title: Effect of soluble receptors to interleukin-1 and tumor necrosis factor alpha on experimentally induced root resorption in rats.
abstract: OBJECTIVE
  In this study, the role of the inflammatory cytokines interleukin-1 (IL-1) and tumor necrosis factor alpha (TNFalpha) in the course of mechanically induced root resorption was investigated.
  
  
  METHODS
  Mechanical induction of root resorption was performed on the upper left first molars in 18 male Wistar rats according to the method of Nakane and Kameyama. Starting on day minus 1, six animals received daily intraperitoneal injections of 2 ml of 1 micro g/ml soluble receptors to IL-1 (sIL-1RII) and another six animals were administered the same dose of soluble receptors to TNFalpha (sTNFalpha-RI). Six animals served as a control. On d 7 the left maxillae were prepared for histological and morphometric analysis of the extent of the root resorption that had developed.
  
  
  RESULTS
  The qualitative and quantitative results demonstrated that in both receptor groups the amount of root resorption was significantly reduced. Especially following systemic application of sTNFalpha-RI, root resorption was nearly completely prevented.
  
  
  CONCLUSIONS
  Our results indicate that IL-1 and more particularly TNFalpha are important for the induction and the further process of mechanically induced root resorption in the rat.
authors.affiliation: Jilin University, Dental School, Department of Orthodontics, Jilin, People's Republic of China.
authors.forename: Dongliang
authors.initials: D
authors.lastname: Zhang
authors.forename: Werner
authors.initials: W
authors.lastname: Goetz
authors.forename: Bert
authors.initials: B
authors.lastname: Braumann
authors.forename: Christoph
authors.initials: C
authors.lastname: Bourauel
authors.forename: Andreas
authors.initials: A
authors.lastname: Jaeger
mesh_terms: D000135:Acid Phosphatase / Q000032:analysis; D000818:Animals; D015415:Biomarkers / Q000032:analysis; D003739:Dental Cementum / Q000473:pathology; D003804:Dentin / Q000473:pathology; D005881:Gingiva / Q000293:injuries / Q000473:pathology; D007375:Interleukin-1 / Q000502:physiology; D007527:Isoenzymes / Q000032:analysis; D008214:Lymphocytes / Q000473:pathology; D008297:Male; D008963:Molar; D010010:Osteoclasts / Q000473:pathology; D010513:Periodontal Ligament / Q000293:injuries / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D017472:Receptors, Interleukin-1 / Q000819:agonists*; D018124:Receptors, Tumor Necrosis Factor / Q000819:agonists*; D012391:Root Resorption / Q000209:etiology* / Q000473:pathology / Q000517:prevention & control; D000071681:Tartrate-Resistant Acid Phosphatase; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology
chemical_list: D015415:Biomarkers; D007375:Interleukin-1; D007527:Isoenzymes; D017472:Receptors, Interleukin-1; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D000135:Acid Phosphatase; D000071681:Tartrate-Resistant Acid Phosphatase