Jing Li1, Xuxia Wang2, Na Li3, Dehua Zhenga1, Yuran Su1, Jun Zhang4. 1. a Student, Department of Orthodontics, School of Stomatology, Shandong University, Jinan, Shandong, China. 2. b Professor and Department Chair, Department of Oral and Maxillofacial Surgery, School of Stomatology, Shandong University, Jinan, Shandong, China. 3. c Physician, Department of Stomatology, Qianfoshan Hospital of Shandong Province, Jinan, Shandong, China. 4. d Professor, Department of Orthodontics, School of Stomatology, Shandong University, Jinan, Shandong, China.
Abstract
OBJECTIVE: To investigate the effect of nicotine exposure on root resorption in an in vivo rat model of orthodontic tooth movement (OTM), and its association with odontoclastogenesis and receptor activator of nuclear factor-kappa B ligand (RANKL) expression. MATERIALS AND METHODS: Forty-eight 10-week-old male Wistar rats were divided into three groups. The negative control group was untreated. The left maxillary first molars in the nicotine-treated group and the positive control group received OTM with an initial force of 0.6 N in the mesial direction. Also, the nicotine-treated group received intraperitoneal injection of nicotine at 7 mg/kg per day. After 21 days, the rats were humanely killed. Eight rats from each group were randomly chosen for crater volume analysis by micro-computed tomography. For the remaining eight rats in each group, specimen slices were generated for histologic examination to determine the odontoclast number and the mean optical density value of RANKL. RESULTS: The resorption volumes in the nicotine-treated group were significantly larger than those in the control groups. Also, the nicotine-treated group displayed significantly higher number of odontoclasts and elevated RANKL expression compared to the control groups. CONCLUSIONS: In an in vivo rat model, nicotine exposure promotes odontoclastogenesis and RANKL expression, evoking aggravated root resorption during OTM.
OBJECTIVE: To investigate the effect of nicotine exposure on root resorption in an in vivo rat model of orthodontic tooth movement (OTM), and its association with odontoclastogenesis and receptor activator of nuclear factor-kappa B ligand (RANKL) expression. MATERIALS AND METHODS: Forty-eight 10-week-old male Wistar rats were divided into three groups. The negative control group was untreated. The left maxillary first molars in the nicotine-treated group and the positive control group received OTM with an initial force of 0.6 N in the mesial direction. Also, the nicotine-treated group received intraperitoneal injection of nicotine at 7 mg/kg per day. After 21 days, the rats were humanely killed. Eight rats from each group were randomly chosen for crater volume analysis by micro-computed tomography. For the remaining eight rats in each group, specimen slices were generated for histologic examination to determine the odontoclast number and the mean optical density value of RANKL. RESULTS: The resorption volumes in the nicotine-treated group were significantly larger than those in the control groups. Also, the nicotine-treated group displayed significantly higher number of odontoclasts and elevated RANKL expression compared to the control groups. CONCLUSIONS: In an in vivo rat model, nicotine exposure promotes odontoclastogenesis and RANKL expression, evoking aggravated root resorption during OTM.
Authors: Fan Yang; Xu Xia Wang; Dan Ma; Qun Cui; De Hua Zheng; Xiao Can Liu; Jun Zhang Journal: Drug Des Devel Ther Date: 2019-11-25 Impact factor: 4.162
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