title: IL-8 and MCP-1 induced by excessive orthodontic force mediates odontoclastogenesis in periodontal tissues.
abstract: OBJECTIVE
  The aim of this study was to investigate how interleukin (IL)-8 (cytokine-induced neutrophil chemoattractant; CINC-1) and monocyte chemotactic protein (MCP)-1/CCL2 contribute to root resorption during orthodontic tooth movement.
  
  
  METHODS
  Forty 6-week-old male 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. We determined the expressions of CINC-1, CXCR2, and MCP-1 proteins in root resorption area using immunohistochemistry. Furthermore, we investigated the effects of compression forces (CF) on IL-8 and MCP-1 production by human periodontal ligament (hPDL) cells. We observed an effect of chemokine treatment on rat odonto/osteoclasts in dentin slices that recapitulated root resorption.
  
  
  RESULTS
  The immunoreactivity for CINC-1/CXCR2 and MCP-1 was detected in odontoclasts and PDL fibroblasts by the orthodontic force of 50 g on day 7. CF increased the secretion and the expression of mRNA of IL-8 and MCP-1 from PDL cells in a magnitude-dependent manner. Moreover, CINC-1 and MCP-1 stimulated osteoclastogenesis from rat osteoclast precursor cells.
  
  
  CONCLUSIONS
  IL-8 (CINC-1) and MCP-1 may therefore facilitate the process of root resorption because of excessive orthodontic force.
authors.affiliation: Department of Orthodontics, Nihon University School of Dentistry at Matsudo, Chiba, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Asano
authors.forename: M
authors.initials: M
authors.lastname: Yamaguchi
authors.forename: R
authors.initials: R
authors.lastname: Nakajima
authors.forename: S
authors.initials: S
authors.lastname: Fujita
authors.forename: T
authors.initials: T
authors.lastname: Utsunomiya
authors.forename: H
authors.initials: H
authors.lastname: Yamamoto
authors.forename: K
authors.initials: K
authors.lastname: Kasai
mesh_terms: D000135:Acid Phosphatase / Q000032:analysis; D000293:Adolescent; D000818:Animals; D001696:Biomechanical Phenomena; D018929:Cell Culture Techniques; D002454:Cell Differentiation / Q000502:physiology; D018932:Chemokine CCL2 / Q000032:analysis*; D054360:Chemokine CXCL1 / Q000032:analysis; D016207:Cytokines / Q000032:analysis*; D003804:Dentin / Q000473:pathology; D005260:Female; D005347:Fibroblasts / Q000502:physiology; D006801:Humans; D007150:Immunohistochemistry; D016209:Interleukin-8 / Q000032:analysis*; D007527:Isoenzymes / Q000032:analysis; D008297:Male; D008963:Molar / Q000473:pathology; D010010:Osteoclasts / Q000502:physiology*; D010513:Periodontal Ligament / Q000166:cytology*; D051381:Rats; D017208:Rats, Wistar; D023063:Receptors, Interleukin-8B / Q000032:analysis; D012391:Root Resorption / Q000473:pathology; D013314:Stress, Mechanical; D000071681:Tartrate-Resistant Acid Phosphatase; D014087:Tooth Movement Techniques
chemical_list: C111835:CCL2 protein, human; C508606:CXCL8 protein, human; C491766:Ccl2 protein, rat; D018932:Chemokine CCL2; D054360:Chemokine CXCL1; C513297:Cxcl1 protein, rat; D016207:Cytokines; D016209:Interleukin-8; D007527:Isoenzymes; D023063:Receptors, Interleukin-8B; D000135:Acid Phosphatase; D000071681:Tartrate-Resistant Acid Phosphatase