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Reduction of orthodontic tooth movement by experimentally induced periodontal inflammation in mice
Authors:Atsuko Okamoto  Tomokazu Ohnishi  Kenjiro Bandow  Kyoko Kakimoto  Norika Chiba  Aya Maeda  Tomohiro Fukunaga  Shouichi Miyawaki  Tetsuya Matsuguchi
Affiliation:Departments of Orthodontics;and Oral Biochemistry, Kagoshima University, Graduate School of Medical and Dental Sciences, Sakuragaoka, Kagoshima, Japan
Abstract:Orthodontic therapy is known to have an aggravating effect on the progression of destructive periodontitis if oral hygiene is not maintained. However, it is largely unknown how active periodontitis affects the velocity of orthodontic tooth movement. In this study, we examined the effect of periodontal inflammation on orthodontic tooth movement using a mouse model. Orthodontic force was applied on the maxillary first molar of mice, with or without ligature wire to induce experimental periodontitis. The distance moved by the first molar was significantly reduced by the ligature-induced experimental periodontitis. Tartrate-resistant acid phosphatase staining revealed that the number of osteoclasts present during orthodontic treatment was lower in the pressure zone of alveolar bone in the presence of periodontal inflammation. Consistently, the expression level of receptor activator of nuclear factor-κB ligand (RANKL) in the pressure zone was decreased in the ligature group. By contrast, experimental periodontitis increased the expression of cyclooxygenase-2 mRNA in the periodontal tissues, while in vitro treatment with prostaglandin E2 decreased extracellular signal-regulated kinase phosphorylation and RANKL expression induced by mechanical stress in osteoblasts. Taken together, these results suggest that the orthodontic force-induced osteoclastogenesis in alveolar bone was inhibited by the accompanying periodontal inflammation, at least partly through prostaglandin E2, resulting in reduced orthodontic tooth movement.
Keywords:orthodontic therapy    osteoclast    receptor activator of nuclear factor-κB ligand
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