Comparison of acetaminophen, ibuprofen, and nabumetone therapy in rats with pulpal pathosis.

The purpose of this study was to determine if daily treatment with acetaminophen, ibuprofen, or nabumetone would alter prostaglandin E2 (PGE2)/leukotriene B4 (LTB4) synthesis in exposed, infected dental pulp and periradicular tissue in rats. Dental pulp of the bilateral first and second mandibular molars were exposed for 15 or 24 days. Rats were divided into four groups. A daily pharmacological oral dose of one of the medications or the suspending solution alone was administered to the designated group. Eicosanoids were extracted from pulpal and periradicular tissues and assayed. PGE2 was significantly elevated in pulp-exposed, nontreated rats and was significantly reduced in the ibuprofen- and nabumetone-treated groups. LTB4 was significantly increased in all pulp-exposed groups at 15 days when compared with control nonexposed groups. Results showed that only ibuprofen reduced LTB4 in the exposed dental pulp at 24 days, although it did not do so at 15 days. Repetitive treatment with acetaminophen did not suppress PGE2/LTB4 in pulp-exposed molars.

Expression of blood group-related glycoconjugates in the junctional and other oral epithelia of rodents.

BACKGROUND: The junctional epithelium (JE) attaches the gingiva to the non-vital tooth surface and has other unusual properties which protect the underlying periodontal tissues. The JE differs from other gingival and oral epithelia in its unusual expression of cytokeratins typical of both stratifying and of simple epithelia, a phenotypic pattern possibly related to its specialized functions. METHODS: The patterns of differentiation of rodent gingival and other epithelia were examined using monoclonal antibodies against various glycoconjugates which are expressed on epithelial cell surfaces and provide an alternative marker system for regionally-differing patterns of cell maturation. RESULTS: Markers that are typical of basal cells in other stratifying epithelia were expressed by all cell strata of JE. JE lacked differentiation markers typical of other stratifying oral epithelial but showed suprabasal expression of markers typically expressed by simple epithelia and specialized epithelia, such as taste buds. CONCLUSIONS: The phenotype of rodent JE differs from that of other oral epithelia and the pattern of differentiation assessed by its expression of glycoconjugates parallels that for other phenotypic markers, such as cytokeratins. Differentiation of rodent JE is similar to that of human JE. The functional significance of these patterns of expression is not yet clear but the markers characterizing this unusual epithelium in rodents may be associated with its behavior in periodontal disease and of value to experimental studies of its development.

Influence of connective tissues on the in vitro growth and differentiation of murine epidermis.

Various experiments indicate that normal growth and differentiation of murine epithelia in vivo are dependent on dermal influences, and the growth-enhancing effects of various connective tissue elements have also been demonstrated in vitro. Such effects were examined by the in vitro growth of murine epidermis on various substrata (collagen, lens capsule) at the air/medium interface with various connective tissue elements or cells apposed to the undersurface of the supporting matrix. Patterns of epithelial growth, morphology and differentiation were examined by histology, electron microscopy, gel electrophoresis and antibody staining. Growth and differentiation varied with differing substrata but good patterns of growth and morphology, and appropriate expression of cytoplasmic and cell surface differentiation markers, were found only in specimens grown in association with dermal elements. It is concluded that diffusible factors of dermal origin facilitate epithelial growth and differentiation.

Keratin expression in taste bud cells of the circumvallate and foliate papillae of adult mice.

The patterns of keratin expression of taste buds in murine oral mucosa were examined using a panel of antibodies with various specificities for cytokeratins. The patterns for taste buds differed markedly from those of the surrounding epithelium but no regional differences in the staining patterns of the taste buds themselves were detected. The taste buds and the ducts of von Ebner's glands were strongly stained by monoclonal antibodies (mAbs) against cytokeratins (K) 8, 18 and 19, those typically expressed by simple epithelia. Merkel cells, which are also present in the oral epithelium and may correspond to the type III cells in taste buds, stained for K8 and K18 but not K19. None of the mAbs against simple epithelial keratins stained the stratifying epithelium of the trench wall or of the oral mucosa. Antibodies with specificity for keratins that are expressed as differentiation products of the mucosal epithelium did not stain taste buds. The staining pattern of the epithelium of the trench wall indicated that it expressed some keratins typical of stratifying epithelia but lacked the full pattern of differentiation of the adjacent mucosal epithelia. Staining within the taste buds was not homogeneous but no clear differences of keratin staining could be directly related to the subtypes of cells constituting them. The markedly differing patterns of keratin expression between taste buds and the adjacent epithelium raises questions about the type of inductive signals that produce and maintain these patterns.

Patterns of cytokeratin expression in human gingival epithelia.

Specimens of human gingiva were collected from teenage and adult subjects and frozen sections were stained with an extensive panel of monoclonal antibodies with defined specificities for individual cytokeratins. The results indicated different and distinctive patterns of keratin expression by the oral gingival, oral sulcular and the junctional epithelia. It was observed that epithelium with staining characteristics of sulcular epithelium extended over the gingival crest onto the oral surface of the gingiva. Junctional epithelium showed the unusual pattern of co-expression of keratins typical of the stratifying and of the simple epithelial phenotypes. The patterns of gingival keratin expression are compared with those of other mucosal epithelia. The findings are discussed in relation to mechanisms that may determine or influence the junctional epithelial phenotype.

Isolation of subpopulations of murine epidermal cells using monoclonal antibodies against differentiation-related cell surface molecules.

Monoclonal antibodies (mAbs) against epithelial cells were prepared by immunization of rats with lyophilized murine epithelia. Screening against tissue sections and epithelial cell suspensions permitted identification of mAbs against surface molecules that are expressed early in cell differentiation. Staining with these mAbs followed by fluorescence-activated cell sorting enabled isolation of subpopulations of basal epithelial cells. Staining these subpopulations with antibodies against known differentiation markers (cytokeratins and bullous pemphigoid antigen) and measurements of cell size indicated that they represented fractions of the basal cell population in sequential stages of early differentiation. Labeling mice with bromodeoxyuridine at various times prior to cell isolation showed that the least-differentiated basal cells cycle more slowly than those at later stages, data which support the concept of a differentiation-related, hierarchical pattern of organization of the proliferative compartment.

Replacement of Langerhans cells in murine palate.

Palates from C3H mice were implanted onto prepared graft beds in histocompatible F1 hybrid mice. Biopsies taken 1, 2, 4, 8, and 16 wk later were prepared to demonstrate Langerhans cells (LC) of C3H and F1 (host) origin. After 1 wk only occasional LC (all of C3H origin) were present. By 2 wk total LC numbers had increased to a level approximately 50% greater than in control (non-implanted) palate, with most of this increase due to C3H LC proliferation. From 4 through 16 wk total LC numbers were not significantly different from those of control palate. During weeks 2 through 16 the percentages of LC of F1 origin were 31, 70, 39, and 19% respectively. These results indicate an increased proliferation of C3H LC with an initial migration of F1 LC which stops as C3H LC numbers increase.

Age-associated changes in Langerhans cells of murine oral epithelium and epidermis.

Oral mucosa and skin of older individuals are immunologically less responsive to a range of allergens, but it is not known whether this is due to changes in the number of Langerhans cells or to impaired cell function. EDTA-separated epithelial sheets from the cheek and palate mucosa, and from ear aN< footpad skin of three-month-old and 24-month-old C57BL/6NNia mice were stained for ATPase, beta-glucuronidase activity and Iab-surface antigen to demonstrate Langerhans cells. The general distribution of such cells was unchanged with age, but those in epithelia from the old mice were more varied in shape, with irregular celL bodies and more elongated dendritic processes. The numerical density of Langerhans cells in old mice was reduced by 30-59 per cent compared with that in young mice.

Lectin binding to murine oral mucosa and skin.

Carbohydrates on epithelial cell surfaces of oral mucosa and skin from various anatomical regions of C3H mice were demonstrated with fluoresceinated lectins. With an individual lectin, all tissues showed a similar pattern of binding: most lectins showed binding to the cell surfaces of all nucleated cell layers although that to basal cells was often weaker and was occasionally absent. The corneocytes did not typically bind lectins except that the follicular keratin of the tail showed a uniform and intense fluorescence with several lectins. Basement membrane bound all lectins. The results indicate that detectable changes occur in the cell-surface carbohydrate composition as cells differentiate but that cell-surface carbohydrates do not differ markedly from one region to the next. Lectin binding may provide a convenient method of detecting functional changes in normal cells and in cells which have undergone experimental or pathological changes.