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The aim of the present study was to describe changes which could be regarded as a result of neoplastic rather than inflammatory processes. Fifty-five weeks after 6 weeks of DMBA application to the cheek pouches of 5 male hamsters there were 4 types of lesion : larger ulcerated sessile ; smaller non-ulcerated sessile ; non-ulcerated pedunculated ; conical projections. These and the rest of the pouches were examined by scanning electron and light microscopy. The interlesional mucosa, non-ulcerated sessile lesions and conical projections were covered by flat polygonal cells with either a honeycomb surface pattern of interconnecting microridges, or microridges arranged into more parallel lines. Cell imprints and boundaries were formed by linear ridges, grooves or both. Pedunculated lesions had flat smooth-surfaced cells and cells with a honeycomb surface pattern. None of these lesions were carcinomas by light microscopy but the ulcerated sessile lesions were. The appearance of the cells on the ulcerated lesions varied : flat, with a variable number of short microvilli that were often knob-like, isolated short microridges, or both ; plump, giving a cobblestone appearance with surfaces that were smooth, covered by microvilli, short microridges or both. Such appearances have been described as characteristic for dysplastic and malignant stratified squamous epithelium in a number of sites. Further study of both experimental and naturally occurring mucosal disease is needed to validate this.

Cytokeratin (CK) expression in untreated, paraffin-treated or dimethylbenzanthracene (DMBA)-treated hamster cheek pouch epithelium was investigated utilizing monoclonal antibodies AE1 or AE3, which react with type I or type II CKs, respectively, and by in situ hybridization utilizing type I CK-specific probes. The latter were isolated from a cDNA library of hamster cheek pouch mRNA and designated CK 13 and CK 10 based on their respective homologies (> 95% amino acids) with murine CK 13 and human CK 10. Treatment of hamster cheek pouch epithelium with DMBA resulted in increased expression of type I CK, detected immunohistochemically with monoclonal AE1, but decreased expression of type II CKs detected with AE3. Despite an overall increase in type I CKs, in situ hybridization demonstrated differential expression of type I CKs with altered distribution of CK 13 mRNA and reduced expression of CK 10 mRNA, providing additional sensitive markers for DMBA-associated changes in CKs. These changes were constant at 2 to 22 weeks in the pre-neoplastic and neoplastic epithelium following the initial application of DMBA.

Canalicular adenomas from five patients were examined by light and electron microscopy. All patients were over 50 years of age; 4 of the lesions were from the upper lip, 4 were cystic, 2 showed capsular invasion and 1 was multifocal. Histopathologically there were epithelial duct-like or canalicular structures cut at various angles and epithelial islands surrounded by hyalinized and mucinous connective tissue that contained little collagen. Ultrastructurally the epithelial islands contained many small lumina and connective tissue islands. The characteristic epithelial cell was columnar or cuboidal, extended from the lumina to the connective tissue, had almost straight lateral cell boundaries with desmosomes that predominated near the lumina, and possessed gap junctions and a small number of tight junctions. Their main cytoplasmic constituents were ribosomes, mitochondria, rough-surfaced endoplasmic reticulum and microfilaments. These findings show that canalicular adenomas are truly monomorphic and support the concept that they are derived from the cells of excretory ducts.

Hyperplasia in the hamster cheek pouch was examined using 4 different hyperplastic agents: oil of turpentine 50% v/v in liquid paraffin; vitamin A palmitate 10% w/v in liquid paraffin; 12-O-tetradeconyl-phorbol-13-acetate 16nM in acetone; and ethylphenylpropiolate 0.04mM in acetone. Acetone, paraffin and untreated control groups were also examined. Cheek pouches were painted 3 times a week for up to 4 weeks with each solution. Samples were removed and prepared for light microscopy 24 hours after 2 weeks of painting and 24 hours, 6, 12 and 18 weeks after 4 weeks of painting. Hyperplasia was produced by application of turpentine, vitamin A and TPA after 2 weeks of application. Further increases in epithelial width occurred after 4 weeks of painting in the turpentine and vitamin A groups but a decrease was seen in the TPA group. Six weeks (vitamin A and TPA groups) or 12 weeks (turpentine group) after the completion of treatment the epithelium had a normal histological appearance. No differences between the control or EPP treated cheek pouch mucosa could be detected. Turpentine and vitamin A can be used as models of reversible hyperplasia in the hamster cheek pouch.

Lesions induced in hamster cheek pouch using dimethylbenz(alpha)anthracene were studied by transmission electron microscopy and compared with normal tissue. Features regarded as suggestive of progression towards malignancy were: increased numbers of membrane-bound vesicles in basal cells, gaps in the lamina densa associated with widening of the lamina lucida and an irregular epithelial-connective tissue junction, the presence of cerebriform cells and frequent close association of 2 or more intra-epithelial cells (lymphocytes, cerebriform cells, Langerhans cells).

A report of an aggressive, peripheral nerve-sheath tumour that presented as a lump on the alveolar mucosa near the mental foramen is presented. Although the tumour was detected in the periphery and appeared to extend centrally, extensive surgery suggested that the tumour had its origins in the infra-temporal fossa.

Mucosa from the hard and soft palates, molar gingiva, cheek and dorsal surface of the tongue of the rat was examined in the light microscope, following Mallory's triple connective tissue stain, and in the scanning and transmission electron microscopes. The epithelium covering the hard palate, gingiva, the smooth band of mucosa at the junction of the hard and soft palates, intermediate zones of the soft palate, fungiform papilla-like structures in the central zone of the soft palate, the fungiform papillae, and the more superficial part and posterior surfaces of the filiform papillae of the tongue all exhibited complete orthokeratinization. The oral surfaces of the epithelial cells in all these areas had a honeycomb pattern of interconnecting ridges surrounding depressions. Imprints of the overlying cells that had been desquamated were apparent, and the lateral boundaries between the cells were formed by two raised ridges separated by a gap. The epithelium covering the cheek, central zone of the soft palate apart from the fungiform papilla-like structures, lateral zones of the soft palate, gingival crevice, and the mucosa between the fungiform and filiform papillae of the tongue all exhibited incomplete orthokeratinization. The oral surfaces of the epithelial cells in all these areas were relatively smooth and did not exhibit a honeycomb pattern of interconnecting ridges. Imprints of the overlying cells that had been desquamated and the lateral boundaries between the cells were only very occasionally found. In the transmission electron microscope the outlines of the cells were compatible with the surface patterns seen in the scanning electron microscope. The possible relationships between the degree of orthokeratinization and ultrastructure of the various epithelia are discussed.

The supeerficial and deep surfaces of the cells of the stratum corneum from the hard palate of the rat were examined in the scanning electron mictroscope. The appearances were compared with those seen in thin sections. In the scanning electron microscope, the superficial surface of each epithelial cell, whether it was situated on the exposed surface or more deepley within the epithelium, had a honeycomb surface pattern of inteerconnecting ridges surrounding depressions. Lateral cell boundaries consisted of two ridges separated by a gap, and the imprints of the edges of the overlying cells were formed by single raised ridges which crossed on to adjacent cells. The deep surface of the cells was covered by microvilli, a deepo groove separated teh margins of adjacent cells, and the imprints of the cell boundaries of the underlying cells were formed by shallower grooves which also crossed on to adjacet cells, The sectionaal appearance of the stratum corneum, as seen in the transmissison electron microscope, confirmed that the cells at different levels overlapped. It also confirmed that the microvilli and grooves on teh deepo surface of the cells were truly complementary and intimately related to the depressions and ridges on the superficial surfaces of opposing cells.

Oral hairy leukoplakia is generally found only in HIV-seropositive individuals or in those who are at risk of developing this infection; its occurrence is accepted to be a reliable predictor for the development of AIDS in those patients who are not already suffering from this disease. This report describes an 18-year-old male who was proven to be HIV-seronegative, was not in any of the at-risk groups associated with this infection, but who had the typical features of oral hairy leukoplakia, clinically and histologically. In such individuals these lesions should be described as hairy leukoplakia-like lesions.

The effects of four different hyperplastic agents and of the carcinogen DMBA on cytokeratin expression in hamster cheek pouch epithelia were compared. Reversible hyperplasia was produced by the application of either oil of turpentine, vitamin A or TPA. No hyperplastic changes were produced by application of EPP. Apart from the transient appearance of a 45 kDa cytokeratin in one group treated with vitamin A, the immunohistochemical staining patterns and immunoblot profiles of cytokeratins from cheek pouches treated with each of the hyperplastic agents were identical to controls. Following application of DMBA, the cytokeratins stained with increased intensity in the spinous and granular cell layers. This was associated with increased amounts of 42-56 kDa cytokeratins and decreased production of 62-75 kDa cytokeratins. Monoclonal antibody AE1 detected a 45 kDa cytokeratin in extracts of DMBA-treated epithelia that was not detected in untreated epithelial extracts. Monoclonal antibody AE3 detected an additional 54 kDa cytokeratin band in extracts of DMBA-treated epithelia. These cytokeratin changes were present in preneoplastic epithelia and maintained in neoplastic epithelia.