Melanocyte localization and distribution in human cholesteatoma.

INTRODUCTION: Melanocytes in skin are derived from the neural crest and colonize the epidermis in the first trimester of gestation. Melanocytes have been observed in the nasopharyngeal, inner ear and oral mucosa and should therefore be present in the middle ear mucosa. AIMS: To identify and determine the distribution of melanocytes in human cholesteatoma and normal meatal skin in Caucasian adults. MATERIAL AND METHODS: Human cholesteatoma (n=18) and normal meatal skin samples (n=10) were investigated immunohistochemically with anti-HMB-45 and MART-1 antibodies. Localization and distribution of melanocytes were assessed in the epidermis and cholesteatoma using an automatic analyzing system. RESULTS: Regular skin exhibited melanocytes within the epidermis and accounted for 10% of the total cell number. They occurred partly as membrane-bound clusters. Cholesteatoma matrix melanocytes were observed in the basal layer and exhibited an oval or roundmorphology. Decreased numbers of melanocytes in the basal layer correlated with keratinization within cholesteatoma samples. Melanocytes revealed monomorphous nuclei, abundant cytoplasm containing particles of melanin. Found adjacent to glands and blood vessels, melanocytes were also scattered among the mesenchymal cells. Accounting for 2-6% of the total cell number within the squamous epithelium, melanocyte density was significantly lower in cholesteatoma tissue than in skin. CONCLUSIONS: The melanocyte distribution pattern was different when comparing the epithelia of skin and cholesteatoma. The presence of melanocytes in cholesteatoma may be due to an ingrowth, consequently controlled by keratinocyte-derived signals. In terms of the pathogenesis of cholesteatoma, neither squamous metaplasia nor melanocyte metaplasia can be excluded by our data.

The management of carotid artery rupture.

Carotid artery rupture is fortunately an uncommon complication of head and neck cancer treatment. Eleven episodes of carotid artery rupture following irradiation and major head and neck resection were identified over a 6-year period. We review our experience and discuss the predisposing factors that can cause this complication, important aspects of management and outcome. During this 6-year period, 11 episodes of carotid artery rupture were treated in our unit. All patients had received prior irradiation (more than 60 Gy) and undergone a major surgical resection or resections. The average age was 59 years; all patients had a salivary fistula, local infection and a manifest 'herald bleed' just before their major carotid artery rupture. These patients were resuscitated, taken to theatre and the neck explored, with control of the vessel and debridement of necrotic tissue. Soft tissue coverage was in the form of a flap. Many of the factors predisposing to carotid artery rupture can be ameliorated or treated early in order to avoid this complication. Early and aggressive nutritional support together with correction of haematological abnormalities promote wound healing and prevent tissue breakdown. The detection and treatment of infection also reduces fistula formation and wound compromise. We present our protocol for the early, aggressive management of these patients with carotid artery rupture.