Orthodontic root resorption (ORR) occurs in tooth movements during orthodontic treatment, although the degree varies depending on the patient. Many ORRs recorded in orthodontic clinics are not severe and are localized in the root surface and apex. Eventually, the repair mechanism of the absorption site occurs by cementogenesis, without any clinical problem. However, in orthodontic practice, cases of tooth roots that are absorbed extensively and cause tooth sway, which greatly affects tooth function and safety, are rarely reported. Kaley et al. (1) showed that ORR occurred in most patients who received orthodontic treatment, of which 3% had severe ORR (absorption of more than a quarter of the root length) in the maxillary central incisors. Many factors are involved in the process of ORR. Risk factors in orthodontic treatment include prolonged treatment and abnormal root morphology (2) , strong orthodontic power (3) and tooth movement (4). Some of the patientʼs risk factors include genetic factors (5) , history of dental trauma (6) , and allergies (7) , but the cause is still unclear. In the study of Yamaguchi et al. (8) , receptor activator of NF-Kappa B ligand (RANKL) was received when compression force (CF) was added to human periodontal ligament (hPDL) cells derived from patients with severe ORR. RANKL, as well as inflammatory cytokine expres-Correspondence to：

Background: Transforming growth factor-β (TGF-β) signaling is an important protein network in bone metabolism. However, the relationship between TGF-β and orthodontically induced inflammatory root resorption (OIIRR) during orthodontic treatment is not well understood. This study aimed to observe TGF-β1 expression on the compressed side of the periodontal ligament (PDL) during orthodontic treatment, and to examine the involvement of TGF-β1 in orthodontic root resorption.Materials and Methods: In vivo experiments, 12weekold male Wistar rats applied to 50g of heavy orthodontic force for 7 days. Then, we determined tartrateresistant acid phosphatase (TRAP) and TGF-β1 positive expression levels in resorbed cementum using immunohistochemical analysis. In vitro, the effects of a heavy compression force (4.0 g/ cm 2 ) with/without SB -431542 (an inhibitor of TGF-β1) on TGF-β1, receptor activator of nuclear factor kappa -B ligand (RANKL) , and interleukin -6 (IL -6) production levels were measured using human PDL (hPDL) cells.Results: In vivo, in the 50g group, the immunoreactivity of TRAP and TGF-β1 with resorption lacunae was determined on day 7. In vitro, TGF-β1, RANKL, and IL -6 production increased in the 4.0 g/cm² group compared to that in the control group in hPDL cells. Moreover, treatment with SB -431542 inhibited the production of these factors. Conclusion:The results suggest that TGF-β1 may aggravate the OIIRR by increasing the production of RANKL and IL -6 from hPDL cells.

Background Wnt signaling is valuable protein network involved in bone metabolism; however, its relationship in bone resorption and formation during orthodontic treatment is currently unknown. Purpose This study examined Wnt5a expression on the compression side in an in vivo experimental rat tooth movement model. The study then investigated the relation of compression force(CF)to Wnt5a expression from human periodontal ligament(PDL)cells. Material and Methods In vivo, to movement the maxillary first molar, we added 10 g of orthodontic force to twenty male rats for seven days. We assessed the production of tartrate-resistant acid phosphatase (TRAP) and Wnt5a protein in rats alveolar bone through an immunohistochemical analysis. In vitro, we examined the effect of compression force(CF)on Wnt5a expression using the human PDL(hPDL)cells. Results We observed resorption lacunae with the multinuclear cells in rat alveolar bone during tooth movement in the 10g group. We observed Wnt5a immunoreactivity on day seven with orthodontic force in the PDL tissue. Wnt5a expression increased for timedependent maner after addition of CF in hPDL cells. Conclusion Given these findings, the Wnt signaling response to optimum orthodontic force appears to stimulate resorption of alveolar bone in the orthodontic tooth movement.