Recently, corticotomy-assisted orthodontic treatments have gathered increasing clinical attention and have been applied more frequently. This technique evolved from traditional corticotomies on the buccal and palatal sides to buccal flapless corticotomies. Accumulating clinical studies suggest that this method leads to accelerated tooth movement, augmented alveolar bone and improved periodontal tissue health. This paper provides an overview of the development of this surgical technique and clinical research results.

Objective: To study the change of STAT1 expression in the anterior cingulate cortex on rats under orthodontic force, and to further explore the roles of STAT1 and related JAK-STAT1 signaling pathway in the mediation and regulation of pain during tooth movement. Methods: 112 male Sprague-Dawley (SD) rats (225±25 g) were used in this study. They were randomly divided into experimental groups (96 rats) and control groups (16 rats). All rats were installed bilateral maxillary device for tooth movement models. Rats in the experimental groups were applied 80g orthodontic force on both sides and were divided into six subgroup 4 h, 12 h, 24 h, 2 d, 3 d, 7 d, with 16 rabbits in each subgroup. The control groups were only installed the same orthodontic devices, without the application of orthodontic force. Brain tissue of the anterior cingulate cortex was isolated after 4 h, 12 h, 24 h, 2 d, 3 d, 7 d since experiment, and the expression level of STAT1 and p-STAT1 was analyzed with the method of immunofluorescence and PCR. Results : For the immunofluorescence result, there was significant difference in STAT1 expression between control groups and different experimental groups at different time points in total (P < 0.05). The STAT1 expression amount in the 4 h group decreased significantly when compared with the control group (P < 0.05); to the 2 d group, the difference is still statistically significant (P < 0.01). 3 d group, 7 d group and control group had no statistically significant difference. The STAT1 expression amount in 4 h group, 12 h group, 24 h group was significantly lower than that in 3 d and 7 d groups, differences were statistically significant (P < 0.05). The STAT1 expression in the 2 d group was significantly lower than that of 7 d (42.35 ± 5.77) group, the difference was statistically significant (P < 0.05). There was significant difference in p-STAT1 expression between control groups and different experimental groups at different time points in total (F = 623.518, P < 0.05). The p-STAT1 expression amount in experimental groups were higher than that in the control group (P < 0.05). The p-STAT1 expression in 4 h group was lower than that in 12 h and 24 h group and higher than that in 2 d, 3 d and 7 d groups, of which the differences were statistically significant (P < 0.05). The p-STAT1 expression in 12 h group was lower than that in 24 h group and higher than that in 2 d, 3 d and 7 d groups, of which the differences were statistically significant (P < 0.05). For the PCR result, the expression of mRNA in STAT1 of experimental groups of 4 h, 12 h, 24 h, 2 d, 3 d, 7 d and the control groups were not statistically significant (P > 0.05). Conclusions After applying orthodontic force, the expression of STAT1 decreased transiently and the expression of p-STAT1 increased transiently. The reduction of STAT1 was probably caused by the phosphorylation of STAT1 and decrease in the translation level of STAT1, rather than changes in the transcriptional levels. The orthodontic pain might be related with the activation of STAT1 into phosphorylated STAT1.