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Background: Inflammatory bowel disease (IBD) and periodontitis are closely associated; however, whether there is a causal association between them is unclear. To explore the existence of causation between genetically proxied inflammatory bowel disease (IBD), including Crohn's disease (CD) and ulcerative colitis (UC), and periodontitis, using a bidirectional two-sample Mendelian randomization analysis. Results:The genetic variants were obtained from the summary statistics of genome-wide association studies of IBD, CD, UC, and periodontitis. To investigate the potential causal association between genetic liability for IBD, including CD and UC, and periodontitis, we used random-effects inverse-variance weighted as primary method with weighted median, MR Egger regression as complementary methods, and a series of sensitivity analyses. Using 175, 148, and 113 single-nucleotide polymorphisms as instrumental variables for IBD, CD, and UC, respectively, we did not find a significant effect of genetically proxied IBD and its subtypes on periodontitis. Applying six single-nucleotide polymorphisms for periodontitis, we did not find a significant effect of the genetic liability for periodontitis on IBD, CD, and UC either. Sensitivity analyses did not reveal horizontal pleiotropy and heterogeneity. Conclusions: No causation in the forward or reverse direction was noted. Our resultssuggest that the treatment of one of these two conditions might not affect the other and help predict what future large-scale RCTs will show.

Objective Emerging evidence shows the clinical consequences of patient with COVID-19 and periodontitis are not promising, and periodontitis is a risk factor. Periodontitis and COVID-19 probably have a relationship. Hence, this study aimed to identify the common molecular mechanism that may help to devise potential therapeutic strategies in the future. Material and methods We analyzed two RNA-seq datasets for differential expressed genes, enrichment of biological processes, transcription factors (TFs) and deconvolution-based immune cell types in periodontitis, COVID-19 and healthy controls. Relationships between TFs and mRNA were established by Pearson correlation analysis, and the common TFs-mRNA regulatory network and nine co-upregulated TFs of the two diseases was obtained. The RT-PCR detected the TFs. Results A total of 1616 and 10201 DEGs from periodontitis and COVID-19 are found. Moreover, nine shared TFs and common biological processes associated with lymphocyte activation involved in immune response were identified across periodontitis and COVID-19. The cell type enrichment revealed elevated plasma cells among two diseases. The RT-PCR further confirmed the nine TFs up-regulation in periodontitis. Conclusion The pathogenesis of periodontitis and COVID-19 is closely related to the expression of TFs and lymphocyte activation, which can provide potential targets for treatment.

Background Previous observational and epidemiological studies have reported the association between periodontitis (PD) and non-alcoholic fatty liver disease (NAFLD). However, evidence from long-term randomized controlled trials (RCTs) is lacking. Therefore, this study aimed to explore the causal relationship between PD and NAFLD. Methods Genetic information for individuals of European ancestry with PD (17,353 clinically diagnosed cases and 28,210 controls) and NAFLD (8,434 clinically diagnosed cases and 770,180 controls) were obtained using published genome-wide association study statistics, following which we conducted two-sample bivariate Mendelian randomisation (MR) analyses. Various techniques such as inverse-variance weighted (IVW), weighted median, and MR-Egger regression methods were used to calculate the causal relationship between exposure and the result. Results No causal effect of genetically determined PD on NAFLD existed (odds ratio [OR] = 0.99, 95% confidence interval [CI]: 0.90–1.10, P = 0.95). Furthermore, no causal effect of NAFLD on PD was observed in the reverse MR analysis (OR = 1.02, 95% CI: 0.92–1.13, P = 0.63). No heterogeneity was observed between individual single nucleotide polymorphisms pursuant to the heterogeneity assessment (Q > 0.1). Horizontal pleiotropy pursuant to the outcomes of MR-Egger regression and MR Pleiotropy RESidual Sum and Outlier overall tests (P > 0.1) were less likely to distort the causal relationship between PD and NAFLD. Conclusion Collectively, we did not find substantial evidence to support a causal association between PD and NAFLD in this bidirectional MR study. Clinical relevance: Periodontitis does not seem to be a risk factor for worsening of non-alcoholic fatty liver disease.

We investigated the changes of labial soft tissue contours with different jumping spaces after immediate implant placement and restoration (IIPR) in the maxillary esthetic area and also provided a long-term stability measurement for the changing trend of soft tissue contour. First, an intraoral pre-operation scanning was used to obtain a digital impression (baseline) of 32 patients with single tooth loss in the maxillary esthetic area. After minimally invasive extraction, the implant had been embedded at the alveolar socket’s palatal side with flapless surgery. A low replacement bone substitute material (Bio-oss bone powder) was then implanted in the jumping space and covered with platelet-rich fibrin (PRF) and screw retention temporary crown was worn. All patients had been separated into three groups based on the jumping space: group A (horizontal defect dimension [HDD] ≤ 2 mm), group B (2 mm < HDD ≤ 3 mm), and group C (HDD > 3 mm) and the digital impressions were obtained in the first, third and sixth month after the operation. The linear changes in peri-implant soft tissue volume, labial gingival margin level, and soft tissue profile were quantitatively analyzed by Geomagic Studio 2013, and the esthetic effect was assessed using the pink esthetic score (PES). The volume of labial soft tissue decreased continuously within six months after IIPR, particularly in the first three months. The changes of gingival mucosa levels, the average thickness of soft tissue contour volume and the linear change of submarginal level decreased gradually across the three groups, with the largest change of submarginal level being at 5 mm. The size of jumping space was moderately negatively correlated with the level and average thickness of gingival mucosa and the linear changes of 3 mm and 5 mm under gingival margin, while there was no significant correlation with PES and the linear change of the 1 mm under the gingival margin. Therefore, enough jumping spaces should be set aside during the immediate implantation to reduce the contour alterations of the soft tissue. Generally, IIPR of upper anterior teeth can achieve esthetic satisfaction, and the level of soft tissue around the implant can be well preserved.