Cholesteatoma là gì? Các công bố khoa học về Cholesteatoma

Cholesteatoma is a non-neoplastic, keratinising lesion which has two forms: congenital and acquired. Congenital cholesteatoma develops behind a normal, intact tympanic membrane, whilst acquired cholesteatoma is associated with a defect in the tympanic membrane. The pathological substrate of cholesteatoma is keratinising stratified squamous epithelium, but the origin of this epidermal tissue in the middle ear is controversial. Here, we review the most relevant and recent evidence for the principal aetiopathogenic theories of both forms of cholesteatoma, in the light of recent otopathological findings.

Congenital cholesteatoma is most plausibly explained by the persistence of fetal epidermoid formation. Conclusive ‘proof’ awaits the unambiguous demonstration of the metamorphosis of an epidermoid nidus into a lesionin vivo.

Acquired cholesteatoma may develop by various mechanisms: immigration, basal hyperplasia, retraction pocket and/or trauma (iatrogenic or non-iatrogenic). However, squamous metaplasia of the normal cuboidal epithelium of the middle ear is a highly unlikely explanation. Chronic inflammation seems to play a fundamental role in multiple aetiopathogenic mechanisms of acquired cholesteatoma. Therefore early treatment of inflammatory conditions might reduce their sequelae, perhaps by preventing the development of hyperplastic papillary protrusions.

Continued otopathological, cellular and molecular research would enhance our limited understanding of cholesteatoma and may lead to new therapeutic strategies for this erosive disease, which often defies surgical treatment.

The process of connective tissue breakdown in chronic otitis media is described in the context of recent advances in our understanding of collagen degradation and bone resorption. The significance of the initial step in collagen breakdown, brought about by the action of a specific collagen dissolving enzyme is emphasized in terms of recent studies in other chronic inflammatory diseases characterized by connective tissue breakdown.

Bone resorption, a characteristic feature of chronic otitis media, requires the breakdown of collagen, which comprises over 90 percent of bone protein. Evidence in support of collagenase in bone resorption from adjacent tissue (in this case, inflammatory connective tissue) would require identification of the enzyme in cells involved in the inflammatory process adjacent to the resorbing bone.

Collagenase was found localized in frozen sections of canal wall skin, middle ear granulation and in cholesteatoma by a specific binding of the enzyme with an antiserum produced against purified human skin collagenase. The antigen antibody complex was labelled with f luorescein. Collagenase appeared in the subepithelial connective tissue of cholesteatoma, granulation tissue from the middle ear and the dermis of canal skin; but was not seen in the keratin layer, epithelium or the epidermal appendages. The enzyme appeared within certain fibroblasts, macrophages and endo‐thelial cells of capillary buds. Collagenase enhanced by chronic inflammation attacks the intact collagen molecule, making it susceptible to further digestion by other proteases that are also products of inflammation. This process brings about resorption of connective tissue and bone.

Objective/Hypothesis Management of chronic otitis media with cholesteatoma remains controversial. The purpose of the study is to examine factors associated with the surgical approach to manage cholesteatoma.

Study Design A retrospective review.

Methods A retrospective review was made of all primary cases of mastoid surgery for cholesteatoma performed at an otological center between 1995 and 2000. During the study period, 486 ears underwent surgery for cholesteatoma. Data included procedures performed, location and extent of the disease, residual and recurrent disease, complications, reasons for staging the surgery, and duration of follow‐up.

Results The canal wall remained intact in 68.5% of ears. The majority of the remainder of the patients underwent a canal wall down technique with mastoid obliteration. Residual cholesteatoma was found in 26.9% of second procedures and in 2.7% of third procedures.

Conclusions The majority of patients with cholesteatoma can be adequately managed with a canal intact tympanomastoidectomy with staging. Otolaryngologists should consider a two‐staged procedure as a viable management approach for chronic otitis media with cholesteatoma.

We prefer the intact canal wall technique for tympanoplasty with mastoidectomy, but use a canal wall down procedure in up to 25 % of oases. Creating a round cavity with a large meatus is imperative if one is to obtain a trouble-free ear. The five types of canal wall down procedures are defined, as are our indications for using them. Results in 19 only hearing ears and 19 labyrinthine fistula cases are presented, along with 64 tympanoplasty cases.

After a mean follow-up period of 7.3 years, a recurrence was found in 43 (12.3 percent) out of 349 consecutive patients undergoing surgical treatment for acquired cholesteatoma. The great majority of residual cholesteatomas detected in the ‘second-look’ operations arose from the oval window area.Chronic otorrhoea and a reperforation were the most common signs of late recurrences. In eight ears a recurrent cholesteatoma developed from a retraction pocket. The recurrence rate was higher in children than in adults. The type of surgical technique had no significant effect on recurrence rate. Recurrences were more frequent in pre-operatively discharging ears than in dry ears. Some suggestions have been made to improve the results of surgery for cholesteatoma.

We previously reported the localization of interleukin 1 in the epithelial layer of human cholesteatomas. On the basis of other studies that showed interleukin 1 can stimulate fibroblasts and macrophages to produce collagenases and prostaglandins, we then proposed that interleukin 1 may play an important role in cholesteatoma‐related bone resorption, also. Our immunocytochemical study involving more human cholesteatoma samples revealed the presence of interleukin 1 in bone cells and monocytes in the region of active bone destruction. In the present study, the effect of interleukin 1 on these cells found at the bone resorption site was examined. By radioimmunoassay, interleukin 1 was shown to stimulate the production of prostaglandin E2 by osteoblasts in vitro. Interleukin 1 also promoted the migration and multinucleation of bone marrow‐derived monocytes. These osteoclast‐like cells formed from monocytes contained tartrate‐resistant acid phosphatase, and caused the resorption of the devitalized bone in vitro. Above findings suggest that interleukin 1 could cause the bone destruction in cholesteatomas, not only by stimulating the local bone cells, but also by recruiting monocytes for osteoclastic bone resorption.