title: TNF-alpha receptor expression correlates with histologic activity of otosclerosis.
abstract: OBJECTIVE
  Otosclerosis is an inflammatory bone remodeling disorder of the human otic capsule, which might be characterized by variable levels and unique expression pattern of TNF-alpha receptors.
  
  
  BACKGROUND
  Histologic characteristics of otosclerosis have been well described during the latest decades; however, the grading of different histopathologic and clinical stages has not been attributed precisely to the molecular biology of the pathologically increased metabolism of osteoclast-osteoblast axis.
  
  
  METHODS
  Forty otosclerotic- and 40 nonotosclerotic ankylotic stapes footplates (n = 80; men, 29; women, 51) were histologically analyzed: conventional hematoxylin-eosin staining and tumor necrosis factor-alpha receptor I and II (TNFRI/II)-specific immunofluorescent assay was performed.
  
  
  RESULTS
  Active otosclerosis (Grades I-II; n = 24) was featured by increased expression of TNFRII and moderate expression of TNFRI; inactive cases (Grades III-IV) were characterized by permanent expression of TNFRI; however, TNFRII-specific immunoreaction was absent. Nonotosclerotic stapes specimens showed a negligible TNFR expression. Tumor necrosis factor receptor expression pattern showed a strong correlation with the histologic activity of otosclerosis (chi2 test; p < 0.001).
  
  
  CONCLUSIONS
  Detection of elevated TNFR expression demonstrates activated osteoclast metabolism and inflammatory pathways in otosclerosis. Different etiopathogenesis of otosclerotic and nonotosclerotic stapes ankylosis should be distinguished. Administration of monoclonal anti-TNF-alpha antibody may be a reasonable option in the medical treatment of active stages of otosclerosis.
authors.affiliation: Department of Otolaryngology Head and Neck Surgery, Medical and Health Scinece Center, University of Debrecen, Debrecen, Hungary.
authors.forename: Péter
authors.initials: P
authors.lastname: Csomor
authors.forename: István
authors.initials: I
authors.lastname: Sziklai
authors.forename: Tamás
authors.initials: T
authors.lastname: Karosi
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000844:Ankylosis / Q000473:pathology; D002356:Cartilage / Q000473:pathology; D019902:Chondrocytes / Q000378:metabolism / Q000473:pathology; D018450:Disease Progression; D005260:Female; D015870:Gene Expression / Q000502:physiology; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D010040:Otosclerosis / Q000235:genetics* / Q000473:pathology*; D018124:Receptors, Tumor Necrosis Factor / Q000235:genetics*; D047888:Receptors, Tumor Necrosis Factor, Type I / Q000096:biosynthesis / Q000235:genetics; D047889:Receptors, Tumor Necrosis Factor, Type II / Q000096:biosynthesis / Q000235:genetics; D013199:Stapes / Q000473:pathology; D055815:Young Adult
chemical_list: D018124:Receptors, Tumor Necrosis Factor; D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II