LAUSR

Periodontal accelerate osteogenesis orthodontics (PAOO) is an extension of described techniques that surgically alter the alveolar bone; however, the specific mechanism underlying the technique is not completely understood. The aim of the present study was to evaluate the roles of microRNA (miR)-21 during PAOO. Sprague-Dawley rats were divided into the following four groups: i) Group tooth movement (TM), underwent TM and were administered normal saline (NS); ii) Group PAOO, underwent PAOO + TM and were administered NS; iii) Group agomiR-21, underwent PAOO + TM and were administered agomiR-21; and iv) Group antagomiR-21, underwent PAOO + TM and were administered antagomiR-21. To validate the rat model of PAOO, morphological analyses were performed and measurements were collected. Reverse transcription-quantitative PCR, western blotting and immunohistochemical staining were performed to examine the expression levels of programmed cell death 4 (PDCD4), activin A receptor type 2B (ACVR2b), receptor activator of NF-κΒ ligand (RANKL) and C-Fos. Dual-luciferase reporter assays were performed to validate PDCD4 as a target of miR-21 in vitro. Following 7 days of treatment, the TM distance of group PAOO was longer compared with groups TM and antagomiR-21 (P<0.05), but shorter compared with group agomiR-21 (P<0.05). Tartrate-resistant acid phosphatase staining indicated that following treatment with agomiR-21, osteoclast activity was notably increased, whereas the mRNA and protein expression levels of PDCD4 were notably decreased compared with group PAOO. The mRNA and protein expression levels of RANKL and C-Fos in group agomiR-21 were notably increased compared with group PAOO, whereas group antagomiR-21 displayed the opposite pattern (P<0.05). With regard to ACVR2b, no significant differences were observed among the group agomiR-21 and antagomiR-21 compared with group PAOO. Bioinformatics analysis predicted that PDCD4 was a potential target gene of miR-21, and dual-luciferase reporter assays demonstrated that miR-21 directly targeted PDCD4. In conclusion, the present study demonstrated that miR-21 serves an important role during PAOO-mediated orthodontic TM.