Th17-cells in atopic dermatitis stimulate orthodontic root resorption
Article first published online: 25 DEC 2012
© 2012 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
Volume 19, Issue 7, pages 683–693, October 2013
How to Cite
Oral Diseases (2013) 19, 683–693
- Issue published online: 19 AUG 2013
- Article first published online: 25 DEC 2012
- Accepted manuscript online: 4 DEC 2012 04:39AM EST
- Manuscript Accepted: 25 NOV 2012
- Manuscript Revised: 15 OCT 2012
- Manuscript Received: 29 AUG 2012
- Japan Society for the Promotion of Science. Grant Numbers: C:22592297, C:23792449, C:23593044
- T-helper 17 cells;
- receptor activator of NF-kB ligand;
- root resorption;
- atopic dermatitis
The aim of this study was to investigate how atopic dermatitis (AD) contributes to root resorption during orthodontic tooth movement.
Materials and Methods
Atopic dermatitis model mice and wild-type mice were subjected to an excessive orthodontic force (OF) to induce movement of the upper first molars. The expression levels of the tartrate-resistant acid phosphatase (TRAP), IL-17, IL-6, and RANKL proteins were determined in the periodontal ligament (PDL) by an immunohistochemical analysis. 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.
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.
Th17 cells may therefore be associated with the deterioration of root resorption of AD mice, and may explain why AD patients are more susceptible to root resorption than healthy individuals when an excessive OF is applied.