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Cell wall-anchored polypeptides of the antigen I/II family are produced by many species of oral streptococci. These proteins mediate adhesion of streptococci to salivary glycoproteins and to other oral microorganisms and promote binding of cells to collagen type I and invasion of dentinal tubules. Since infections of the root canal system have a mixed anaerobic bacterial etiology, we investigated the hypothesis that coadhesion of anaerobic bacteria with streptococci may facilitate invasive endodontic disease. Porphyromonas gingivalis ATCC 33277 cells were able to invade dentinal tubules when cocultured with Streptococcus gordonii DL1 (Challis) but not when cocultured with Streptococcus mutans NG8. An isogenic noninvasive mutant of S. gordonii , with production of SspA and SspB (antigen I/II family) polypeptides abrogated, was deficient in binding to collagen and had a 40% reduced ability to support adhesion of P. gingivalis . Heterologous expression of the S. mutans SpaP (antigen I/II) protein in this mutant restored collagen binding and tubule invasion but not adhesion to P. gingivalis or the ability to promote P. gingivalis coinvasion of dentin. An isogenic afimbrial mutant of P. gingivalis had 50% reduced binding to S. gordonii cells but was unaffected in the ability to coinvade dentinal tubules with S. gordonii wild-type cells. Expression of the S. gordonii SspA or SspB polypeptide on the surface of Lactococcus lactis cells endowed these bacteria with the abilities to bind P. gingivalis , penetrate dentinal tubules, and promote P. gingivalis coinvasion of dentin. The results demonstrate that collagen-binding and P. gingivalis -binding properties of antigen I/II polypeptides are discrete functions. Specificity of antigen I/II polypeptide recognition accounts for the ability of P. gingivalis to coinvade dentinal tubules with S. gordonii but not with S. mutans . This provides evidence that the specificity of interbacterial coadhesion may influence directly the etiology of pulpal and periapical diseases.

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.

A two-year-old boy with S. pneumoniae-associated haemolytic-uraemic syndrome (HUS) was treated with antibiotics and early peritoneal dialysis. The haemolysis and thrombocytopenia improved following a change in transfusion therapy to washed blood products and exchange transfusion. The exchange transfusion was performed after the red cell polyagglutination test had become negative and was associated with a dramatic improvement in haematocrit, platelet count and renal function. We suggest that transfusions of washed blood products (which do not provide anti-T-cryptantigen immunoglobulin) are more effective than standard blood products in this disease. In addition, the combination of early dialysis and appropriately timed exchange transfusion may have contributed to a nearly complete recovery from this potentially lethal form of HUS.

Mucus-producing adenopapillary carcinoma is a rare neoplasm of the oral cavity. The literature is reviewed and a case described, with histological and ultrastructural findings of a tumour which involved the upper lip and recurred following local excision.

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.

Cell surface proteins SspA and SspB in Streptococcus gordonii and SpaP in Streptococcus mutans are members of the antigen I/II family of polypeptides produced by oral streptococci. These proteins are adhesins and mediate species-specific binding of cells to a variety of host and bacterial receptors. Here we show that antigen I/II polypeptides are involved in the attachment of oral streptococci to collagen and that they also determine the ability of these bacteria to invade human root dentinal tubules. Wild-type S. gordonii DL1 (Challis) cells showed heavy invasion of tubules to a depth of approximately 200 microm, whereas the abilities of cells of isogenic mutant strains OB220 (sspA) and OB219 (sspA sspB) to invade were 50 and >90% reduced, respectively. Likewise, wild-type S. mutans NG8 cells invaded dentinal tubules, whereas cells of isogenic mutant strain 834 (spaP) did not. The invasive abilities of strains OB220 and OB219 were restored by heterologous expression of S. mutans SpaP polypeptide in these strains. The extents of tubule invasion by various wild-type and mutant strains correlated with their levels of adhesion to type I collagen, a major component of dentin. Furthermore, S. gordonii DL1 cells exhibited a growth response to collagen by forming long chains. This was not shown by ssp mutants but was restored by the expression of SpaP in these cells. The production of SspA polypeptide by S. gordonii DL1, but not production of SspB polypeptide by strain OB220 (sspA), was enhanced in the presence of collagen. These results are the first to demonstrate that antigen I/II family polypeptides bind collagen and mediate a morphological growth response of streptococci to collagen. These antigen I/II polypeptide activities are critical for intratubular growth of streptococci and thus for establishment of endodontic infections.

The purpose of this study was to evaluate the sheep as a suitable animal model in which to compare periodontal wound healing after surgically induced Class II furcation defects were treated with different guided tissue regeneration (GTR) membranes. 22 mandibular second premolar sites in 11 sheep were used. The experimental design included untreated control teeth, sites treated by surgery alone, and others where surgery included placement of either Gore-Tex Periodontal Material (GTPM) or Gore-Tex Soft Tissue Patch (GTSTP). Sheep were killed 7 wk after surgery. Mesiodistal sections through decalcified second mandibular premolars were evaluated histologically. Histomorphometric analysis of digitized images allowed both area and linear measurements of newly regenerated furcal tissues. Percentage areas of cementum, bone, epithelium and connective tissue filling the furcation region were calculated. Coronal regeneration of alveolar bone and cementum were expressed as a percentage of the original height of the defect. Mean values for each group were subsequently analysed by 1-way ANOVA. Significantly greater regeneration was achieved with both of the GTR membranes, by comparison with the non-GTR surgical control group, with respect to percentage areas of cementum, bone and connective tissue, and the linear measurement of cementum (p < or = 0.05). This study demonstrates successfully the use of the sheep animal model for GTR research, and shows that few differences exist between GTR healing when either GTPM or GTSTP is used in the treatment of class II furcation defects.

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.

A clinical study determined the whitening effect of a 10 percent carbamide peroxide gel on the teeth of 10 subjects. Histological evaluation of the effect of this agent on human tooth pulps and hamster cheek pouch tissues was also undertaken. The gel provided a modest, but unpredictable, whitening of discoloured teeth. A localised mild to moderate inflammatory response was found in some of the pulps of teeth that had been bleached. No soft-tissue changes were observed in the hamster cheek pouches.

Temporalis muscle flaps were evaluated in sheep. Flaps placed following discectomy were examined at 2, 4, 12, and 24 weeks. Histologic evaluation showed avascular necrosis and subsequent displacement and loss of tissue from the joint resulting in close contact between the condyle and fossa. Muscle flaps placed lateral to the joint in operative controls were examined at 4, 12, and 24 weeks. This muscle remained viable while undergoing fibrous replacement. Although the surface layers of the condyle and fossa were initially lost, the tissues were reformed with time. This experiment showed that in the sheep, temporalis muscle does not withstand functional loading within the joint. However, despite the lack of interpositional material, the condyle and fossa can remodel.

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.

A 42-year-old female presented with a 2.5 cm symptomless swelling on the left lateral surface of the tongue. Histologically, there were large, often pleomorphic, fibroblast-like and histiocyte-like cells, multinucleate giant cells and cells of variable morphology. Many of the cells had abundant vesicular cytoplasm. There were also aggregations of neutrophilic or eosinophilic leukocytes, or both. The cells in some areas formed a fascicular or storiform pattern, or both. Ultrastructurally, the vesicular appearance was due mostly to markedly dilated endoplasmic reticulum, but many of the neoplastic cells contained some lipid. There were some myofibroblasts and a few xanthofibroblasts. The cells of variable morphology had many of the ultrastructural features of the fibroblast and histiocyte-like cells. There were also some small undifferentiated cells with minimal cytoplasm. These ultrastructural features confirmed the histological diagnosis of malignant fibrous histiocytoma.

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.