title: Th17-cells in atopic dermatitis stimulate orthodontic root resorption.
abstract: OBJECTIVE
  The aim of this study was to investigate how atopic dermatitis (AD) contributes to root resorption during orthodontic tooth movement.
  
  
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Orthodontics, Nihon University School of Dentistry at Matsudo, Chiba, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Yamada
authors.forename: M
authors.initials: M
authors.lastname: Yamaguchi
authors.forename: M
authors.initials: M
authors.lastname: Asano
authors.forename: S
authors.initials: S
authors.lastname: Fujita
authors.forename: R
authors.initials: R
authors.lastname: Kobayashi
authors.forename: K
authors.initials: K
authors.lastname: Kasai
mesh_terms: D000135:Acid Phosphatase / Q000032:analysis; D000328:Adult; D000818:Animals; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D018929:Cell Culture Techniques; D018920:Coculture Techniques; D003876:Dermatitis, Atopic / Q000276:immunology* / Q000473:pathology; D004195:Disease Models, Animal; D005260:Female; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood; D020381:Interleukin-17 / Q000032:analysis / Q000097:blood; D015850:Interleukin-6 / Q000032:analysis; D007527:Isoenzymes / Q000032:analysis; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D053244:Osteoprotegerin / Q000032:analysis; D010513:Periodontal Ligament / Q000276:immunology / Q000473:pathology; D053245:RANK Ligand / Q000032:analysis; D012391:Root Resorption / Q000276:immunology* / Q000473:pathology; D013314:Stress, Mechanical; D000071681:Tartrate-Resistant Acid Phosphatase; D058504:Th17 Cells / Q000276:immunology*; D014087:Tooth Movement Techniques / Q000009:adverse effects; D055815:Young Adult
chemical_list: D020381:Interleukin-17; D015850:Interleukin-6; D007527:Isoenzymes; D053244:Osteoprotegerin; D053245:RANK Ligand; D007073:Immunoglobulin E; D000135:Acid Phosphatase; C000605511:Acp5 protein, mouse; D000071681:Tartrate-Resistant Acid Phosphatase
keywords: IL-17; T-helper 17 cells; atopic dermatitis; receptor activator of NF-kB ligand; root resorption