Chronic periodontitis is a multifactorial polygenetic disease with an increasing number of associated factors that have been identified over recent decades. Longitudinal epidemiologic studies have demonstrated that the risk factors were related to the progression of the disease. A traditional multivariate regression model was used to find risk factors associated with chronic periodontitis. However, the approach requirement of standard statistical procedures demands individual independence. Multilevel modelling (MLM) data analysis has widely been used in recent years, regarding thorough hierarchical structuring of the data, decomposing the error terms into different levels, and providing a new analytic method and framework for solving this problem. The purpose of our study is to investigate the relationship of clinical periodontal index and the risk factors in chronic periodontitis through MLM analysis and to identify high-risk individuals in the clinical setting.Fifty-four patients with moderate to severe periodontitis were included. They were treated by means of non-surgical periodontal therapy, and then made follow-up visits regularly at 3, 6, and 12 months after therapy. Each patient answered a questionnaire survey and underwent measurement of clinical periodontal parameters.Compared with baseline, probing depth (PD) and clinical attachment loss (CAL) improved significantly after non-surgical periodontal therapy with regular follow-up visits at 3, 6, and 12 months after therapy. The null model and variance component models with no independent variables included were initially obtained to investigate the variance of the PD and CAL reductions across all three levels, and they showed a statistically significant difference (P < 0.001), thus establishing that MLM data analysis was necessary. Site-level had effects on PD and CAL reduction; those variables could explain 77-78% of PD reduction and 70-80% of CAL reduction at 3, 6, and 12 months. Other levels only explain 20-30% of PD and CAL reductions. Site-level had the greatest effect on PD and CAL reduction.Non-surgical periodontal therapy with regular follow-up visits had a remarkable curative effect. All three levels had a substantial influence on the reduction of PD and CAL. Site-level had the largest effect on PD and CAL reductions.
To investigate whether visceral adipose tissue-derived serine protease inhibitor (vaspin) can alleviate the inhibitory effect of high-glucose (HG) culture on the proliferation and osteogenic differentiation of human periodontal ligament stem cells (PDLSCs) and to preliminarily explore the underlying mechanisms.
Porphyromonas gingivalis (P. gingivalis), one of the most important pathogens of periodontitis, is closely associated with the aggravation and recurrence of periodontitis and systemic diseases. Antibacterial peptide LL-37, transcribed from the cathelicidin antimicrobial peptide (CAMP) gene, exhibits a broad spectrum of antibacterial activity and regulates the immune system. In this study, we demonstrated that LL-37 reduced the number of live P. gingivalis (ATCC 33277) in HaCaT cells in a dose-dependent manner via an antibiotic-protection assay. LL-37 promoted autophagy of HaCaT cells internalized with P. gingivalis. Inhibition of autophagy with 3-methyladenine (3-MA) weakened the inhibitory effect of LL-37 on the number of intracellular P. gingivalis. A cluster of orthologous groups (COGs) and a gene ontology (GO) functional analysis were used to individually assign 65 (10%) differentially expressed genes (DEGs) to an "Intracellular trafficking, secretion, and vesicular transport" cluster and 306 (47.08%) DEGs to metabolic processes including autophagy. Autophagy-related genes, a tripartite motif-containing 22 (TRIM22), and lysosomal-associated membrane protein 3 (LAMP3) were identified as potentially involved in LL-37-induced autophagy. Finally, bioinformatics software was utilized to construct and predict the protein–protein interaction (PPI) network of CAMP-TRIM22/LAMP3-Autophagy. The findings indicated that LL-37 can reduce the quantity of live P. gingivalis internalized in HaCaT cells by promoting autophagy in these cells. The transcriptome sequencing and analysis also revealed the potential molecular pathway of LL-37-induced autophagy.
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