Reduction of orthodontic tooth movement by experimentally induced periodontal inflammation in mice.
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-kappaB 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 E(2) 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 E(2), resulting in reduced orthodontic tooth movement.
Okamoto
Atsuko
A
Department of Orthodontics, Kagoshima University, Graduate School of Medical and Dental Sciences, Sakuragaoka, Kagoshima, Japan.
Ohnishi
Tomokazu
T
Bandow
Kenjiro
K
Kakimoto
Kyoko
K
Chiba
Norika
N
Maeda
Aya
A
Fukunaga
Tomohiro
T
Miyawaki
Shouichi
S
Matsuguchi
Tetsuya
T
D016475:3T3 Cells; D000135:Acid Phosphatase / Q000032:analysis; D016301:Alveolar Bone Loss / Q000473:pathology / Q000503:physiopathology; D000539:Alveolar Process / Q000473:pathology / Q000503:physiopathology; D000818:Animals; D015415:Biomarkers / Q000032:analysis; D051546:Cyclooxygenase 2 / Q000032:analysis; D015232:Dinoprostone / Q000494:pharmacology; D004195:Disease Models, Animal; D048049:Extracellular Signal-Regulated MAP Kinases / Q000187:drug effects; D007527:Isoenzymes / Q000032:analysis; D008297:Male; D008437:Maxilla / Q000473:pathology / Q000503:physiopathology; D051379:Mice; D008810:Mice, Inbred C57BL; D008815:Mice, Inbred Strains; D008963:Molar / Q000503:physiopathology; D010006:Osteoblasts / Q000187:drug effects / Q000473:pathology; D010010:Osteoclasts / Q000473:pathology / Q000502:physiology; D010518:Periodontitis / Q000473:pathology / Q000503:physiopathology*; D010766:Phosphorylation; D053245:RANK Ligand / Q000032:analysis / Q000187:drug effects; D013314:Stress, Mechanical; D000071681:Tartrate-Resistant Acid Phosphatase; D014087:Tooth Movement Techniques
D015415:Biomarkers; D007527:Isoenzymes; D053245:RANK Ligand; C077623:Ptgs2 protein, mouse; D051546:Cyclooxygenase 2; D048049:Extracellular Signal-Regulated MAP Kinases; D000135:Acid Phosphatase; D000071681:Tartrate-Resistant Acid Phosphatase; D015232:Dinoprostone