Christian Kirschneck1, Jochen Fanghänel2, Ulrich Wahlmann3, Michael Wolf4, J Camilo Roldán5, Peter Proff6. 1. Department of Orthodontics, University Medical Centre of Regensburg, Franz-Josef-Strauß-Allee 11, D-93053 Regensburg, Germany. Electronic address: christian.kirschneck@ukr.de. 2. Department of Orthodontics, University Medical Centre of Regensburg, Franz-Josef-Strauß-Allee 11, D-93053 Regensburg, Germany. Electronic address: jochen.fanghaenel@ukr.de. 3. Department of Maxillofacial Surgery, University Medical Centre of Regensburg, Franz-Josef-Strauß-Allee 11, D-93053 Regensburg, Germany. Electronic address: ulrich.wahlmann@ukr.de. 4. Department of Orthodontics, Rheinische Friedrich Wilhelm University of Bonn, Welschnonnenstraße 17, D-53111 Bonn, Germany. Electronic address: michael.wolf@uni-bonn.de. 5. Director of the Division of Pediatric Facial Plastic Surgery and Craniofacial Anomalies, Catholic Children's Hospital Wilhelmstift, Liliencronstraße 130, D-22149 Hamburg, Germany; Lecturer at the Department of Cranio-Maxillofacial Surgery, University Medical Centre of Regensburg, Franz-Josef-Strauß-Allee 11, D-93053 Regensburg, Germany. Electronic address: jc.roldan@kkh-wilhelmstift.de. 6. Department of Orthodontics, University Medical Centre of Regensburg, Franz-Josef-Strauß-Allee 11, D-93053 Regensburg, Germany. Electronic address: peter.proff@ukr.de.
Abstract
BACKGROUND: Many adult orthodontic patients suffer from chronic periodontitis with recurrent episodes of active periodontal inflammation. As their number is steadily increasing, orthodontists are more and more frequently challenged by respective treatment considerations. However, little is currently known regarding interactive effects on undesired dental root resorption (DRR), tooth movement velocity, periodontal bone loss and the underlying cellular and tissue reactions. MATERIAL AND METHODS: A total of 63 male Fischer344 rats were used in three consecutive experiments employing 21 animals each (A/B/C), randomly assigned to 3 experimental groups (n=7, 1/2/3), respectively: (A) CBCT; (B) histology/serology; (C) RT-qPCR-(1) control; (2) orthodontic tooth movement (OTM) of the first/second upper left molars (NiTi coil spring, 0.25N); (3) OTM with experimentally induced periodontitis (cervical silk ligature). After 14days of OTM, we quantified blood leukocyte level, DRR, osteoclast activity and relative gene expression of inflammatory and osteoclast marker genes within the dental-periodontal tissue as well as tooth movement velocity and periodontal bone loss after 14 and 28 days. RESULTS: The experimentally induced periodontal bone loss was significantly increased by concurrent orthodontic force application. Periodontal inflammation during OTM on the other hand significantly augmented the extent of DRR, relative expression of inflammatory/osteoclast marker genes, blood leukocyte level and periodontal osteoclast activity. In addition, contrary to previous studies, we observed a significant increase in tooth movement velocity. CONCLUSIONS: Although accelerated tooth movement would be favourable for orthodontic treatment, our results suggest that orthodontic interventions should only be performed after successful systematic periodontal therapy and paused in case of recurrent active inflammation.
BACKGROUND: Many adult orthodontic patients suffer from chronic periodontitis with recurrent episodes of active periodontal inflammation. As their number is steadily increasing, orthodontists are more and more frequently challenged by respective treatment considerations. However, little is currently known regarding interactive effects on undesired dental root resorption (DRR), tooth movement velocity, periodontal bone loss and the underlying cellular and tissue reactions. MATERIAL AND METHODS: A total of 63 male Fischer344 rats were used in three consecutive experiments employing 21 animals each (A/B/C), randomly assigned to 3 experimental groups (n=7, 1/2/3), respectively: (A) CBCT; (B) histology/serology; (C) RT-qPCR-(1) control; (2) orthodontic tooth movement (OTM) of the first/second upper left molars (NiTi coil spring, 0.25N); (3) OTM with experimentally induced periodontitis (cervical silk ligature). After 14days of OTM, we quantified blood leukocyte level, DRR, osteoclast activity and relative gene expression of inflammatory and osteoclast marker genes within the dental-periodontal tissue as well as tooth movement velocity and periodontal bone loss after 14 and 28 days. RESULTS: The experimentally induced periodontal bone loss was significantly increased by concurrent orthodontic force application. Periodontal inflammation during OTM on the other hand significantly augmented the extent of DRR, relative expression of inflammatory/osteoclast marker genes, blood leukocyte level and periodontal osteoclast activity. In addition, contrary to previous studies, we observed a significant increase in tooth movement velocity. CONCLUSIONS: Although accelerated tooth movement would be favourable for orthodontic treatment, our results suggest that orthodontic interventions should only be performed after successful systematic periodontal therapy and paused in case of recurrent active inflammation.
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