A 42-year-old woman presented with a painful swelling of the left parotid gland; a mass found on palpation was surgically resected. Histopathology revealed a sialolith and mild multifocal chronic inflammatory infiltrate. In addition, multiple scattered foci of sebaceous-type glands admixed with salivary gland acini were seen. Many of the foci revealed nearly complete replacement of the serous acini by sebaceous glandular epithelium (Figure). Isolated single sebaceous-type cells admixed with salivary acini were not seen, nor was there any preferential localization of these glands in areas of chronic inflammation.
The earliest description of sebaceous units in salivary glands was published by Hamperl in 1931.1 Auclair et al2 reported that sebaceous differentiation occurs in about 10.5% to 42% of normal parotid glands. Sebaceous differentiation is commonly seen in periductal locations in interlobular ducts. It may present as single, isolated, sebaceous-type cells within serous or mucinous salivary acini or as fully developed sebaceous glands.2 A mixed serous and sebaceous gland with near complete acinar replacement by the sebaceous glandular epithelium is rare. It is not known if sebaceous neoplasms of salivary gland, such as sebaceous adenoma, sebaceous lymphadenoma, or sebaceous carcinoma, arise from these aberrantly differentiated glands.
A few investigators have attempted to explain such aberrant locations of sebaceous glands. They are thought to be the result of either (1) sebaceous metaplasia within ectodermally derived ductal epithelium or (2) developmentally derived from dermis and therefore representative of glandular heterotopia. A good discussion with illustrations showing the presence of sebaceous elements in salivary glands is found in Sternberg's Histology for Pathologists.3 In a discussion by Martinez-Madrigal et al, however, the authors discount an embryological origin for these glands, since they believe that parotid gland development is not along a “line of closure.” Contrary to their views, embryological studies and texts explain that the parotid gland (which contains the highest distribution of sebaceous elements among all salivary glands) is formed as an outgrowth in relation to the line along which the maxillary and mandibular processes fuse to form the embryonic cheek. A recent study of 21 fetuses at different gestational ages confirmed this finding.4 Thus, Stensen duct is generally considered ectodermal in origin. The periductal location of sebaceous glands supports the theory that these may be developmentally related to the lines of fusion and therefore are ectodermally derived (similar to Fordyce disease). Presence of these glands even in normal parotid glands and no obvious association with chronic inflammatory lesions argue against a metaplastic process. Lastly, given such a high prevalence of sebaceous glands in the parotid, it is possible that sebaceous glands represent a normal but variable component of the salivary gland without a closely studied functional or anatomical significance.
Functionally, sebaceous glands in skin arise as an outgrowth of the external root sheaths of hair follicles. Sebaceous glands secrete sebum, and in skin they are thought to have bacteriostatic, emollient, and barrier functions in humans, and additionally function as pheromone producers in lower animals. Sebum is implicated in the pathogenesis of acne. Sebaceous glands do not have any known physiological function as a component of salivary tissue. If the sebaceous glands in salivary glands are as highly distributed,2 and if they are functionally active, then the glossary buds are constantly coated by sebum—a dysgeusic thought.