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Objective: The aim of this study was to investigate how T-helper (Th) 17 cells and interleukin (IL)-17 contribute to root resorption during orthodontic tooth movement. Materials and methods: Experiment 1: Rheumatoid arthritis (RA) model mice and wild type mice were subjected to the orthodontic force (OF) to induce root resorption (heavy OF) of the upper first molars. The double-immunofluorescence analysis for IL-17/CD4 was performed to detect Th17 cells in the periodontal ligament (PDL). Experiment 2: Atopic dermatitis (AD) model mice and wild type mice were subjected to the heavy OF to induce movement of the upper first molars. The expression levels of the tartrate-resistant acid phosphatase (TRAP), IL-17, IL-6, and receptor activator of nuclear factor kappaB ligand (RANKL) proteins were determined in the PDL by an immunohistochemical analysis. Moreover, the fluorescent localization immunoassay was performed to detect Th17 cells. Furthermore, the effects of the compression force on co-cultures of CD4+ cells from AD patients or healthy individuals and human PDL cells were investigated with regard to the levels of secretion and mRNA expression of IL-17, IL-6, RANKL, and osteoprotegerin (OPG). Results: Experiment 1: The double-immunofluorescence analysis for IL-17/CD4 detected immunoreaction. Experiment 2: The immunoreactivities for TRAP, IL-17, IL-6, and RANKL in the AD group were found to be significantly increased. The double-immunofluorescence analysis for IL-17/CD4 detected immunoreaction. The secretion of IL-17, IL-6 and RANKL, and the mRNA levels of IL-6 and RANKL in the AD patients were increased compared with those in healthy individuals. Conclusion: Th17-producing IL-17 may be associated with the deterioration of orthodontic root resorption. [ABSTRACT FROM AUTHOR]

Objective: Orthodontically induced inflammatory root resorption (OIIRR) is one of the most difficult to predict accidental symptom in orthodontic treatment. Orthodontic forces are known to produce mechanical damage and inflammatory reactions in the periodontal ligament (PDL). Notch signaling pathway is a highly conserved cell signaling system that plays an important role in various cell differentiation processes including bone homeostasis. However, the role of Notch signaling in tooth movement and root resorption in orthodontic treatment has not fully understood. We examined the effects of orthodontic force on Notch and Jagged1(Notch ligand) expression in human PDL (hPDL) cells in vitro, andthe expression of Jagged1, RANKL and IL-6 in root resorption area during experimental tooth movement in rats. Materials and Methods: Different compression forces (CF) were applied to hPDL cells for up to 24h. With/without γ-secretase inhibitor (GSI; inhibitor of Notch signaling). The expression of Jagged1, RANKL and IL-6 mRNA was determined by using real-time PCR. In animal study, rats were subjected to an orthodontic force of 10 or 50g with a closed coil spring. Experimental tooth movement was undertaken for 7days. Each sample was prepared for HE and immunohistochemistry staining for TRAP, Jagged1, RANKL and IL-6 in root resorption area. Results: CF increased the expression of Jagged1, RANKL and IL-6mRNA from hPDL cells. Moreover, GSI suppresses CF-induced expression of these mRNA. On days 7, immunoreactivity for Jagged1, RANKL and IL-6 was detected in odontoclasts with an orthodontic force of 50g, but not 10g. Conclusions: These results indicate that CF may modulate the mRNA expression of RANKL and IL-6 via Notch signaling in hPDL cells. Notch signaling might be involved in the progress of inflammation in PDL tissue and the incidence of severe root resorption during orthodontic treatment. [ABSTRACT FROM AUTHOR]