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Summary Table

Category	Details
Risk Factors	History of recurrent acute otitis media (AOM), chronic otitis media (COM), prior tympanostomy tube insertion, middle ear surgery, chronic inflammation of the middle ear mucosa
Etiology	Hyaline degeneration and dystrophic calcification of the submucosal connective tissue in response to chronic inflammation
Patient Presentation	Progressive conductive hearing loss; often discovered incidentally on otoscopy in a patient with a history of repeated ear infections during childhood
Classic Physical Exam	White, chalky, horseshoe-shaped plaques on the tympanic membrane (TM); TM mobility is reduced on pneumatic otoscopy; the TM is often intact
Key Diagnostic Results	Audiometry shows conductive hearing loss with an air-bone gap; CT temporal bone reveals calcified deposits in the middle ear; tympanometry shows a flat or stiffened (type B or As) curve
Management	Observation if hearing is adequate; hearing aids for mild-moderate loss; tympanoplasty with ossicular chain reconstruction for functionally relevant conductive hearing loss
Keywords	"White patches on the tympanic membrane," "history of recurrent otitis media," "chalk-like plaques," "conductive hearing loss," "prior ear tubes"

1. Pathophysiology

Tympanosclerosis is the end result of a chronic inflammatory healing response within the middle ear and tympanic membrane. When the middle ear mucosa is subjected to repeated episodes of infection or trauma (including tympanostomy tube placement), the body mounts an inflammatory reaction that damages the lamina propria of the TM and the submucosal connective tissue of the middle ear.

During this healing process, fibroblasts deposit excessive collagen, which then undergoes hyaline degeneration. Over time, dystrophic calcification occurs within this hyalinized tissue, producing dense plaques of calcium and phosphate crystals. This is not metastatic calcification (serum calcium is normal); it is a local tissue response in previously damaged tissue.

When the process is limited to the TM (called myringosclerosis), it typically has minimal functional impact. The white plaques are visible but rarely cause meaningful hearing loss on their own. However, when calcification extends into the middle ear cavity proper and involves the ossicular chain, oval window niche, or round window, the ossicles become fixed or encased in calcium deposits. This fixation disrupts the normal mechanical vibration pathway from the TM through the malleus, incus, and stapes to the oval window. The result is a conductive hearing loss with a preserved sensorineural component, producing the characteristic air-bone gap on audiometry.

The reason this condition is strongly linked to recurrent AOM in childhood is that repeated cycles of mucosal edema, neutrophilic infiltration, and resolution create the cumulative tissue damage needed to trigger this irreversible fibrocalcific response.

2. Classification and Clinical Manifestation

Type	Location	Clinical Impact	Exam Finding
Myringosclerosis	Confined to the tympanic membrane (lamina propria)	Usually no functional hearing loss; incidental finding	White, chalky plaques visible on otoscopy; TM intact
Intratympanic tympanosclerosis	Middle ear mucosa, ossicular chain, oval/round window niche	Conductive hearing loss (can be moderate to severe)	TM may appear normal or show plaques; reduced TM mobility; air-bone gap on audiometry
Mixed	Both TM and middle ear involvement	Variable hearing loss depending on degree of ossicular fixation	Combination of visible TM plaques and conductive deficit

The clinical distinction that matters most for exam purposes is between myringosclerosis (cosmetically apparent but functionally benign) and intratympanic tympanosclerosis (functionally relevant because it impairs ossicular mechanics). A vignette showing white TM plaques with normal hearing points toward myringosclerosis alone. A vignette showing white TM plaques with a conductive hearing loss indicates middle ear involvement and raises the question of surgical management.

3. Diagnostic Workup

Test	Role	Expected Finding
Otoscopy	Best initial test	White, dense, calcified plaques on the TM; TM usually intact
Pneumatic otoscopy	Functional screening	Reduced or absent TM mobility
Pure tone audiometry	Quantify hearing loss	Conductive hearing loss with air-bone gap; bone conduction thresholds are normal
Tympanometry	Assess middle ear compliance	Type As (reduced compliance/stiff system) or Type B (flat) curve
CT temporal bone (HRCT)	Most accurate test for middle ear involvement	Calcified plaques around ossicles, oval window, or round window niche
Surgical exploration	Gold standard for ossicular status	Direct visualization of ossicular fixation and extent of sclerotic deposits

The workup begins with otoscopy, which is the best initial step. The classic finding of white, chalk-like plaques on the TM in a patient with a history of recurrent ear infections is often enough to make the clinical diagnosis. The next step is audiometry to determine whether there is a functionally relevant hearing deficit. If audiometry reveals a conductive hearing loss with an air-bone gap, this tells you the disease has extended beyond the TM into the middle ear.

Tympanometry supports the diagnosis by demonstrating a stiffened middle ear system (type As curve), but it is not the confirmatory test. When surgical planning is needed, high-resolution CT of the temporal bone is ordered to map the extent of calcification and determine whether the ossicular chain, oval window, or round window is involved. This guides the surgeon in planning reconstruction.

The true gold standard for defining the degree of ossicular involvement is intraoperative exploration, since CT can underestimate or overestimate the extent of fixation. However, for exam purposes, CT temporal bone is the best non-invasive confirmatory test.

4. Management and Treatment

Clinical Scenario	Management
Myringosclerosis with normal hearing	Observation only; no treatment needed
Mild conductive hearing loss, patient tolerates it	Hearing aid fitting; regular audiometric follow-up
Functionally relevant conductive hearing loss affecting daily life	Tympanoplasty with ossicular chain reconstruction (ossiculoplasty)
Extensive ossicular fixation involving the stapes footplate	Stapedectomy or stapedotomy with prosthesis placement (higher risk of sensorineural loss)
Oval or round window involvement with dense calcification	Surgery carries elevated risk; hearing aid may be the safer option

Observation is the first-line approach when hearing is preserved. Many patients with myringosclerosis alone require no intervention at all. The white plaques are cosmetically notable but functionally irrelevant.

When a conductive hearing loss develops and affects communication or quality of life, a hearing aid is the least invasive option and is appropriate for patients who are not surgical candidates or who prefer a conservative approach.

Surgical intervention is reserved for patients with a meaningful air-bone gap (typically greater than 20-30 dB) who desire restoration of natural hearing. The procedure involves tympanoplasty with removal of sclerotic plaques and ossicular chain reconstruction using autograft (reshaped incus) or alloplastic prostheses (titanium partial or total ossicular replacement prostheses, PORP or TORP).

When the stapes footplate is involved, the surgery becomes more complex and carries a risk of sensorineural hearing loss from inadvertent inner ear trauma. In cases of dense calcification around the oval window, the surgeon must weigh the benefit of hearing restoration against the risk of a dead ear. In these situations, a hearing aid is often the safer recommendation.

There is no medical therapy (no medication dissolves the calcified plaques). Antibiotics and steroids treat active infection but do not reverse established tympanosclerosis.

5. Differential Diagnosis and Distractors

Differential Diagnosis	Why It Looks Similar	Key Discriminator
Otosclerosis	Both cause conductive hearing loss with an intact TM	Otosclerosis has a normal-appearing TM (no white plaques); audiometry may show a Carhart notch (dip at 2000 Hz on bone conduction); no history of recurrent otitis media; often bilateral with family history
Cholesteatoma	Both can occur after chronic ear disease and cause hearing loss	Cholesteatoma presents with a retraction pocket or marginal perforation with whitish, pearly debris and foul-smelling otorrhea; it is destructive (erodes bone), whereas tympanosclerosis is a reparative process
Chronic suppurative otitis media (CSOM)	Both share a history of recurrent infection	CSOM presents with persistent ear discharge through a perforated TM; tympanosclerosis has an intact TM with calcified plaques and no active drainage
Middle ear effusion (OME)	Both can show reduced TM mobility and conductive hearing loss	OME shows an amber or dull TM with visible fluid level or air-fluid interface; tympanometry shows type B curve but without calcified plaques on otoscopy
Ossicular discontinuity (post-traumatic)	Both cause conductive hearing loss with an intact TM	History of head trauma; tympanometry may show type Ad (hypercompliant) curve rather than the stiff type As curve seen in tympanosclerosis

6. Traps and High-Yield Pearls

The most common way students lose points on tympanosclerosis questions is by confusing it with otosclerosis. Both conditions cause conductive hearing loss with an intact tympanic membrane, but the distinguishing feature is the appearance of the TM itself. White, chalky plaques on the TM in a patient with a history of childhood ear infections equals tympanosclerosis. A normal-appearing TM with progressive conductive hearing loss, a family history, and a Carhart notch equals otosclerosis. If the vignette mentions prior tympanostomy tubes, this is a strong clue pointing toward tympanosclerosis.

A second trap is overestimating the clinical importance of myringosclerosis. When a vignette describes white plaques on the TM but audiometry is normal, the answer is observation. Students sometimes select surgical intervention because the TM looks abnormal, but the plaques themselves are benign when hearing is intact.

Finally, remember that tympanosclerosis is an irreversible, end-stage scarring process. No medical therapy reverses it. If a question asks for the treatment of tympanosclerosis and includes an antibiotic or steroid among the answer choices, that is a distractor. The only interventions that matter are hearing aids and surgery.

The core competency being tested is the ability to recognize the classic visual finding on otoscopy, connect it to the patient's history of chronic ear disease, differentiate it from otosclerosis, and select the appropriate management based on the degree of hearing loss.

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