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This article presents accounts of two patients with cholesteatoma of the tympanic part of the temporal bone, located immediately lateral to the tympanic annulus (and with an intact tympanic membrane).
The tympanic part of the temporal bone forms all of the anterior and inferior walls and a part (inferior and medial) of the posterior wall of the external acoustic meatus. The anterior horn is separated by the glaserian petrotympanic fissure from the petrous part and squama.
Cholesteatoma of the ear is, from a topographical point of view, a syndrome, because it includes cholesteatoma of the middle ear (located in the tympanic cavity, in the mastoid process, or in both) and cholesteatoma of the petrous air cells (anterior air cells, posterior air cells, and apical cells).
Simultaneously, many categories of "common" middle-ear cholesteatoma exist, including congenital (or primitive) cholesteatoma with an intact eardrum, described by House in 1953 [4]. The invagination theory explains the cholesteatoma that occurs in the case of the retraction pocket or adhesive otitis media.
Secondary, acquired cholesteatoma, with a perforation of the eardrum, is explained by the epithelial invasion theory.
It has been shown that severe deficiency of vitamin A may provoke keratinized epithelium formation. Cholesteatoma in chronic otitis media and mastoiditis may accumulate the keratin mass slowly and may create some complications. Cholesteatoma may be found in very rare cases behind an intact tympanic membrane without a prior history of otorrhea. We admitted PI, a 12-year-old girl, to our clinic on September 20, 1999, for mucopurulent otorrhea in the right ear, which occurred 4 months earlier after repeated bathing in the swimming pool.
Otoscopic examination of the right ear revealed a huge granulation tissue that filled the entire external auditory canal and was covered with mucopurulent discharge. Radiological and tomographic examinations of the right ear (in Schuller and Chausse III views) showed bone-destructive lesions of the inferior wall of the EAM (Fig. We drilled the cavity (and a part of the inferior wall of the EAM) and removed a bloody granulation tissue. A long, postoperative course ensued, owing to recurrent granulation tissue that necessitated repeated removals. We admitted PS, a 28-year-old woman, to our clinic on February 12, 2002, for fetid, persistent otorrhea of the right ear, associated with ipsilateral hemicrania and temporomandibular arthralgia with an important reduction of temporomandibular joint mobility. Between 1984 and 2002, the patient had four other similar events, of which one episode in 1988 was noticeable, when trismus and functional impotence of the right temporomandibular joint were added to the initial symptomatology and feeding by a tube was imposed for 3 months. In December 2001, the patient had the last episode with violent, permanent, and progressive right otalgia associated with ipsilateral hemicrania and trismus but without otorrhea and hearing loss. In January 2002, we admitted the patient to our clinic for the aforementioned symptomatology. After the suction of discharge and removal of the cholesteatoma, the tympanic membrane became visible and was seen to be intact and mobile (but a little thicker), with its landmarks present. Radiological and tomographic examinations (in Schuller and Chausse III views) revealed normal pneumatization of both mastoid processes and the presence of a large bone erosion, relatively well delimited in a double sac, of the right tympanic part of the temporal bone, suggestive of cholesteatoma (Fig.
We blindly elevated and totally removed the sac of cholesteatoma, which necesitated massive drilling of the inferior wall of the EAM. For hemostatic purposes, we filled the entire postoperative cavity and the EAM with compressed Gelfoam and added auriculotemporal packing. Cholesteatoma of the EAM is a rare pathological finding that entails some different entities. Another hypothesis involves an atypical coloboma auris as a point of departure, developing into such a cholesteatoma. Tympanoplasty or reconstruction of the middle ear hearing mechanism serves the purpose of rebuilding the ear drum. The procedure for a Tympanoplasty with or without Ossiculoplasty takes between 30 minutes and 2 hours, under general or local anesthesia. An excellent result may be expected in 90% of cases although failure to improve is not a complication. Unless control of infection is the reason for surgery, tympanoplasty is an elective procedure. Note that the best hearing results are obtained when there is no damage to any of the hearing bones.
In cases where the hearing bones are not re-constructable, or when tympanoplasty and ossiculoplasty fail, BAHA implants may be indicated. There is also a newly opened car park building located in the lane way behind Lakeside Drive, however you will need to enter our rooms through the front entrance. The lesions were located deep in the anterior and inferior walls of the canal, especially in the vaginal process of the tympanic part.

The glaserian fissure consists of the chorda tympani nerve, Raw's anterior malleal ligament, and Nager's anterior tympanic artery and veins. However, at the same time, the epidermal plug and hyperkeratinized epidermis of the external auditory meatus (EAM) belong to the same pathogenic and histopathological category [1-3].
It is explained by embryological theory as remnant embryonic cells from the first branchial cleft. Sade in 1979 considered it like an epithelial migration defect with an attical retraction pocket [5].
The squamous keratinized epithelium invades through the tympanic membrane perforation into the middle ear along the contact guidance surface. The basal cell hyperplasia theory explained the occurrence of cholesteatoma as resulting from the invasion of the subepithelial tissue by proliferative epithelial cells. We treated her for 4 months with drops into the ear canal of borated alcohol and rifampicin solutions, without any improvement of symptoms. After otomicroscopical examination, we removed the granulation tissue and noticed a fetid, purulent discharge and massive keratin debris with bone erosion of the inferior wall of the EAM. Radiological examination of the right ear of patient 1 (12-year-old girl) showed bone-destructive lesions of the inferior wall of the external auditory meatus.
Reepithelialization of the postoperative cavity was slow and lasted for approximately 3 months. The apparent onset of the disease is placed in 1984, with violent right otalgia and fetid, mucopurulent otorrhea, apparently in the presence of an acute pharyngoamygdalitis. General antibiotic therapy, local suction, and local instillation of antibiotic agents were undertaken. Despite massive antibiotic therapy, the symptoms did not abate; on the contrary, a fetid, pulsatile, green-yellowish, viscid discharge developed additionally. The physical examination revealed trismus due to the right temporomandibular arthralgia and right submandibular lymphadenopathy (1.5 cm in size). Radiological examination of patient 2 (28-year-old woman) revealed normal pneumatization of both mastoid processes and the presence of a large erosion of the right tympanic part of the temporal bone, suggestive of cholesteatoma.
We made a semicircular incision of the inferior wall of the right EAM and removed the entire sac of cholesteatoma. Surgical exploration of the cholesteatomatous cavity confirmed the imaging examination: The cavity had no communication with the tympanic cavity and mastoid process. After a couple of weeks of antibiotic therapy, a very good-and surprisingly short-postoperative course followed (with the disappearance of trismus and of all the symptoms). Keratosis obturans is, for some authors, considered to be in the same field as cholesteatoma.
The pathogenesis of cholesteatoma of the tympanic part of the temporal bone involves some hypotheses.
The differential diagnosis could include the following entities: cervical Bezold's otomastoiditis, Mouret's jugodigastric otomastoiditis, cancer of the EAM, ceruminoma of the EAM, glomus jugulare tumor, and epidermal plug. The approach is often noninvasively done through the ear canal, although some extensive cases require an incision behind the ear. Success depends almost as much on the ability of the body to heal and preserve the reconstruction as it does on the surgeon's skill. If any of the bones need to be replaced, the final result is never as good as the original equipment.
These more severe cases required surgical correction (removal of the sac of cholesteatoma) with very good results.
During the intrafetal period of ontogenesis and sometimes in postnatal life, the vaginal process presents a small foramen (of Huschke) that represents a nonossified part of the plate. The tympanomastoid fissure separates the posterior horn from the mastoid process, and it is a landmark of the fallopian aqueduct and facial nerve. The squamous metaplastic theory takes into consideration the metaplasia of the mucous membrane of the middle ear into squamous keratinized epithelium. No evidence exists to support the hypothesis that cholesteatoma can develop by metaplasia of the mucous membrane [7]. The tympanic membrane was intact and mobile but thicker, matted, and bearing preserved landmarks. Microbiological assessment of the ear discharge revealed an infection with Pseudomonas aeruginosa , sensitive to gentamicin, carbenicillin, colistin sulfate, norfloxacin, and ceftriaxone. We decided on a surgical approach and operated on October 4, 1999, with the patient under general anesthesia.
Accidentally, we opened the canal of the chorda tympani nerve during surgery and damaged the nerve.

In 1999, a tonsillectomy was performed, on the supposition that this was the point of infection. Otoscopic and otomicroscopical examinations revealed fetid, mucopurulent discharge in the right EAM, huge masses of whitish keratin debris, and a huge erosion of the anterior and inferior walls of the EAM in their medial third.
We found a large cavity (some 1.5-2 cm toward the anterior and inferior walls of the right EAM). Keratosis obturans is caused by a combination of hyperkeratosis and failure of normal epithelial migration of the EAM's skin. Aberrant air cells that have migrated into the plate of the tympanic part might be a plausible explanation for this kind of cholesteatoma. The skin of the meatus is relatively thick (similar to the integument of the auricle) in the cartilaginous part of the meatus. The tiny amount of graft material usually comes from the patient's own tissue in the ear or behind the ear and is not ever noticed. Fortunately, even those cases that fail may be revised and have the same high degree of expected good result.
If the ear drum perforation is not repaired, ear plugs are recommended to protect the middle ear from contamination when bathing.
There are synthetic bones that replace any combination of damage to the three natural hearing bones. Sade in 1971 sustained the theory, showing that the mucous cells are pluripotent cells when they are stimulated by infection [5].
However, in this pathogenesis, the basal membrane must be altered so that the lamina propria may be invaded by the epithelium. The cholesteatomatous masses often are infected and, when accompanied by bone erosion, can lead to severe complications. We made a semicircular endomeatal incision on the inferior wall of the meatus and elevated and fully removed the entire cholesteatomatous sac. For hemostatic purposes, we filled both the cavity and the EAM with compressed Gelfoam and added an auriculotemporal packing. We found the inner one-third of the anterior wall of the tympanic part of the temporal bone both completely eroded toward the parotic region and changed into a fibrous wall.
However, the skin in the bony portion of the meatus is very thin, and it appears completely different, like a mucous membrane. The technique usually involves patching the hole from the undersurface of the drum after the hole has been prepped. As a general statement, success in restoring hearing without complication is the usual outcome in simple perforations. A distinct category is cholesteatoma of the postoperative cavities (in radical mastoidectomy). Ombredanne and Porte in 1962) [8] and Schucknecht in 1989 [9] described cholesteatoma of the EAM occurring in association with congenital aural atresia.
The changes in the behavior of this EAM integument could be the starting point of the cholesteatoma of the tympanic part of the temporal bone.
However, individual outcomes vary and are related to the severity of the disease present before surgery.
Persistent post-operative dizziness is almost unheard of after surgery limited to the repair of an eardrum perforation and uncommon after rebuilding the ear bones, although post op nausea from anesthesia is not uncommon. A special case is posttraumatic cholesteatoma, when trauma allows an enclave of the epithelial tissue into the middle ear. Meatoplasty of the postoperative cavity is contrary to the concept of cholesteatoma definition.
Sometimes, it persists into adult life as an anatomical variation, and the skin of the EAM is invaginated into the opening and under the inferior wall of the meatus [10]. Therefore, cholesteatoma is not considered to be the last stage of adhesive otitis media; on the contrary, the two are considered to be different entities. Surgery must also be adapted to the local situation, often requiring a laborious and iterative operation.

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