The main components, both intrinsic (laminin and type IV collagen) and extrinsic (fibronectin), of the basement membrane (BM) were analyzed by immunohistochemical methods in normal, dysplastic and neoplastic laryngeal mucosa specimens. The material was obtained from 35 patients who had undergone surgery for glottic or supraglottic cancer. Fibronectin proved to be absent from normal mucosa whereas an immunopositivity was observed close to the dysplastic epithelium, especially around inflammatory cells. Positivity increased as the degree of dysplasia increased from LIN I to LIN III. A strong staining was also seen around nests of well and moderately differentiated squamous cell carcinoma. These findings are in agreement with the theories about the main sites of origin for fibronectin, both from plasma and connective tissue. Laminin and type IV collagen showed the same staining characteristics. In normal and mild dysplastic samples a regular and continuous positivity was found at the boundaries between the epithelium and the mesenchymal stroma. Focal discontinuities were present in areas of intense subepithelial inflammation only. Interruptions and reduplications were more evident in severely dysplastic epithelium. In invasive squamous cell carcinomas a strong correlation has been found between the degree of cell differentiation and the pattern of distribution of the intrinsic BM components. Immunostaining was usually evident and continuous around nests of well differentiated squamous cell carcinoma, whereas positivity progressively decreased in moderately and poorly differentiated neoplasms. Furthermore, staining for intrinsic BM components was also related to the pattern of tumor growth: continuous around the "pushing" edge of neoplastic growth and discontinuous when the neoplastic front had an "invading" appearance. These observations tend to support the theory which considers neoplastic growth a cyclic process. BM components are most likely synthesized during the phases of quiescence and reabsorbed during the phase of invasiveness, following shifts in neoplastic cell metabolism.