Background:In periodontal connective tissue cells, the vitamin D pathway has been elucidated, and vitamin D 3 in the main storage form, 25-hydroxy vitamin D 3 (25[OH]D 3 ), and the functional form, 1,25-dihydroxy vitamin D 3 (1,25[OH] 2 D 3 ), have been found to induce the expression of human cationic antimicrobial protein (hCAP-18)/LL-37. Moreover, synergistic effects between Toll-like receptor agonists and 25(OH)D 3 have been reported. This research aimed at extending the vitamin D pathway to vitamin D 3 and CYP27A1 in human periodontal ligament cells (hPDLCs) to further explore its function in periodontal inflammatory reaction.Methods: Vitamin D 3 was used to stimulate hPDLCs in the presence or absence of Porphyromonas gingivalis lipopolysaccharide (Pg-LPS). Conversely, CYP27A1 RNA interference was performed to further validate the findings. The mRNA expression of hCAP-18 was determined with real-time polymerase chain reaction. Monocyte chemotactic protein-1 (MCP-1) and interleukin-8 (IL-8) were also detected. The cell supernatant levels of LL-37 were detected with enzyme-linked immunosorbent assay.Results: Vitamin D 3 significantly enhanced the generation of hCAP-18/LL-37. A combination of Pg-LPS and vitamin D 3 significantly promoted hCAP-18/LL-37 expression. When the expression of CYP27A1 was knocked down with RNA interference, the induction of hCAP-18/LL-37 expression was significantly inhibited. Therefore, the mRNA levels of MCP-1 and IL-8 in hPDLCs were significantly decreased through the vitamin D pathway. Conclusion:The vitamin D pathway from vitamin D 3 to hCAP-18/LL-37 exists in hPDLCs, and CYP27A1 might be involved in periodontal immune defense.

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Background 2019 Coronavirus disease (COVID-19) is an infectious disease caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The COVID-19 pandemic has already had a serious influence on human existence, causing a huge public health concern for countries all around the world. Because SARS-CoV-2 infection can be spread by contact with the oral cavity, the link between oral illness and COVID-19 is gaining traction. Through bioinformatics approaches, we explored the possible molecular mechanisms linking the COVID-19 and periodontitis to provide the basis and direction for future research. Methods Transcriptomic data from blood samples of patients with COVID-19 and periodontitis was downloaded from the Gene Expression Omnibus database. The shared differentially expressed genes were identified. The analysis of Gene Ontology, Kyoto Encyclopedia of Genesand Genomes pathway, and protein–protein interaction network was conducted for the shared differentially expressed genes. Top 5 hub genes were selected through Maximal Clique Centrality algorithm. Then mRNA-miRNA network of the hub genes was established based on miRDB database, miRTarbase database and Targetscan database. The Least absolute shrinkage and selection operator regression analysis was used to discover possible biomarkers, which were then investigated in relation to immune-related genes. Results Fifty-six shared genes were identified through differential expression analysis in COVID-19 and periodontitis. The function of these genes was enriched in regulation of hormone secretion, regulation of secretion by cell. Myozenin 2 was identified through Least absolute shrinkage and selection operator regression Analysis, which was down-regulated in both COVID-19 and periodontitis. There was a positive correlation between Myozenin 2 and the biomarker of activated B cell, memory B cell, effector memory CD4 T cell, Type 17 helper cell, T follicular helper cell and Type 2 helper cell. Conclusion By bioinformatics analysis, Myozenin 2 is predicted to correlate to the pathogenesis and immune infiltrating of COVID-19 and periodontitis. However, more clinical and experimental researches are needed to validate the function of Myozenin 2.