Histochemical detection of lectin binding was carried out using the HRP-conjugated lectin method in hyperkeratinized lesions including leukoplakia, carcinoma in situ, Paget's disease, keratoacanthoma, and condyloma acuminatum. The lectins used for demonstrating sugar residues were: Con A (hexose), PNA and RCA-1 (Gal), DBA and SBA (GalNAc), UEA -1 (Fuc), and WGA (GlcNAc). Lectin binding in normal squamous epithelium showed regional distribution patterns of keratinized, spinous and basal layer types. Histochemical localization of lectin binding was generally at the cellular surface and in the intercellular substance and sometimes in the cytoplasm of normal epithelial cells. Dysplastic cells or carcinoma cell, in contrast, displayed a loss of cellular surface and intercellular staining. Paget's cells were devoid of lectin staining. In keratoacanthoma and condyloma specimens, spinous cells, which were PAS-positive, showed an intense PA/Con A-HRP staining and moderate binding by other lectins, which was somewhat decreased when compared with that in the surrounding intact epithelium. The cytochemical distribution of epithelial lectin binding might be indicative of the expression of normal stratification and keratinocytic differentiation , and the disappearance of this typical epithelial pattern may suggest severe dysplasia and malignancy.

The lectin-binding patterns of the cells involved in amelogenesis and dentinogenesis in developing teeth of rats were studied. Undifferentiated odontogenic epithelia exhibited very slight staining with almost all of the lectins examined. The lectin-staining affinities of secretory ameloblasts could be divided into two categories: Concanavalin-A (Con-A), Wheat germ agglutinin (WGA) and Soybean agglutinin (SBA) binding occurred from the middle to apical cytoplasm, whereas Ricinus communis agglutinin-I (RCA-I) and Ulex europeus I (UEA-I) binding predominated in the basal regions. The cells of the stratum intermedium exhibited relatively strange lectin staining, which appeared to be dependent on ameloblastic maturation. The basement membranes in undifferentiated epithelia were markedly positive for lectin binding. Odontoblasts showed moderate Con-A staining on the apical side of the cells, as well as slight-to-moderate reactions with WGA and SBA. Pulp cells and dental papillae showed slight-to-moderate lectin staining, and predentin and dentin were also moderately positive for Con-A and RCA-I binding and slightly so for WGA and SBA. The lectin-binding affinities were enhanced during the formation of enamel and dentin, and appeared to be dependent on the degree of cellular differentiation in ameloblasts and odontoblasts.

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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.

Immunohistochemical detection of lactoforrin (LF), lysozyme (LZ) and carcinoembryonie antigen (CEA) was made in obstructive adenitis of the submandibular glands. Atrophic and altered acinar cells in the early stage of the lesion stained strongly for I.F, whereas they were unreactive or stained slightly for LZ. Ductal cells usually stained for LZ Staining for CEA was strong and irregularly distributed in altered acinar cells. Duct‐like structures and dilated ductal segments in the chronic stage were generally negative for LF LZ and CEA. Secretory components in luminal cavities gave abundant staining for LF. LZ and CEA. Histocytes which infiltrated into the connective tissue in the later stage showed a positive LZ reaction.