It is well known that cell surface glycoconjugates play an important role in cell proliferation, adhesion and differentiation. The aim of this investigation was to define the changes of the glycoconjugate saccharidic moieties in the epidermis and derma of patients affected by several skin pathologies such as seborrheic keratosis, lichen planus, granuloma annulare and palmoplantaris keratoderma. Bioptical specimens from skin lesions as well as from normal skin were fixed in Carnoy's fluid and routinely processed. The sections were treated with HRP-lectins (PNA, DBA, SBA, WGA, ConA, LTA and UEAI). Cytochemical controls were performed for specificity of lectin-sugar reaction. Some sections were pre-treated with neuraminidase prior to staining with HRP lectins. In comparison with normal human skin, epidermal lectin binding pattern in the considered diseases showed considerable qualitative and quantitative variations. In general, in all the considered pathologies, a lack and/or a decrease in lectin binding at the epidermal layers was observed; among the various diseases, differences in cellular localisation of the sugar residues were also noted. In such respect, an exception was represented by seborrheic keratosis, where the cells of the basal layer showed PNA reactivity, which was absent in the basal layer of the normal skin. Although seborrheic keratosis and lichen planus have been studied by others authors, our findings are not in total accordance concerning lectin binding; this is probably due to the different fixatives employed. Our findings seem to reveal significant changes in keratinocyte glycoconjugate oligosaccharides in the previously mentioned diseases, providing clues to their pathogenesis.