Open AccessAlteration of cell surface carbohydrates associated with ordered and disordered proliferation of oral epithelia: a lectin histochemical study in oral leukoplakias, papillomas and carcinomas
Author(s) -
Vigneswaran N.,
Peters K.P.,
Hornstein O. P.,
Diepgen T. L.
Publication year - 1990
Publication title -
cell proliferation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.647
H-Index - 74
eISSN - 1365-2184
pISSN - 0960-7722
DOI - 10.1111/j.1365-2184.1990.tb01108.x
Subject(s) - peanut agglutinin , agglutinin , soybean agglutinin , griffonia simplicifolia , wheat germ agglutinin , lectin , dysplasia , biology , microbiology and biotechnology , cell , epithelial dysplasia , pathology , chemistry , biochemistry , medicine , genetics
. Cell surface carbohydrates in healthy oral mucosa (n = 15), leukoplakias without ( n = 48) and with (n = 62) dysplasia, oral papillomas (n = 6) and squamous cell carcinomas (SCCs) (n – 40) were examined using the lectins peanut agglutinin (PNA), Ulex europaeus agglutinin I (UEA I), soybean agglutinin (SBA), Helix pomatia agglutinin (HPA), and Griffonia simplicifolia agglutinin I (GS I‐B 4 ). Binding of these lectins in formalin‐fixed, paraffin‐embedded tissues was demonstrated using either the peroxidase‐anti‐peroxidase (PAP) method or the avidin‐biotin method. Healthy oral epithelia revealed binding sites for these lectins mostly in the suprabasal keratinocytes with occasional PNA binding also in their basal cells. Unlike healthy mucosa, a number of leukoplakias without and with dysplasia revealed receptor sites for UEA I also in their basal layer. Only those keratinocytes undergoing squamoidal differentiation exhibited SBA binding. Staining patterns of UEA I and SBA did not vary significantly between either leukoplakias without and with dysplasia or papillomas and SCCs. Conversely, a reduction or lack of binding sites for PNA (Galβl‐3GalNAc), HPA (D‐GalNAcα) and GS I‐B 4 (αD‐Gal) was observed more frequently in leukoplakias with dysplasia and SCCs contrasting their counterparts lacking epithelial dysplasia. Cell surface glycosyl residues play an important role in the regulation of cell proliferation and epithelial growth. Aberrant glycosylation in oral dysplastic leukoplakias and carcinomas leading to the lack of the relevant terminal sugar residues from their cell surface carbohydrates is probably a major reason for the hyper‐/ disordered proliferation.