Objectives The present study was designed to investigate the effects of microRNA‐21 (miR‐21) on orthodontic tooth movement. Methods The orthodontic tooth movement model was established in C57BL/6 and miR‐21−/− mice with or without implantation of activated T cells. Histological and histomorphometrical analyses were performed by hematoxylin–eosin staining. Tartrate‐resistant acid phosphate staining was used to analyze the osteoclast numbers during tooth movement. Enzyme‐linked immunosorbent assay, reverse transcription polymerase chain reaction, and immunohistochemistry analysis were used to examine the expression of RANKL and OPG. Results In miR‐21−/− mice, the distance of tooth movement was retarded, the osteoclast number was decreased, and serum RANKL expression was strongly reduced. MiR‐21 promoted the secretion of RANKL from activated T cells. Furthermore, activated T cells could partially rescue the decreased orthodontic tooth movement distance in miR‐21−/− mice. MiR‐21 was shown to promote orthodontic tooth movement by modulating the RANKL/OPG balance in T cells. Conclusions The impact of miR‐21 on tooth movement was better elucidated, furthering our understanding of its role and clinical applications in orthodontics.

Periodontal ligament stem cell- (PDLSC-) mediated periodontal tissue regeneration has recently been proposed for the new therapeutic method to regenerate lost alveolar bone and periodontal ligament. It was reported that both autogenic and allogeneic PDLSCs could reconstruct damaged periodontal tissues but the regeneration effects were not consistent. The effective methods to improve the properties of PDLSCs should be further considered. In this study, we investigated if D-mannose could affect the immunomodulatory properties of hPDLSCs. After being pretreated with D-mannose, hPDLSCs could inhibit T cell proliferation and affect T cell differentiation into Treg cells. We found that less IL-6 could be detected in D-mannose-pretreated hPDLSCs. In the D-mannose pretreatment group, induced Treg cell number would decrease if increased IL-6 levels could be detected. Our data uncovered a previously unrecognized function of D-mannose to regulate the immunomodulatory function of PDLSCs and that IL-6 might play a key role in this process. The results provided a property method to improve PDLSC-based periodontal regeneration.

Cover image © Lijia Guo Images The cover image is based on the Original Article* MicroRNA‐21 promotes orthodontic tooth movement by modulating the RANKL/OPG balance in T cells by Lili Wu et al., https://doi.org/10.1111/odi.13239.

Objectives. The aim of this study was to investigate the effect of nitric oxide (NO) on orthodontic tooth movement and the regulatory effect on bone formation. Design. A mouse orthodontic tooth movement model was established to measure the level of releasing NO. Besides, orthodontic tooth movement distance and the bone formation in the tension side of the orthodontic tooth were also analyzed. In vitro, human periodontal ligament stem cells (hPDLSCs) were cultured under tensile force stimulation. The production of NO and the expression level of nitric oxide synthase (NOS) were detected after mechanical stimulation. Furthermore, the downstream cellular signaling pathway regulated by NO was also explored. Results. The generation of NO steadily increased throughout the orthodontic tooth movement in mice. Orthodontic tooth movement was decreased in the NOS inhibitor group while it was accelerated in the NO precursor group. Force-induced NO promoted the osteogenic differentiation of human hPDLSCs under tensile force stimulation. And force-induced NO in hPDLSCs regulated the PI3K/Akt/β-catenin signal pathway. Conclusion. NO is involved in the regulation of orthodontic tooth movement and promotes bone formation on the tension side of the orthodontic tooth. The PI3K/Akt/β-catenin pathway is one of the downstream cell signal transduction pathways of NO in the orthodontic process.