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1. |
Permeability of rodent junctional epithelium to exogenous protein |
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Journal of Periodontal Research,
Volume 23,
Issue 2,
1988,
Page 81-86
A. W. Romanowski,
C. A. Squier,
C. A. Lesch,
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摘要:
It has generally been assumed that oral sulcular epithelium, being nonkeratinized, is a vulnerable region which allows bacterial products to pass from the gingival sulcus to the subjacent connective tissue. It has also been suggested that inducing keratinization of the oral sulcular epithelium might create a better barrier to such material. However, this approach ignores the effect of a permeable junctional epithelium, for if exogenous material penetrates this epithelium then the presence of keratinization may be unimportant. Rats possess an orthokeratinized oral sulcular epithelium and so represent what might be considered as an ideal sulcus lining. The protein tracers horseradish peroxidase or microperoxidase were instilled into the gingival sulcus of anesthetized rats. After 1 h, the animals were killed and fixative applied topically and by perfusion. The mandibles were detached, decalcified in EDTA to permit removal at the gingival attachment and sectioning, reacted with diaminobenzidine and H2O2to visualize the tracer, and prepared for light and electron microscopic examination. Controls consisted of: a) animals that had not been treated with horseradish peroxidase, and b) horseradish peroxidase‐treated animals incubated without H2O2. Microscopic examination revealed penetration of the tracers through the junctional epithelium and into the underlying connective tissue, but never through the adjacent oral sulcular and gingival epithelium. These results suggest that material placed in the sulcus can enter the connective tissue via the junctional epithelium even when the adjacent oral sulcular epithelium forms a keratinized barrie
ISSN:0022-3484
DOI:10.1111/j.1600-0765.1988.tb01338.x
出版商:Blackwell Publishing Ltd
年代:1988
数据来源: WILEY
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2. |
Gingival tissue‐produced inhibition of platelet aggregation and the loss of inhibition in streptozotocin‐induced diabetic rats |
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Journal of Periodontal Research,
Volume 23,
Issue 2,
1988,
Page 87-90
Keiichiroh Kawamura,
Toshihiro Dohi,
Kazuharu Tamal,
Masaharu Shirakawa,
Hiroshi Okamoto,
Akira Tsujimoto,
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摘要:
Addition of medium incubated with normal rat gingival tissue to platelet‐rich plasma inhibited ADP‐induced platelet aggregation. The ability of rat gingiva to produce activity inhibiting platelet aggregation was enhanced by the addition of arachidonic acid. Diabetic rat gingiva failed to inhibit platelet aggregation but did produce the anti‐platelet aggregating activity in the presence of arachidonic acid. Indomethacin blocked the production of anti‐platelet aggregating activity. There was no difference in conversion of [1‐14C]arachidonic acid to prostaglandins by normal and diabetic rat gingiva. These results suggest that an arachidonic acid metabolite released from gingiva during incubation inhibits platelet aggregation, and the synthesis of the metabolite is impaired in diabetic rat gingiva. A decrease in availability of arachidonic acid may be a causal factor of the defect in diabetic ra
ISSN:0022-3484
DOI:10.1111/j.1600-0765.1988.tb01339.x
出版商:Blackwell Publishing Ltd
年代:1988
数据来源: WILEY
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3. |
Culture and characterization of rat junctional epithelium |
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Journal of Periodontal Research,
Volume 23,
Issue 2,
1988,
Page 91-99
Leonard C. Altman,
Caron L. Nelson,
Brian Povolny,
Philip Fleckman,
Beverly A. Dale,
Ronald V. Maier,
Carl Soderland,
Coralle Baker,
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摘要:
Junctional epithelium, which forms the interface between the gingival tissues and the teeth, is a unique nondifferentiating, nonkeratinizing simple epithelium with essentially no gradient of cytoplasmic alterations. The purpose of this study was to develop methods for obtaining and culturing junctional epithelial cells and characterizing these cells with monoclonal antibodies and by keratin analysis. Microsurgical methods were developed to obtain pure specimens of junctional epithelium from the interproximal molar regions of pathogen‐free rats. Specimens of palatal and free gingival epithelia were also taken. The tissue explants were cultured by three methods; an explant technique using 3T3 fibroblasts as feeder cells, a procedure which used cloning rings to isolate primary epithelial outgrowths, and growth in small chambers coated with solubilized basement membrane. Specimens from the three oral epithelia grew well by all methods and appeared homogenous by phase contrast microscopy. Immunocytochemical analysis of fresh specimens by antikeratin antibody staining showed differences in the staining patterns of the three oral epithelia and suggested the absence of 54 and 40 kD keratins from these tissues. Junctional, palatal and gingival epithelial cells grown by the cloning ring technique stained positively with the monoclonal antibody 34βE12 which stains all stratified epithelia and identifies 66 and 57 kD keratins, but failed to stain with antibodies to vimentin and desmin which are intermediate filament proteins in mesenchymal and muscle cells, respectively, Junctional epithelial cells grown on solubilized basement membrane showed positive staining with antidesmoplakin antibodies I and II, which identify desmosomal plaque proteins, and negative staining with the keratin‐specific monoclonal antibody AE2. Gingival cells grown by the same technique had the opposite staining pattern with these antibodies. Cells grown by the 3T3 feeder cell method were analyzed for their cytokeratin content by SDS polyacrylamide gel electrophoresis and immunoblotting using the keratin‐specific monoclonal antibodies AEl and AE3. The keratin patterns in freshly explanted tissues all differed, indicating that these oral epithelia are indeed different in vivo. Further, the keratin patterns in extracts of subconfluent and confluent cultured oral epithelial cells differed from those in the freshly isolated tissues, but were similar for the different epithelia. Specifically, subconfluent cultures of the three epithelia had identical keratin patterns, but differed from those of confluent cultures which were themselves identical. This report presents methods for obtaining and culturing junctional epithelium, and data which indicate that junctional cells differ from other oral epithelia in cytokeratin and desmosomal protein compo
ISSN:0022-3484
DOI:10.1111/j.1600-0765.1988.tb01340.x
出版商:Blackwell Publishing Ltd
年代:1988
数据来源: WILEY
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4. |
Investigation of the distribution of cementum‐associated lipopolysaccharides in periodontal disease by scanning electron microscope immunohistochemistry |
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Journal of Periodontal Research,
Volume 23,
Issue 2,
1988,
Page 100-106
F. J. Hughes,
D. W. Auger,
F. C. Smales,
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摘要:
Previous work in our laboratory has suggested that cementum‐associated LPS is confined to the surface of affected roots. In order to localize the distribution of cementum‐associated LPS more precisely, an immunogold/silver labelling system has been utilized to demonstrate LPS on scanning electron microscope images of scaled, extracted teeth. With this technique, antibody binding to the specimen is detected by electron probe X‐ray microanalysis of the bound silver label. Most of the detectable LPS was found to be associated with bacteria and calculus which persisted on the root surface despite the scaling of the specimens. Smaller amounts of bound LPS were also detected on the cuticle and surface cementum layers of the affected root surfaces, but in places where some of the underlying cementum had been removed no LPS was detected. These results cast some doubt on the importance of the removal of cementum‐bound endotoxins in the treatment of periodontal disease. From these results it is postulated that the principal therapeutic effect of extensive cementum removal by root planing is that it facilitates the removal of plaque and calculus from resorption lacunae, which were a prominent feature of the affected root s
ISSN:0022-3484
DOI:10.1111/j.1600-0765.1988.tb01341.x
出版商:Blackwell Publishing Ltd
年代:1988
数据来源: WILEY
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5. |
Progenitor cell kinetics during guided tissue regeneration in experimental periodontal wounds |
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Journal of Periodontal Research,
Volume 23,
Issue 2,
1988,
Page 107-117
J. Iglhaut,
I. Aukhil,
D. M. Simpson,
M. C. Johnston,
G. Koch,
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摘要:
The present investigation compared the premitotic labelling of cells in the bone and periodontal ligament (PDL) compartments apical to a surgically created fenestration wound containing a “periodontal space.” Buccal fenestration wounds (3x3 mm) were made at midroot level in 4Macaca fascicularismonkeys. The exposed root surfaces were planed and a piece of millipore filter was placed over each fenestration prior to flap replacement. Wounding in the different dentition segments and sacrifice of monkeys were scheduled to provide observation periods of I h I, 2, 3, 7 and 21 d in each monkey. One hour prior to sacrifice, tritiated thymidine (1 μCi/gm body weight) was administered intravenously. Autoradiographs were used to determine the labeling index (L.I.) of fibroblast‐like cells in each of the three following histologic compartments: PDL, alveolar bone adjacent to the apical border of the fenestration, and the wound proper. No significant differences in the L.I. between the bone and PDL tissue compartments were noted for nearly all of the observation periods. L.I. in the PDL peaked at 2 d while the alveolar bone demonstrated two peaks of activity, one at 2 d and the other at 7 d. Labeled cells first appeared at the edge of the wound proper at 3 d. At 7 d, labeled cells were noted throughout the wound compartment indicating continued activity of migrated cells. The 21‐d specimens demonstrated a few labeled cells in the wound compartment and a reduction of mitotic activity in the adjacent PDL and bone compartments to almost normal levels. The results of the present investigation suggest that both the bone and PDL tissue compartments supply cells to a periodontal wound containing a surgically created periodontal space. Moreover, some of the cells which migrate into the potential space formed by the physical barrier continue to prepare for mitosis as they
ISSN:0022-3484
DOI:10.1111/j.1600-0765.1988.tb01342.x
出版商:Blackwell Publishing Ltd
年代:1988
数据来源: WILEY
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6. |
Regulation of collagen production in fibroblasts cultured from normal and phenytoin‐induced hyperplastic human gingiva |
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Journal of Periodontal Research,
Volume 23,
Issue 2,
1988,
Page 118-121
A. S. Narayanan,
D. F. Meyers,
R. C. Page,
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摘要:
We have studied how collagen production is regulated in fibroblasts obtained from normal and phenytoin‐induced hyperplastic human gingiva. Collagen production was determined as collagenase digestible radioactivity and degradation was examined by adding labelled procollagen to the cultures and by pulselabelling in the presence of lysosomal inhibitors. Collagen mRNA levels were measured using a [35S]‐UTP labelled proα[1]probe. The normal and phenytoininduced fibroblasts did not degrade collagen extracellularly and lysosomal inhibitors did not enhance collagen production in either culture. Collagen production by the cultures correlated with mRNA levels, and in 2 of 3 phenytoin‐induced fibroblasts, which produced more collagen than other cells. collagen mRNA levels were higher. We conclude that collagen production in gingival fibroblasts is primarily regulated by the mRNA levels and that overproduction of collagen by cells from phenytoin‐induced hyperplastic gingiva results from an increased steady state level of collagen mRNA and not decreased collagen deg
ISSN:0022-3484
DOI:10.1111/j.1600-0765.1988.tb01343.x
出版商:Blackwell Publishing Ltd
年代:1988
数据来源: WILEY
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7. |
Polyclonal induction of IgG antibody forming cells by stimulation withActinomycesviscosus T14V |
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Journal of Periodontal Research,
Volume 23,
Issue 2,
1988,
Page 122-126
Yasushi Harada,
Hiro‐o Ito,
Yasuo Miki,
Shigeyuki Ebisu,
Hiroshi Okada,
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摘要:
Actinomyces viscosushas been shown to possess the potential for polyclonal B cell activation (PBA), but this activation mechanism is still not well understood. In this report, the T cell and/or macrophage requirement for PBA and the development of IgG producing plasma cells were investigated in the murine system by using an ultrasonicated extract from A.viscosusT14V (Av. sup). The results were as follows: 1. Av.sup activated B cells polyclonally without any participation of T cells and macrophages. 2. Av.sup could induce IgG as well as IgM antibody forming cells (AFC) polyclonally. IgG AFC were induced from surface IgG‐positive (sIgG+) B cells (memory B cells, which had been immunized with antigens), but not from sIgG−B cells. Therefore, circulating memory B cells may be activated by microbial components at periodontally diseased sites and these may contribute to the formation of an IgG‐producing B cell‐rich
ISSN:0022-3484
DOI:10.1111/j.1600-0765.1988.tb01344.x
出版商:Blackwell Publishing Ltd
年代:1988
数据来源: WILEY
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8. |
Re‐epithelialization of a palatal connective tissue graft transplanted in a non‐keratinized alveolar mucosa: A histological and biochemical study in humans |
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Journal of Periodontal Research,
Volume 23,
Issue 2,
1988,
Page 127-133
J. P. Ouhayoun,
M. H. Sawaf,
J. C. Goffaux,
D. Etienne,
N. Forest,
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摘要:
This study was undertaken to evaluate the type of tissue obtained after transplantation of a connective tissue graft, from the same palatal donor site, into a non‐keratinized oral mucosa in humans. In 6 human volunteers, a thick palatal epithelio‐connective tissue graft was excised, split into two thinner grafts (a thin epithelio‐connective tissue graft and a connective tissue graft) and transplanted into controlateral areas lacking keratinized gingiva. The biopsies, excised 3 months post‐operatively, were examined using routine histology, immunofluore‐scence techniques with different anticy to keratin antibodies and biochemical techniques with non‐equilibrium two‐dimensional gel electrophoresis. The results show that the epithelio‐connective tissue grafts display the histological and biochemical characteristics of keratinized gingiva, whereas the connective tissue grafts expressed features belonging both to keratinized and non‐keratinized gingival tissues. It is concluded that the deep palatal connective tissue does not have the full potential to induce non‐keratinized epithelial cells to keratinize and that a gingival or palatal connective tissue graft without its overlying epithelium is not likely to yield genui
ISSN:0022-3484
DOI:10.1111/j.1600-0765.1988.tb01345.x
出版商:Blackwell Publishing Ltd
年代:1988
数据来源: WILEY
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9. |
Indomethacin or flurbiprofen treatment of periodontitis in beagles: Effect on crevicular fluid arachidonic acid metabolites compared with effect on alveolar bone loss |
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Journal of Periodontal Research,
Volume 23,
Issue 2,
1988,
Page 134-138
R. C. Williams,
S. Offenbacher,
M. K. Jeftcoat,
T. H. Howell,
H. G. Johnson,
C. M. Hall,
W. J. Wechter,
P. Gotdhaber,
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摘要:
The effect of two non‐steroidal anti‐inflammatory drugs, indomethacin and flurbiprofen, on the progression of alveolar bone loss and on the crevicular fluid (CF) levels of four arachidonic acid metabolites was compared in 16 beagle dogs over a 12‐month period. Standardized radiographs were used to measure the rate of bone loss. Radioimmunoassay was used to measure CF levels of PGE2, PGF2α, TxB2and 6K‐PGF1α. Following a 6‐month pretreatment baseline period, 5 dogs were dosed daily with 1.0 mg/kg indomethacin, 5 dogs were dosed daily with 0.02 mg/kg flurbiprofen, and 6 dogs were dosed with empty gelatin capsules for a 6‐month period. With the administration of either indomethacin or flurbiprofen. the CF levels of PGE2, PGF2α, and TxB2were similarly significantly decreased; 6K‐PGF1αlevels were not altered. Indomethacin and flurbiprofen did not have a similar effect on reducing the rate of alveolar bone loss. Flurbiprofen significantly decreased rate of bone loss from baseline whereas indomethacin did not. The data indicate that indomethacin and flurbiprofen inhibit CF arachidonic acid metabolite levels in a similar manner, but not rate of bone loss. The data suggest that flurbiprofen's striking effect on inhibiting rate of bone loss cannot be solely attributed to simple cyclooxygenase inhibition with a reduction in CF pro
ISSN:0022-3484
DOI:10.1111/j.1600-0765.1988.tb01346.x
出版商:Blackwell Publishing Ltd
年代:1988
数据来源: WILEY
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10. |
The effect of interleukin‐1 β on hyaluronic acid synthesized by adult human gingival fibroblastsin vitro |
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Journal of Periodontal Research,
Volume 23,
Issue 2,
1988,
Page 139-147
P. Mark Bartold,
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摘要:
The effect of recombinant interleukin‐1β (IL‐lβ) on hyaluronic acid synthesis by human gingival fibroblasts was studied. IL‐1bT caused a dose‐dependent increase in the incorporation of (3lucosamine into hyaluronic acid. The35S/35H ratios of labeled macromolecules did not change regardless of the presence or absence of TL‐lβ and indicates stimulation of hyaluronic acid synthesis. Inhibition of cell proliferation by hydroxyurea caused an increase in hyaluronic acid synthesis. The effect of IL‐1β on hyaluronic acid synthesis in the presence of hydroxyurea was increased over untreated and IL‐lβ‐treated controls, but equivalent to the hydroxyurea‐treated controls. Thus the effect of IL‐1β on hyaluronic acid synthesis may be independent of cell proliferation. Furthermore, inhibition of prostaglandin E2 synthesis by indomethacin abolished the effect of IL‐1β on hyaluronic acid synthesis. Inhibition of new protein synthesis by cycloheximide negated the effect of IL‐β on hyaluronic acid synthesis. This may be related to inhibition of new hyaluronate synthetase synthesis, since IL‐1β stimulated the level of hyaluronate synthetase activity. Sepharose CL‐2B chromatography revealed that most of the newly synthesized hyaluronic acid was of large molecular size. The cells exposed to IL‐1β retained more large molecular size hyaluronic acid in their cell layer environment than did the control cells. These responses by fibroblasts to IL‐1
ISSN:0022-3484
DOI:10.1111/j.1600-0765.1988.tb01347.x
出版商:Blackwell Publishing Ltd
年代:1988
数据来源: WILEY
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