Immunohistochemical Localization of T-helper 17 Cells, IL-17, and RANKL during Root Resorption Induced by Excessive Orthodontic Force in the Mouse Model of T Cell-mediated Autoimmune Disease

Abstract

Orthodontically induced inflammatory root resorption is a common complication associated with orthodontic tooth movement. 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. Fifteen male 8-week-old SKG/Jcl mice (rheumatoid arthritis (RA) group) and 15 male 8-week-old BALB/cAJcL mice (wild type group) were subjected to an excessive orthodontic force of 25 g to induce a mesially tipping movement of the upper first molars for nine days. The expression levels of the cathepsin K, IL-17, IL-17 receptor (IL-17R), receptor activator of nuclear factor kappa B (RANK) ligand (RANKL), and RANK proteins were determined in the resorbed lacunae of the mouse periodontal ligament (PDL) by an immunohistochemical analysis. Following the experimental tooth movement in vivo,resorption lacunae with multinucleated cells were observed in both groups. The immunoreactivities for cathepsin K, IL-17, IL-17R, RANKL, and RANK in the RA group were found to be significantly increased in the PDL tissue subjected to the orthodontic force on day 9 compared with the control group. The double-immunofluorescence analysis for IL-17/CD4 detected immunoreactivity in the PDL. The results of this study suggest that the Th17 cell response to excessive orthodontic force may lead to the progression of root resorption by increasing the expression of IL-17, RANKL, and RANK.