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T‐helper 17 cells mediate the osteo/odontoclastogenesis induced by excessive orthodontic forces
Author(s) -
Hayashi N,
Yamaguchi M,
Nakajima R,
Utsunomiya T,
Yamamoto H,
Kasai K
Publication year - 2012
Publication title -
oral diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.953
H-Index - 87
eISSN - 1601-0825
pISSN - 1354-523X
DOI - 10.1111/j.1601-0825.2011.01886.x
Subject(s) - periodontal fiber , osteoclast , interleukin , bone resorption , chemistry , immunohistochemistry , in vitro , resorption , interleukin 17 , western blot , microbiology and biotechnology , receptor , medicine , dentistry , inflammation , biology , cytokine , biochemistry , gene
Oral Diseases (2012) 18 , 375–388 Objective: The aim of this study was to investigate how T‐helper 17 cells (Th17 cells), interleukin (IL)‐17, and interleukin‐6 contribute to root resorption during orthodontic tooth movement. Materials and Methods: Fifteen male 6‐week‐old Wistar rats were subjected to orthodontic force of 10 or 50 g to induce a mesially tipping movement of the upper first molars for 7 days. The expression levels of TRAP, IL‐17, the IL‐17 receptor (IL‐17R), and IL‐6 proteins were determined in periodontal ligament (PDL) by immunohistochemical analysis. Moreover, the fluorescent localization immunoassay was performed to detect Th17 cells. Furthermore, the effects of IL‐17 on IL‐6 release were investigated using human PDL cells in vitro . The effect of IL‐17 on osteoclastogenesis was evaluated by TRAP staining, actin ring staining, and the pit formation assay. Results: The immunoreactivity for Th17, IL‐17, IL‐17R, and IL‐6 was detected in PDL tissue subjected to the orthodontic force on day 7. IL‐17 increased the release of IL‐6 from human periodontal ligament cells in a time‐dependent manner. Moreover, IL‐17 stimulated osteoclastogenesis from human osteoclast precursor cells, and these effects were partially suppressed by an anti‐IL‐6 antibody. Conclusion: These results suggest that Th17 cells may aggravate the process of orthodontically induced inflammatory root resorption.