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Objectives: In order to predict the patients' prognosis with tongue squamous cell carcinoma (SCC), this study set out to develop a clinically useful and trustworthy prognostic nomogram. Subjects and Methods: The Surveillance, Epidemiology, and End Results (SEER) Program was used to compile clinical information on patients with tongue SCC between 2010 and 2015. The likelihood of Cancer‐Specific Survival (CSS) and Overall Survival (OS) for specific patients was predicted using a prognostic nomogram created with the help of the RStudio software. The nomogram's predictive ability was evaluated using the consistency index (C‐index) and decision curve analysis, and the nomogram was calibrated for 1‐, 2‐, 3‐, 5‐, and 10‐year CSS and OS. Results: Patients numbering 6453were enrolled in this study. The primary cohort (3895) and validation cohort (2558) were each randomly assigned. Sex, age, tumor‐node‐metastasis (TNM) stage, surgery, chemotherapy, and radiation were significant risk factors for OS, whereas age, TNM stage, surgery, chemotherapy, and radiotherapy were significant risk factors for CSS. Additionally, C‐index and calibration curves indicated that the prognostic nomogram prediction and the actual observation in both cohorts would be very coherent. Conclusions: The predictive nomogram created in this study can offer patients with tongue SCC customized treatment and survival risk assessment. [ABSTRACT FROM AUTHOR]

Background: An increasing number of studies have shown that dysregulated miR-589-3p is associated with multiple diseases. However, the role of miR-589-3p in osteogenic differentiation of periodontal ligament stem cells (PDLSCs) remains unknown. This study aimed to explore the biological function and potential molecular mechanism of miR-589-3p in osteogenic differentiation of PDLSCs. Methods: GSE159508 was downloaded from Gene Expression Omibus (GEO, http://www.ncbi.nlm.nih.gov/geo/). Differentially expressed miRNAs between osteogenic induction PDLSCs versus non-induction PDLSCs were obtained by R software. miR-589-3p mimic and miR-589-3p inhibitor and corresponding negative control were obtained and to identify the role of miR-589-3p in osteogenic differentiation of PDLSCs. ALP staining and ARS were used to evaluate ALP activity and mineralization, respectively. The targeted binding relationship between miR-589-3p and ATF1 was predicted and verified by target prediction analysis and dual-luciferase assay. Furthermore, the functional mechanism based on miR-589-3p and ATF1 in osteogenic differentiation of PDLSCs was further investigated through rescue experiments. Results: According to the cut-off criteria with log 2 FC > 1.0 and P < 0.05, 514 differentially expressed miRNAs were identified between osteogenic induction and non-induction PDLSCs, including 309 upregulated miRNAs and 205 downregulated miRNAs. Compared with control PDLSCs, miR-589-3p expression level was notably increased in PDLSCs that underwent osteogenic induction. The overexpression of miR-589-3p promoted the cell viability of PDLSCs, while the low expression of miR-589-3p had the opposite effect. The dual luciferase reporter assay verified that ATF1 was proved to be a direct target of miR-589-3p in PDLSCs. And overexpressed miR-589-3p reduced the expression of ATF1. Overexpression of miR-589-3p enhanced the osteogenic capacity of PDLSCs, as demonstrated by increases in ALP activity, matrix mineralization, and RUNX2, OCN and OSX expression. In addition, the rescue experiments confirmed that overexpressed ATF1 restored the effects of overexpressed miR-589-3p on cell proliferation and osteogenic differentiation of PDLSCs. Conclusion: miR-589-3p could down-regulate the expression of ATF1, thereby promote the proliferation and osteogenic differentiation of PDLSCs. This finding may provide a new therapeutic target for molecular therapy of periodontitis. [ABSTRACT FROM AUTHOR]

Background and Objectives: Periodontal pathogens initiate various diseases and induce inflammatory host responses. The activation of inflammasomes triggers caspase‐1 and interleukin (IL)‐1β‐mediated pyroptosis via gasdermin D (GSDMD). Differentiated embryo chondrocyte 2 (Dec2) is a transcription repressor that controls the expression of genes involved in innate immune and inflammatory responses. However, the effects of Dec2 on inflammasome‐induced pyroptosis in periodontal tissues remain elusive. This study aimed to characterize the activation of Dec2 inflammasomes that contribute to P. gingivalis lipopolysaccharide (LPS)‐induced pyroptosis and its functional and regulatory importance in periodontal inflammation. Materials and Methods: Human gingival fibroblasts (HGFs) and human periodontal ligament fibroblasts (HPDLFs) were stimulated with P. gingivalis LPS in vitro. An experimental periodontitis mouse model (wild‐type (WT) and Dec2KO) was established to profile periodontal pyroptosis. Results: The results demonstrate that P. gingivalis LPS activates caspase‐1, caspase‐11, and NF‐κB in HGFs and in HPDLFs. siRNA knockdown of Dec2 stimulated the induction and further upregulated LPS‐induced pyroptosis in HGFs and HPDLFs, resulting in the release of IL‐1β. Further, a deficiency of Dec2 alleviated periodontal pyroptosis via the transcriptional induction of GSDMD. In addition, P. gingivalis‐induced IL‐1β expression and Dec2‐deficient mice subsequently increased the inflammatory effect of P. gingivalis in HGFs and in HPDLFs, confirming the importance of Dec2 in the activation of inflammasomes and the regulation of pyroptosis. Conclusion: Our results demonstrate that Dec2 alleviates periodontal pyroptosis by regulating the expression of NF‐κB, caspase‐1 and GSDMD, suggesting that Dec2 is a crucial component of inflammasome activation and subsequent pyroptosis. [ABSTRACT FROM AUTHOR]

Objective: Nail biting leads to a variety of health issues. Habit reversal treatment is a major approach to cease nail biting, but is often ineffective since patients continue to suffer from anxiety, a major trigger. This study investigated whether the potential anxiety relief provided by auricular acupressure could improve the efficacy of habit reversal treatment, as evidenced by improved stomatological and other outcomes. Methods: In a pragmatic, randomized, crossover, pilot clinical trial, 83 nail biters (8–12 years old) received habit reversal treatment in combination with either auricular acupressure intended to reduce anxiety (Method A) or placebo auricular acupressure (Method B). The alternative protocol was employed after a two-month washout period. The primary outcome measured was the 41-item child self-reported version of the Screen for Child Anxiety Related Emotional Disorders, while the secondary outcomes were the nail growth status (NS), which represented the fingernail growth of each finger during habit reversal treatment, simplified plaque index (SPI), and the simplified gingival index (SGI) as measures of oral health. A paired sample t-test was used to assess the differences between Methods A and B, and the differences in the anxiety scores, NS, SGI, and SPI between the baseline and each time point. Results: Forty-one children successfully completed both arms of the treatments and attended all appointments. There were significant differences in the efficacy of habit reversal treatment, the anxiety score, the nail status, and the SGI in favor of Method A (p < 0.001). Conclusion: Auricular acupressure appears to improve the efficacy of habit reversal treatment, likely by reducing anxiety. [ABSTRACT FROM AUTHOR]

Aim Tumour necrosis factor-alpha ( TNF- α) plays a critical role in the pathogenesis of periodontal disease. TNF-α gene polymorphisms can influence the TNF- α production. Many studies have focused the association between TNF-α gene promoter polymorphisms and periodontitis risk, but these results are still controversial. Materials and Methods A meta-analysis was performed to assess the effect of TNF-α −308G/A (rs1800629), −238G/A (rs361525) and −863C/A (rs1800630) polymorphisms on either chronic ( CP) or aggressive periodontitis (AgP) risk. Odds ratios ( ORs) along with their 95% confidence intervals ( CIs) were calculated to assess the strength of the association. Forty-six studies involving 5186 cases and 6683 controls were retrieved and analyzed. Results The TNF-α −308G/A AA genotype was associated with increased CP risk in Asians, non-smoking Asians and Caucasians, and this polymorphism was significantly associated with elevated risk of AgP in Asians and Caucasians. Asian individuals carrying AA genotype had a significantly increased risk for −863C/A. No significant association was identified between TNF −238G/A polymorphism and CP. Conclusions These findings supported that TNF-α −308G/A and −863C/A polymorphisms may contribute to the susceptibility of periodontitis. [ABSTRACT FROM AUTHOR]