title: Increased gene expression of Toll-like receptors and antigen-presenting cell-related molecules in the onset of experimentally induced furcation lesions of endodontic origin in rat molars.
abstract: BACKGROUND
  Early immunopathogenic mechanisms behind pulp infection-induced furcal inflammation have not been well understood. To address the immunopathology of the pulp infection-induced furcal region of the periodontal ligament (PDL), we performed immunohistochemical and quantitative gene expression analyses for toll-like receptors (TLRs) in the furcal PDL of rat molars subjected to unsealed or sealed pulpotomy.
  
  
  METHODS
  Furcal inflammation in rat molars was generated by making unsealed pulpotomies that were exposed to the oral environment for 24 hours. Pulpotomized teeth sealed with a temporary filling material and untreated normal teeth served as controls. Gene expression was analyzed with laser capture real-time polymerase chain reaction for TLR-2, TLR-4, and antigen presenting cell (APC)-related molecules (class II MHC, CD83, and CD86). Immunohistochemistry for TLR-2 and TLR-4 was also performed.
  
  
  RESULTS
  Messenger RNA expression levels of TLRs and the APC-related molecules in the furcal periodontal ligament were significantly up-regulated in teeth with unsealed pulpotomy. Immunohistochemistry for unsealed pulpotomized teeth revealed that TLRs-expressing cells were predominantly distributed within the PDL beneath the furcal dentin.
  
  
  CONCLUSIONS
  These results suggested the involvement of innate immune mechanisms involving TLRs and resulting activation of APCs in the early pathogenesis of pulp infection-induced furcal inflammation.
authors.affiliation: Pulp Biology and Endodontics, Graduate School, Tokyo Medical and Dental University, Tokyo, Japan.
authors.forename: Uraiwan
authors.initials: U
authors.lastname: Chokechanachaisakul
authors.forename: Tomoatsu
authors.initials: T
authors.lastname: Kaneko
authors.forename: Takashi
authors.initials: T
authors.lastname: Okiji
authors.forename: Reika
authors.initials: R
authors.lastname: Kaneko
authors.forename: Mitsuhiro
authors.initials: M
authors.lastname: Kaneko
authors.forename: Jun
authors.initials: J
authors.lastname: Kawamura
authors.forename: Mitsuhiro
authors.initials: M
authors.lastname: Sunakawa
authors.forename: Hideaki
authors.initials: H
authors.lastname: Suda
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D000938:Antigen-Presenting Cells / Q000276:immunology* / Q000502:physiology; D003782:Dental Pulp / Q000276:immunology* / Q000502:physiology; D003789:Dental Pulp Exposure / Q000276:immunology*; D004195:Disease Models, Animal; D005786:Gene Expression Regulation; D007150:Immunohistochemistry; D008297:Male; D010513:Periodontal Ligament / Q000276:immunology / Q000502:physiology; D011672:Pulpotomy; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017208:Rats, Wistar; D012389:Root Canal Obturation; D051195:Toll-Like Receptor 2 / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D051197:Toll-Like Receptor 4 / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D019227:Tooth Apex / Q000276:immunology* / Q000502:physiology
chemical_list: D012333:RNA, Messenger; D051195:Toll-Like Receptor 2; D051197:Toll-Like Receptor 4