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

International Journal of Oral Science 2018年第1期10卷 27-35页

作者： Chia-Ying Yang Hyeran Helen Jeon ahmed alshabab Yu Jin Lee Chun-Hsi Chung Dana T. Graves 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

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.

关键词：中国牙科口腔医学

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