Endolaryngeal microsurgery at the anterior glottal commissure: controversies and observations.

There are a number of tenets regarding endolaryngeal microsurgical management of disease that involves and/or encroaches upon the anterior glottal commissure (AGC). They include avoidance of 1) bilateral epithelial incisions near the AGC, 2) removal of papillomatosis in the AGC, and 3) resection of bilateral keratosis with atypia or carcinoma at the AGC. During the last 6 years, 115 patients underwent microsurgical management of disease at the AGC: carcinoma in 20 (T1 in 15 and T2 in 5), keratosis in 41, papillomatosis in 20, and polypoid corditis (Reinke's edema) in 34. No patients with polypoid corditis developed a synechia or web. All cancers were successfully resected en bloc; 1 of the 20 patients developed a microscopic local failure that was successfully re-resected endoscopically. Eleven of the 20 cancers required excision of part of the supraglottis to establish adequate exposure for the glottic cancer resection. Eight of 15 patients with bilateral keratosis underwent staged resections. Fourteen of 15 patients with bilateral papillomatosis required staged resections. Twelve of the total 115 patients presented with a web secondary to prior microsurgery, and 3 developed a new, clinically insignificant web. The complications of management of disease in or near the AGC described by other authors were not noted in this series. This success was primarily the result of improved exposure in the AGC, which was achieved by use of larger and better-designed laryngoscopes and by resection of supraglottic tissue as necessary. Positioning these prototype laryngoscopes was facilitated by the use of elevated-vector suspension and external counterpressure.

Cricothyroid subluxation: a new innovation for enhancing the voice with laryngoplastic phonosurgery.

Laryngoplastic phonosurgery has evolved to become a dominant treatment modality for paralytic dysphonia. Current surgical procedures have addressed primarily the position of the musculomembranous vocal fold and the arytenoid in the axial and vertical planes. However. dynamic range capabilities and vocal flexibility have been limited secondary to the flaccid, denervated vocal fold tissue. Therefore. a new procedure was conceived to enhance the acoustic vocal outcome from operations that reposition the vocal edge. Cricothyroid (CT) subluxation was designed as a technique to increase the distance between the cricoarytenoid joint and the insertion of the anterior commissure ligament. Cricothyroid subluxation was done without complication in 9 patients who underwent combined adduction arytenopexy and medialization laryngoplasty, and in 4 patients with medialization laryngoplasty alone. Postoperative stroboscopic assessment was done in all of the 13 patients, while complete analysis of vocal function was available in 10 of the 13 patients; this revealed improvement (as a group) on almost all objective measures over the preoperative state. All patients who underwent CT subluxation had a normal maximum frequency range (pitch variation of more than 2 octaves), as compared with 22% of a prior similar cohort of patients who did not undergo CT subluxation. All patients who underwent CT subluxation had normal glottal airflow and a normal noise-to-harmonics ratio. Cricothyroid subluxation is a relatively easily adjustable procedure that increases the length and viscoelastic tension of the denervated vocal fold. The modified biomechanical properties resulted in improved vocal outcome in all of our patients, which was most remarkable in terms of maximal range capabilities. Cricothyroid subluxation enhanced the postoperative voice of patients regardless of whether they required medialization laryngoplasty alone or whether they also required adduction arytenopexy.

Protuberant fibro-osseous lesions of the temporal bone: a unique clinicopathologic diagnosis.

OBJECTIVE: The objective of the study was to describe the clinical presentation and treatment of exophytic fibro-osseous temporal bone lesions, a clinical entity never previously reported, and to consider the differential diagnosis. STUDY DESIGN: The design of the study was a retrospective case review. SETTING: The setting was a tertiary referral center. PATIENTS: Two patients diagnosed with exophytic fibro-osseous temporal bone lesions were included in the study. INTERVENTION: The intervention used was surgical excision. MAIN OUTCOME MEASURE: The main outcome measures were clinical, radiographic, and histopathologic examination. RESULTS: There was no evidence of recurrence at 15 and 17 months after surgery. CONCLUSION: Although fibro-osseous lesions of the temporal bone have been previously reported, there have been no reported cases of an exophytic variant.

Expression of p53 protein in human middle ear cholesteatomas: pathogenetic implications.

BACKGROUND: Cholesteatoma is a destructive lesion of the middle ear or mastoid process or both. The molecular and cellular defects that result in the clinical hallmarks of acquired and congenital cholesteatomas, namely invasion, migration, uncoordinated proliferation, altered differentiation, aggressiveness, and recidivism, are unknown. Determining the existence of defects in the normal biology, biochemistry, and genetic complement of the major cellular constituents comprising a cholesteatoma (i.e., fibroblasts and keratinocytes) is critical to the understanding of the pathogenesis of cholesteatomas. It has been speculated that the development of human cholesteatomas is due, in part, to the altered control of cellular proliferation, which tilts the balance toward the aggressive, invasive growth of squamous epithelium within the middle ear. However, whether this altered control is due to defects in the mechanisms and underlying genes that control proliferation, or to cytokines released from infiltrating inflammatory cells, or to some other mechanism is unknown. The nuclear phosphoprotein p53 tumor suppressor gene plays a critical regulatory role in cell cycle control and apoptosis. In the current article, the authors have analyzed congenital, primary and secondary acquired, and recurrent cholesteatomas for the altered expression of p53 and Ki-67, a marker of active proliferation. METHODS: p53 and Ki-67 expression was determined by immunohistochemical assays using specific monoclonal antibodies. RESULTS: The authors' results indicate that p53 is elevated 9- to 20-fold in all cholesteatomas when compared to the expression of p53 in normal postauricular skin or tympanic membrane. However, there is no concomitant increase in Ki-67 expression in cholesteatomas. CONCLUSIONS: These data indicate a defect in cholesteatomas in the mechanisms that p53 engages (i.e., cell cycle control or apoptosis or both). In addition, these data further suggest that there is no intrinsic difference between any clinicopathologic group of cholesteatomas, at least with respect to p53-expression and, presumably, p53 function.

DNA analysis of human cholesteatomas.

HYPOTHESIS: The hypothesis tested in this article is that if cholesteatomas are a low-grade squamous cell neoplasm, then evidence of genetic instability, in the form of abnormal or aneuploid amounts of DNA, should be evident. BACKGROUND: Cholesteatoma is a destructive lesion of the middle ear and/or mastoid process that produces complications by erosion of the temporal bone. The clinical hallmarks of cholesteatomas, namely invasion, migration, uncoordinated proliferation, altered differentiation, aggressiveness, and recidivism, are traits typically associated with the neoplastic cell. However, there is little evidence to support or refute the speculation that cholesteatomas are a low-grade squamous cell neoplasm. the existence of defects in the genetic complement of the major cellular constituents comprising a cholesteatoma, fibroblasts and keratinocytes, would support the speculation that cholesteatomas are a neoplasm, since cancers commonly manifest quantitative and qualitative alterations in the normal euploid complement of genetic information, resulting in a cell that has an abnormal or aneuploid amount of DNA. METHODS: DNA content (ploidy) within cholesteatoma tissues was measured by flow cytometry and image analysis. RESULTS: The DNA content of 11 human cholesteatomas and nine postauricular skin specimens was analyzed using flow cytometry, while the DNA content of 10 cholesteatoma specimens was analyzed using image analysis. Interpretable data was obtained from 10 cholesteatoma specimens and six postauricular skin specimens. One cholesteatoma specimen demonstrated an abnormal aneuploid DNA content, whereas the remaining nine cholesteatomas and the six postauricular skin specimens demonstrated a normal euploid DNA content. CONCLUSIONS: We conclude that, due to the lack of overt genetic instability, as evidenced by the presence of a normal euploid DNA content, cholesteatomas are not low-grade neoplasms.

Altered regulation of cell surface peptidases in human cholesteatoma.

Cholesteatoma is a destructive process involving an accumulation of desquamated keratin arising from squamous epithelium that pathologically has invaded the middle ear or mastoid process. The clinical hallmarks of cholesteatomas, namely invasion of healthy tissues, migration, unrestrained proliferation, aggressiveness, recidivism, and uncoordinated differentiation predict the existence of defects in the normal biology and biochemistry of the cellular constituents that compose a cholesteatoma, as well as in the cellular interactions between these cells, the surrounding normal tissue, and the host. In the current report, we analyzed 11 cholesteatomas and matched healthy tissue for altered expression in four different cell surface peptidases, aminopeptidase A, aminopeptidase N, dipeptidyl peptidase IV, and neutral endopeptidase. We suggest that peptidases may modulate cell growth and differentiation by inactivating stimulatory signals (or conversely, by activating inhibitory signals).

Beta-2 transferrin: limitations of use as a clinical marker for perilymph.

Beta-2 transferrin is a protein marker that can be used in the clinical setting to reliably identify the presence of cerebrospinal fluid (CSF). Recent literature has suggested that beta-2 transferrin can also be used as a clinical marker for perilymph. This study investigates the use of a beta-2 transferrin assay as a method to identify the presence of perilymph. Twenty-two patients were enrolled in the study. Fluid samples were obtained intraoperatively and tested for the presence of beta-2 transferrin. As expected, four CSF samples collected were positive for beta-2 transferrin; however, four known perilymph samples collected from patients undergoing cochlear implantation were negative for beta-2 transferrin, seven of nine known perilymph samples obtained during stapedectomies were negative for beta-2 transferrin, and four of five samples collected during middle ear explorations for fistula were negative for beta-2 transferrin. With current methodology beta-2 transferrin does not appear to be a reliable clinical marker for perilymph in the operative setting.