Objective: The present study aimed to summarize and update the evidence regarding the association between periodontitis and psoriasis.Methods: The present systematic review was conducted under the guidelines of Transparent Reporting of Systematic Reviews and Meta‐Analyses (PRISMA) and was recorded in the PROSPERO database, under registration number CRD42017063799. Three databases (MEDLINE, Embase, and Cochrane Library) were searched up to March 2020. Case–control or cohort studies assessing the association between periodontitis and psoriasis were identified. Quantitative synthesis was conducted with meta‐analysis.Results: A total of 13 studies (11 case–control and two cohort studies) assessing the association between periodontitis and psoriasis were included. Of these 13 articles, 9 showed the prevalence of periodontitis or psoriasis. Therefore, meta‐analyses were conducted with data retrieved from the nine studies included. Pooled effect estimate for nine studies showed that patients with periodontitis associated with a higher risk of psoriasis with a pooled OR of 2.87 (95% CI, 1.75–4.69).Conclusions: This systematic review demonstrated a positive association between periodontitis and psoriasis; however, a causal relationship cannot be established. Due to the weak evidence, caution should be taken when interpreting the results regarding periodontal parameters. Well‐designed prospective studies are necessary to evaluate interactions between both diseases.

Qian Cheng, MD/Ying-Ying Su, PhD/Xin Wang, PhD/Su Chen, PhD: Purpose: To identify whether or not immediate loading yields different clinical outcomes from conventional loading of single-tooth implants in the esthetic zone. Materials and Methods: Various databases (MEDLINE/PubMed, Cochrane [CENTRAL], and Embase) were searched electronically to find articles published in the English language from January 2000 to April 2018. Only randomized controlled clinical trials (RCTs) that compared conventional and immediate implant loading with a minimum follow-up period of 1 year or more were considered. Available data were pooled for meta-analysis using the Review Manager software. Results: Seven RCTs were included. There was no significant difference between immediate and conventional loading protocols on implant survival at the 1-year follow-up (risk ratio [RR] = 0.99; 95% confidence interval [CI]: 0.95 to 1.02). The differences regarding marginal bone loss between the two protocols were statistically insignificant (mean difference [MD] = 0.03 mm; 95% CI: ?0.09 to 0.15 mm at the 1-year follow-up, and MD = ?0.01 mm; 95% CI: ?0.16 to 0.15 mm at the 2-year follow-up). Soft tissue changes following different loading protocols revealed no significant differences in the mesial papillae (MD = 0.30 mm; 95% CI: ?0.25 to 0.85 mm), the distal papillae (MD = ?0.00 mm; 95% CI: ?0.42 to 0.42 mm), and the midfacial mucosa (MD = ?0.33 mm; 95% CI: ?1.17 to 0.50 mm) at the 1-year follow-up. The esthetic outcomes and patient satisfaction were reported in two and three RCTs, respectively. Conclusion: A short-term follow-up of single-tooth implants in the esthetic zone showed that the loading protocols (conventional or immediate loading) are not likely to influence the clinical outcomes, including implant survival and peri-implant stability of soft and hard tissues.

DNA methylation is an important epigenetic modification critical to the regulation of gene expression during development. To date, little is known about the role of DNA methylation in tooth development in large animal models. Thus, we carried out a comparative genomic analysis of genome-wide DNA methylation profiles in E50 and E60 tooth germ from miniature pigs using methylated DNA immunoprecipitation-sequencing (MeDIP-seq). We observed different DNA methylation patterns during the different developmental stages of pig tooth germ. A total of 2469 differentially methylated genes were identified. Functional analysis identified several signaling pathways and 104 genes that may be potential key regulators of pig tooth development from E50 to E60. The present study provided a comprehensive analysis of the global DNA methylation pattern of tooth germ in miniature pigs and identified candidate genes that potentially regulate tooth development from E50 to E60.

Mesenchymal stem cells (MSCs) treatment has emerged as a promising approach for treating Sjögren’s syndrome (SS). Impaired immunoregulatory activities of bone marrow mesenchymal stem cells (BMMSCs) are found in both SS patients and animal models, and the underlying mechanism is poorly understood. Increased expression of BMP6 is reported to be related to SS. The aim herein was to determine the effects of BMP6 on BMMSCs function. BMMSCs were isolated from SS patients and NOD mice and showed a high level of BMP6 expression. The effects of BMP6 on BMMSCs function were investigated using in vitro BMMSCs differentiation and in vitro and in vivo T cell proliferation and polarization assays. BMP6 increased osteogenic differentiation of BMMSCs and inhibited the immunomodulatory properties of BMMSCs. BMP6 enhanced T cell proliferation and Th1/Th17 differentiation in a T cell-BMMSC coculture system. Mechanistically, BMP6 downregulated PGE2 and upregulated IFN-gamma via Id1 (inhibitor of DNA-binding protein 1). Neutralizing BMP6 and knockdown of Id1 could restore the BMMSCs immunosuppressive function both in vitro and in vivo. The present results suggest a novel role of Id1 in BMP-mediated MSCs function, which may contribute to a better understanding of the mechanism of action of MSCs in treating autoimmune diseases.

Tongue squamous cell carcinoma (TSCC) is an aggressive oral cancer with a high incidence of metastasis and poor prognosis. We aim to identify and verify potential biomarkers for TSCC using bioinformatics analysis. To begin with, we examined clinical and RNA expression information of individuals with TSCC from the Gene Expression Omnibus (GEO) database. Differential expression analysis and functional analysis were conducted. Multiple machine-learning strategies were next employed to screen and determine the hub gene, and receiver operating characteristic (ROC) analysis was used to assess diagnostic value. Semaphorin3C (SEMA3C) was identified as a critical biomarker, presenting high diagnostic accuracy for TSCC. In the validation cohorts, SEMA3C exhibited high expression levels in TSCC. The high expression of SEMA3C was a poor prognostic factor in TSCC by the Kaplan–Meier curve. Based on the Gene Ontology (GO) analysis, SEMA3C was mapped in terms related to cell adhesion, positive regulation of JAK-STAT, positive regulation of stem cell maintenance, and positive regulation of NF-κB activity. Single-cell RNA sequencing (ScRNA-seq) analysis showed cells expressing SEMA3C were predominantly tumor cells. Then, we further verified that SEMA3C had high expression in TSCC clinical samples. In addition, the knockdown of SEMA3C suppressed the proliferation, migration, and invasion of TSCC cells in vitro. This study is the first to report the involvement of SEMA3C in TSCC, suggesting that upregulated SEMA3C could be a novel and critical potential biomarker for future predictive diagnostics, prevention, prognostic assessment, and personalized medical services in TSCC.