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Long‐term sequential receptor activator of NF‐κB ligand (RANKL) and osteoprotegrin (OPG) expression in lipopolysaccharide‐induced rat periapical lesions
Authors:Fu‐Hsiung Chuang  Chi‐Cheng Tsai  Jeng‐Huey Chen  Ker‐Kong Chen  Yuk‐Kwan Chen  Ying‐Chu Lin
Affiliation:1. School of Dentistry, College of Dental Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan;2. Division of Conservative Dentistry, Department of Dentistry, Kaohsiung Medical University Chung‐Ho Memorial Hospital, Kaohsiung, Taiwan;3. PhD Program, School of Dentistry, College of Dental Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan;4. College of Dental Medicine, Chung‐Shan Medical University, Taichung, Taiwan;5. Division of Oral Pathology and Diagnosis, Department of Dentistry, Kaohsiung Medical University Chung‐Ho Memorial Hospital, Kaohsiung, Taiwan;6. Department of Oral Hygiene, College of Dental Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan
Abstract:J Oral Pathol Med (2012) 41 : 186–193 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. Materials: 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. Conclusion: 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.
Keywords:lipopolysaccharide  OPG  osteoclast  periapical lesion  RANKL  rat
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