title: Expression of Toll-like receptors 2 and 4 and the OPG-RANKL-RANK system in inflammatory external root resorption and external cervical resorption.
abstract: OBJECTIVE
  To investigate and compare the expression of the pathogen recognition receptors Toll-like receptor (TLR) 2 and TLR4, and the hard tissue resorption triad osteoprotegerin (OPG)-receptor activator of nuclear factor kappa-B ligand (RANKL)-receptor activator of nuclear factor kappa-B (RANK) in external inflammatory root resorption of endodontic origin (ER) and external cervical root resorption (ECR) by immunohistochemistry.
  
  
  METHODS
  Formalin-fixed, paraffin-embedded archival specimens collected from teeth that were diagnosed clinically, radiographically and histopathologically with either ER (n = 9) or ECR (n = 9) were processed for immunohistochemistry to investigate and compare levels of TLR2, TLR4, OPG, RANKL, RANK, CD3, CD19 and CD83 expression. The histological features were evaluated via haematoxylin and eosin stain. Taylor's modification of the Brown and Brenn Gram stain was used for examining the presence and distribution of bacteria. All stained slides were digitally photographed and qualitatively analysed, and F test and unpaired Student's t-test were used for statistical analysis.
  
  
  RESULTS
  Both ER and ECR showed similar immuno-histopathology characteristics of a fibrovascular connective tissue with varying degrees of inflammatory infiltrate consisting of T and B lymphocytes, dendritic cells, polymorphonuclear lymphocytes and plasma cells. Colonies of bacteria were identified in the majority of lesions, and this correlated with the cellular expression of TLR2 and TLR4 in all lesions. Similarly, all lesions showed a significantly higher (P < 0.05) level of cells expressing RANKL than OPG, indicating hard tissue resorption processes where active in the lesions.
  
  
  CONCLUSIONS
  The immunohistopathology patterns of ECR samples were consistent with the bacteria-driven ER specimens, suggesting bacteria-induced inflammation may be involved in ECR.
authors.affiliation: Faculty of Dentistry, University of Otago, Dunedin, New Zealand.
authors.forename: Y P
authors.initials: YP
authors.lastname: Lin
authors.forename: R M
authors.initials: RM
authors.lastname: Love
authors.forename: L T
authors.initials: LT
authors.lastname: Friedlander
authors.forename: H F
authors.initials: HF
authors.lastname: Shang
authors.forename: M H
authors.initials: MH
authors.lastname: Pai
mesh_terms: D006801:Humans; D007249:Inflammation / Q000378:metabolism; D053244:Osteoprotegerin / Q000378:metabolism*; D053245:RANK Ligand / Q000378:metabolism*; D053246:Receptor Activator of Nuclear Factor-kappa B / Q000378:metabolism*; D012391:Root Resorption / Q000378:metabolism*; D051195:Toll-Like Receptor 2 / Q000378:metabolism*; D051197:Toll-Like Receptor 4 / Q000378:metabolism*; D019237:Tooth Cervix / Q000378:metabolism*
chemical_list: D053244:Osteoprotegerin; D053245:RANK Ligand; D053246:Receptor Activator of Nuclear Factor-kappa B; C505686:TNFRSF11A protein, human; C506030:TNFRSF11B protein, human; C505688:TNFSF11 protein, human; D051195:Toll-Like Receptor 2; D051197:Toll-Like Receptor 4
keywords: OPG; RANK; RANKL; Root resorption; Toll-like Receptor