Histologic subclassification of the cystadenolymphoma of the parotid gland

Abstract

Cystadenolymphomas (CAL) of the parotid gland are variable in their epithelial differentiation and the ratio of the epithelial tumor component to lymphoid stroma. Two hundred and seventy five cases of CAL from the files of the Salivary Glands Register of the Institute of Pathology, University of Hamburg (1965–1979) were analysed. Their pathogenesis from parenchyma included in regional lymph nodes is discussed. The following Subclassification was established. Depending on to the ratio of epithelial tumor component to lymphoid stroma, three subtypes were distinguished. Subtype 1, “typical CAL” with an epithelial tumor component of 50%, amounted to 77% of all cases of CAL studied. Oncocytic differentiation and focal metaplasia to goblet cells or squamous epithelium was also found. 13.5% of CAL were classified as subtype 2, “stroma-poor CAL” with an epithelial tumor component of 70 to 80%). The tumor structure was similar to that of an oncocytoma in places. Two per cent of the CAL were in subtype 3, “stroma-rich CAL” with an epithelial tumor component of only 20 to 30%. Subtype 3 was found solely in men. The average age at presentation (61 years) was slightly lower than that of all the cases studied (65 years). In 7.5% of the cases large areas of squamous cell metaplasia and regressive changes was found within a CAL. These cases were classified as subtype 4 (“metaplastic CAL”). The average age was 67 years. The case histories showed that 20% of these metaplastic CAL had previously been irradiated. Bilateral CAL was found in 7.5% of the cases. In 4% multifocal CAL occurred in the parotid gland unilaterally. Recurrences were observed in 2% of all CAL. Carcinoma in CAL is rare (we found two cases in our own material). In 50% of all cases reported radiotherapy was mentioned in the case histories. Malignant tumors coincident with CAL were recorded in 3% of the cases. The lymphoid stroma showed reaction patterns similar to those of the regional lymph nodes. These included granulomatous changes (foreign body granuloma with cholesterol deposits, tuberculosis) and tumor metastases. In the neighborhood of oncocytic tumor epithelium focal accumulations of plasma cells forming IgA and IgG were found. Metaplasia to squamous epithelium is believed to be caused by circulatory disturbances, irradiation, and other noxae. In the differential diagnosis of the stroma-poor subtype 2, oncocytoma and cystic sialadenoma must be excluded, and in the differential diagnosis of subtype 4 (the metaplastic CAL), sebaceous adenoma, mucepidermoid tumor, squamous cell carcinoma, lymphoepithelioma, and other non-tumorous lesions of the parotid gland (lymphoepithelial cysts, myoepithelial parotitis) must be ruled out. Our findings suggest that CAL develops from parenchyma included in parotid lymph nodes with the oncocytic ductal epithelium representing the neoplastic component.