Journal of periodontal research最新文献

{"title":"Systemic RVX-208 Attenuates Experimental Periodontitis Through Inflammatory Host Modulation.","authors":"Sheikh Alam, Simrah Ansari, Birtan T Yilmaz, David J Cohen, James Sugai, Caroline Carrico, Melissa Morgan, Matthew S Halquist, Sinem Esra Sahingur, Barbara D Boyan, Zvi Schwartz, William V Giannobile, Zhao Lin","doi":"10.1111/jre.70183","DOIUrl":"https://doi.org/10.1111/jre.70183","url":null,"abstract":"<p><strong>Aims: </strong>This study investigated whether systemic treatment of RVX-208, a selective BET protein inhibitor, could ameliorate experimental periodontitis in a prophylactic setting and examined transcriptomic changes associated with RVX-208 in vitro.</p><p><strong>Methods: </strong>Porphyromonas gingivalis (Pg) lipopolysaccharide (LPS) was injected into gingiva in mice twice a week for 6 weeks to induce periodontitis. RVX-208 or vehicle was administered via oral gavage every Monday-Friday, beginning 1 week before LPS injection and continuing for 7 weeks. The periodontal bone loss and osteoclastic activity were evaluated through micro-CT and histological analyses. THP-1 human monocytic cells were treated with Pg bacteria, with or without RVX-208 and JQ1, and RNA-sequencing was performed.</p><p><strong>Results: </strong>Pg LPS delivery led to periodontal bone loss in mice. Compared with vehicle, systemic treatment of RVX-208 reduced alveolar bone loss and the number of tartrate-resistant acid phosphatase (TRAP) positive cells. In vitro, RVX-208 suppressed the expression of a set of inflammatory genes in THP-1 cells and led to a more moderate and limited effect on transcriptome compared to pan-BET inhibitor JQ1.</p><p><strong>Conclusion: </strong>Systemic RVX-208 treatment reduced periodontal bone loss in a prophylactic setting in this experimental periodontitis model. In THP-1 cells, RVX-208 suppresses the global inflammatory response induced by Pg.</p>","PeriodicalId":16715,"journal":{"name":"Journal of periodontal research","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149149208","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Measuring the Wrong Variable: The Case for an Inflammatory Burden Axis in Oral-Systemic Research.","authors":"Karim El Kholy, Thomas E Van Dyke","doi":"10.1111/jre.70182","DOIUrl":"https://doi.org/10.1111/jre.70182","url":null,"abstract":"<p><p>Oral-systemic research often proposes an inflammatory mechanism while relying on measures of accumulated periodontal destruction; because staging records largely irreversible past damage, a treated and stable patient remains classified as Stage III while a patient with less destruction carries a substantially greater current inflammatory burden. This Perspective proposes an inflammatory burden axis for research use alongside clinical classification and introduces inflammatory burden-years, a time-integrated exposure that can be estimated from serial periodontal charting.</p>","PeriodicalId":16715,"journal":{"name":"Journal of periodontal research","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149137315","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Periodontal Salutogenesis: Why Are Some People Resistant to Oral Microbial Dysbiosis and Destructive Inflammation?","authors":"Bruno G Loos, Magda Feres, William V Giannobile, Hatice Hasturk, Egija Zaura","doi":"10.1111/jre.70173","DOIUrl":"https://doi.org/10.1111/jre.70173","url":null,"abstract":"<p><p>Periodontitis research has traditionally focused on pathogenesis; however, understanding why some individuals remain resistant to the disease may be even more important. The concept of salutogenesis (\"salutology\") has evolved around the capacity to remain resilient to life's stressors. An individual's sense of coherence (SOC) is based on generalized resistance resources (GRRs), including physiological, biological, material, psychological, interpersonal, and sociocultural factors. This review focuses mainly on physiological and biological resistance resources and briefly considers psychosocial coping, which together can generate actions that mitigate periodontal stressors, that is, periodontal risk factors. We focus on dental biofilm compositions compatible with resistance to periodontal destruction and host responses that promote homeostasis and resolve inflammation. Putative physiological and biological salutogenic factors described here are summarized in a five-cluster model. First, people may be resistant to periodontitis because their dental biofilm communities do not promote inflammation and exhibit resilience that maintains eubiosis. Furthermore, inherited DNA variants may modulate non-destructive, tolerant immunological and inflammatory responses. Protective epigenetic factors may also induce trained immunity with enhanced protective and inflammation-resolving capacity. Lifestyle-related salutogenic factors for periodontal health are better understood because they are also associated with general health. From an oral health standpoint, maintaining a consistent and effective daily oral hygiene routine is a straightforward way to protect against gingivitis. In addition, we emphasize dietary components that may support the resolution of inflammation, including specific omega-6 and omega-3 polyunsaturated fatty acids that serve as precursors of specialized pro-resolving mediators (e.g., lipoxins and resolvins); sufficient vitamins and other micronutrients may also be salutogenic. More broadly, systemic health may protect against systemic inflammation and its adverse effects on distant tissues and organs, including the periodontium. Finally, the absence of plaque-retentive factors in the dentition may be salutogenic by helping to prevent the transition from eubiosis to dysbiosis. We propose that resistance to periodontitis does not depend on any single cluster or specific factor but on individually variable, combined, and synergistic effects of multiple factors that maintain eubiosis, immune tolerance, and resolution of gingival inflammation. The key pillars of salutogenesis support a more holistic interpretation of resistance to periodontitis. This state-of-the-art review provides new insights into potential mechanisms that maintain periodontal health and enhance resistance to the onset of periodontitis.</p>","PeriodicalId":16715,"journal":{"name":"Journal of periodontal research","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149127849","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Periodontitis GWAS Reveal Immune-Biased Heritability Without Gingival Cell-Type Resolution.","authors":"Chengze Wang, Wenyue An, Mengna Lin, Ying Wang, Guoli Yang","doi":"10.1111/jre.70179","DOIUrl":"https://doi.org/10.1111/jre.70179","url":null,"abstract":"<p><p>Three methodologically distinct analyses partition periodontitis common-variant heritability across 27 gingival cell types. They agree on an immune-over-stromal direction but nominate three different top cell types, and a low-power analysis inverts the fibroblast signal; the current periodontitis GWAS therefore cannot resolve heritability to a single gingival cell type.</p>","PeriodicalId":16715,"journal":{"name":"Journal of periodontal research","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149127837","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Why Peri-Implant Tissues Are Susceptible to Inflammatory Breakdown-Single-Cell Transcriptomics Reveals Immune Priming in Clinically Healthy Peri-Implant Mucosa and CXCR2⁺ Neutrophil Activation in Peri-Implantitis.","authors":"Yi-Rao Lai, Jia-Ji Mo, Xin-Xin Ding, Rui-Ying Chen, Xiao-Lei Lv, Mario Romandini, Hong-Chang Lai, Shu-Jiao Qian","doi":"10.1111/jre.70180","DOIUrl":"https://doi.org/10.1111/jre.70180","url":null,"abstract":"<p><strong>Aim: </strong>Peri-implant tissues are more susceptible than gingiva to rapid inflammatory breakdown, but the cellular basis of this vulnerability remains unclear. This study investigated (1) whether clinically healthy peri-implant mucosa already displays an immune landscape distinct from healthy gingiva, and (2) which cellular states and molecular pathways characterize the transition from peri-implant health to peri-implantitis.</p><p><strong>Methods: </strong>An integrative single-cell RNA-sequencing analysis was performed using clinically healthy pre-loading peri-implant mucosa (n = 3), healthy gingiva (n = 17), and peri-implantitis tissues (n = 3). Healthy peri-implant mucosa was first compared with a healthy gingival reference atlas to define the baseline peri-implant immune niche. Disease-associated changes were then examined by comparing healthy peri-implant and peri-implantitis tissues. Key findings were validated in independent tissue cohorts comprising healthy gingiva, clinically healthy peri-implant mucosa, and peri-implantitis (n = 6 participants per group) using multiplex immunofluorescence, immunohistochemistry, and reactive oxygen species (ROS) detection.</p><p><strong>Results: </strong>Clinically healthy peri-implant mucosa showed greater immune-cell enrichment than healthy gingiva, most notably within the myeloid compartment. Among myeloid cells, a CXCR2⁺ neutrophil subset exhibited the highest baseline signature for neutrophil extracellular trap (NET) formation, indicating an immune-enriched state with enhanced NET-associated transcriptional potential, despite clinical health. In peri-implantitis, this CXCR2⁺ neutrophil subset expanded further and displayed increased oxidative, chemotactic, and NET-associated programs, supported by tissue validation of MPO, CXCR2, CitH3, and ROS signals. Cell-cell communication analysis nominated fibroblast-derived CXCL signaling as a potential contributor to CXCR2⁺ neutrophil recruitment. NSUN6, an RNA modification enzyme, was enriched in disease-associated CXCR2⁺ neutrophils, and NSUN6 knockdown in neutrophil-like cells attenuated CXCR2⁺ cell enrichment and NET-associated marker expression.</p><p><strong>Conclusion: </strong>Clinically healthy peri-implant mucosa before functional loading is not immunologically equivalent to gingiva, but represents an immune-primed niche that may lower the threshold for inflammatory breakdown. These findings may not be directly generalized to long-term functionally loaded implants. Peri-implantitis is characterized by amplification of an oxidative CXCR2⁺ neutrophil state, with fibroblast-derived CXCL-CXCR2 signaling and NSUN6-associated neutrophil activation emerging as candidate pathways for future diagnostic and therapeutic investigation.</p>","PeriodicalId":16715,"journal":{"name":"Journal of periodontal research","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149111114","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of Early Occlusal Therapy in Stage III and IV Periodontitis: A Prospective Cohort Study.","authors":"Rodolfo Gianserra, Michele La Rocca, Vittorio Gianserra, Nicholas Gianserra, Ludovico Sbordone","doi":"10.1111/jre.70174","DOIUrl":"https://doi.org/10.1111/jre.70174","url":null,"abstract":"<p><p>The combined protocol of dental splinting and occlusal adjustment was associated with greater short-term improvements in PD, CAL, and BOP following nonsurgical periodontal therapy in teeth with severe mobility.</p>","PeriodicalId":16715,"journal":{"name":"Journal of periodontal research","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149111152","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Peri-Implant Radiographic Measurements Compared With Intra-Surgical Assessments: Diagnostic Accuracy and Reproducibility.","authors":"Era Kakar, Parham Hazrati, Andrea Laureti, Zhaozhao Chen, Hom-Lay Wang","doi":"10.1111/jre.70169","DOIUrl":"https://doi.org/10.1111/jre.70169","url":null,"abstract":"<p><p>Not all peri-implant radiographic measurements. Across eight calibrated examiners, emergence angle and defect width were highly reproducible, but defect height, defect angle, and distal bone levels varied widely and underestimated the true defect size measured intrasurgically. Calibration and multi-examiner averaging matter.</p>","PeriodicalId":16715,"journal":{"name":"Journal of periodontal research","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149075085","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Systemic Impact of Peri-Implantitis: A Systematic Review.","authors":"Antonio Liñares, Stephane Kerner, Juan Blanco, Eduardo Montero, Maria Clotilde Carra","doi":"10.1111/jre.70167","DOIUrl":"https://doi.org/10.1111/jre.70167","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Aim: &lt;/strong&gt;To systematically evaluate the available evidence regarding the association between peri-implantitis and systemic inflammatory biomarkers and/or systemic diseases, and to assess whether peri-implantitis treatment influences systemic inflammatory burden. Particular attention was given to the methodological limitations of the available evidence and the potential role of residual confounding.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;A systematic review and meta-analysis were conducted in accordance with PRISMA guidelines. Electronic searches were performed in MEDLINE, Embase, Scopus, and Web of Science from inception to December 2025, and updated in April 2026. Observational studies comparing systemic inflammatory biomarkers and/or presence of systemic diseases between individuals with and without peri-implantitis, as well as interventional studies evaluating the impact of any peri-implantitis treatment on the systemic inflammatory burden, were included. Random-effects meta-analyses were performed using Hedges' g (standardized mean difference).&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Of 2399 records screened, 21 studies were included in the qualitative synthesis. Fourteen observational studies evaluated systemic inflammatory biomarkers, three randomized clinical trials assessed the effect of peri-implantitis treatment on systemic outcomes, and four observational studies investigated associations with systemic diseases. Comparative meta-analysis demonstrated significantly higher conventional CRP concentrations in patients with peri-implantitis than in healthy implant controls (Hedges' g = 3.73; 95% CI: 0.63-6.83; p = 0.02), although heterogeneity was considerable (I&lt;sup&gt;2&lt;/sup&gt; = 99%). In contrast, no significant differences were observed for high-sensitivity CRP (hsCRP) (Hedges' g = -0.29; 95% CI: -0.61 to 0.04; p = 0.09; I&lt;sup&gt;2&lt;/sup&gt; = 2%), IL-6, TNF-α, IL-10, or IL-1β. Evidence regarding systemic diseases was limited and heterogeneous, precluding quantitative synthesis. Interventional studies suggested modest and predominantly short-term reductions in selected inflammatory biomarkers following peri-implantitis treatment, whereas consistent improvements in systemic metabolic outcomes were not demonstrated.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;Current evidence suggests that patients with peri-implantitis may exhibit higher circulating conventional CRP concentrations in some observational studies. However, this finding should be interpreted cautiously given the substantial heterogeneity of the pooled analysis, the absence of significant differences for high-sensitivity CRP, and the limited control of major confounding factors, in particular previous or concomitant periodontitis and other shared inflammatory and metabolic risk factors. Consequently, it remains uncertain whether peri-implantitis represents an independent source of systemic inflammation or rather reflects a susceptible host phenotype characterized by shared inflammatory and metab","PeriodicalId":16715,"journal":{"name":"Journal of periodontal research","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149069844","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Periodontitis, Edentulism, and Accelerated Biological Aging: A Population-Based Study of Epigenetic Clocks.","authors":"Yi-Ning Chen, Lu Wang, Mario Romandini, Dominique S Michaud","doi":"10.1111/jre.70163","DOIUrl":"https://doi.org/10.1111/jre.70163","url":null,"abstract":"<p><strong>Aim: </strong>To examine whether periodontitis and its ultimate sequela (edentulism) are associated with accelerated epigenetic aging in older adults.</p><p><strong>Methods: </strong>A total of 1 926 adults aged ≥ 50 years with DNA-methylation (DNAm) and oral health data from the NHANES 1999-2002 cycles were included. Periodontitis (stages/grades) and edentulism were classified using the 2018 AAP/EFP framework via the ACES system. Epigenetic age acceleration was estimated using genome-wide DNAm for four clocks: HannumAge, HorvathAge, PhenoAge, and GrimAge2Mort. Survey-weighted linear regression models, adjusted for relevant confounders, assessed the relationship between periodontal status and epigenetic age acceleration.</p><p><strong>Results: </strong>In fully adjusted models, Stage III-IV periodontitis was associated with higher biological age acceleration compared with healthy/gingivitis/Stage I for three of the four clocks examined: PhenoAge +2.12 years (95% CI 0.64-3.59), HannumAge +1.48 years (0.34-2.62), and GrimAge2Mort +1.35 years (0.52-2.63). Associations with edentulism were stronger in 3 of the clocks: HorvathAge +1.31 years (0.00-2.62), HannumAge +1.92 years (0.72-3.12), and GrimAge2Mort +1.77 years (0.90-2.65). Accelerated aging was also observed in individuals with Grade B/C periodontitis for HorvathAge (+1.04 years; 0.35-1.72), HannumAge (+0.93 years; 0.26-1.60), and GrimAge (+0.55 years; 0.03 = 1.07), when compared with health/gingivitis/Grade A. Associations were also observed between mean interproximal CAL and age acceleration in all four clocks.</p><p><strong>Conclusion: </strong>Severe and higher-grade periodontitis, as well as edentulism, are associated with higher epigenetic aging acceleration, suggesting that these oral conditions may reflect-or potentially contribute to-systemic biological aging.</p>","PeriodicalId":16715,"journal":{"name":"Journal of periodontal research","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149025100","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Periodontitis, Tooth Loss, and Risk of Cognitive Impairment and Dementia: A Systematic Review With Meta-Analysis.","authors":"Ryan T Demmer, David Watson, Charlene E Goh, Lyubov D Slashcheva, Sarah E Tom, Miao Xian Zhou, Moritz Kebschull, Souvik Sen, James M Noble, Panos N Papapanou","doi":"10.1111/jre.70177","DOIUrl":"https://doi.org/10.1111/jre.70177","url":null,"abstract":"<p><strong>Aim: </strong>To systematically review and meta-analyze cohort studies evaluating associations of gingival inflammation, periodontitis, and tooth loss with cognitive decline and incident mild cognitive impairment or dementia.</p><p><strong>Methods: </strong>PROSPERO-registered searches of MEDLINE, Embase, Scopus, Web of Science, and the Cochrane Library identified cohort studies from inception through October 10, 2025, with a PubMed update on June 24, 2026. Random-effects meta-analyses pooled adjusted hazard ratios (HRs) for dementia/MCI; cognitive function outcomes were summarized qualitatively. Risk of bias (RoB) was assessed using the Newcastle-Ottawa Scale.</p><p><strong>Results: </strong>Fifty-nine studies met inclusion criteria; 28 contributed to dementia/MCI meta-analyses. Severe periodontitis (HR: 1.16; 95% CI: 1.06-1.27; I² = 0%; Q-test p = 0.49), periodontitis of unspecified severity (HR: 1.45; 95% CI: 1.21-1.73; I² = 98%; Q-test p < 0.001), edentulism (HR: 1.26; 95% CI: 1.19-1.33), and low tooth count (HR: 1.27; 95% CI: 1.14-1.42; I² = 94%; Q-test p < 0.001) were associated with elevated dementia/MCI risk. RoB was low in 31 studies (53%), moderate in 25 (42%), and high in 3 (5%); inadequate confounder adjustment was common. Meta-regression showed stronger estimates for ICD-code periodontitis definitions (fold change (FC) = 1.44 95% CI: 1.04-2.01), older cohorts (FC per year = 1.02 95% CI: 1.00, 1.05), and weaker estimates with lower RoB (FC per NOS star = 0.81 95% CI: 0.73-0.92). Follow-up duration, cohort age, and RoB were not associated with tooth-count estimates.</p><p><strong>Conclusion: </strong>Periodontitis and tooth loss are associated with modestly higher dementia/MCI risk and poorer cognitive function, but heterogeneity, residual confounding, and bias temper causal interpretation. Longitudinal studies with rigorous baseline cognition assessment and intervention studies are needed.</p>","PeriodicalId":16715,"journal":{"name":"Journal of periodontal research","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148977057","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}