Suppressing STAT3 activation impairs bone formation during maxillary expansion and relapse

作者全名："Xiao, Xiaoyue; Chen, Jianwei; Zhai, Qiming; Xin, Liangjing; Zheng, Xinhui; Wang, Si; Song, Jinlin"

作者地址："[Xiao, Xiaoyue; Zhai, Qiming; Xin, Liangjing; Zheng, Xinhui; Wang, Si; Song, Jinlin] Chongqing Med Univ, Coll Stomatol, Chongqing Key Lab Oral Dis & Biomed Sci, Municipal Key Lab Oral Biomed Engn Chongqing Highe, Chongqing, Peoples R China; [Chen, Jianwei] Sichuan Univ, West China Hosp Stomatol, State Key Lab Oral Dis, Chengdu, Peoples R China; [Chen, Jianwei] Sichuan Univ, West China Hosp Stomatol, Natl Clin Res Ctr Oral Dis, Chengdu, Peoples R China; [Wang, Si; Song, Jinlin] Chongqing Med Univ, Stomatol Hosp, 426 Songshi North Rd, Chongqing, Peoples R China"

通信作者："Wang, S; Song, JL (通讯作者)，Chongqing Med Univ, Stomatol Hosp, 426 Songshi North Rd, Chongqing, Peoples R China."

来源：JOURNAL OF APPLIED ORAL SCIENCE

ESI学科分类：CLINICAL MEDICINE

WOS号：WOS:000991233000001

JCR分区：Q2

影响因子：2.2

年份：2023

卷号：31

期号：　

开始页：　

结束页：　

文献类型：Article

关键词：Bone formation; Maxillary expansion; STAT3 protein

摘要："Objectives: The mid-palatal expansion technique is commonly used to correct maxillary constriction in dental clinics. However, there is a tendency for it to relapse, and the key molecules responsible for modulating bone formation remain elusive. Thus, this study aimed to investigate whether signal transducer and activator of transcription 3 (STAT3) activation contributes to osteoblast-mediated bone formation during palatal expansion and relapse. Methodology: In total, 30 male Wistar rats were randomly allocated into Ctrl (control), E (expansion only), and E+Stattic (expansion plus STAT3-inhibitor, Stattic) groups. Micro-computed tomography, micromorphology staining, and immunohistochemistry of the mid-palatal suture were performed on days 7 and 14. In vitro cyclic tensile stress (10% magnitude, 0.5 Hz frequency, and 24 h duration) was applied to rat primary osteoblasts and Stattic was administered for STAT3 inhibition. The role of STAT3 in mechanical loading -induced osteoblasts was confirmed by alkaline phosphatase (ALP), alizarin red staining, and western blots. Results: The E group showed greater arch width than the E+Stattic group after expansion. The differences between the two groups remained significant after relapse. We found active bone formation in the E group with increased expression of ALP, COL-I, and Runx2, although the expression of osteogenesis-related factors was downregulated in the E+stattic group. After STAT3 inhibition, expansive force-induced bone resorption was attenuated, as TRAP staining demonstrated. Furthermore, the administration of Stattic in vitro partially suppressed tensile stress-enhanced osteogenic markers in osteoblasts. Conclusions: STAT3 inactivation reduced osteoblast-mediated bone formation during palatal expansion and post -expansion relapse, thus it may be a potential therapeutic target to treat force-induced bone formation."

基金机构：　

基金资助正文：