摘要:

Phenotypic differences existin vivabetween junctional (JE) and oral gingival (OGE) epithelia and anin vitrosystem has been developed that maintains phenotypic differences. This system, which permitsin vitrostudies of factors that may influence the epithelial phenotype, was used to investigate the effects of retinoic acid (RA) on epithelial expression of various markers known to distinguish JE from OGE. Primary cultures of JE and OGE were initiated from defined gingival regions and were subcultured and grown for 48 h in 96‐well plates or on multiple‐well slides. Control cultures were grown in medium supplemented with delipidized serum and all‐trans RA was added to experimental groups. Other cultures were grown in a defined RA‐free medium. Cultures were examined using monoclonal antibodies against cytokeratins, vimentin, and ICAM‐1 and binding displayed by indirect immunocytochemical staining. Staining reactions were assessed by direct microscopic observation and assayed by spectrophotometric quantitation. The results showed that RA had minor effects on the marker expression of JE but markedly enhanced expression of cytokeratins 8, 18, 19, vimentin and ICAM‐1 in OGE. These markers, which normally distinguish JE from OGE, were expressed at levels approaching or exceeding those of control JE cultures. These observations indicate that RA responsive mechanisms affect the phenotypes expressed by epitheliain vitroand suggest that such mechanisms may be related to the different phenotypic patterns expressed by gingival epith

ISSN:0022-3484    

DOI:10.1111/j.1600-0765.1996.tb00468.x

出版商:Blackwell Publishing Ltd    

年代:1996

数据来源: WILEY

摘要:

Bacteria can indirectly affect the course of periodontal diseases by activating host cells to produce and release inflammatory mediators and cytokines. These mediators and cytokines, manifest potent proinflammatory and catabolic activity and may play key roles in local amplification of the immune response as well as in periodontal tissue breakdown. This study tested the effect ofActinobacillus actinomycetemecomitans (Aa)andCampylobacter rectus (Cr)challenge on PGE2, IL‐1β, IL‐6 and IL‐8 production by human gingival fibroblasts (HGF). Contact‐inhibited HGF were prepared and formalin‐killed bacterial cells (AaJP2, ATCC 29523&33384 and Cr ATCC 33238) at 106‐109were added to the HGF. Culture supernatants were collected at varying time intervals and analyzed for cytokine and mediator content. All concentrations ofAaJP2 and Cr ATCC 33238 suppressed IL‐1β production up to approximately 50% during the initial 3‐12‐h period. No bacterial concentration tested was able to increase IL‐1β production above the maximum basal levels. Both bacterial species stimulated production of IL‐6 and IL‐8.AaJP2 did not affect PGE2levels significantly, whereasCrATCC 33238 was stimulatory only at the highest concentration tested (109). There were no significant differences among the threeAastrains with respect to IL‐1β production. However, Aa ATCC 29523 and ATCC 33384 were less capable of stimulating IL‐6 secretion and more efficient in stimulating. IL‐8 production than Aa JP2. In general. Cr was the most potent enhancer of cyto‐kine and mediator production by HGF. In conclusion,AaandCrare capable of amplifying the local immune response and promoting periodontal tissue inflammation by stimulating

ISSN:0022-3484    

DOI:10.1111/j.1600-0765.1996.tb00469.x

出版商:Blackwell Publishing Ltd    

年代:1996

数据来源: WILEY

摘要:

Cigarette smoking is a major risk factor in the development and further progression of periodontitis. However, little is known regarding the pathogenesis of smoking‐related periodontal diseases. The purpose of this study was to examine the effects of nicotine, alone and in combination with lipopolysaccharide (LPS), on monocyte secretion of bone‐resorbing factors, PGE2and IL‐1β. Peripheral blood monocytes (PBM) were isolated by counterflow centrifugal elutriation from 15 healthy, non‐smoking donors. PBM were incubated for 24 h in RPMI 1640 containing nicotine (0, 50 μg/ml, I μg/ml, 10 μg/ml and 100 μg/ml) with or without 10 μg/mlPorphyromonas gingivalisLPS orEscherichia coliLPS. Culture supernatants were assayed for PGE2and IL‐1β by ELISA. None of the nicotine preparations resulted in significant PBM secretion of PGE2and IL‐1β above that of unstimulated cultures. However, PGE2release was potentiated 1.7‐fold by the combination of P. gingivalis LPS and 10 μg/ml nicotine relative toP. gingivalisLPS alone (p<0.05, one‐way ANOVA). Prostaglandin E3release also was potentiated 3.5‐fold byP. gingivalisLPS and 100 μg/ml nicotine relative toP. gingivalisLPS alone (p<0.00001, one‐way ANOVA) and 3.1‐fold byE. coliLPS and 100 μg/ml nicotine relative toE. coliLPS alone (p<0.00001, I. one‐way ANOVA). IL‐1β secretion was lower for either LPS plus 100 μg/ml nicotine relative to LPS alone, although not significantly. These data demonstrate upregulation of LPS‐mediated monocyte secretion of PGE2by nicotine and suggest a potential role for nico

ISSN:0022-3484    

DOI:10.1111/j.1600-0765.1996.tb00470.x

出版商:Blackwell Publishing Ltd    

年代:1996

数据来源: WILEY

摘要:

Tenascin is a large oligomeric glycoprotein of the extracellular matrix that is expressed prominently during embryonic development and wound healing. Previous studies on tenascin expression in wounds have used immunohistochem‐istry to describe the expression of tenascin in wounds. The present study used in situ hybridization to identify the cells expressing tenascin mRNA in healing wounds. The results demonstrate that the cells of the basal layer of epidermis, migrating over the heating wound, are expressing the mRNA for tenascin. Intense expression was seen during the first three days after wounding, but after seven days, after the epithelium had grown to cover the wound, no tenascin transcripts were seen in epithehall cells. The epithelial cells elsewhere in the skin were devoid of tenascin transcripts at all stages examined. Previously, prominent immunohistological staining for tenascin has been located in wounds bellow the emigrating epithelial cells and it has been thought to be synthesized by stromal cells upon epithelial induction. Our findings in the present study indicate that tenascin is produced by epithelial cells, which apparently are induced to produce tenascin as they migrate after woundin

ISSN:0022-3484    

DOI:10.1111/j.1600-0765.1996.tb00471.x

出版商:Blackwell Publishing Ltd    

年代:1996

数据来源: WILEY

摘要:

We studied histamine‐induced Ca2+mobilization in human periodontal ligament (HPDL) cells. Histamine induced a transient rise in intracellular Ca2+([Ca2+]i) and maintained a sustained phase in the presence of extracellular Ca2+. In the absence of extracellular Ca2+, the transient peak was slightly reduced and the sustained phase was decreased to the basal level. The initial rise in [Ca2+]iwas attributed to two components: intracellular Ca2+release and Ca2+influx, whereas the sustained phase was due to Ca2+influx. After depletion of intracellular Ca2+stores with thapsigargin, a known Ca2+‐ATPase inhibitor, histamine‐induced increase in [Ca2+]iwas significantly reduced, suggesting histamine induces Ca2+release from inositol 1,4,5‐trisphosphate [Ins(l,4,5)P3]‐ and thapsigargin‐sensitive Ca2+stores. Histamine‐induced peak in [Ca2+]iwas increased dose‐dependently in the presence and absence of extracellular Ca2+. The histamine‐mediated response in [Ca2+]iwas specifically attenuated by chlorpheniramine (H1antagonist) but not by cimetidine (H2antagonist), clearly indicating that activation of H1receptor mediates histamine‐induced Ca2+mobilization. We next examined the effect of histamine on inositol phosphates formation. Histamine stimulated the formation of inositol phosphates which changed time‐dependently. In particular, the formation of Ins(1,4,5)P3was increased significantly for 10 s. The histamine‐induced Ca2+mobilization caused an increase of prostaglandin E2(PGE2) release which was reduced in excluding extracellular Ca2+. These results indicate that activation of histamine H1receptor induces the accumulation of Ins(l,4,5)P3and the following transient increase in [Ca2+]i, and elicits the release of PGE2which may be

ISSN:0022-3484    

DOI:10.1111/j.1600-0765.1996.tb00472.x

出版商:Blackwell Publishing Ltd    

年代:1996

数据来源: WILEY

摘要:

Saline extraction of the periodontopathic bacterium,Actinobacillus actinomycetemcomitans, releases surface‐associated material (SAM), a complex mixture of proteins and carbohydrates with potent biological actions on isolated bone and on various mammalian cell populations. In this study, the relative ability of the SAM from 5 organisms, implicated in the pathology of periodontal disease, to stimulate human mesenchymal and myelomonocytic cells to synthesize the pro‐inflammatory cytokines ‐ interleukin (IL)‐1β, IL‐6 and tumour necrosis factor (TNF)α has been investigated. The bacteria investigated wereActinobacillus actinomycetemcomitans, Eikenella corrodens, Porphyromonas gingivalis, Prevotella intermediaandCampylobacter rectus. Human cells were exposed to a four log order range of concentrations of the SAM, or of Escherichia coli lipopolysaccharide, to provide full agonist dose responses in order to allow comparison of the potency and efficacy of each SAM, All SAMs demonstrated the capacity to stimulate human gingival fibroblasts (HGFs), human peripheral blood mononuclear cells (PBMCs) or the myelomonocytic cell line ‐ Mono‐Mac‐6 to release one or all of the cytokines assayed. Activity was heat‐ and trypsin‐sensitive suggesting that the active components were proteinaceous. However, there were substantial differences in the potency and efficacy of each SAM when compared on a concentration basis (w/v). The most active SAM was fromA. actinomycetemcomitanswith those fromE. corrodensandP. gingivalisbeing slightly less active. The least active cytokine‐stimulating SAMs were fromC. rectusandPr. intermedia. One major difference between the SAMs andE. coliLPS was the inability of the former to stimulate HGFs to release IL‐1β or TNFα although they could stimulate PBMCs to release these cytokines. This may have relevance to the pathology

ISSN:0022-3484    

DOI:10.1111/j.1600-0765.1996.tb00473.x

出版商:Blackwell Publishing Ltd    

年代:1996

数据来源: WILEY

摘要:

Cyclosporine (CsA) is a selective immunosuppressant widely used in clinical therapy. Like phenytoin and nifedipine, the drug is associated with gingival overgrowth. This study considers the interaction of CsA and prostaglandin I2(PGI2), in particular the action of the drug on gingival tissuein vitroandin vivo. The PGI2‐synthesis of rat, rabbit and human gingival tissue was examined by bioassay.In vivoCsA‐therapy reduces gingival PGI2‐synthesis. The results furthermore show a dose‐dependent inhibition of PGI2‐synthesis by CsA (1–100 μg/ml) in vitro. PGI2‐synthesis fromin vivoCsA‐pretreated probes was further dose‐dependently diminished by in vitro addition of CsA. As PGI2exerts an antiproliferative activity via cAMP‐elevation, the drug‐induced inhibition of PGI2production is claimed to be responsible for gingival hyperplasia i

ISSN:0022-3484    

DOI:10.1111/j.1600-0765.1996.tb00474.x

出版商:Blackwell Publishing Ltd    

年代:1996

数据来源: WILEY

摘要:

The aim of the present study was to investigate whether incipient periodontal disease breakdown could be associated with changes in gingival crevicular fluid (GCF) acute‐phase protein levels. In addition, the potential of clinical indices to act as predictors of significant attachment level (AL) change was investigated. AL measurements were taken at baseline and 3 months using the Florida Probe stent handpiece from a total of 384 sites in 38 patients. The average standard deviation of duplicate AL measurements was 0.423. When the tolerance method was used to detect significant AL change, 3.9% of the sites lost attachment. When a less stringent criterion of AL change of ≥1 mm was used 9.9% of the sites lost attachment during the 3‐month period. With the exception of probing depth, baseline clinical parameters failed to predict AL change. Fourteen active periodontitis sites that demonstrated significant attachment loss were paired to stable periodontitis sites within the same patient. The levels of four acute‐phase proteins, namely α2‐macroglobulin (α2‐M), α1‐antitrypsin (α1‐AT), transferrin (TF) and lactoferrin (LF), and also albumin (Alb) were assessed in the same gingival crevicular fluid sample using sandwich ELISAs. Results were expressed either as ng/30 s and ng/μg Alb. Acute‐phase protein levels in GCF failed to differentiate between active and stable periodontitis sites at baseline. In conclusion, the degree of gingival inflammation of the tissues adjacent to the crevice/pocket seems to influence the levels of protease inhibitors and iron‐binding proteins in GCF to a greater extent than

ISSN:0022-3484    

DOI:10.1111/j.1600-0765.1996.tb00475.x

出版商:Blackwell Publishing Ltd    

年代:1996

数据来源: WILEY

ISSN:0022-3484    

DOI:10.1111/j.1600-0765.1996.tb00476.x

出版商:Blackwell Publishing Ltd    

年代:1996

数据来源: WILEY

摘要:

We examined the site specificity of fluoride (F) distribution in human dental calculus. Teeth with supra‐ and subgingival calculus were obtained from patients who resided in non‐fluoridated areas in Japan and China. Sequential layers of the dental calculus (30 μm thick) were abraded by an abrasive micro‐sampling technique and fluoride and phosphorus in the powdered samples were analyzed. Fluoride concentrations were highest in the outer, lowest in the middle and intermediate in the inner layers of dental calculus in general. In the outermost layers fluoride concentrations were highest in calculus found near the tooth cervix both in supra‐ and subgingival calculus. Fluoride concentrations decreased markedly toward the apical region in subgingival calculus. while it did not change toward the incisal or occlusal region in supragingival calculus. In the inner layers, fluoride concentrations in both supra‐ and subgingival calculus were not affected by position on the teeth. Fluoride concentrations in subgingival calculus near the apex were lower than in supragingival calculus near the incisal or occlusal region. It was concluded that the fluoride concentrations differ in different regions of dental calculus, probably due to their different mechanisms of

ISSN:0022-3484    

DOI:10.1111/j.1600-0765.1996.tb00477.x

出版商:Blackwell Publishing Ltd    

年代:1996

数据来源: WILEY