RANKL deletion in periodontal ligament and bone lining cells blocks orthodontic tooth movement

作     者：Chia-Ying Yang Hyeran Helen Jeon Ahmed Alshabab Yu Jin Lee Chun-Hsi Chung Dana T. Graves 

作者机构：Department of Orthodontics School of Dental Medicine University of Pennsylvania Philadelphia PA USA Department of Pedodontics School of Dental Medicine University of Pennsylvania Philadelphia PA USA 

出 版 物：《International Journal of Oral Science》 (国际口腔科学杂志（英文版）)

年 卷 期：2018年第10卷第1期

页      面：27-35页

核心收录：

学科分类：10[医学] 

基　　金：supported by NIDCR grants R01DE017732 and R01AR0600 the Schoenleber Pilot Grant from the University of Pennsylvania School of Dental Medicine 

主　　题：DEPENDENT UP-REGULATION OSTEOCLAST DIFFERENTIATION ALKALINE-PHOSPHATASE MECHANICAL VIBRATION PDL FIBROBLASTS GENE-TRANSFER B-CELLS EXPRESSION TISSUE COMPRESSION 

摘      要：The bone remodeling process in response to orthodontic forces requires the activity of osteoclasts to allow teeth to move in the direction of the force applied. Receptor activator of nuclear factor-κB ligand(RANKL) is essential for this process although its cellular source in response to orthodontic forces has not been determined. Orthodontic tooth movement is considered to be an aseptic inflammatory process that is stimulated by leukocytes including T and B lymphocytes which are presumed to stimulate bone resorption. We determined whether periodontal ligament and bone lining cells were an essential source of RANKL by tamoxifen induced deletion of RANKL in which Cre recombinase was driven by a 3.2 kb reporter element of the Col1α1 gene in experimental mice(Col1α***+.RANKLf/f) and compared results with littermate controls(Col1α***-.RANKLf/f). By examination of Col1α***+.ROSA26 reporter mice we showed tissue specificity of tamoxifen induced Cre recombinase predominantly in the periodontal ligament and bone lining cells. Surprisingly we found that most of the orthodontic tooth movement and formation of osteoclasts was blocked in the experimental mice, which also had a reduced periodontal ligament space. Thus, we demonstrate for the first time that RANKL produced by periodontal ligament and bone lining cells provide the major driving force for tooth movement and osteoclastogenesis in response to orthodontic forces.