TNF-alpha receptor expression correlates with histologic activity of otosclerosis.
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.
Csomor
Péter
P
Department of Otolaryngology Head and Neck Surgery, Medical and Health Scinece Center, University of Debrecen, Debrecen, Hungary.
Sziklai
István
I
Karosi
Tamás
T
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
D018124:Receptors, Tumor Necrosis Factor; D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II