Histochemical studies of obstructive adenitis in human submandibular salivary glands. II. Lectin binding and keratin distribution in the lesions

Abstract

Lectin‐binding profiles and keratin distribution in obstructive adenitis of human submandibular glands (SMGs) are reported and compared those of normal SMGs. Histologically, obstructive changes in the SMGs included acinar atrophy, duct‐like structure formation in the early stage, and disappearance of acinar cells and dilation of ductal segments in the later, chronic stage. The following lectins were used: Con A (Glc. Man), PNA(Gal, GalNAc). RCA1I(Gal), DBA(GalNAc). SBA(Gal, Gal‐NAc). UEA‐1(α‐L‐Fuc) and WGA((GlcNAC, NeuNAc). Lectin staining in atrophie acinar cells was usually reduced except for SUA binding and was irregularly distributed in altered acinar and ductal epithelia. Binding of DBA and UEA‐1 lectins were particularly intense along the luminar borders of ductal segments in the lesions. Immunohistochemically detectable keratins were characterized by intense staining in atrophie acinar cells and in all the ductal segments, whereas normal acinar cells, either serous or mucous, were negative.

Vascular endothelial cell participation in formation of lymphoepithelial lesions (epi-myoepithelial islands) in lymphoepithelial sialadenitis (benign lymphoepithelial lesion)

“…These cells were sometimes in the process of forming vessel walls but at other times were not yet assembled into blood vessels. Although the duct epithelial nature of their constituent cells has been well investigated by ultrastructural [2,5,9,11,19,28,32,35,40,41] and immunohistochemical [3,15,16,21,22,26,27,32,38] studies, there has been no postulation of endothelial cell participation in the formation of LELs. Only Qin et al [29] reported von Willebrand factor-immunopositive capillaries in the inflammatory stroma, suggesting that an efficient blood supply elucidates regeneration and proliferation of epithelial cells in the formation of the LELs in a general sense.…”

“…EMIs were first investigated using electron microscopy (EM) in the 1960s [2,5,9,11,19,28,32,35,40,41] and were shown to be composed of both duct epithelial and myoepithelial cells. However, immunohistochemical studies for cytoskeletal proteins were introduced in this lesion in the 1980s, which indicated that cells with duct epithelial characteristics are mainly responsible for the EMI formation [3,15,16,21,22,26,27,32,38]. In addition to the EM studies, these immunohistochemical studies have also indicated that the EMIs are composed of not only epithelial cells but also of other inflammatory cells, as not all of the constituent cells of EMIs are immunolabeled for epithelial cytoskeletal proteins.…”

Monoclonal antibody to keratin K8.12 expression in ductal basal cells of obstructive lesions and in outer tumor cells of salivary pleomorphic adenomas.

“…This histopathology of obstructed salivary gland lesions has been well established, and the keratin staining pattern of the lesions has also been reported with the use of polyclonal antibody (24,28). Existence of K8.12 staining in ductal basal cells of obstructive lesions was first noted in the present study.…”

“…Early obstructive lesions mainly showed ductal dilation and a little atrophy of acinar compartments accompanied by infiltrating inflammatory cells. When long-standing obstruction occured in the glands, almost all acinar cells disappeared or degenerated with fibrous tissue replacement and ductal segments remained in a fibrous stroma (24).…”

Expression of involucrin in human salivary gland lesions and tumors.

“…In the present study, ductal epithelia and acinar cells, either serous or mucous, of normal glands indicated negative staining as did duct-like structures in obstructive sialadenitis. Keratin staining is strongly evident in epithelial architecture, i.e., normal ductal segments of salivary glands and duct-like structures of sialadenitis (2,3,6,12). This finding suggests that the duct-like structures in obstructive salivary lesions have less tendency to terminal keratinization.…”