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Neuro-rehabilitation Approach for Sudden Sensorineural Hearing Loss
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Published on: January 25, 2016

Otosclerosis: an organ-specific inflammatory disease with sensorineural hearing loss

István Sziklai1, Tamás József Batta, Tamás Karosi

  • 1Department of Otorhinolaryngology, Head and Neck Surgery, Medical and Health Science Center, University of Debrecen, Debrecen, Hungary.

European Archives of Oto-Rhino-Laryngology : Official Journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : Affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery
|April 3, 2009
PubMed

Insights

Persistent measles virus (MV) infection in otosclerosis causes inflammation and sensorineural hearing loss (SNHL). Non-inflammatory stapes ankylosis does not lead to SNHL, differentiating it from otosclerosis.

Area of Science:

  • Otolaryngology
  • Virology
  • Pathology

Background:

  • Otosclerosis is an inflammatory condition of the otic capsule linked to persistent measles virus (MV) infection.
  • Tumor necrosis factor-alpha (TNF-alpha) release in active otosclerosis may cause sensorineural hearing loss (SNHL) by affecting outer hair cells.
  • Non-otosclerotic stapes ankylosis is non-inflammatory and theoretically should not cause SNHL.

Purpose of the Study:

  • To investigate the role of measles virus (MV) and TNF-alpha in otosclerosis-related sensorineural hearing loss (SNHL).
  • To differentiate the histopathological and etiological factors contributing to stapes fixation and associated hearing loss.
  • To correlate audiological findings with histopathological and virological results in stapes fixation.

Main Methods:

  • Histopathological examination (hematoxylin-eosin staining) of 248 stapes footplates.
  • Detection of measles virus (MV), osteopontin (OPG), and TNF-alpha using RT-PCR.
  • Measurement of anti-measles IgG levels in serum via ELISA.
  • Correlation of preoperative audiological data with histopathology.

Main Results:

  • Measles virus (MV) was detected exclusively in otosclerotic stapes footplates, confirming its association with the disease.
  • Elevated bone conduction thresholds, particularly at high frequencies, were observed in otosclerotic patients, correlating with hearing loss duration.
  • Osteopontin (OPG) mRNA expression was lower in TNF-alpha positive samples, irrespective of MV presence.
  • Non-otosclerotic stapes ankylosis accounted for approximately one-third of stapes fixation cases and did not result in high-frequency SNHL.

Conclusions:

  • Persistent MV infection and subsequent TNF-alpha release are key factors in the development of SNHL in otosclerosis.
  • Histological evidence of otosclerosis strongly correlates with MV presence and inflammation.
  • Non-otosclerotic stapes fixation is a distinct entity that does not cause high-frequency SNHL, highlighting the inflammatory nature of otosclerosis.

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