Otosclerosis

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Otosclerosis
Other namesOtospongiosis
Gray919.png
Chain of ossicles and their ligaments. (Stapes visible near center right.)
Specialty Otorhinolaryngology

Otosclerosis is a condition of the middle ear where portions of the dense enchondral layer of the bony labyrinth remodel into one or more lesions of irregularly-laid spongy bone. As the lesions reach the stapes the bone is resorbed, then hardened (sclerotized), which limits its movement and results in hearing loss, tinnitus, vertigo or a combination of symptoms. [1] [2] [3] [4] The term otosclerosis is something of a misnomer: much of the clinical course is characterized by lucent rather than sclerotic bony changes, so the disease is also known as otospongiosis.

Contents

Etymology

The word otosclerosis derives from Greek ὠτός (ōtos), genitive of οὖς (oûs) "ear" [5] + σκλήρωσις (sklērōsis), "hardening". [6]

Presentation

The primary form of hearing loss in otosclerosis is conductive hearing loss (CHL) whereby sounds reach the ear drum but are incompletely transferred via the ossicular chain in the middle ear, and thus partly fail to reach the inner ear (cochlea). This can affect one ear or both ears. On audiometry, the hearing loss is characteristically low-frequency, with higher frequencies being affected later. [7]

Sensorineural hearing loss (SNHL) has also been noted in patients with otosclerosis; this is usually a high-frequency loss, and usually manifests late in the disease. The causal link between otosclerosis and SNHL remains controversial. Over the past century, leading otologists and neurotologic researchers have argued whether the finding of SNHL late in the course of otosclerosis is due to otosclerosis or simply to typical presbycusis.[ citation needed ]

Most patients with otosclerosis notice tinnitus (head noise) to some degree. The amount of tinnitus is not necessarily related to the degree or type of hearing impairment. Tinnitus develops due to irritation of the delicate nerve endings in the inner ear. Since the nerve carries sound, this irritation is manifested as ringing, roaring or buzzing. It is usually worse when the patient is fatigued, nervous or in a quiet environment.[ citation needed ]

Causes

Otosclerosis can be caused by both genetic and environmental factors, such as a viral infection (like measles). [8] [9] [10] Ribonucleic acid of the measles virus has been found in stapes footplate in most patients with otosclerosis. [11] Populations that have been vaccinated against measles had a significant reduction in otosclerosis. [12] While the disease is considered to be hereditary, its penetrance and the degree of expression is so highly variable that it may be difficult to detect an inheritance pattern. Most of the implicated genes are transmitted in an autosomal dominant fashion. One genome-wide analysis associates otosclerosis with variation in the RELN gene. [13]

Loci include:

Name OMIM Locus
OTSC1 166800 15q26.1
OTSC2 605727 7q
OTSC3 608244 6p
OTSC4 611571 16q
OTSC5 608787 3q22-q24
OTSC7 611572 6q13
OTSC8 612096 9p13.1-q21.11

Pathophysiology

The pathophysiology of otosclerosis is complex. The key lesions of otosclerosis are multifocal areas of sclerosis within the endochondral temporal bone. [14] These lesions share some characteristics with Paget's Disease, but they are not thought to be otherwise related. Histopathological studies have all been done on cadaveric temporal bones, so only inferences can be made about progression of the disease histologically. It seems that the lesions go through an active "spongiotic" or hypervascular phase before developing into "sclerotic" phase lesions. There have been many genes and proteins identified that, when mutated, may lead to these lesions. Also there is mounting evidence that measles virus is present within the otosclerotic foci, implicating an infectious etiology (this has also been noted in Paget's Disease). [15]

Conductive hearing loss (CHL) in otosclerosis is caused by two main sites of involvement of the sclerotic (or scar-like) lesions. The best understood mechanism is fixation of the stapes footplate to the oval window of the cochlea. This greatly impairs movement of the stapes and therefore transmission of sound into the inner ear ("ossicular coupling"). Additionally the cochlea's round window can also become sclerotic, and in a similar way impair movement of sound pressure waves through the inner ear ("acoustic coupling").

CHL is usually concomitant with impingement of abnormal bone on the stapes footplate. This involvement of the oval window forms the basis of the name fenestral otosclerosis. The most common location of involvement of otosclerosis is the bone just anterior to the oval window at a small cleft known as the fissula ante fenestram. The fissula is a thin fold of connective tissue extending through the endochondral layer, approximately between the oval window and the cochleariform process, where the tensor tympani tendon turns laterally toward the malleus.

The mechanism of sensorineural hearing loss in otosclerosis is less well understood. It may result from direct injury to the cochlea and spiral ligament from the lytic process or from release of proteolytic enzymes into the cochlea. There are certainly a few well documented instances of sclerotic lesions directly obliterating sensory structures within the cochlea and spiral ligament, which have been photographed and reported post-mortem. Other supporting data includes a consistent loss of cochlear hair cells in patients with otosclerosis; these cells being the chief sensory organs of sound reception. A suggested mechanism for this is the release of hydrolytic enzymes into the inner ear structures by the spongiotic lesions.

Diagnosis

Otosclerosis is traditionally diagnosed by characteristic clinical findings, which include progressive conductive hearing loss, a normal tympanic membrane, and no evidence of middle ear inflammation. The cochlear promontory may have a faint pink tinge reflecting the vascularity of the lesion, referred to as the Schwartz sign.[ citation needed ]

Approximately 0.5% of the population will eventually be diagnosed with otosclerosis. Post-mortem studies show that as many as 10% of people may have otosclerotic lesions of their temporal bone, but apparently never had symptoms warranting a diagnosis. Caucasians are the most affected race, with the prevalence in the Black and Asian populations being much lower. In clinical practice otosclerosis is encountered about twice as frequently in females as in males, but this does not reflect the true sex ratio. When families are investigated it is found that the condition is only slightly more common in women. [16] Usually noticeable hearing loss begins at middle-age, but can start much sooner. The hearing loss was long believed to grow worse during pregnancy, but recent research does not support this belief. [17] [18]

Differential testing

Audiometry

Fixation of the stapes within the oval window causes a conductive hearing loss. In pure-tone audiometry, this manifests as air-bone gaps on the audiogram (i.e. a difference of more than 10 dB between the air-conduction and bone-conduction thresholds at a given test frequency). However, medial fixation of the ossicular chain impairs both the inertial and osseotympanic modes of bone conduction, increasing the bone-conduction thresholds between 500 Hz and 4 kHz, and reducing the size of air-bone gaps. As 2 kHz is the resonant frequency of the ossicular chain, the largest increase in bone-conduction threshold (around 15 dB) occurs at this frequency – the resultant notch is called Carhart's notch and is a useful clinical marker for medial ossicular-chain fixation. [19]

Tympanometry measures the peak pressure (TPP) and peak-compensated static admittance (Ytm) of the middle ear at the eardrum. As the stapes is ankylosed in otosclerosis, the lateral end of the ossicular chain may still be quite mobile. Therefore, otosclerosis may only slightly reduce the admittance, resulting in either a shallow tympanogram (type AS), or a normal tympanogram (type A). Otosclerosis increases the stiffness of the middle-ear system, raising its resonant frequency. This can be quantified using multi-frequency tympanometry. Thus, a high resonant-frequency pathology such as otosclerosis can be differentiated from low resonant-frequency pathologies such as ossicular discontinuity.[ citation needed ]

In the absence of a pathology, a loud sound (generally greater than 70 dB above threshold) causes the stapedius muscle to contract, reducing the admittance of the middle ear and softening the perceived loudness of the sound. If the mobility of the stapes is reduced due to otosclerosis, then stapedius muscle contraction does not significantly decrease the admittance. When acoustic reflex testing is conducted, the acoustic reflex thresholds (ART) cannot be determined when attempting to measure on the affected side. Also, a conductive pathology will attenuate the test stimuli, resulting in either elevated reflex thresholds or absent reflexes when the stimulus is presented in the affected ear and measured in the other ear. [20]

CT imaging

Imaging is usually not pursued in those with uncomplicated conductive hearing loss and characteristic clinical findings. Those with only conductive hearing loss are often treated medically or with surgery without imaging. The diagnosis may be unclear clinically in cases of sensorineural or mixed hearing loss and may become apparent only on imaging. Therefore, imaging is often performed when the hearing loss is sensorineural or mixed.[ citation needed ]

A high-resolution CT shows very subtle bone findings. However, CT is usually not needed prior to surgery.[ citation needed ]

Otosclerosis on CT can be graded using the grading system suggested by Symons and Fanning. [21]

Treatment

Several approaches have been used in the treatment of otosclerosis, including medical, surgical and amplification. Technological innovations in hearing aid technology and cochlear implants are now being used to substitute or complement other interventions. [22]

Medical

Earlier workers suggested the use of calcium fluoride; now sodium fluoride is the preferred compound. Fluoride ions inhibit the rapid progression of disease. In the otosclerotic ear, there occurs formation of hydroxylapatite crystals which lead to stapes (or other) fixation. The administration of fluoride replaces the hydroxyl radical with fluoride leading to the formation of fluorapatite crystals. Hence, the progression of disease is considerably slowed down and active disease process is arrested. This treatment cannot reverse conductive hearing loss, but may slow the progression of both the conductive and sensorineural components of the disease process. Otofluor, containing sodium fluoride, is one treatment. Recently, some success has been claimed with a second such treatment, bisphosphonate medications that inhibit bone destruction. [23] [24] [25] However, these early reports are based on non-randomized case studies that do not meet standards of clinical trials. [26] There are numerous side-effects to both pharmaceutical treatments, including occasional stomach upset, allergic itching, and increased joint pains which can lead to arthritis. [27] In the worst case, bisphosphonates may lead to osteonecrosis of the auditory canal itself. [28] Finally, neither approach has been proven to be beneficial after the commonly preferred method of surgery has been undertaken.

Surgical

Endoscopic Stapedotomy Endoscopic view of Stapedotomy.jpg
Endoscopic Stapedotomy
Endocopic view of the ear with the piston inserted into the stapedotomy View of Piston.jpg
Endocopic view of the ear with the piston inserted into the stapedotomy

There are various methods to treat otosclerosis. However the method of choice is a procedure known as stapedectomy. [29] Early attempts at hearing restoration via the simple freeing of the stapes from its sclerotic attachments to the oval window were met with temporary improvement in hearing, but the conductive hearing loss would almost always recur. A stapedectomy consists of removing a portion of the sclerotic stapes footplate and replacing it with a middle ear implant that is secured to the incus. This procedure restores continuity of ossicular movement and allows transmission of sound waves from the eardrum to the inner ear. A modern variant of this surgery called a stapedotomy, is performed by drilling a small hole in the stapes footplate with a micro-drill or a laser, and the insertion of a piston-like prothesis. The success rate of either surgery depends greatly on the skill and the familiarity with the procedure of the surgeon. [17] However, comparisons have shown stapedotomy to yield results at least as good as stapedectomy, with fewer complications, and thus stapedotomy is preferred in normal circumstances. [30] Recently, Endoscopic stapedotomy has been gaining popularity since its first description by Professor Tarabichi in 1999. [31] The endsocope provides much better view of the stapes footplate without removal of bone to access that structure. [32]

Amplification

Although hearing aids cannot prevent, cure or inhibit the progression of otosclerosis, they can help treat the largest symptom, hearing loss. Hearing aids can be tuned to specific frequency losses. However, due to the progressive nature of this condition, use of a hearing aid is palliative at best. Without eventual surgery, deafness is likely to result.[ citation needed ]

Society and culture

Notable cases

Related Research Articles

<i>Stapes</i> Bone in the middle ear

The stapes or stirrup is a bone in the middle ear of humans and other animals which is involved in the conduction of sound vibrations to the inner ear. This bone is connected to the oval window by its annular ligament, which allows the footplate to transmit sound energy through the oval window into the inner ear. The stapes is the smallest and lightest bone in the human body, and is so-called because of its resemblance to a stirrup.

<span class="mw-page-title-main">Cochlea</span> Snail-shaped part of inner ear involved in hearing

The cochlea is the part of the inner ear involved in hearing. It is a spiral-shaped cavity in the bony labyrinth, in humans making 2.75 turns around its axis, the modiolus. A core component of the cochlea is the organ of Corti, the sensory organ of hearing, which is distributed along the partition separating the fluid chambers in the coiled tapered tube of the cochlea.

<span class="mw-page-title-main">Vestibulocochlear nerve</span> Cranial nerve VIII, for hearing and balance

The vestibulocochlear nerve or auditory vestibular nerve, also known as the eighth cranial nerve, cranial nerve VIII, or simply CN VIII, is a cranial nerve that transmits sound and equilibrium (balance) information from the inner ear to the brain. Through olivocochlear fibers, it also transmits motor and modulatory information from the superior olivary complex in the brainstem to the cochlea.

Stapedectomy is a surgical procedure in which the stapes bone is removed from the middle ear and replaced with a prosthesis.

<span class="mw-page-title-main">Conductive hearing loss</span> Medical condition

Conductive hearing loss (CHL) occurs when there is a problem transferring sound waves anywhere along the pathway through the outer ear, tympanic membrane (eardrum), or middle ear (ossicles). If a conductive hearing loss occurs in conjunction with a sensorineural hearing loss, it is referred to as a mixed hearing loss. Depending upon the severity and nature of the conductive loss, this type of hearing impairment can often be treated with surgical intervention or pharmaceuticals to partially or, in some cases, fully restore hearing acuity to within normal range. However, cases of permanent or chronic conductive hearing loss may require other treatment modalities such as hearing aid devices to improve detection of sound and speech perception.

<span class="mw-page-title-main">Sensorineural hearing loss</span> Hearing loss caused by an inner ear or vestibulocochlear nerve defect

Sensorineural hearing loss (SNHL) is a type of hearing loss in which the root cause lies in the inner ear or sensory organ or the vestibulocochlear nerve. SNHL accounts for about 90% of reported hearing loss. SNHL is usually permanent and can be mild, moderate, severe, profound, or total. Various other descriptors can be used depending on the shape of the audiogram, such as high frequency, low frequency, U-shaped, notched, peaked, or flat.

<span class="mw-page-title-main">Weber test</span> Screening test for hearing

The Weber test is a screening test for hearing performed with a tuning fork. It can detect unilateral (one-sided) conductive hearing loss and unilateral sensorineural hearing loss. The test is named after Ernst Heinrich Weber (1795–1878). Conductive hearing ability is mediated by the middle ear composed of the ossicles: the malleus, the incus, and the stapes. Sensorineural hearing ability is mediated by the inner ear composed of the cochlea with its internal basilar membrane and attached cochlear nerve. The outer ear consisting of the pinna, ear canal, and ear drum or tympanic membrane transmits sounds to the middle ear but does not contribute to the conduction or sensorineural hearing ability save for hearing transmissions limited by cerumen impaction.

The Rinne test is used primarily to evaluate loss of hearing in one ear. It compares perception of sounds transmitted by air conduction to those transmitted by bone conduction through the mastoid. Thus, one can quickly screen for the presence of conductive hearing loss.

<span class="mw-page-title-main">Audiogram</span> Graph showing audible frequencies

An audiogram is a graph that shows the audible threshold for standardized frequencies as measured by an audiometer. The Y axis represents intensity measured in decibels (dB) and the X axis represents frequency measured in hertz (Hz). The threshold of hearing is plotted relative to a standardised curve that represents 'normal' hearing, in dB(HL). They are not the same as equal-loudness contours, which are a set of curves representing equal loudness at different levels, as well as at the threshold of hearing, in absolute terms measured in dB SPL.

<span class="mw-page-title-main">Bone-anchored hearing aid</span>

A bone-anchored hearing aid (BAHA) is a type of hearing aid based on bone conduction. It is primarily suited for people who have conductive hearing losses, unilateral hearing loss, single-sided deafness and people with mixed hearing losses who cannot otherwise wear 'in the ear' or 'behind the ear' hearing aids. They are more expensive than conventional hearing aids, and their placement involves invasive surgery which carries a risk of complications, although when complications do occur, they are usually minor.

<span class="mw-page-title-main">Round window</span>

The round window is one of the two openings from the middle ear into the inner ear. It is sealed by the secondary tympanic membrane, which vibrates with opposite phase to vibrations entering the inner ear through the oval window. It allows fluid in the cochlea to move, which in turn ensures that hair cells of the basilar membrane will be stimulated and that audition will occur.

Hearing loss with craniofacial syndromes is a common occurrence. Many of these multianomaly disorders involve structural malformations of the outer or middle ear, making a significant hearing loss highly likely.

Electric acoustic stimulation (EAS) is the use of a hearing aid and a cochlear implant technology together in the same ear. EAS is intended for people with high-frequency hearing loss, who can hear low-pitched sounds but not high-pitched ones. The hearing aid acoustically amplifies low-frequency sounds, while the cochlear implant electrically stimulates the middle- and high-frequency sounds. The inner ear then processes the acoustic and electric stimuli simultaneously, to give the patient the perception of sound.

<span class="mw-page-title-main">Tympanosclerosis</span> Medical condition

Tympanosclerosis is a condition caused by hyalinization and subsequent calcification of subepithelial connective tissue of the tympanic membrane and middle ear, sometimes resulting in a detrimental effect to hearing.

Bone-conduction auditory brainstem response or BCABR is a type of auditory evoked response that records neural response from EEG with stimulus transmitted through bone conduction.

SoundBite Hearing System is a non-surgical bone conduction prosthetic device that transmits sound via the teeth. It is an alternative to surgical bone conduction prosthetic devices, which require surgical implantation into the skull to conduct sound.

<span class="mw-page-title-main">Persistent stapedial artery</span> Blood vessel anomaly

A persistent stapedial artery (PSA) is a rare anomaly in human anatomy where the stapedial branch of posterior auricular artery, or simply stapedial artery, remains within the ear of a fetus after the first ten weeks of pregnancy. Whilst not problematic for the majority of people with the anomaly, it can cause difficulties with hearing.

Causes of hearing loss include ageing, genetics, perinatal problems, loud sounds, and diseases. For some kinds of hearing loss the cause may be classified as of unknown cause.

<span class="mw-page-title-main">Diagnosis of hearing loss</span>

Identification of a hearing loss is usually conducted by a general practitioner medical doctor, otolaryngologist, certified and licensed audiologist, school or industrial audiometrist, or other audiometric technician. Diagnosis of the cause of a hearing loss is carried out by a specialist physician or otorhinolaryngologist.

A middle ear implant is a hearing device that is surgically implanted into the middle ear. They help people with conductive, sensorineural or mixed hearing loss to hear. 

References

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  2. ↑ Uppal S, Bajaj Y, Rustom I, Coatesworth AP (October 2009). "Otosclerosis 1: the aetiopathogenesis of otosclerosis". International Journal of Clinical Practice. 63 (10): 1526–30. doi: 10.1111/j.1742-1241.2009.02045.x . PMID   19769709. S2CID   11989071.
  3. ↑ Ealy, Megan; Smith, Richard J. H. (2011). "Otosclerosis". Medical Genetics in the Clinical Practice of ORL. Advances in Oto-Rhino-Laryngology. 70: 122–129. doi:10.1159/000322488. ISBN   978-3-8055-9668-8. PMID   21358194.
  4. ↑ Chole, Richard A.; McKenna, Michael (March 2001). "Pathophysiology of Otosclerosis". Otology & Neurotology. 22 (2): 249–257. doi:10.1097/00129492-200103000-00023. ISSN   1531-7129. PMID   11300278. S2CID   36262295 . Retrieved 2022-10-07.
  5. ↑ οὖς, Liddell & Scott, A Greek–English Lexicon
  6. ↑ σκλήρωσις, Liddell & Scott, A Greek–English Lexicon
  7. ↑ Danesh AA, Shahnaz N, Hall JW (April 2018). "The Audiology of Otosclerosis". Otolaryngologic Clinics of North America. 51 (2): 327–342. doi:10.1016/j.otc.2017.11.007. PMID   29397946.
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  12. ↑ Niedermeyer HP, Arnold W (2008). "Otosclerosis and measles virus - association or causation?". ORL; Journal for Oto-Rhino-Laryngology and Its Related Specialties. 70 (1): 63–9, discussion 69–70. doi:10.1159/000111049. PMID   18235207. S2CID   9284681.
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  14. ↑ Niedermeyer HP, Arnold W (2002). "Etiopathogenesis of otosclerosis". ORL; Journal for Oto-Rhino-Laryngology and Its Related Specialties. 64 (2): 114–9. doi:10.1159/000057789. PMID   12021502. S2CID   2134033.
  15. ↑ Quesnel, Alicia M.; Ishai, Reuven; McKenna, Michael J. (April 2018). "Otosclerosis". Otolaryngologic Clinics of North America. 51 (2): 291–303. doi:10.1016/j.otc.2017.11.001. PMID   29397947.
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  17. 1 2 de Souza C, Glassock M (2003). Otosclerosis and Stapedectomy: Diagnosis, Management & Complications. New York, NY: Thieme. ISBN   978-1-58890-169-9.
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  21. ↑ Lee TC, Aviv RI, Chen JM, Nedzelski JM, Fox AJ, Symons SP (August 2009). "CT grading of otosclerosis". AJNR. American Journal of Neuroradiology. 30 (7): 1435–9. doi: 10.3174/ajnr.a1558 . PMC   7051554 . PMID   19321627.
  22. ↑ Batson, Lora; Rizzolo, Denise (February 2017). "Otosclerosis: An update on diagnosis and treatment". Journal of the American Academy of Physician Assistants. 30 (2): 17–22. doi:10.1097/01.JAA.0000511784.21936.1b. ISSN   1547-1896. PMID   28060022. S2CID   31467710.
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  24. ↑ "Use of bisphosphonates for otosclerosis" Archived 2014-10-28 at the Wayback Machine , Fresh Patents.
  25. ↑ Chris De Souza, Michael E. Glasscock, Otosclerosis and Stapedectomy: Diagnosis, Management, and Complications, Thieme, 2004.
  26. ↑ Chole RA & McKenna M, "Pathophysiology of otosclerosis", Otology & Neurotology, 22(2): 249–257, 2001.
  27. ↑ Otosclerosis Archived 2009-12-27 at the Wayback Machine at the American Hearing Research Foundation, Chicago, Illinois 2008.
  28. ↑ Polizzotto MN, Cousins Polizzotto & Schwarer AP, "Bisphosphonate-associated osteonecrosis of the auditory canal", British Journal of Haematology , 132(1): 114, 2005.
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  30. ↑ Thamjarayakul T, Supiyaphun P, & Snidvongs K, "Stapes fixation surgery: Stapedectomy versus stapedotomy", Asian Biomedicine, 4(3): 429–434, 2010.
  31. ↑ Tarabichi M (January 1999). "Endoscopic middle ear surgery". The Annals of Otology, Rhinology, and Laryngology. 108 (1): 39–46. doi:10.1177/000348949910800106. PMID   9930539. S2CID   40931362.
  32. ↑ Moneir W, Abd El-Fattah AM, Mahmoud E, Elshaer M (September 2018). "Endoscopic stapedotomy: Merits and demerits". Journal of Otology. 13 (3): 97–100. doi:10.1016/j.joto.2017.11.002. PMC   6291631 . PMID   30559773.
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  35. ↑ Charles Higham, Howard Hughes: The Secret Life.
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  40. ↑ Adam Savage [@donttrythis] (November 4, 2010). "@jayyoozee Yes I wear a hearing aid. Not from the explosions tho. It's a congenital condition. Titanium earbones on my left side" (Tweet) – via Twitter.
  41. ↑ John Cornforth Archived 15 February 2011 at the Wayback Machine , biotechnology-innovation.com.au
  42. ↑ "Zak Abel talks Love Over Fear, major label turmoil, and coping with hearing loss". headlinermagazine.net. Retrieved 24 October 2023.
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