The findings of this study showing suppressed cellular proliferation and infrequent p53 dysfunction in snuff lesions may partly explain why dysplastic changes are seldom seen in mucosal lesions induced by the Scandinavian type of snuff.
Differences in the expression of cytokeratins (CK) in specimens obtained from snuff-affected oral epithelium of the maxillary vestibular sulcus and clinically normal sulcular epithelium were studied by indirect immunofluorescence staining with a panel of monoclonal antibodies (MAbs). CK 14, a marker of stratified squamous epithelium was not seen expressed in 3/11 of the snuff user's specimens. Terminal differentiation markers, typical of cornified epithelia (CK 1, 9, 10 and 11), were detected suprabasally in the snuff user's keratosis but not in the normal control epithelium. The use of snuff seemed to change the CK staining pattern of the mucosa so that it resembles more that of a cornified type of epithelium. Simple epithelial-type CK were included in the study in order to establish the CK profile of the snuff-induced keratosis, for comparison with normal and dysplastic lesions. MAb to CK 7 and 19 showed reactivity in the basal cells and suprabasally whereas the monospecific MAb anti-CK 7 showed suprabasal staining both in the control and affected epithelia. By using MAbs, we found no immunoreactivity against CK 18 either in normal or affected epithelia, whereas we found suprabasal reaction (5/11) against CK 8 in the snuff user's epithelia. The two MAbs demonstrating the expression of CK 19, normally confined to the basal cells of the stratified squamous epithelium, showed variable patterns of expression both in basal cells and suprabasally in the snuff lesions. The results show that use of oral snuff causes some alterations in the CK expression pattern of the affected epithelium. Whether the alterations are indicative of a premalignant change is, however, uncertain. The results encourage further studies on the subject.
We have shown, by using two monoclonal antibodies (143DB7 and 100EB2), that the expression of the extracellular matrix protein tenascin (Tn) is increased in the connective tissue of biopsies taken from snuff users' and tobacco smokers' oral mucosa. In normal oral mucosa Tn was seen to underlie the epithelium as a thin delicate band. The most increase in Tn reaction was observed in snuff users' mucosa while the immunoreaction in smokers' mucosa was less conspicuous. Often the most prominent Tn reaction took place in association with round cell inflammatory infiltration, indicating epithelial irritation. Tn has been shown to take part in epithelial-mesenchymal interactions during embryogenesis, wound healing and tumorigenesis. Here, a superficial epithelial irritant has been shown to cause conspicuous alterations not only in the epithelial cell layers but also in the underlying connective tissue by increasing its Tn content. As a result of our findings we suggest a further link for Tn in a dynamic epithelial-mesenchymal interplay by virtue of this marked connective tissue reaction in snuff users' and smokers' oral mucosa.
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