The European Journal of Orthodontics Advance Access originally published online on July 16, 2008
The European Journal of Orthodontics 2008 30(4):336-345; doi:10.1093/ejo/cjn012
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Cellular and extracellular factors in early root resorption repair in the rat
* Department of Orthodontics, University of Bonn, Germany
** Dental School, Jilin University, People's Republic of China
Address for correspondence Professor A. Jäger, Department of Orthodontics, University of Bonn, Welschnonnenstrasse 17, 53111 Bonn, Germany, E-mail: a.jaeger{at}uni-bonn.de
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The aim of this study was to investigate the role of extracellular matrix components, such as collagen type I, fibronectin, and osteopontin (OPN) during cementum repair following experimentally induced tooth movement, and to characterize the cells taking part in the regenerative process. The upper right first molars were moved mesially in 21 three-month-old male Wistar rats using a coil spring with a force of 0.5 N. After 9 days, the appliance was removed and the animals were killed in groups of three immediately after withdrawal of the force and 5, 7, 10, 12, 14, and 17 days later. Three rats served as non-experimental control animals. The maxillae were prepared and processed for histological analysis.
Together with the disappearance of the multinucleated odontoclasts from the resorption lacunae, signs of repair were visible 5 days after the release of the orthodontic force. The first signs of cementum repair were seen on day 10. The newly produced cementum was of the acellular extrinsic fibre type (AEFC) and reattachment was achieved with the principal periodontal ligament (PDL) fibres orientated almost perpendicular to the root surface. The initial interface formed between the old and new cementum, as well as the new AEFC, was characterized by a strong immunoreaction with OPN and collagen I antibody, but only a weak immunoreaction with the fibronectin antibody. Only a small number of mononuclear cells, which were involved in the repair process, showed a positive immunoreaction with the osteoblastic lineage markers runt-related transcription factor 2 and osteocalcin. These same cells stained sparsely with muscle segment homeobox homologue 2, but not with the E11 antibody. Thus, most of the cells associated with this reparative activity on the surface of the lacunae were differentiated PDL cells of the fibroblastic phenotype. Cells with a defined osteoblastic phenotype seemed to be of minor importance in this repair process.
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