circRNA CDR1as (CDR1as) has been demonstrated to play important roles in a variety of inflammation-related diseases by acting as miRNA sponges. The present study is aimed at investigating the potential roles of CDR1as in the proliferation of human periodontal ligament stem cells (PDLSCs) under an inflammatory condition induced by Porphyromonas gingivalis-derived lipopolysaccharide (LPS). Human periodontal ligament cells (PDLCs) were isolated from periodontal ligament tissue, and PDLSCs were sorted from PDLCs based on the STRO-1 expression through fluorescence-activated cell sorting. We further found that CDR1as was significantly downregulated in LPS-treated PDLSCs compared to untreated cells, as well as in normal periodontal ligament tissues compared to periodontitis tissues. Knockdown of CDR1as promoted LPS-induced proliferative inhibition of PDLSCs, whereas overexpression of CDR1as alleviated the LPS-induced proliferative ability of PDLSCs. Mechanistically, CDR1as functioned as an miR-7 sponge to activate the ERK signal pathway to mediate the inhibition effect of LPS on cell proliferation. Taken together, our findings revealed the effects of the interacting pair of CDR1as/miR-7 on the proliferation ability of PDLSCs within their surrounding inflammatory microenvironment of periodontitis.

Aim To ascertain the anti‐inflammation mechanism of catechins in lipopolysaccharide‐treated human dental pulp cells (HDPCs). Methods Expression of tumor necrosis factor (TNF)‐α, interleukin (IL)‐1β, and IL‐6 was measured using quantitative polymerase chain reaction (qPCR) and enzyme‐linked immunosorbent assays. The anti‐inflammatory mechanism was explored by examining activation of nuclear factor‐kappa B (NF‐κB) signaling using qPCR, Western blotting, and immunofluorescence staining. Results Human dental pulp cells proliferation was not affected by treatment with epigallocatechin (ECG) or epigallocatechin 3‐gallate (EGCG). mRNA expression of the pro‐inflammatory cytokines TNF‐α, IL‐1β, and IL‐6 was decreased significantly in ECG‐ and EGCG‐treated HDPCs. Subsequently, the effects of ECG and EGCG upon activation of NF‐κB signaling were evaluated by Western blotting and immunofluorescence staining. Expression of p‐p65 protein in HDPCs treated with ECG, EGCG, or an NF‐κB inhibitor (Bay 11‐7082) was lower than that in HDPCs treated with lipopolysaccharide, data that were consistent with the location of p65 protein according to immunofluorescence staining. Conclusions Catechin could reduce lipopolysaccharide‐stimulated inflammation in HDPCs by inhibiting activation of the NF‐κB pathway.

Objectives To better guide clinicians to choose the appropriate chairside system, we compared and evaluated the morphology of crowns generated by three different biogeneric design modes (biogeneric copy (BC), biogeneric individual (BI), and biogeneric reference (BR)) of the CEREC software. Methods Maxillary and mandibular casts were obtained from twelve volunteers and digital impressions were acquired. All ceramic crown preparations of all right maxillary central incisors were prepared and digital impressions were taken. Then, crowns were automatically designed under BC, BI and BR modes separately and their morphologies were evaluated by six doctors. The "optimal fitting alignment" and "3D analysis" functions of the Geomagic Qualify software were carried out between original teeth and auto-generated full crowns. The auto-generated crowns were modified by a technician according to clinical criteria and the adjustment time was recorded. The discrepancies between technician modified crowns and the auto-generated full crowns were evaluated with the same functions in the Geomagic Qualify software. Results The subjective evaluation results of BC group were significantly better than those of BI and BR group (p < 0.05). Compared with the original teeth and modified crowns, auto-generated crowns in BC group all had the smallest differences, followed by BR and BI group (p < 0.05). BC group needed the shortest adjustment time than BI and BR group (p < 0.05).

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