title: Toll-like receptor 2 knockout mice showed increased periapical lesion size and osteoclast number.
abstract: BACKGROUND
  The aim of this study was to characterize the formation and progression of experimentally induced periapical lesions in TLR2 knockout (TLR2 KO) mice.
  
  
  METHODS
  Periapical lesions were induced in molars of 28 wild type (WT) and 27 TLR2 KO mice. After 7, 21, and 42 days, the animals were euthanized, and the mandibles were subjected to histotechnical processing. Hematoxylin-eosin-stained sections were examined under conventional light microscopy for the description of pulpal, apical, and periapical features and under fluorescence microscopy for the determination of the periapical lesion size. The subsequent sections were evaluated by tartrate resistant acid phosphatase histoenzymology (osteoclasts), Brown and Brenn staining (bacteria), and immunohistochemistry (RANK, RANKL, and OPG). Data were analyzed by the Mann-Whitney U and Kruskal-Wallis tests (α = 0.05).
  
  
  RESULTS
  The WT group showed significant differences (P < .05) in the periapical lesion size and the osteoclast number between 7 and 42 days and between 21 and 42 days. In the TLR2 KO group, significant differences (P < .05) in the periapical lesion size and the osteoclast number were found between 7 days and the other periods. There was a significant difference (P < .05) between the 2 types of animal regarding the periapical lesion size, which was larger in the TLR2 KO animals. No significant differences (P > .05) were found between WT and TLR2 KO mice related to the pulpal, apical, and periapical features; bacteria localization; and immunohistochemical results (except for RANK expression).
  
  
  CONCLUSIONS
  TLR2 KO animals developed larger periapical lesions with a greater number of osteoclasts, indicating the important role of this receptor in the host's immune and inflammatory response to root canal and periradicular infection.
authors.affiliation: Department of Pediatric Clinics, Preventive and Community Dentistry, School of Dentistry of Ribeirão Preto, University of São Paulo, Ribeirão Preto, São Paulo, Brazil. raquel@forp.usp.br
authors.forename: Raquel Assed Bezerra
authors.initials: RA
authors.lastname: da Silva
authors.forename: Paula Dariana Fernandes
authors.initials: PD
authors.lastname: Ferreira
authors.forename: Andiara
authors.initials: A
authors.lastname: De Rossi
authors.forename: Paulo
authors.initials: P
authors.lastname: Nelson-Filho
authors.forename: Lea Assed Bezerra
authors.initials: LA
authors.lastname: Silva
mesh_terms: D000818:Animals; D002452:Cell Count; D003790:Dental Pulp Necrosis / Q000276:immunology / Q000382:microbiology / Q000473:pathology*; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D009504:Neutrophils; D010010:Osteoclasts / Q000378:metabolism / Q000473:pathology*; D053244:Osteoprotegerin / Q000378:metabolism; D010485:Periapical Periodontitis / Q000276:immunology* / Q000382:microbiology / Q000473:pathology*; D053245:RANK Ligand / Q000378:metabolism; D053246:Receptor Activator of Nuclear Factor-kappa B / Q000378:metabolism; D051195:Toll-Like Receptor 2 / Q000235:genetics* / Q000502:physiology*
chemical_list: D053244:Osteoprotegerin; D053245:RANK Ligand; D053246:Receptor Activator of Nuclear Factor-kappa B; C493486:Tlr2 protein, mouse; D051195:Toll-Like Receptor 2