title: Possible inflammatory mediators in tympanosclerosis development.
abstract: OBJECTIVE
  Tympano/myringosclerosis is a sequelae following otitis media, causing hearing disability. There is no curative treatment for this condition. In order to illuminate the correlation of inflammatory mediators in otitis media and tympanosclerosis development, the present study was performed.
  
  
  METHODS
  In an animal model, Streptococcus pneumonia bacteria were inoculated to the middle ear. Furthermore, biopsies were harvested during surgery, from children suffering from secretory otitis media and from patients with already established tympanosclerosis. The early inflammatory parameters were investigated in the rat model as well as in the patient material. The lymphocytic population, macrophages, interleukin-6, inducible nitric oxide synthase and MHC class II were studied by immunohistochemistry and by mRNA in situ hybridization.
  
  
  RESULTS
  Myringosclerosis was produced in 30% of the rats studied. Macrophages were the first cells to invade the middle ear after induction of otitis media, followed by B-cells and T-cells. IL-6 m-RNA was found as early as 1 h after inoculation. Cells, expressing inducible nitric oxide synthase, seemed to be activated macrophages. Osteoclast like cells, positive in immunohistechemical macrophage staining, were found close to the insertion of the tympanic membrane. The human specimens showed a more immunological active stage in the secretory otitis media group as compared to the specimens with tympanosclerosis.
  
  
  CONCLUSIONS
  The immunocompetent cells and some mediators are presented time dependently in otitis media and a possible reaction sequence, leading to differentiation of macrophages into osteoclasts is presented. This may lead to tympanosclerosis development.
authors.affiliation: Department of Plastic and Reconstructive Surgery/Otorhinolaryngology, Karolinska Hospital, Karolinska Institute, 171 76, Stockholm, Sweden. marie.forseni@ood.ki.se
authors.forename: Marie
authors.initials: M
authors.lastname: Forséni Flodin
authors.forename: Malou
authors.initials: M
authors.lastname: Hultcrantz
mesh_terms: D000818:Animals; D001707:Biopsy, Needle; D002908:Chronic Disease; D004195:Disease Models, Animal; D006801:Humans; D018836:Inflammation Mediators / Q000032:analysis*; D008264:Macrophages; D008297:Male; D010010:Osteoclasts; D010033:Otitis Media / Q000150:complications*; D051381:Rats; D017207:Rats, Sprague-Dawley; D018570:Risk Assessment; D012598:Sclerosis / Q000209:etiology / Q000473:pathology; D012680:Sensitivity and Specificity; D012720:Severity of Illness Index; D013045:Species Specificity; D014432:Tympanic Membrane / Q000378:metabolism* / Q000473:pathology*
chemical_list: D018836:Inflammation Mediators