Otosclerosis is one of most common causes of acquired hearing loss. It is reported that about 13% of the U.S. population has nonclinical otosclerosis (histologic oto-sclerosis); however, incidence of clinical disease ranges from 0.5% to 1.0%. Individuals with otosclerosis complain about progressive hearing loss. Symptoms usually become apparent between ages 20 and 45. Otosclerosis is a metabolic bone disease that uniquely affects the temporal bone and ossicles and is characterized by abnormal bone remodeling. The stimulus to initiate bone remodeling in oto-sclerosis is still unknown, but recent studies associate this event with measles virus infection. Mature bone in the area of the oval window on the medial wall of the tympanic cav-ity, which separates the middle ear from the internal ear, is removed by osteoclasts and replaced with much thicker immature (woven) bone. Since the footplate of the stapes normally resides and freely vibrates within the oval window to allow the transmission of sound into the internal ear, the bone remodeling in this area results in fixation of the stapes into the surrounding bone. The cemented (or frozen in place) stapes does not vibrate and prevents sound waves from reaching the perilymphatic fluid space of the internal ear, causing conductive hearing loss. The treatment of otosclerosis includes several options: phar-macologic treatment to suppress bone remodeling with fluorides and bisphosphonates, amplification of sounds with hearing aids, and surgical removal of the stapes (stapedectomy) with subsequent implantation of a pros-thesis between the incus and the oval window. Surgery is usually the most effective method of managing otosclero-sis; more than 90% of patients experience complete elim-ination of conductive hearing loss.
 FOLDER 25.2 Clinical Correlation: Hearing Loss—Vestibular Dysfunction