## 4 Discussion
However, in healthy alveolar bone, in the process of post-extraction healing, and even with osteoporosis, HFV stimulates growth and increases tissue density and bone volume, promoting a process of osteogenesis [3; 13; 24; 25]. This is possible because the alveolar bone is a mechanosensitive tissue that reacts to different external mechanical stimuli, adapting the bone mass and structure in a continuous remodeling process [15; 16]. In addition, in the oral environment, the periodontal ligament has mechanoreceptors that respond to external mechanical stimuli known as Ruffini type I, which is characterized by having two types of response, both a fast adaptation response, located near the center of resistance of the tooth, and a slow adaptation, located near the apex. The fast adaptationis activated only when there is a mechanical load of pressure, while the slow adaptation depends on the frequency and magnitude of load for the transmission of the impulse [12]. At the same time, the vibratory stimulus propagates through the tissues, demonstrating that the anabolic effects are not only localized to the area of application but also affect the areas adjacent to it. However, the effect decreases the further away the application site is [13; 24]. It is important to note that the anabolic effect on the alveolar bone of LFV and HFV results from activation of the canonical Wnt signaling pathway [14; 15; 16]. This signaling pathway acts through Wnt ligands such as Wnt10B. Initially, Wnt proteins bind to the Frizzled receptor and Lrp5/6 co-receptor found on the cell membrane, which causes a concentration of \(\beta\)-catenin within osteoblasts, inhibiting the degradation of phosphorylated \(\beta\)-catenin through the ubiquitin-proteasome pathway; the concentration of \(\beta\)-catenin within the cytoplasm of osteoblasts results in the translocation of this enzyme within the nucleus, where it binds to TCF/LEF transcription factors and regulates the expression of RUNX2 [33]. [PERSON] et al. reported an increase in the Wnt gene expression upon application of 120 Hz vibrations [13]. This coincides with the results of [PERSON] et al., who report that osteoblasts of mandibular origin had an overexpression of the Wnt10b gene after being subjected to vibrations of 120 Hz [14]. There are other factors that favor the anabolic effect when vibratory stimuli are used, such as the reduction of the activity and quantity of osteoclasts [6; 25; 26]. This is consistent with the results obtained by [PERSON] et al., who observed that the amount of recurrence was lower in rats that received vibrations of 30 Hz during a retention period [6]. Furthermore, a decrease in the number of osteoclasts was shown, thus preventing tooth displacement. These results are similar to those reported by [PERSON] et al., who showed that the use of LFV decreased sclerostin, which caused a decrease in the number of osteoclasts [26]. These results are consistent with the downregulation of the SOST gene in osteoblasts subjected to vibration reported by [PERSON] et al. in their in vitro study [15]. The SOST gene encodes the protein sclerostin and is mainly secreted by osteocytes and cells of the periodontal ligament, whose function is to inhibit bone formation by binding competitively to the Wnt co-receptor, LRP5/6; sclerostin causes phosphorylation and degradation of beta-catenin and hinders the activation of osteoblasts [34; 35]. In this sense, a decrease in the SOST gene represents an inhibition of the bone resorption process. Therefore, a decrease in the SOST gene helps to reduce tooth movement by decreasing the activity of the osteoclasts, which is the objective in a post-orthodontic retention stage or when a bone resorption process is to be halted [6; 26]. Only two studies have an experimental design that simulated a clinical situation of orthodontic retention [9; 26]. [PERSON] et al. reported that there was no significant difference in using or not using vibrations in the retention period [26]. On the other hand, [PERSON] et al.