title: Expression of RANKL and OPG in middle ear cholesteatoma tissue.
abstract: OBJECTIVE
  The objective of this study was to investigate how the expression of the RANK-RANKL-OPG system mediates the formation and differentiation of osteoclasts and causes bone resorption in cholesteatoma.
  
  
  METHODS
  An immunohistochemical analysis was carried out in 22 cholesteatoma tissues obtained during middle ear surgery and 15 normal postauricular skin tissues to examine the expression of RANKL and OPG.
  
  
  RESULTS
  All 22 cases of cholesteatoma and the 15 cases of normal postauricular skin expressed RANKL and OPG. The count and rate of RANKL-positive cells in cholesteatoma was significantly higher than in normal postauricular skin. The count and rate of OPG-positive cells in normal postauricular skin was significantly higher than in cholesteatoma. The ratio of the positive expression rates of RANKL and OPG in cholesteatoma was statistically higher than in normal postauricular skin.
  
  
  CONCLUSIONS
  We provide evidence suggesting that RANKL, which activates osteoclasts, plays a significant role in the mechanism of bone destruction in cholesteatoma, and that the ratio of RANKL to OPG may be a reliable indicator of bone destruction in cholesteatoma.
authors.affiliation: Department of Otolaryngology, College of Medicine, Hanyang University, Seoul, Korea.
authors.forename: Jin-Hyeok
authors.initials: JH
authors.lastname: Jeong
authors.forename: Chul-Won
authors.initials: CW
authors.lastname: Park
authors.forename: Kyung
authors.initials: K
authors.lastname: Tae
authors.forename: Seung-Hwan
authors.initials: SH
authors.lastname: Lee
authors.forename: Dae-Hyun
authors.initials: DH
authors.lastname: Shin
authors.forename: Kyung-Rae
authors.initials: KR
authors.lastname: Kim
authors.forename: Yong-Wook
authors.initials: YW
authors.lastname: Park
mesh_terms: D015415:Biomarkers / Q000378:metabolism; D002352:Carrier Proteins / Q000096:biosynthesis*; D018424:Cholesteatoma, Middle Ear / Q000378:metabolism* / Q000473:pathology; D018450:Disease Progression; D006023:Glycoproteins / Q000096:biosynthesis*; D006801:Humans; D007150:Immunohistochemistry; D066298:In Vitro Techniques; D008562:Membrane Glycoproteins / Q000096:biosynthesis*; D010010:Osteoclasts / Q000378:metabolism* / Q000473:pathology; D053244:Osteoprotegerin; D011379:Prognosis; D053245:RANK Ligand; D053246:Receptor Activator of Nuclear Factor-kappa B; D018160:Receptors, Cytoplasmic and Nuclear / Q000096:biosynthesis*; D018124:Receptors, Tumor Necrosis Factor / Q000096:biosynthesis*; D012189:Retrospective Studies
chemical_list: D015415:Biomarkers; D002352:Carrier Proteins; D006023:Glycoproteins; D008562:Membrane Glycoproteins; D053244:Osteoprotegerin; D053245:RANK Ligand; 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