SummaryThe expression of laminin and fibronectin isoforms varies with cellular maturation and differentiation and these differences may well influence cellular processes such as adhesion and motility. The basement membrane (BM) of fetal oral squamous epithelium contains the laminin chains, α2, α3, α5, β1, β2, β3, γ1 and γ2. The BM of adult normal oral squamous epithelium comprises the laminin chains, α3, α5, β1, β3, γ1 and γ2. A re-expression of the laminin α2 and β2 chains could be shown in adult hyperproliferative, dysplastic and carcinomatous lesions.In dysplasia and oral squamous cell carcinoma (OSCC), multifocal breaks of the BM are present as indicated by laminin chain antibodies. These breaks correlate to malignancy grade in their extent. Moreover, in the invasion front the α3 and γ2 chain of laminin-5 can immunohistochemically be found outside the BM within the cytoplasm of budding carcinoma cells and in the adjacent stroma. The correlation between the morphological pattern of invasive tumour clusters and a laminin-5 immunostaining in the adjacent stroma may suggest, first, that a laminin-5 deposition outside the BM is an immunohistochemical marker for invasion and second, that OSCC invasion is guided by the laminin-5 matrix. Expression of oncofetal fibronectins (IIICS de novo glycosylated fibronectin and ED-B fibronectin) could be demonstrated throughout the stromal compartment. However, the ED-B fibronectin synthesizing cells (RNA/RNA in situ hybridization) are confined to small stroma areas and to single stroma and inflammatory cells in the invasion front. A correlation of the number of ED-B fibronectin synthesizing cells to malignancy grade could not be seen. ED-B fibronectin mRNA-positive cells seem to be concentrated in areas of fibrous stroma recruitment with a linear alignment of stromal fibro-/myofibroblasts (desmoplasia). Double staining experiments (ED-B fibronectin in situ hybridization and α-smooth muscle actin immunohistochemistry) indicated that the stroma myofibroblasts are a preferential source of ED-B fibronectin. In conclusion, in OSCC, a fetal extracellular matrix conversion is demonstrable. Tumour cells (laminin α2 and β2 chain) and recruited stromal myofibroblasts (oncofetal ED-B fibronectin) contribute to the fetal extracellular matrix milieu.

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A case report of a multifocal oncocytic adenomatous hyperplasia occurring in a parotid gland is presented. The differential diagnosis of (multicystic) Warthin's tumor is discussed.

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The basaloid squamous cell carcinoma (BSCC) is a variant of squamous cell carcinoma, having histologically distinctive features and appearing in the oral cavity, upper respiratory tract and esophagus. Histological hallmarks are the presence of a basaloid component in intimate association with squamous cell carcinoma. The basaloid component is characterized by tightly packed nests of cells with scant cytoplasm and hyperchromic nuclei without visible nucleoli and an increased mitosis rate. Basaloid squamous cell carcinoma is said to have a higher malignant potential than common oral squamous cell carcinoma with an increased incidence of regional lymph-node metastases and distant metastases. Our finding of a Ki-67 index of 30% and the immunohistochemical demonstration of p53 protein speaks well for enhanced aggressive biological behavior. The differential diagnosis includes the adenoid cystic, mucoepidermoid, neuroendocrine, adenosquamous and conventional oral squamous cell carcinoma. Because of early dissemination, radical surgical treatment and additional radiation therapy are considered necessary. Our findings indicate that partial clinical and histological tumor regression occurs after systemic neoadjuvant chemotherapy.