title: Elevated level of tenascin and matrix metalloproteinase 9 correlates with the bone destruction capacity of cholesteatomas.
abstract: OBJECTIVE
  Bone destruction is a key step in the progression of cholesteatomas. Some of the lesions can grow without affecting the surrounding anatomic structures, whereas others can cause severe bone destruction despite their limited size. This study aims to identify factors that could play important role during the invasion of the disease.
  
  
  METHODS
  Cholesteatoma tissue samples were examined immunohistochemically. Tissue samples were arranged on the basis of bone destruction (destructive cholesteatomas [DC] and nondestructive cholesteatomas [NDC]). Double-immunofluorescent labeling was performed to detect simultaneously 1) tenascin (TN) and cytokeratin; 2) matrix metalloproteinase 9 (MMP-9) and TN; 3) TN and Ki-67. An in situ apoptosis detection kit was used to detect apoptotic cells. External auditory canal skin samples were used as control.
  
  
  RESULTS
  1) In DCs, more widespread stromal TN labeling was seen compared with NDCs or external auditory canal skin samples. 2) More enhanced MMP-9 staining was detected in DCs compared with NDCs. 3) The proportion of Ki-67-positive cells in DC samples was significantly higher than in NDCs. 4) The percentage of apoptotic cells was higher in NDC than in DC samples.
  
  
  CONCLUSIONS
  Our present study demonstrates that levels of TN, MMP-9, and proliferative activity are increased in cholesteatomas. It has also been shown that increased levels of TN, MMP-9-positive cells, and proliferative activity of the lesions, as well as decreased levels of apoptosis, can be linked to more aggressive clinical behavior of cholesteatomas. Our findings also indicate that TN and MMP-9 can be key molecules of bone destruction during cholesteatoma progression.
authors.affiliation: Department of Otorhinolaryngology Head and Neck Surgery, Medical and Health Science Center, University of Debrecen, Debrecen, Hungary.
authors.forename: Attila
authors.initials: A
authors.lastname: Juhász
authors.forename: István
authors.initials: I
authors.lastname: Sziklai
authors.forename: Zsuzsa
authors.initials: Z
authors.lastname: Rákosy
authors.forename: Szilvia
authors.initials: S
authors.lastname: Ecsedi
authors.forename: Róza
authors.initials: R
authors.lastname: Adány
authors.forename: Margit
authors.initials: M
authors.lastname: Balázs
mesh_terms: D000293:Adolescent; D000328:Adult; D017209:Apoptosis; D015415:Biomarkers / Q000032:analysis; D049109:Cell Proliferation; D002648:Child; D018424:Cholesteatoma, Middle Ear / Q000378:metabolism / Q000473:pathology; D018450:Disease Progression; D004432:Ear, Middle; D005260:Female; D006801:Humans; D007633:Keratins / Q000032:analysis / Q000096:biosynthesis; D019394:Ki-67 Antigen / Q000032:analysis / Q000096:biosynthesis; D008297:Male; D020780:Matrix Metalloproteinase 9 / Q000032:analysis / Q000096:biosynthesis*; D013701:Temporal Bone / Q000473:pathology*; D019063:Tenascin / Q000032:analysis / Q000096:biosynthesis*
chemical_list: D015415:Biomarkers; D019394:Ki-67 Antigen; D019063:Tenascin; D007633:Keratins; D020780:Matrix Metalloproteinase 9