To evaluate the clinical effect of endoscopic-assisted subgingival scaling and root planning (SRP) in the treatment of periodontitis.

PubMed, EMBASE, The Cochrane Library, Web of Science, CNKI, WanFang Data, and VIP databases were searched for randomized controlled trials (RCTs) related to endoscopy-assisted SRP. The search time limit was from the establishment of the database to September 15, 2021. The outcome indicators included in the study included the plaque index (PLI), probing depth (PD), attachment loss (AL), and bleeding index (BI). Review Manager 5.4 and Stata 12.0 software were used for the meta-analysis.

A total of 111 studies were retrieved, and 5 quantitative studies were included after screening. Meta-analysis showed that for sites with 4 mm ≤ PD < 6 mm, 3 and 6 months after treatment, there was no significant difference in the PD value between the endoscope assisted group and the simple SRP group (P > 0.05); for sites with PD ≥ 6 mm, the PD value of the endoscope assisted group was smaller than that of the simple SRP group 3 and 6 months after treatment. The difference between the two groups was statistically significant (P < 0.05), but there was no significant difference in PLI, Al or BI between the two groups (P > 0.05).

Compared with simple SRP, the auxiliary use of endoscopy has a better effect on reducing PD in deep periodontal pockets (PD ≥ 6 mm). However, for clinical indicators such as PLI, AL, and BI, there was no difference between the therapeutic effects of the two methods.

To evaluate the clinical effect of enamel matrix derivative(EMD) assisted with connective tissue graft(CTG) in the treatment of gingival recession.

Search The Cochrane Library, PubMed, EMbase, Web of Science, Wanfang Public Database, VIP database and CNKI to search for randomized controlled trials of EMD in the treatment of gingival recession. The search period is from the establishment of the databases to October 3, 2022. The test group was treated with EMD+CTG, while the control group was treated with CTG alone. Meta-analyses were performed using Review Manager 5.4.1 and Stat12.0.

Meta analysis results showed that only 12 months after treatment, there was a statistically significant difference in the PD and CAL outcome indicators between the EMD assisted treatment group and the control group [MD_PD=-0.10, 95% CI (-0.19, -0.01), P = 0.03], [MD_CAL=-0.38, 95% CI (-0.71, -0.04), P = 0.03]. There was no significant difference between the test group and the control group in other indicators.

EMD assisted CTG in the treatment of gingival recession may be beneficial to the reduction of PD and CAL.

To explore the bidirectional causal relationship between 731 immune cell phenotypes and recurrent aphthous ulcers (RAU) using Mendelian randomization (MR).

A two-sample bidirectional MR study was conducted using publicly available genome-wide association study (GWAS) summary statistics for 731 immune cell phenotypes and the RAU GWAS summary data from the FinnGen consortium. The inverse-variance weighted (IVW) method was used as the primary analysis tool, with supplementary analyses including the weighted median (WM) method, MR-Egger regression, weighted mode, and simple mode. Sensitivity analyses were conducted using Cochran's Q test, the mendelian randomization pleiotropy residual sum and outlier (MR-PRESSO) method for detecting pleiotropy and outliers, and leave-one-out cross-validation. Furthermore, differential analysis was performed using a clinical cohort dataset from the Gene Expression Omnibus (GEO) to further validate the MR results.

In the forward MR analysis, 731 immune cell phenotypes were considered as exposures and RAU as the outcome. Among them, 52 immune cell phenotypes showed a significant causal effect on RAU (P < 0.05). After false discovery rate (FDR) correction, two immune phenotypes remained significantly associated with RAU risk: with increased monocyte-derived myeloid suppressor cells (M-MDSC) (OR = 1.06; 95% CI: 1.03-1.09) and CD33 on granulocytic myeloid-derived suppressor cells (G-MDSC) (OR = 1.06; 95% CI: 1.03-1.09), the risk of RAU also increased. In reverse MR, RAU was found to have a significant causal effect on two immune cell phenotypes (P < 0.05), but no significant effects were found after FDR correction. Sensitivity analysis showed no significant heterogeneity between SNPs (P > 0.05). Differential analysis of the GEO dataset revealed that the characteristic genes of myeloid-derived suppressor cells (MDSC) (CTBS, IPMK, and UBA3) were significantly upregulated in RAU (P < 0.05).

The MR results of 731 immune cell phenotypes suggest that M-MDSC and CD33 molecules on G-MDSC may be risk factors for RAU development. The clinical GEO dataset further validated that MDSC may play a role in RAU, while RAU did not show a significant causal association with the 731 immune cell phenotypes.