Background: Despite the popularity of clear aligner treatment, the effect of the thickness of these aligners has not been fully investigated. The objective of this study was to assess the effects of incisor torque compensation with different thicknesses of clear aligner on the three-dimensional displacement tendency of teeth in cases of extraction.Methods: Three-dimensional finite element models of the maxillary dentition with extracted first premolars, maxilla, periodontal ligaments, attachments, and aligners were constructed and subject to Finite Element Analysis (FEA). Two groups of models were created: (1) with 0.75 mm-thick aligners and (2) with 0.5 mm-thick aligners. A loading method was developed to simulate the action of clear aligners for theen masseretraction of the incisors. Power ridges of different heights were applied to both groups to mimic torque control, and the power ridges favoring the translation of the central incisors were selected. Then, we used ANSYS software to analyze the initial displacement of teeth and the principle stress on the PDL.Results: Distal tipping, lingual tipping and extrusion of the incisors, distal tipping and extrusion of the canines, and mesial tipping and intrusion of the posterior teeth were all generated by clear aligner therapy. With the 0.5 mm-thick aligner, a power ridge of 0.7 mm could cause bodily retraction of the central incisors. With the 0.75 mm-thick aligner, a power ridge of 0.25 mm could cause translation of the central incisors. Aligner torque compensation created by the power ridges generated palatal root torque and intrusion of the incisors, intrusion of the canines, mesial tipping and the intrusion of the second premolar; these effects were more significant with a 0.75 mm-thick aligner. After torque compensation, the stress placed on the periodontal ligament of the incisors was distributed more evenly with the 0.75 mm-thick aligner.Conclusions: The torque compensation caused by power ridges can achieve incisor intrusion and palatal root torque. Appropriate torque compensation with thicker aligners should be designed to ensure bodily retraction of anterior teeth and minimize root resorption, although more attention should be paid to the anchorage control of posterior teeth in cases of extraction.

Objective. Periodontitis is a chronic inflammatory disease that causes loss of periodontal support tissue. Our objective was to investigate the mechanism by which METTL3‐mediated N6‐methyladenosine modification regulates the osteogenic differentiation through lncRNA in periodontal mesenchymal stem cells in patients with periodontitis (pPDLSCs). Material and Methods. We carried out a series of experiments, including methylated RNA immunoprecipitation‐PCR, quantitative real‐time polymerase chain reaction, and western blotting. The expressions of alkaline phosphatase (ALP), Runx2, Col1, Runx2 protein level, ALP staining, and Alizarin red staining were used to demonstrate the degree of osteogenic differentiation. Results. We found that METTL3 was the most significantly differentially expressed methylation‐related enzyme in pPDLSCs and promoted osteogenic differentiation of pPDLSCs. METTL3 regulated the stability and expression of lncRNA CUTALP, while lncRNA CUTALP promoted osteogenic differentiation of pPDLSCs by inhibiting miR‐30b‐3p. At different time points of osteogenic differentiation, lncRNA CUTALP expression was positively correlated with Runx2, while miR‐30b‐3p showed the opposite pattern. The attenuated osteogenic differentiation induced by METTL3 knockdown was recovered by lncRNA CUTALP overexpression. The attenuated osteogenic differentiation induced by lncRNA CUTALP knockdown could be reversed by the miR‐30b‐3p inhibitor. Conclusions. In summary, METTL3/lncRNA CUTALP/miR‐30b‐3p/Runx2 is a regulatory network in the osteogenic differentiation of pPDLSCs.

Transient receptor potential ankyrin 1 (TRPA1) molecule is an important type of transient receptor potential (TRP) cation channels, which can cause extracellular Ca²⁺ to flow into cells after activation. TRPA1 plays an important role in acute and chronic pain, inflammation, kidney disease, cough and asthma, osteoarthritis, cardiovascular disease, obesity, diabetes, and other diseases. In this study, the expression of interleukin (IL)‐1β, IL‐6, and IL‐8 in periodontal ligament stem cells (PDLSCs) treated by lipopolysaccharide (LPS) and the effect of LPS on PDLSCS proliferation were detected. Meanwhile, the change in TRPA1 expression in PDLSCs treated by LPS was also assessed. By knocking down the expression of TRPA1 and using the TRPA1 antagonist HC‐030031, the expression of IL‐1β, IL‐6, and IL‐8 in PDLSCs treated by LPS was downregulated. After LPS stimulation, the proliferation ability of PDLSCs decreased, the gene expression and secretion of IL‐1β, IL‐6, and IL‐8 increased and the gene and protein expression of TRPA1 were upregulated. Reducing the expression of TRPA1 can effectively inhibit the increase of gene expression of IL‐1β, IL‐6, and IL‐8 after LPS stimulation, and pretreatment of PDLSCs with HC‐030031 can also achieve the above effect. And research has found that HC‐030031 can inhibit the phosphorylation level of JNK in PDLSCs treated by LPS. The use of JNK inhibitor JNK‐IN‐8 can also reduce the expression of IL‐1β, IL‐6, and IL‐8 in PDLSCs. Finally, this study found LPS could cause the upregulation of TRPA1, and the inhibition of TRPA1 could produce an anti‐inflammatory effect in PDLSCs treated by LPS due to its inhibition of JNK phosphorylation.