Journal of Dental Research最新文献

{"title":"Epithelial Rests of Malassez Form a Wnt-Dependent Mechanoresponsive Network.","authors":"B Liu,I Lambrichts,E Chang,M M Torabi,F Aellos,P C Ochweri,I Evens,M R James,M A Hakeam,C Huang,J B Brunski,F Hermans,J A Helms","doi":"10.1177/00220345261455868","DOIUrl":"https://doi.org/10.1177/00220345261455868","url":null,"abstract":"Epithelial rests of Malassez (ERMs) constitute a 3-dimensional epithelial meshwork extending from the tooth apex to the junctional epithelium (JE). This position, coupled with observations from a variety of injury models, suggests that ERMs may be involved in sensing disruptions to the mechanical integrity of the periodontium. To test this hypothesis, finite element modeling was employed to predict strain states in tissues surrounding ERMs (e.g., the periodontal ligament [PDL], supracrestal connective tissues, and the JE), which, by virtue of their attachment to the tooth surface, experience distortional strains during mastication. An in vivo hyper-loading mouse model was employed to map these distortional strains to location-specific and time-dependent morphological changes in ERMs. Quantitative immunohistochemistry was used to interrogate ERMs for changes in the expression of Piezo1, β4 integrin, plectin, YAP, TRPV4, and phosphorylated FAK. Collagen and oxytalan fiber organization around ERMs was compared between normal- and hyper-loading conditions. Axin2CreERT2;R26RmTmG/+ mice were used to lineage-trace Wnt-responsive ERMs under normal and hyper-loading conditions, and Wnt signaling from ERMs and the JE was disrupted using K14CreERT2;Wlsfl/fl mice. Collectively, these analyses predicted that hyper-loading produced high distortional strains in the JE and supracrestal connective tissues, which correlated with sites of ERM enlargement. ERMs expressed mechanosensory proteins, whose levels were significantly elevated by hyper-loading. Load-activated ERMs were Wnt-responsive, and if Wnt secretion was blocked, then ERMs no longer expressed mechanosensory proteins and no longer enlarged in response to hyper-loading. A deterioration in the JE attachment and the PDL followed. Thus, the ERM network is positioned to sense distortional strains produced by mastication; they possess the molecular machinery to sense and respond to masticatory forces and, via a Wnt-dependent mechanism, coordinate tissue-level responses to mechanical loading in the PDL, supracrestal connective tissues, and the JE.","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":"260 1","pages":"220345261455868"},"PeriodicalIF":7.6,"publicationDate":"2026-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148408365","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":"Periodontitis-Aggravated Diabetic Kidney Disease with Altered Glycolysis.","authors":"Y Shi,X Zhu,J Li,Y Liu,C Li,Y Yang,X He,H Liu","doi":"10.1177/00220345261455840","DOIUrl":"https://doi.org/10.1177/00220345261455840","url":null,"abstract":"Diabetic kidney disease (DKD) is a leading cause of end-stage renal disease, and its progression is influenced by metabolic and inflammatory factors beyond hyperglycemia. Periodontitis, a common chronic inflammatory disease, has been associated with adverse renal outcomes in diabetes, but the underlying mechanisms remain unclear. The objective of this study is to evaluate the impact of experimental periodontitis (EP) on DKD progression and its association with renal glycolytic alterations. EP was induced in male db/db mice using silk ligation combined with Porphyromonas gingivalis administration. Renal function, histopathology, inflammatory responses, and glycolytic metabolism were assessed in vivo. Transcriptomic datasets were integrated for pathway analysis, and in vitro experiments were performed in human proximal tubular epithelial (HK-2) cells. EP significantly exacerbated kidney dysfunction and renal fibrosis in diabetic mice without further increasing fasting blood glucose levels. These changes were accompanied by enhanced epithelial-mesenchymal transition (EMT) activation in renal tubular cells. Diabetic kidneys exhibited increased expression of glycolytic-related enzymes and lactate accumulation and decreased adenosine triphosphate levels and NAD+/NADH ratios; these alterations were further aggravated by EP. Bioinformatic analysis revealed enrichment of EMT- and mTORC1-related pathways in DKD with periodontitis. Pharmacologic inhibition of mammalian target of rapamycin (mTOR) partially attenuated EP-associated renal dysfunction, fibrosis, partial EMT, and glycolytic alterations. In HK2 cells, tumor necrosis factor-α amplified high-glucose-induced (mTOR)/hypoxia-inducible factor-1α (HIF-1α) activation, glycolysis, and EMT; these alterations were attenuated by rapamycin or HIF-1α silencing. Together, these findings suggest that periodontitis is associated with aggravated DKD through altered glycolysis, partial EMT, and fibrosis. The mTOR/HIF-1α axis may represent a linking pathway between periodontal inflammation and metabolic and phenotypic alterations in renal tubular cells.","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":"251 1","pages":"220345261455840"},"PeriodicalIF":7.6,"publicationDate":"2026-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148372792","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":"Gold Nanoparticles Enhance the Antibacterial and Osteogenic Properties of Polyetheretherketone.","authors":"H Tang,J Yan,X Zhan,Y Qin,M Bai,H Lin,D Xia","doi":"10.1177/00220345261454554","DOIUrl":"https://doi.org/10.1177/00220345261454554","url":null,"abstract":"Polyetheretherketone (PEEK) is a promising implant material due to its excellent physicochemical properties and bonelike mechanical strength. However, its inherent lack of antibacterial and osteogenic activities limits broader clinical application. In this study, gold nanoparticles of three sizes were synthesized and immobilized onto the PEEK surface via polydopamine-assisted deposition, constructing a functional coating. The results demonstrated that the coated PEEK exhibited significantly enhanced antibacterial performance, which was more pronounced with smaller nanoparticle sizes. Moreover, the modified surface favored the early adhesion of bone mesenchymal stem cells. Both in vitro and in vivo experiments confirmed that this coating effectively promoted the osseointegration of PEEK implants. In summary, this work presents a potential surface treatment strategy to endow PEEK with enhanced osteogenic and antimicrobial properties.","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":"37 1","pages":"220345261454554"},"PeriodicalIF":7.6,"publicationDate":"2026-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148372791","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":"Reorienting Oral Health Promotion through Systems Thinking","authors":"D. Duijster, M. de Jong-Lenters, C.M.C. Volgenant","doi":"10.1177/00220345261453896","DOIUrl":"https://doi.org/10.1177/00220345261453896","url":null,"abstract":"The impact of oral health promotion efforts is hampered by a predominant focus on individual behavior and clinically oriented prevention, which addresses only a narrow part of the complex systems that influence oral disease outcomes. This article applies systems thinking to reorient oral health promotion toward deeper structural and societal determinants. The Action Scales Model (ASM) is introduced as a practical framework that distinguishes 4 interconnected levels at which action can be taken: events (what is happening), structures (how the system is organized), goals (what the system is set up to achieve), and beliefs (the assumptions and values that legitimize those goals and structures). Using the ASM, the oral health care and public health systems are examined to reveal where current efforts are concentrated and where opportunities for transformation lie. Most activity remains at the event level, where behavior change programs and treatment‑oriented care dominate. Structural features, such as financing mechanisms, workforce organization, and weak integration of oral health within public health systems, reinforce this narrow focus. At deeper levels, prevailing goals and beliefs continue to emphasize individual responsibility and market‑driven delivery rather than equity, prevention, and societal well-being. Meaningful system change requires shifting these underlying goals and beliefs, reframing oral health as a socially determined outcome and therefore a collective responsibility. While the ASM cannot fully capture complex realities, it offers a useful methodological framework to support reflection, dialogue, and more coherent system‑level action in oral health promotion.","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":"34 1","pages":""},"PeriodicalIF":7.6,"publicationDate":"2026-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148365193","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":"Porphyromonas gingivalis-Induced NETs Mediate Neuroinflammation via TLR4 Activation.","authors":"L Xu,Y Zhou,H Chen,J Zhuang,Y Jiang,T Li,Z He,Z Song,W Zhou","doi":"10.1177/00220345261425925","DOIUrl":"https://doi.org/10.1177/00220345261425925","url":null,"abstract":"Periodontitis, caused by periodontal pathogens such as Porphyromonas gingivalis, is a risk factor for Alzheimer's disease (AD) progression. Neutrophils, which are abundant in patients with periodontitis, release neutrophil extracellular traps (NETs) to resist microbial infection. We explored the mechanism and effects of P. gingivalis-induced NETs on the relationship between periodontitis and neuroinflammation. A murine periodontitis model was established via oral local application of P. gingivalis with or without tak242 (TLR4 inhibitor). Maxillary bones were evaluated via micro-computed tomography. The proportion of neutrophils was determined by flow cytometry. NET formation and morphology were analyzed via a cell-free DNA kit, a neutrophil elastase enzyme-linked immunosorbent assay (ELISA) and myeloperoxidase ELISA kit, reverse transcription polymerase chain reaction (RT-PCR), western blotting and immunofluorescence. Behavior tests were used to investigate cognitive ability. Neuroinflammation was assayed by immunohistochemistry (IHC) and RT-PCR. Amyloid precursor protein (APP) processing was measured by IHC. In vitro experiments explored the functional mechanism underlying the effects of P. gingivalis-induced NETs on the neuron-glia unit. We observed significant alveolar bone resorption with elevated neutrophil count and increased NET formation in mice with periodontitis. Cognitive abilities were impaired by periodontitis. Neuroinflammation manifested as glia activation and upregulated inflammatory cytokines, and APP processing was altered by the elevated expression of APP and PSEN1. These changes were specifically reversed by tak242. In vitro, P. gingivalis-induced NETs mediated M1 polarization in BV2 cells and changed APP processing in N2a cells, along with the activation of TLR4/Myd88/NF-κB and GSK3β/Akt, which is consistent with the in vivo findings. In conclusion, P. gingivalis-induced NETs play pivotal roles in the relationship between neuroinflammation and cognitive impairment. Furthermore, the effects of P. gingivalis-induced NETs on neuron-glia unit were related to TLR4 activation.","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":"74 1","pages":"220345261425925"},"PeriodicalIF":7.6,"publicationDate":"2026-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148348842","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oral Burden of Sjögren Disease: A Systematic Review and Meta-analysis","authors":"Á. Heizer, M. Kisgergely, B. Szabó, Z. Sipos, J. Lee, X. Qian, G. Varga, P. Hegyi, K. Márton","doi":"10.1177/00220345261450057","DOIUrl":"https://doi.org/10.1177/00220345261450057","url":null,"abstract":"Primary Sjögren disease (pSjD) is associated with a wide range of oral manifestations, including mucosal alterations such as oral ulcers, stomatitis, angular cheilitis, papillary atrophy, and tongue fissuration, as well as oral sequelae of sicca symptoms, including dysphagia, dysgeusia, and chewing difficulties. In addition to these oral findings, pSjD also presents with systemic manifestations such as arthritis, cutaneous vasculitis, and involvement of internal organs. This systematic review and meta-analysis aimed to assess the risk of oral disorders and differences in cariological and periodontal indices in pSjD patients compared with controls. The systematic search was conducted in PubMed, EMBASE, and CENTRAL on November 8, 2024 (PROSPERO: CRD42024608240). Studies meeting the eligibility criteria included adult patients with pSjD. Primary outcomes included the odds ratio (OR) and prevalence of oral disorders as well as the mean difference (MD) and single mean values of dental indices. Meta-analyses were performed using random-effects models to calculate pooled outcome measures and corresponding 95% confidence intervals (CIs). Seventy-five studies were included in the systematic review, with 49 eligible for meta-analysis. The following oral disorders showed increased risk: candidiasis (OR: 10.5; CI: 6.99 to 15.79), dysphagia (OR: 26.78; CI: 20.94 to 34.25), dysgeusia (OR: 17; CI: 4.52 to 63.96), stomatitis (OR: 2.65; CI: 2.17 to 3.23), angular cheilitis (OR: 6.31; CI: 1.94 to 20.53), papillary atrophy (OR: 6.68; CI: 1.12 to 42.16), and fissured tongue (OR: 11.72; CI: 3.42 to 40.18). Patients with pSjD were found to have fewer teeth (MD: −2.16; CI: −4.27 to −0.05) and a higher decayed, missing, filled teeth (MD: 4.72; CI: 3.01 to 6.43) and decayed, missing, filled surfaces (MD: 20.45; CI: 10.16 to 30.74) scores. Furthermore, periodontal parameters showed no significant differences. Patients with pSjD have up to a 30-fold higher risk of developing various oral disorders, emphasizing the need for preventive dental care and early recognition.","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":"33 1","pages":""},"PeriodicalIF":7.6,"publicationDate":"2026-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148322016","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":"Gingival Fibroblast-Driven Osteoimmunology via the IL-33-ILC2-IL-13 Axis.","authors":"Y Sato,T Kondo,K Otake,S Ambo,A Ashry,K Engkatanachai,H Egusa","doi":"10.1177/00220345261449746","DOIUrl":"https://doi.org/10.1177/00220345261449746","url":null,"abstract":"Tooth extraction is a fundamental dental intervention for managing oral infections; however, the resulting tooth loss is associated with systemic health risks, including cognitive decline and increased mortality. Alveolar bone resorption following tooth extraction significantly alters jaw morphology, complicating subsequent functional rehabilitation. Despite its clinical significance, the cellular and molecular mechanisms governing bone regeneration within extraction sockets remain poorly understood. Here, we identified group 2 innate lymphoid cells (ILC2s) as pivotal regulators of alveolar bone regeneration following tooth extraction. Using single-cell RNA sequencing and flow cytometry, we demonstrated that ILC2s accumulate and persist within extraction sockets beyond the acute inflammatory phase. Genetic lymphocyte ablation revealed that loss of all ILCs severely impairs bone formation, highlighting their essential role in socket regeneration. Following tooth extraction, ILC2s exhibited increased interleukin (IL)-13 production and promoted bone formation via IL-13-mediated activation of bone marrow-derived mesenchymal stromal cells. Single-cell RNA sequencing and histological analyses suggested that gingival fibroblasts are a major source of IL-33 in extraction sockets during mucosal healing. IL-33 activated ILC2s, increasing IL-13 production and promoting osteogenesis, whereas IL-33 neutralization suppressed ILC2 activation and impaired socket bone regeneration. Collectively, these findings suggest that the gingival fibroblast-IL-33-ILC2-IL-13 axis may contribute to the regulation of alveolar bone regeneration following tooth extraction. This study provides a biological basis for developing novel therapeutic strategies to optimize postextraction bone preservation.","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":"5 1","pages":"220345261449746"},"PeriodicalIF":7.6,"publicationDate":"2026-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148299271","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":"FSTL3-Driven Cuproptosis Resistance and EPCs Promote OSCC Metastasis.","authors":"S-R Li,Z-Z Wu,W-D Wang,W-T Mo,Q Wang,E-L Yang,W-Y Wang,Q-C Yang,H Li,T-F Wu,Z-J Sun","doi":"10.1177/00220345261442182","DOIUrl":"https://doi.org/10.1177/00220345261442182","url":null,"abstract":"Lymph node metastasis, critically dependent on evasion of cancer cell death, drives poor prognosis in oral squamous cell carcinoma (OSCC). Through CRISPR-Cas9 screening in OSCC cell lines with divergent metastatic potential, we identified follistatin-like 3 (FSTL3) as a master regulator of lymph node metastasis. Fstl3 knockdown drastically suppressed metastasis. Mechanistically, FSTL3 loss induced cuproptosis susceptibility by suppressing SLC25A10, triggering mitochondrial succinate accumulation. Succinate promoted succinylation and upregulation of dihydrolipoamide S-acetyltransferase (DLAT), essential for cuproptosis execution, thereby crippling metastatic spread. Crucially, FSTL3 simultaneously orchestrates an immunosuppressive tumor microenvironment. FSTL3 recruits erythroid progenitor cells (EPCs) into tumor sites by upregulating CCR5 on EPCs. Concurrently, FSTL3-exposed EPCs exhibited elevated CD73 and PD-L1, establishing an immunosuppressive niche that promotes metastasis. Consequently, FSTL3 depletion in immunotherapy-resistant tumors unleashed potent antitumor immunity and synergized with immunotherapy. Our findings establish FSTL3 as a pivotal node coordinating dual metastasis mechanisms: cuproptosis resistance and immune evasion. Targeting FSTL3 disrupts both adaptive programs, effectively inhibiting lymph node metastasis. This work nominates FSTL3 as a therapeutic target; combining FSTL3 inhibition with immunotherapy represents a promising dual-targeting strategy to improve OSCC outcomes by simultaneously disabling cancer cell survival and immune escape.","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":"22 1","pages":"220345261442182"},"PeriodicalIF":7.6,"publicationDate":"2026-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147702218","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":"AI in Oral Health Surveillance: Critical Review","authors":"Z. Chen, P. Liu, K. Han, P. Liao, Y. Yang, M.C.M. Wong, C.K.Y. Yiu, E.C.M. Lo","doi":"10.1177/00220345261434568","DOIUrl":"https://doi.org/10.1177/00220345261434568","url":null,"abstract":"Artificial intelligence (AI) holds transformative potential for advancing oral health surveillance by streamlining data collection, integration, and dissemination. This review critically synthesizes AI applications in oral health surveillance, highlighting its roles in 1) mapping population-level trends and oral health inequities using machine learning on epidemiological data; 2) enabling remote screening of oral diseases/conditions, including caries, oral hygiene, gingivitis, oral cancer, and malocclusion from intraoral images via computer vision models; and 3) integrating multimodal data through emerging large language models (LLMs) to enhance precision public health. We clarify the comparative strengths of distinct AI modeling for processing the primary data types in surveillance: structured clinical records, unstructured images, and integrated multimodal data. Traditional machine learning methods have been effectively applied to map population-level oral health disparities and identify risk factors but are constrained to structured data. Computer vision methods excel in individual-level diagnostics using intraoral photographs. To translate such capability into scalable surveillance, it is recommended to establish standardized imaging protocols for nonclinical settings, develop scalable models for fine-grained feature extraction, and implement reliable evaluation. These steps are essential to address pervasive challenges, including inconsistent image quality, domain shift, prevalence imbalance, and cost-effectiveness constraints. The future of AI-driven oral health surveillance lies in developing dental-adapted multimodal LLMs (MLLMs). Such MLLMs are uniquely capable of synthesizing disparate data streams, from structured clinical data to heterogeneous imaging modalities (e.g., intraoral photographs and radiographs), or even biomolecular data. This integration capacity facilitates a paradigm shift, moving current applications in dental consultation and clinical decision support toward a novel, tiered system for population-level monitoring. Such a system would provide actionable insights for public health policymaking via spatiotemporal analysis and causal inference. Next-generation AI-driven oral health surveillance systems can only succeed when built on a strong foundation of rigorous ethical principles and safeguards.","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":"68 1","pages":""},"PeriodicalIF":7.6,"publicationDate":"2026-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147641404","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":"Response to Letter to the Editor: “Tooth Loss in Individuals with Dementia: A Swedish Register-Based Cohort Study”","authors":"M. Mohammadi, J. Holmer, H. Imberg, H. Albrektsson, M. Eriksdotter, K. Buhlin","doi":"10.1177/00220345261435933","DOIUrl":"https://doi.org/10.1177/00220345261435933","url":null,"abstract":"","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":"112 1","pages":""},"PeriodicalIF":7.6,"publicationDate":"2026-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147635826","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}