## 4 Discussion  
As demonstrated in the literature, traditional orthodontics treatment acts as a trigger on the periodontal tissues [26; 38; 39]. Traditional orthodontic techniques have been described as causing damage to dental and periodontal tissues, such as recessions and root resorption [33; 40; 41; 42]. Based on the protocols used in conventional orthodontics, profound changes in the periodontium were observed, such as thickening in the traction's zone and thinning in the compression's zone, with the appearance of areas of necrosis and bone remodeling. The current gold standard is represented by Piezsurgery(r), which aims to improve tooth alignment without adverse effects on periodontal structures through a standardized surgical practice protocol [43; 44; 45; 46; 47; 48]. Gingival inflammation is related to the increase in inflammatory cytokines and/or MMPs in the periodontal ligament, and the turning on of inflammatory tissue destruction by gingival fibroblasts and periodontal ligament has been proposed. Despite these functional and regional corrections, the role of gum tissue has been neglected with regard to orthodontic treatment [49; 50]. To focus on biological events in gingival tissue, a prerequisite for this study was the exclusion of gingival tissue subjected to orthodontic improvement and the observation of primary subcellular mutations. In this study, a real-time RT-PCR was necessary since this allows a relatively reliable quantification of RNA, unlike conventional RT-PCR; without taking into account the number of PCR cycles, it quickly shows results in time real. The IL-1 beta and MMP-9 mRNA levels were significantly high at all pressure sites for a relatively long period of time (2 weeks), and no substantial change was noted in the group of false activation, indicating that the changes were mainly due to pressure stimulation on the gum tissue. Although many studies have pointed out growing pro-inflammatory cytokines in the periodontal ligament, the direct efficiency of the mechanical load on beta IL-1 from gingival fibroblasts is not yet clear. [PERSON] et al. demonstrated a voltage-induced increase in IL-6 secretion in tendon fibroblasts [51]. [PERSON] et al. found that the inflammatory response of tendon fibroblasts depended on the intensity of the traction, with an anti-inflammatory response at low levels and a proinflammatory response at high levels of strength [52]. Changes in IL-1 beta mRNA levels in this research mostly agree with those described in a previous report on IL-1 beta secretion from gingival crevicular fluid. However, a relatively constant increase can be noted. The decline in IL-1 beta on day 14 can be attributable to a decrease in the level of forces caused by the absence of reactivation, but the cytokines may be refractory to the application of a reactivation [53]. [PERSON] et al. reported that the concentration of IL-1 beta in gingival crevicular fluid rose and returned to baseline levels in 14-28 days [54]. However, a sustained increase of IL-1 beta in the pressure side of the gingival tissue set against with  
Figure 3: Average IL-2 values over time with standard deviation. the traction site was a new discovery of our study, implying a possible role of gingival soft tissues in tissue remodeling [50,54]. In our research, the expression of MMP-9 was increased by performing orthodontic microsurgery followed by orthodontic loading. MMP-2 and MMP-9 were previously found, both in the pressure and PDL side, during orthodontic movements to assist collagen abasement. [PERSON] et al. reported, through in situ hybridization technique, that MMP-9 mRNA in the periodontal ligament was increased within 7 days of orthodontic loading and decreased after 14 days [55]. The primary increase in those key mRNA points in the gingiva suggest the following possibilities:  
1. mRNAs could be directly implicated in gingival inflammation and/or destruction of the soft tissues surrounding the moving tooth;
2.