Journal of oral pathology最新文献

Ten biopsies of oral Kaposi's sarcoma were examined histologically and ultrastructurally. Histologically, early and late tumor stages could be differentiated. On the ultrastructural level, endothelial-like and spindle-shaped tumor cells were revealed. Tumor cells associated with vessel-like spaces showed partly interrupted basal membranes, Weibel-Palade bodies, desmosomes and tight-junctions, while spindle-shaped cells lacked these ultrastructural features of endothelial cells. Within the cytoplasm of endothelial-like cells, aggregates of tubular structures were observed. Histological and ultrastructural findings in oral Kaposi sarcoma are comparable to those of such other organs as skin and intestines. The ultrastructural findings indicate an endothelial origin, at least of endothelial-like tumor cells.

Lesions were created in the incisor enamel organs of adult rats by a single dose of tetracycline, and the secretory products in these lesions were examined with the transmission electron microscope. The following abnormal products were found: 1) circumscribed areas of a mottled uncalcified material within the enamel; 2) an uncalcified material consisting of tubules with dimensions similar to the crystal coat of normal enamel, 3) spherical calcified masses which at their periphery resemble normal enamel; 4) layers of a basal lamina-like material in the extracellular spaces between Tomes' processes, and an attachment site-like modification of the cell borders next to this material. It is suggested a) that the enamel tubule is a primary secretory product of the ameloblast; in normal enamel it would support the growth of the crystal; b) that, in the lesion, enamel can grow by diffusion of precursors from distant ameloblasts, while rat enamel normally grows only in direct contact with the ameloblast cell membrane.

Pulpectomies were performed on 22 immature premolars (44 root canals) from 3 young dogs. The root canals remained unfilled and the access cavities were sealed with amalgam. After observation periods of 7, 15 and 45 days, the apical and periapical regions of the teeth were evaluated histopathologically. Hard tissue formation was found in 32 open apices. The apical calcification occurred only in specimens with intracanal vital tissue. The severity of periapical inflammatory response had no relationship to the presence or absence of apical hard tissue formation. No apical bridging was seen in specimens where epithelial proliferation had occurred.

One thousand seven hundred and three consecutive cases from a microscopic slide exchange with 10 institutions were evaluated for extent of agreement (or disagreement) defined as: A) complete agreement (85.8%). B) Disagreement--difference in diagnostic terminology, no significant pathologic or clinical implications (1.4%); C) disagreement--difference in diagnosis with pathologic significance only (7.7%); C1 disagreement--difference in diagnosis with pathologic significance only, radiographic interpretation necessary (1.1%); D) disagreement--major significance for prognosis and/or treatment (4.0%). Trends in disagreement were identified in the following tissue/location categories: mesenchymal lesions, minor salivary gland tumors, odontogenic tumors, fibro-osseous lesions, and benign epithelial lesions. These are discussed in relation to the oral pathology literature. All disagreements with significance for prognosis and/or patient treatment were evaluated retrospectively in an attempt to resolve the disparities. The implications for peer review, continuing education, and teaching programs are addressed.

One of the features of epithelial dysplasia at the histological level is known as "loss of cellular adherence" in which adjacent epithelial cells appear more widely separated from each other than in normal tissues. In this study we examine the effects of the carcinogen DMBA on the epithelium of the hamster cheek-pouch with particular emphasis on the dimensions of the intercellular spaces. DMBA-induced lesions were processed for electron microscopy and assigned to hyperplasia, dysplasia and carcinoma groups, using defined criteria on toluidine blue-stained 1 micron Araldite sections. Untreated pouches were used as a control. At the light-microscopical level, intercellular spaces in hyperplastic epithelium appeared similar to those present in untreated tissue but increased progressively in dysplastic and carcinomatous lesions. Spaces were generally wider between basal and spinous cells than between granular cells, although wide variations were observed between tissue blocks demonstrating similar histological features and also within adjacent areas of the same block. At the ultrastructural level, untreated and hyperplastic tissue showed only occasional focal separations of adjacent plasma membranes; these spaces were more frequent between cells of lower strata. In sections from dysplasias and carcinomas, spaces were always extensive and were occupied by numerous villous or foliate membrane-bound cytoplasmic extensions. These were often attached to each other by desmosomes of apparently normal morphology but of a lower frequency than in untreated epithelium. The increased epithelial separation as indicated by the increased intercellular spaces during chemical carcinogenesis may be a result of any or all of the following factors: desmosomal disruption or their failure to develop; the production of cell-surface molecules which are less adhesive; inflammatory oedema and direct alterations on intercellular junctions and cell-surface components by infiltrating inflammatory cells.

Surface markers of human gingival fibroblasts in vitro were investigated using monoclonal and heterologous antisera against a range of cell surface antigens, together with rosetting techniques to characterize surface receptors for IgG and C3. WI-38 fibroblasts and human peripheral blood monocytes were used as control cells. Human gingival fibroblasts exhibited complement receptors and beta2-microglobulin, as did WI-38 cells. Ten per cent of the human gingival fibroblasts were positive for HLA-DR antigens and additionally exhibited a granulocyte antigen not apparent on WI-38 cells. Monolayers of the gingival fibroblasts were further exposed for short periods to varying concentrations of enzymes (trypsin, collagenase and neuraminidase), bacterial extracts (lipopolysaccharide and lipoteichoic acid) and crude supra- and subgingival plaque sonicates. Surface-marker analysis was then carried out. The most noticeable effects were obtained with Vibrio cholerae neuraminidase which enhanced C3 receptor and surface antigen expression, and supragingival plaque sonicate which depressed the expression of HLA-DR and granulocyte antigens while not affecting beta2-microglobulin expression. Trypsin reduced antigen expression to a degree, but its effects were mainly on cell adherence.