (Peer Review of Electronic Search Strategies) and utilized established databases, including Medline/PubMed, Embase, Web of Science, and Scopus, alongside machine learning tools for sorting the most impactful EV studies for SG diseases.</p>","PeriodicalId":94075,"journal":{"name":"Journal of dental research","volume":" ","pages":"704-714"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143712479","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":"The Roles and Molecular Mechanisms of HIF-1α in Pulpitis.","authors":"L Shao, Q Wang, B Chen, Y Zheng","doi":"10.1177/00220345251320970","DOIUrl":"10.1177/00220345251320970","url":null,"abstract":"<p><p>Pulpitis is characterized by inflammation within dental pulp tissue, primarily triggered by bacterial infection. Hypoxia-inducible factor-1α (HIF-1α), a key transcriptional regulator, is stabilized under the hypoxic conditions associated with pulpitis. This review examines the roles and molecular mechanisms of HIF-1α in the pathogenesis and progression of pulpitis. Hypoxia in pulpitis prevents the degradation of HIF-1α, leading to its elevated expression. Furthermore, lipopolysaccharide from invading bacteria upregulates HIF-1α transcription through nuclear factor kappa B and mitogen-activated protein kinase pathways. HIF-1α regulates immunity and pulp remodeling in a stage-dependent manner by controlling various cytokines. During the inflammation stage, HIF-1α promotes recruitment of neutrophils and enhances their bactericidal effects by facilitating neutrophil extracellular trap release and M1 macrophage polarization. Concurrently, HIF-1α contributes to programmed cell death by increasing mitophagy. In the proliferation stage, HIF-1α stimulates immune responses involving T cells and dendritic cells. In the remodeling stage, HIF-1α supports angiogenesis and pulp-dentin regeneration. However, excessive pulpitis-induced hypoxia may disrupt vascular dynamics within the pulp chamber. This disruption highlights a critical threshold for HIF-1α, beyond which its effects might accelerate pulp necrosis. Overall, HIF-1α plays a central role in regulating immunity and tissue remodeling during pulpitis. A comprehensive understanding of the physiological and pathological roles of HIF-1α is essential for the advancement of effective strategies to manage irreversible pulpitis.</p>","PeriodicalId":94075,"journal":{"name":"Journal of dental research","volume":" ","pages":"715-724"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143660150","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":"Role of Pink1 in Regulating Osteoclast Differentiation during Periodontitis.","authors":"H Gou, T Wang, Y Chen, Y Zhou, J Li, Y Xu","doi":"10.1177/00220345251315723","DOIUrl":"10.1177/00220345251315723","url":null,"abstract":"<p><p>Periodontitis has recently been recognized as an inflammatory disease caused by oxidative stress, with mitochondrial dysfunction being a key factor leading to oxidative stress. PTEN-induced kinase 1 (PINK1) is an essential protein for mitochondrial quality control, which protects cells from oxidative stress by inducing mitophagy to degrade damaged mitochondria, but its role in periodontitis has not been elucidated. This study aimed to explore the contribution and underlying mechanisms of Pink1 in regulating the differentiation and function of osteoclasts during periodontitis. Here we observed a significant downregulation of PINK1 expression in periodontitis-affected tissues. Then we constructed a periodontitis model in mice with fluorescently labeled mononuclear/macrophages, and the results showed that as the modeling time extended, the alveolar bone destruction gradually worsened and was accompanied by gradually decreased Pink1 expression in osteoclasts and a significantly increased osteoclast number. In vitro experiments further demonstrated a negative correlation between Pink1 and osteoclast differentiation. In addition, alveolar bone destruction in the <i>Pink1</i> knockout mice was significantly more advanced than that in the littermate wild type mice after ligature-induced periodontitis and enhanced osteoclastogenesis and bone-resorptive capacity in vitro. RNA-sequencing analysis and in vitro validation revealed that the absence of Pink1 led to a decrease in oxidative phosphorylation levels and an enhancement of calcium-mediated signaling, specifically the calcineurin-NFATc1 pathway, via an intracellular calcium source. Further mechanistic studies found that the deficiency of Pink1 inhibited mitophagy but strengthened mitochondrial-endoplasmic reticulum coupling, which, by promoting the interaction of Mfn2-IP3R-VDAC1 proteins, increased the concentration of mitochondrial calcium ions, thereby triggering more active osteoclast differentiation. The aforementioned process can be reversed by the IP3R channel inhibitor Bcl-XL. These findings unveiled that Pink1 was involved in osteoclast differentiation by regulating mitochondrial calcium transport mediated by mitochondria-associated endoplasmic reticulum membranes, providing a new theoretical basis for the pathogenesis and treatment of periodontitis.</p>","PeriodicalId":94075,"journal":{"name":"Journal of dental research","volume":" ","pages":"753-762"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143618002","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":"Response to Letter to the Editor, \"Oral Health Research in the WHO African Region between 2011 and 2022: A Scoping Review\".","authors":"A Carrasco-Labra, M Glick","doi":"10.1177/00220345251339397","DOIUrl":"10.1177/00220345251339397","url":null,"abstract":"","PeriodicalId":94075,"journal":{"name":"Journal of dental research","volume":" ","pages":"807"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144175599","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":"TTP as Tumor Suppressor and Inflammatory Regulator in Oral Carcinogenesis.","authors":"D M Ferri, M Ayre, L Ariza Bareño, M Stedile, A V DiGaudio, G Fernandez Ugazio, E C Kordon, P J Blackshear, A Urtreger, A R Raimondi","doi":"10.1177/00220345251316828","DOIUrl":"10.1177/00220345251316828","url":null,"abstract":"<p><p>The stability of messenger RNA (mRNA) is controlled by proteins that bind to adenosine-uridine-rich sequences (AREs) in their 3' untranslated regions (3'UTR), known as AU-binding proteins. One of these proteins is tristetraprolin (TTP; encoded by <i>Zfp36</i>), which promotes degradation of mRNAs with AREs in their 3'UTR. TTP accelerates the decay of its target transcripts, many of which encode proinflammatory mediators that promote tumorigenesis. TTP underexpression has been reported in multiple cancer types. Oral squamous cell carcinoma is an aggressive disease characterized by high morbidity and few therapeutic options. The role of TTP has not been studied in oral epithelium homeostasis nor in its carcinogenesis. Herein, using tissue-specific TTP knockout mice (TTP-KO), we show that TTP expression is relevant for oral epithelium homeostasis. TTP-KO mice developed dysplastic lesions in the tongue along with inflammatory infiltrates in the connective tissue. Analysis of the inflammatory infiltrate revealed the presence of mast cells (MCs), CD45+ cells, and CD11b+ cells, with the MCs being the most abundant cell type and associated with cyclooxygenase-2 expression. Recruitment of MCs was dependent on tumor necrosis factor-α (TNFα) upon TTP ablation in the tongue. Although the infiltration of MCs was dependent on TNFα activity, this did not affect the development of tongue dysplasia. We analyzed the status of the NF-κB pathway, finding its activation. In addition, we demonstrate that K-ras activation combined with <i>Zfp36</i> deletion leads to the rapid onset of the oral tongue phenotype and significantly reduces mouse survival. Our results support the notion that TTP expression protects against oral carcinogenesis, regulates the inflammatory infiltrate, and maintains the epithelial microenvironment, potentially serving as a barrier to tumorigenesis.</p>","PeriodicalId":94075,"journal":{"name":"Journal of dental research","volume":" ","pages":"795-805"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143618005","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":"Release of Bisphenol A from Dental Materials: Risks and Future Perspectives.","authors":"A Tichy, T Srolerova, F Schwendicke","doi":"10.1177/00220345251337728","DOIUrl":"https://doi.org/10.1177/00220345251337728","url":null,"abstract":"<p><p>The gradual phaseout of dental amalgam has contributed to a significant increase in the use of resin-based materials. While these materials offer several desirable properties, concerns persist regarding their biocompatibility, particularly the release of bisphenol A (BPA). BPA is an endocrine-disrupting chemical linked to adverse effects on human health, including reproductive, developmental, and metabolic disorders. Although food contact materials are the primary source of human BPA exposure and the contribution of dental materials is minor, the associated risks cannot be dismissed due to BPA's nonmonotonic dose-response relationship. In 2023, the European Food Safety Authority proposed a 20,000-fold reduction in the tolerable daily intake of BPA to 0.2 ng/kg body weight, citing immune system effects at extremely low doses. This proposal has sparked regulatory and scientific debate, as adopting such a stringent limit would effectively ban the use of BPA in food contact materials and many other products. Given this context, it is essential to assess the release of BPA from dental materials both in vitro and in vivo. However, data interpretation is complicated by methodological inconsistencies, including variations in material composition, specimen preparation, choice of extraction media, experimental duration, and analytical methods. In addition, pivotal differences in reporting results make it difficult to synthesize findings and draw reliable conclusions. This review examines the controversy surrounding BPA, critically evaluates evidence on its release from dental materials, and explores mitigation strategies. By highlighting gaps in knowledge and proposing future research directions, this review aims to provide clinicians, researchers, and policymakers with a clearer understanding of BPA-related complexities, ultimately contributing to patient safety and material innovation.</p>","PeriodicalId":94075,"journal":{"name":"Journal of dental research","volume":" ","pages":"220345251337728"},"PeriodicalIF":0.0,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144311113","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":"Perineural Invasion Exhibits Traits of Neurodegeneration.","authors":"M Zhang, M Yuan, K Asam, Z Gong, T Xie, F Gleber-Netto, M D Santi, Y Kobayashi, E Shimizu, B Aouizerat, M Amit, M D Boada, Y Ye","doi":"10.1177/00220345251334379","DOIUrl":"https://doi.org/10.1177/00220345251334379","url":null,"abstract":"<p><p>Perineural invasion (PNI) frequently occurs in head and neck squamous cell carcinoma (HNSCC), which correlates with poor survival and induces intractable pain and numbness. There is no effective treatment for PNI or associated pain. To gain a better understanding of PNI at the molecular and cellular level, we produced an orthotopic, syngeneic mouse model of PNI by inoculating mouse oral cancer cells into the infraorbital nerve (ION), a nerve that is susceptible to cancer invasion in patients with HNSCC. Mice with PNI in the ION exhibited both evoked and spontaneous nociception and impaired oral function, mimicking human conditions. PNI resulted in a drastic reduction in the proportion and altered mechanical thresholds in mechanically sensitive trigeminal neurons; axon and myelin abnormalities, as well as phagocytic cells, were observed. The tumor bed is marked by CD4⁺ and CD8⁺ T cells, CD68⁺ cells, and F4/80⁺ macrophages, while CD4⁺, CD8⁺, and CD68⁺ immune cells can be found surrounding the nerve. The intraneural niche is predominantly marked by CD68 that does not overlap with F4/80 but instead overlaps with NF200 and MPZ and occasionally with DAPI, suggesting these are likely phagocytic macrophages or Schwann cells. Finally, our RNA sequencing pathway analysis in mouse and human HNSCC found perturbed pathways in neuroinflammation, mitochondrial dysfunction, and cellular metabolism. Additionally, ION-PNI exhibits nerve degenerative features with perturbed pathways that are observed in Alzheimer, Parkinson, and prion diseases. In conclusion, we report a novel, anatomically relevant in vivo model that could be used to study the cellular and molecular mechanisms of PNI-induced neuropathies. Importantly, we found that PNI resembles neurodegenerative diseases with features of altered sensory transduction and conduction, neuroinflammation, and mitochondrial dysfunction, which may underlie peripheral neuropathies, such as pain.</p>","PeriodicalId":94075,"journal":{"name":"Journal of dental research","volume":" ","pages":"220345251334379"},"PeriodicalIF":0.0,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144259698","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}