EPIDERMAL GROWTH-FACTOR, TRANSFORMING GROWTH-FACTOR-ALPHA, AND EPIDERMAL GROWTH-FACTOR RECEPTOR IN LABIAL SALIVARY-GLANDS IN SJOGRENS-SYNDROME

Objective. Epidermal growth factor (EGF) and transforming growth facto r-alpha (TGF-alpha) affect cells through binding to a shared EGF recep tor (EGF-R), which is a transmembrane protein with tyrosine kinase act ivity. They exert trophic effects on vascular endothelial, salivary ac inar, and ductal and mucosal epithelial cells. In Sjogren's syndrome ( SS) focal sialadenitis leads to salivary gland tissue damage, diminish ed salivary flow, and changes in the oral epithelium, a complex referr ed to as xerostomia. We compared the localization of EGF, TGF-alpha, a nd EGF-R in labial salivary glands in SS and in healthy controls. Meth ods. Labial salivary gland tissues of 12 patients with SS and 7 health y controls were stained with the immunohistochemical peroxidase-antipe roxidase method for EGF, TGF-alpha, and EGF-R. Results. Immunoreactivi ty for both EGF and TGF-alpha was found in endothelial cells of blood vessels and in some ductal epithelial cells. TGF-alpha, but not EGF, w as also found in some acinar cells. EGF-R was found in endothelial, ac inar, and salivary duct epithelial cells. There was no difference in t he expression of EGF-R between diseased and healthy specimens, but bot h EGF and TGF-alpha were diminished in SS. Conclusion. The interrelate d localization of EGF-R and its ligands, EGF and TGF-alpha, suggests a n autocrine, juxtacrine, and paracrine mitogenic/trophic role for them and thus a role in the maintenance of the secretory and excretory cel ls of the normal salivary glands. The trophic effects on acinar cells seem not to be mediated by EGF, but more likely by TGF-alpha. The dimi nished expression of EGF and TGF-alpha indicates a failure of this tro phic system in SS, which may contribute to the acinar atrophy and seco ndary changes thereof, including atrophy of the oral mucosa.