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Histochemical studies of obstructive adenitis in human submandibular salivary glands. II. Lectin binding and keratin distribution in the lesions
Author(s) -
Nakai M.,
Tsukitani K.,
Tatemoto Y.,
Hikosaka N.,
Mori M.
Publication year - 1985
Publication title -
journal of oral pathology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.887
H-Index - 83
eISSN - 1600-0714
pISSN - 0904-2512
DOI - 10.1111/j.1600-0714.1985.tb00546.x
Subject(s) - pathology , lectin , ductal cells , serous fluid , keratin , salivary gland , staining , submandibular gland , biology , immunohistochemistry , chemistry , microbiology and biotechnology , medicine
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.