The effect of compression force on periodontal ligament (PDL) plays a critical role in orthodontic tooth movement. However, little is known about this effect on apoptosis and the underlying reactive mechanisms in PDL cells. This study focuses on the application of compression force associated with reactive oxygen species (ROS)-induced apoptosis in PDL cells. Following the application of orthodontic force to maxillary first molars, the molars were investigated using immunohistochemical analysis. The cell cycle and apoptosis were assessed in compression force-treated PDL cells using flow cytometry. Furthermore, we assayed the effect on ROS generation by DCFDA fluorescence. In vivo study revealed an increased number of terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) and caspase 8-positive cells in the orthodontic force group. In our in vitro study model, the compression force increased the G1 phase and apoptotic cells. A large increase in the intracellular ROS levels in human (h) PDL cells was observed in the compression force group. Taken together, these results provide new information on compression force-induced G1 arrest and apoptosis in hPDL cells.
The aim of this study was to investigate the amount of external apical root resorption (EARR) and the release of interleukin (IL)-1 beta in the gingival crevicular fluid (GCF) in subjects treated with a low-force low-friction system. Sixty patients were assigned to two groups of thirty patients each: one group received treatment with self-ligating brackets and the other received conventional ligated edgewise brackets. All patients were treated with extraction of the maxillary first premolars. The EARR of the maxillary central incisors was evaluated on the periapical radiographs and cephalograms, taken before and after orthodontic treatment. The GCF was also collected non-invasively from the mesial and distal sides of central incisors using filter paper strips before and after orthodontic treatment. Enzyme-linked immunosorbent assay (ELISA) kits were used to determine the IL-1 beta levels in the GCF samples.A significant difference was found in the amount of EARR between the patients with selfligating brackets and conventional brackets. The mean amount of EARR was significantly lower for self-ligating brackets than the conventional brackets (p<0.05).The GCF levels of IL-1 beta for the patients with the self-ligating brackets application were significantly lower than for those with the conventional brackets (p<0.05). These results show that the mean amount of EARR and the GCF levels of IL-1 beta are significantly lower in patients treated using low-force low-friction appliances than with the conventional brackets. Therefore, self-ligating brackets may be a useful system for reducing inflammation and EARR.
Remodelling of the periodontium after application of mechanical forces constitutes the basis of clinical orthodontics, and various immunoregulatory molecules are involved in this process. The present study focused on the localizations of the tumor necrosis factor-α (TNF-α)and macrophages in periodontal ligament(PDL)during experimental tooth movement in rats. A total of 15 male 6-weeks-old Wistar rats were subjected to an orthodontic force of 10 g to induce a mesially tipping movement of the upper first molars.Experimental tooth movement was accomplished for seven days. We determined the localization of TNF-α and RM-4(an antibody specific for identification of macrophages)in the PDL during orthodontic tooth movement using immunohistochemistry. Immunoreactivity for TNF-α and RM-4 was detected in PDL fibroblasts in the compressive side by the orthodontic force of 10 g. On the first day after tooth movement, the immunoreactivity of TNF-α and RM-4 was weak. On the third and fifth days, more TNF-α and RM-4 positive reactions in some nucleuses of fibroblasts were recognized than on the first day.Furthermore, these positive reactions were decreased after seven days. Therefore, RM-4 (+)cells involved in the expression of TNF-α may play an important role in the initial reaction of the PDL and in the induction of the osteoclastic bone resorption during orthodontic tooth movement.
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