title: Long-term sequential receptor activator of NF-κB ligand (RANKL) and osteoprotegrin (OPG) expression in lipopolysaccharide-induced rat periapical lesions.
abstract: BACKGROUND
  Long-term sequential expression of receptor activator of NF-κB ligand (RANKL) and osteoprotegrin (OPG) in lipopolysaccharide (LPS)-induced rat periapical lesions has not been studied.
  
  
  METHODS
  Seventy-two 4-week-old Wistar rats were divided into eight experimental groups and one control group (eight animals in each).
  
  
  METHODS
  Lipopolysaccharide-induced periapical lesions were produced in rats by occlusal exposure of the pulp of their lower first molars in all experimental groups but not the control group. The extent of periapical destruction was measured by radiographic imaging. RANKL and OPG mRNA were measured in all tissue sections containing the periapical lesions as well as the control group every week from week 1 to week 8 by real-time quantitative reverse transcription polymerase chain reaction. RANKL and OPG protein were determined by immunohistochemistry. Osteoclasts were identified by enzyme histochemistry.
  
  
  RESULTS
  The sequential changes in the mRNA and protein expression of RANKL and OPG were largely compatible with the occurrence of osteoclasts histologically and enzymes histochemically, as well as the mean areas of the periapical lesions radiographically during long-term observation of the LPS-induced rat periapical lesions.
  
  
  CONCLUSIONS
  This study may be the first to demonstrate the long-term RANKL and OPG expression every week from week 1 to week 8 using LPS to produce periapical infection in a Wistar rat model. The long-term findings of high expressions of RANKL and OPG further extend the potential application of the Wistar rat model for future experimental trials using RANKL inhibitor to evaluate the treatment outcome for LPS-induced rat periapical lesions.
authors.affiliation: School of Dentistry, College of Dental Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.
authors.forename: Fu-Hsiung
authors.initials: FH
authors.lastname: Chuang
authors.forename: Chi-Cheng
authors.initials: CC
authors.lastname: Tsai
authors.forename: Jeng-Huey
authors.initials: JH
authors.lastname: Chen
authors.forename: Ker-Kong
authors.initials: KK
authors.lastname: Chen
authors.forename: Yuk-Kwan
authors.initials: YK
authors.lastname: Chen
authors.forename: Ying-Chu
authors.initials: YC
authors.lastname: Lin
mesh_terms: D000135:Acid Phosphatase / Q000032:analysis; D016301:Alveolar Bone Loss / Q000378:metabolism / Q000473:pathology; D000818:Animals; D015415:Biomarkers / Q000032:analysis; D002452:Cell Count; D003789:Dental Pulp Exposure / Q000150:complications; D004195:Disease Models, Animal; D004926:Escherichia coli; D015726:Giant Cells / Q000473:pathology; D007091:Image Processing, Computer-Assisted; D007150:Immunohistochemistry; D007527:Isoenzymes / Q000032:analysis; D008070:Lipopolysaccharides / Q000009:adverse effects*; D008297:Male; D010010:Osteoclasts / Q000378:metabolism / Q000473:pathology; D053244:Osteoprotegerin / Q000032:analysis*; D010483:Periapical Diseases / Q000209:etiology / Q000378:metabolism / Q000473:pathology*; D053245:RANK Ligand / Q000032:analysis*; D016300:Radiography, Bitewing; D051381:Rats; D017208:Rats, Wistar; D060888:Real-Time Polymerase Chain Reaction; D020133:Reverse Transcriptase Polymerase Chain Reaction; D000071681:Tartrate-Resistant Acid Phosphatase; D013997:Time Factors
chemical_list: D015415:Biomarkers; D007527:Isoenzymes; D008070:Lipopolysaccharides; D053244:Osteoprotegerin; D053245:RANK Ligand; C506032:Tnfrsf11b protein, rat; D000135:Acid Phosphatase; D000071681:Tartrate-Resistant Acid Phosphatase