Ultrastructural studies of the parotid glands in sialadenosis

30 parotid biopsies of patients with sialadenosis--a symmetrical, painless, non-inflammatory, recurrent parotid swelling--were studied by electron microscopy. The patients suffered from different diseases, such as diabetes mellitus, liver diseases, hypertension and other affections. Parotid biopsies from 25 patients with slight parotitis or with oral cancer were used as controls. Morphometric studies reveal that the parotid swelling is caused by an enlargement of acinar cells. In controls the average diameters of the acinar cells are 30 to 40 mu. In sialadenosis the diameters are enlarged to 50 to 70 mu, in some cases to a maximum of 100 mu. Histologically the cytoplasm of the enlarged acinar cells shows either a granular pattern due to a numerical increase in secretory granules or a vacuolar transformation. Ultrastructurally the vacuolar transformed acinar cells also contain an increased number of granules with less electron density than the surrounding cytoplasm. Three types of sialadenosis can be distinguished with regard to the electron density of the acinar granules: a) a dark granular type, b) a pale granular type and c) a mixed granular type. The mixed granular type probably develops from the dark granular form. Alterations leading to the destruction of the myoepithelial cells were observed in all three types of sialadenosis with minimal changes in the dark granular type. Degenerative alterations of the autonomic nervous system are evident in all three groups with most pronounced changes in the pale granular type of sialadenosis. The ultrastructural alterations are interpreted as a disturbance of secretion, probably primarily caused by the degeneration of the autonomic nervous system. The alteration of the autonomic nervous system is suggested to be the common pathogenetic principle in all types of human sialadenosis occurring with different basic diseases. The enlargement of the acinar cells is the result of an intracellular disturbance in the secretory process due to the preceding defect of the autonomous nerval structures.