title: The presence of TNF-alpha and TNFR1 in aseptic root resorption. A preliminary study.
abstract: BACKGROUND
  It is hypothesised that osteoprotegerin (OPG), as an osteoclast antagonist, may offer molecular control over the process of orthodontic root resorption. Previous work investigating OPG in a rat periodontal ligament (PDL) ankylosis model found no inhibitory effect on osteoclasts and odontoclasts when given at a recommended dosage of 2.5 mg/kg. It was considered that traumatically-induced PDL inflammation produces mediators and cytokines with the ability to stimulate clast cell differentiation and counter the effects of OPG.
  
  
  OBJECTIVE
  The present study investigated the presence of Tumour Necrosis Factor Alpha (TNF-alpha) and its receptor Tumour Necrosis Factor Receptor 1 (TNFR1) in a PDL sterile inflammatory model.
  
  
  METHODS
  Dry ice was applied for 15 minutes to the upper right first molar crown of eighteen, 8-week-old, male Sprague-Dawley rats of which 9 were injected with OPG at a dose of 2.5 mg/kg of body weight at the time of freezing. After 7 days, the rats were sacrificed and each maxilla processed for immunohistochemical identification of TNF-alpha and TNFR1.
  
  
  RESULTS
  Results showed the presence of root resorption in varying amounts and locations in both experimental and control rats. Reparative processes appeared greater in the OPG-treated rats, often with the presence of an ankylotic union. Immunolabelling showed the presence of TNF-alpha and TNFR1 in the sterile inflammation located mainly in the interradicular PDL area. More definitive labelling appeared in OPG-treated rats.
  
  
  CONCLUSIONS
  The results indicated that TNF-alpha, and its receptor TNFR1, by their presence, may modify OPG effectiveness by offering an alternative pathway for osteoclast formation, which counters the anti-resorptive effects of OPG.
authors.affiliation: Orthodontic Unit, School of Dentistry, The University of Adelaide, Adelaide, South Australia, Australia.
authors.forename: Linda
authors.initials: L
authors.lastname: Curl
authors.forename: Wayne
authors.initials: W
authors.lastname: Sampson
mesh_terms: D000539:Alveolar Process / Q000473:pathology; D000818:Animals; D003080:Cold Temperature / Q000009:adverse effects; D003782:Dental Pulp / Q000473:pathology; D003790:Dental Pulp Necrosis / Q000473:pathology; D005347:Fibroblasts / Q000473:pathology; D015726:Giant Cells / Q000473:pathology; D005881:Gingiva / Q000473:pathology; D008297:Male; D008963:Molar / Q000473:pathology; D010010:Osteoclasts / Q000187:drug effects; D053244:Osteoprotegerin / Q000494:pharmacology; D010513:Periodontal Ligament / Q000473:pathology; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D047888:Receptors, Tumor Necrosis Factor, Type I / Q000032:analysis*; D012391:Root Resorption / Q000473:pathology*; D020254:Tooth Ankylosis / Q000473:pathology; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis*; D014945:Wound Healing / Q000187:drug effects
chemical_list: D053244:Osteoprotegerin; D047888:Receptors, Tumor Necrosis Factor, Type I; C506032:Tnfrsf11b protein, rat; C506237:Tnfrsf1a protein, rat; D014409:Tumor Necrosis Factor-alpha