title: Expression of receptor activator of nuclear factor kappa B ligand relates to inflammatory bone resorption, with or without occlusal trauma, in rats.
abstract: OBJECTIVE
  Receptor activator of nuclear factor kappa B ligand (RANKL) is an important factor in osteoclast differentiation, activation and survival; however, its involvement in inflammatory bone resorption, with or without occlusal trauma, is unclear. The purpose of the present study was to investigate the distribution of RANKL-expressing cells in rat periodontium during lipopolysaccharide-induced inflammation with or without occlusal trauma.
  
  
  METHODS
  Lipopolysaccharide was injected into rat gingiva of the lower left first molar to induce inflammation. In addition, the occlusal surface of the upper left first molar of rat was raised by placing a gold inlay to induce occlusal trauma in the lower left first molars. The distribution of RANKL-expressing cells was immunohistochemically observed.
  
  
  RESULTS
  In the inflammatory model, many osteoclasts were observed at the apical inter-radicular septum on day 5 and they were reduced by day 10. On the other hand, in the inflammatory model with occlusal trauma, many osteoclasts were still observed on day 10. RANKL expression was similar to the changes in osteoclast number. The expression of RANKL increased in endothelial cells, inflammatory cells and periodontal ligament cells.
  
  
  CONCLUSIONS
  These findings clearly demonstrated that RANKL expression on endothelial cells, inflammatory cells and periodontal ligament cells is involved in inflammatory bone resorption and the expression is enhanced by traumatic occlusion. These results suggest that RANKL expression on these cells is closely involved in the increase of osteoclasts induced by occlusal trauma.
authors.affiliation: Department of Periodontology, Unit of Translational Medicine, Course of Medical and Dental Sciences, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Yoshinaga
authors.forename: T
authors.initials: T
authors.lastname: Ukai
authors.forename: Y
authors.initials: Y
authors.lastname: Abe
authors.forename: Y
authors.initials: Y
authors.lastname: Hara
mesh_terms: D016301:Alveolar Bone Loss / Q000209:etiology / Q000473:pathology*; D000539:Alveolar Process / Q000473:pathology; D000818:Animals; D001862:Bone Resorption / Q000209:etiology / Q000473:pathology*; D002452:Cell Count; D003769:Dental Occlusion, Traumatic / Q000150:complications*; D042783:Endothelial Cells / Q000473:pathology; D004730:Endothelium, Vascular / Q000473:pathology; D004926:Escherichia coli; D007150:Immunohistochemistry; D007249:Inflammation; D008070:Lipopolysaccharides / Q000009:adverse effects; D008297:Male; D008336:Mandibular Diseases / Q000209:etiology / Q000473:pathology; D008963:Molar; D010010:Osteoclasts / Q000473:pathology; D010513:Periodontal Ligament / Q000473:pathology; D053245:RANK Ligand / Q000032:analysis*; D051381:Rats; D011917:Rats, Inbred Lew; D013997:Time Factors
chemical_list: D008070:Lipopolysaccharides; D053245:RANK Ligand