title: Expression of RANKL and OPG mRNA in periodontal disease: possible involvement in bone destruction.
abstract: Periodontitis is a complex, multifactorial process affected by bacterial plaque-components and host defense mechanisms. Inflammation of the periodontitium may lead the destruction of the underlying ligament and alveolar bone. Receptor activator of NF-kappaB ligand (RANKL), a novel TNF receptor-related protein is an important factor for osteoclast differentiation and activation. Given osteolysis by osteoclast has been demonstrated in periodontitis, we hypothesized that RANKL expression may be associated with bone destruction in periodontitis. We used semi-quantitative RT-PCR to compare the gene expression of RANKL and osteoprogerin (OPG), a decoy receptor of RANKL, between moderate and advanced periodontitis, and healthy subjects. The level of RANKL mRNA was highest in advanced periodontitis. In contrast, the level of OPG mRNA in both advanced and moderate periodontitis was lower than that in the healthy group. It appears that the ratio of RANKL to OPG mRNA in periodontitis has increased. To determine the localization of RANKL gene transcripts in gingival tissue at the cellular level, in situ hybridization was performed using digoxigenin-labeled specific riboprobes. RANKL mRNA was expressed in inflammatory cells, mainly lymphocyte and macrophages. In addition, proliferating epithelium in the vicinity of inflammatory cells expressed high levels of RANKL mRNA. In short, our data suggest that up regulation of RANKL mRNA in both inflammatory cells and epithelium may be associated with the activation of osteoclastic bone destruction in periodontitis.
authors.affiliation: Department of Orthopaedic Surgery, Queen Elizabeth II Medical Centre, UWA, WA, Australia.
authors.forename: D
authors.initials: D
authors.lastname: Liu
authors.forename: J K
authors.initials: JK
authors.lastname: Xu
authors.forename: L
authors.initials: L
authors.lastname: Figliomeni
authors.forename: L
authors.initials: L
authors.lastname: Huang
authors.forename: N J
authors.initials: NJ
authors.lastname: Pavlos
authors.forename: M
authors.initials: M
authors.lastname: Rogers
authors.forename: A
authors.initials: A
authors.lastname: Tan
authors.forename: P
authors.initials: P
authors.lastname: Price
authors.forename: M H
authors.initials: MH
authors.lastname: Zheng
mesh_terms: D000328:Adult; D000368:Aged; D001847:Bone Diseases / Q000209:etiology / Q000235:genetics*; D002352:Carrier Proteins / Q000235:genetics*; D005881:Gingiva / Q000378:metabolism; D006023:Glycoproteins / Q000235:genetics*; D006801:Humans; D017403:In Situ Hybridization; D008562:Membrane Glycoproteins / Q000235:genetics*; D008875:Middle Aged; D053244:Osteoprotegerin; D010518:Periodontitis / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D053245:RANK Ligand; D012333:RNA, Messenger / Q000235:genetics*; D053246:Receptor Activator of Nuclear Factor-kappa B; D018160:Receptors, Cytoplasmic and Nuclear / Q000235:genetics*; D018124:Receptors, Tumor Necrosis Factor; D012016:Reference Values; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014158:Transcription, Genetic
chemical_list: D002352:Carrier Proteins; D006023:Glycoproteins; D008562:Membrane Glycoproteins; D053244:Osteoprotegerin; D053245:RANK Ligand; D012333:RNA, Messenger; D053246:Receptor Activator of Nuclear Factor-kappa B; D018160:Receptors, Cytoplasmic and Nuclear; D018124:Receptors, Tumor Necrosis Factor; C505686:TNFRSF11A protein, human; C506030:TNFRSF11B protein, human; C505688:TNFSF11 protein, human