287: Th17-producing IL-17 on periodontal ligament induced root resorption in mouse models of rheumatoid arthritis and atopic dermatitis

Abstract

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.