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  • 1
    Electronic Resource
    Electronic Resource
    Osteocalcin, deoxypyridinoline and interleukin-1β in peri-implant crevicular fluid of patients with peri-implantitis (2002)
    Oxford, UK : Munksgaard International Publishers
    Clinical oral implants research 13 (2002), S. 0 
    Details
    ISSN: 1600-0501
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The aim of the present study was to analyze the levels of osteocalcin, deoxypyridinoline (Dpd) and interleukin-1β as markers of bone metabolism in peri-implant crevicular fluid (PICF) from peri-implantitis patients. PICF was sampled from a total of 34 endosseous titanium implants from 16 patients; nine females (mean age 52.8, range 40–62 years) and seven males (mean age 56.0, range 36–66 years). The implants had been in place for a period of 9–112 months (mean; 35.8 months) since the loading. These sites were categorized as six peri-implantitis, eight peri-implant mucositis and 20 healthy implant. PICF volume from peri-implantitis sites was significantly higher than mucositis and healthy implant sites (P 〈 0.01). Osteocalcin levels in PICF from mucositis sites were significantly higher than healthy implants (P 〈 0.05), whereas peri-implantitis sites were not significantly different from either mucositis or healthy implant sites. Dpd could not be detected in any of the samples examined. IL-1β levels in PICF from peri-implantitis sites were significantly higher than levels from peri-implant mucositis (P 〈 0.05) and healthy implant sites (P 〈 0.01). In conclusion, osteocalcin in PICF may reflect increased local bone turnover around implants. Further, IL-1β should be a useful marker for peri-implant inflammation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1034/j.1600-0501.2002.130610.x
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  • 2
    Electronic Resource
    Electronic Resource
    Smoking cessation increases gingival blood flow and gingival crevicular fluid (2004)
    Oxford, UK : Munksgaard International Publishers
    Journal of clinical periodontology 31 (2004), S. 0 
    Details
    ISSN: 1600-051X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Objectives: The purpose of the present study was to determine the effect of smoking cessation on gingival blood flow (GBF) and gingival crevicular fluid (GCF).Material and Methods: Sixteen male smokers (aged 22–39 (25.3±4.0) years), with no clinical signs of periodontal and systemic diseases, were recruited. The experiment was performed before (baseline) and at 1, 3 and 5 days, and at 1, 2, 4 and 8 weeks after smoking cessation. The status of smoking and smoking cessation was verified by exhaled carbon monoxide (CO) concentration, and by serum nicotine and cotinine concentrations. A laser Doppler flowmeter was used to record relative blood flow continuously, on three gingival sites of the left maxillary central incisor (mid-labial aspect of the gingival margin and bilateral interdental papillae). The GCF was collected at the mesio- and disto-labial aspects of the left maxillary central incisor and the volume was calculated by the Periotron 6000® system. The same measurements except for the GBF were performed on 11 non-smoking controls (four females and seven males), aged 23–27 (24.4±1.2) years.Results: Eleven of 16 smokers successfully completed smoking cessation for 8 weeks. At 1 day after smoking cessation, there was a significantly lower CO concentration than at baseline (p〈0.01). Also, nicotine and cotinine concentrations markedly decreased at the second measurement. The GBF rate of smokers was significantly higher at 3 days after smoking cessation compared to the baseline (p〈0.01). While the GCF volume was significantly increased at 5 days after smoking cessation compared to the baseline (p〈0.01), it was significantly lower than that of non-smokers until 2 weeks after smoking cessation (p〈0.01).Conclusion: The results show that the gingival microcirculation recovers to normal in the early stages of smoking cessation, which could activate the gingival tissues metabolism/remodeling, and contribute to periodontal health.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1600-051X.2004.00476.x
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  • 3
    Electronic Resource
    Electronic Resource
    Enamel matrix derivative (EMDOGAIN®) rapidly stimulates phosphorylation of the MAP kinase family and nuclear accumulation of smad2 in both oral epithelial and fibroblastic human cells (2001)
    Copenhagen : Munksgaard International Publishers
    Journal of periodontal research 36 (2001), S. 0 
    Details
    ISSN: 1600-0765
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: In our previous study, we demonstrated that porcine enamel matrix derivative (EMD) induces p21WAF1/cip1 within 8 hours and subsequently arrests the cell cycle of human oral epithelial cells in G1 phase. In contrast, EMD markedly stimulates the proliferation of gingival fibroblasts without inducing p21WAF1/cip1. To investigate the mechanism of how EMD produces these differential effects, we have focused on the initial response of these two cell types to EMD. In epithelial cell cultures, EMD stimulated cytoskeletal actin polymerization within 30 min and promoted cell adhesion within 3 hours, but EMD had no substantial effects on fibroblastic cell adhesion in our experimental system. EMD failed to stimulate either intracellular Ca2+ mobilization or cAMP production in either cell type. In both epithelial and fibroblastic cells, EMD (25–100 μg/ml) rapidly produced dose-dependent phosphorylation of the mitogen-activated protein kinase (MAPK) family: extracellular signal response kinase (ERK), p38-MAPK (p38-K), and c-Jun–terminal kinase/stress-activated protein kinase (JNK). However, neither inhibitors of MEK (ERK kinase) nor p38-K could block EMD’s anti-proliferative action on epithelial cells. On the other hand, EMD rapidly stimulated translocation of smad2 into the nucleus in both cell types. Spurred by this finding, we assayed for TGF-β1, a ligand for one receptor associated with smad2 activation, and detected significant levels in EMD preparations. The sum of these pharmacological findings indicates that EMD contains at least one bioactive factor, which is most probably TGF-β1 (or TGF-β-like substances). In conjunction with the similarities in the differential growth-modulating actions between EMD and what is known for TGF-β, we suggest that TGF-β might act as the principal growth regulating agent of oral fibroblastic and epithelial cell types in EMD despite being present in only low levels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1034/j.1600-0765.2001.360604.x
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  • 4
    Electronic Resource
    Electronic Resource
    Calcitonin gene-related peptide acts as a mitogen for human Gin-1 gingival fibroblasts by activating the MAP kinase signalling pathway (1999)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of periodontal research 34 (1999), S. 0 
    Details
    ISSN: 1600-0765
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: In many peripheral tissues, calcitonin gene-related peptide (CGRP) is released from peptidergic sensory nerve fibres and acts like a growth factor during tissue development and regeneration. However, the ability of CGRP to influence gingival tissue has not been studied. To address this question, we have now examined the effects of CGRP on the proliferation of human gingival fibroblasts (Gin-1) in vitro. Gin-1 cells have approximately 3100 specific CGRP-binding sites with a Kd of 38.6 pM on their surface. Treatment with CGRP (0.1-100 nM) significantly stimulated cell proliferation in a dose-dependent manner, with maximal effects at 1-10 nM CGRP after 2 d. As one early cellular response to CGRP, p44-MAPK protein (also known as the extracellular signal response kinase [ERK]) was tyrosine- and threonine-phosphorylated within 2 min, and this phosphorylation was sustained for at least 1 h. The dose-response curve of MAPK activation was very similar to that observed for CGRP's stimulation of ceil proliferation. In addition, CGRP's activation of MAPK stimulated its ability to phosphorylate the Elk-1 transcription factor. When cells were pretreated with PD98059, a selective inhibitor of MAPK kinase (also known as MEK), CGRP not only failed to induce phosphorylation of MAPK but also failed to stimulate Gin-1 cell proliferation. Our present data indicate that CGRP rapidly activates the MAPK signalling pathway, an effect which consequently stimulates the proliferation of gingival fibroblasts. Our data demonstrate specific cellular responses to CGRP by gingival fibroblasts and support the possibility that CGRP acts as a targeted local factor in the regulation of development, generation and or regeneration of gingival tissues.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1600-0765.1999.tb02237.x
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  • 5
    Electronic Resource
    Electronic Resource
    TGF-β1 influences early gingival wound healing in rats: an immunohistochemical evaluation of stromal remodelling by extracellular matrix molecules and PCNA (1998)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of oral pathology & medicine 27 (1998), S. 0 
    Details
    ISSN: 1600-0714
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The effect of topically applied transforming growth factor β1 (TGF - β1) on the rat gingival wound healing process after flap surgery was evaluated by immunohistochemistry for extracellular matrix molecules (ECM), such as tenascin, heparan sulfate proteoglycan (HSPG) and type IV collagen, and for proliferating cell nuclear antigen (PCNA) in fibroblasts. TGF-β1 solution was applied to the surgical wound experimental sites. Two μg/μl were applied at the time of the operation, and 1 μg/μl at days 1 and 2 after surgery, with contralateral control sites receiving the vehicle alone. Periodontal tissues were histologically examined at 3 and 7 days post-surgery. Tenascin was found to be more strongly stained in the granulation tissue from experimental sites at 3 days post-surgery. At 7 days post-surgery, HSPG-positive areas in granulation tissue had become smaller and there was a prominent proliferation of PCNA-positive fibroblast-like cells and type IV collagen-positive blood vessels. These results suggest that TGF-β1 applied to surgical wounds influences early proliferation of gingival fibroblast-like cells, the formation of blood vessels, and ECM remodelling. In conclusion, TGF-β1 application appears to promote granulation tissue formation in periodontal wound healing.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1600-0714.1998.tb01913.x
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  • 6
    Electronic Resource
    Electronic Resource
    Levels of tissue inhibitor of metalloproteinases-1 and matrix metalloproteinases-1 and -8 in gingival crevicular fluid following treatment with enamel matrix derivative (EMDOGAIN®) (2001)
    Copenhagen : Munksgaard International Publishers
    Journal of periodontal research 36 (2001), S. 0 
    Details
    ISSN: 1600-0765
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The mechanism of enamel matrix derivative (EMD) action on the periodontal wound healing process is not well understood. However, earlier in vitro studies from our laboratory demonstrated that EMD stimulated the proliferation of both periodontal ligament and gingival fibroblast cells. Therefore, the purpose of this study was to further evaluate the effect of EMD on the early wound healing process by assessing the protein levels of matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) in gingival crevicular fluid (GCF). Sixteen patients, each of whom had one or two pairs of infrabony defects located contralaterally in the same arch, were included in this clinical trial. Thirty-six infrabony defects were randomly assigned treatment with flap surgery plus EMD or flap surgery plus placebo. At baseline and at 2, 4 and 12 week follow-up evaluation visits, GCF was sampled with paper strips. After determination of GCF volume, TIMP-1, MMP-1 and MMP-8 GCF levels were measured by an enzyme-linked immunosorbent assay. Intragroup analysis: At week 2 following surgery, when compared to baseline all parameters in each study group, except MMP-1, significantly increased (p〈0.05). There were no significant differences between 4 or 12 weeks and baseline in either study group. Intergroup analysis: At 4 weeks after surgery, GCF volume and TIMP-1 levels showed a significant decrease (p〈0.05) in the EMD group, when compared to the placebo group. MMP-1 levels at weeks 2, 4 and 12, and MMP-8 levels at weeks 4 and 12 were significantly lower (p〈0.05) in the EMD group compared to the placebo group. EMD compared to placebo treated sites demonstrated a more rapid return to baseline levels of TIMP-1, MMP-1 and MMP-8. These findings suggest that treatment with flap surgery and EMD, compared to flap surgery with placebo, accelerated healing at an earlier stage of wound healing following surgery.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1034/j.1600-0765.2001.360506.x
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  • 7
    Electronic Resource
    Electronic Resource
    Cytostatic action of enamel matrix derivative (EMDOGAIN®) on human oral squamous cell carcinoma-derived SCC25 epithelial cells (2000)
    Copenhagen : Munksgaard International Publishers
    Journal of periodontal research 35 (2000), S. 0 
    Details
    ISSN: 1600-0765
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: During surgical treatment of periodontal disease, enamel matrix derivative (EMD) is topically applied as a substitute for extracellular matrix in order to facilitate regeneration of damaged periodontal tissue. However, the mechanism for EMD action is poorly understood. We have now examined the effects of EMD on the proliferation of oral epithelial (SCC25) cells in vitro. After 3 days of treatments, EMD (25–100 μg/ml) dose-dependently inhibited cell division and concomitantly arrested cell cycle at the G1 phase. Prior to this inhibition, EMD significantly up-regulated p21WAF1/cip1, a cyclin-dependent kinase inhibitor, induced G1-arrest, and inhibited DNA synthesis. In addition, EMD down-regulated expression of cytokeratin-18 (CK18) protein, which was most due to decreased production, but less to increased degradation. However, EMD did not discernibly increase the number of apoptotic cells over 8 days of treatment. These findings indicate (1) that EMD acts as a cytostatic agent, rather than a cytotoxic agent, on epithelial cells, and (2) that this anti-proliferative action is probably due to p21WAF1/cip1-mediated G1-arrest. Furthermore, our in vitro cellular data clearly verify and provide an explanation for the clinical observation that EMD application suppresses the down-growth of junctional epithelium onto dental root surfaces, a process that frequently interferes with the formation of new connective tissue attachments.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1034/j.1600-0765.2000.035005291.x
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  • 8
    Electronic Resource
    Electronic Resource
    Anti-TGF-β antibody blocks enamel matrix derivative-induced upregulation of p21WAF1/cip1 and prevents its inhibition of human oral epithelial cell proliferation (2002)
    Oxford, UK : Munksgaard International Publishers
    Journal of periodontal research 37 (2002), S. 0 
    Details
    ISSN: 1600-0765
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: We have previously demonstrated that porcine enamel matrix derivative (EMD) contains TGF-β1 (or a TGF-β-like substance), and that EMD rapidly translocates smad2, which is an effector of the TGF-β signaling pathway, into the nucleus and modulates the proliferation of both human gingival fibroblastic and oral epithelial cells in a cell type-specific manner. To investigate the involvement of TGF-β in the growth modulatory action of EMD, two approaches have been used in the present study: i) a neutralizing anti-TGF-β antibody to block EMD action, and ii) authentic porcine TGF-β1 to compare with EMD. Both in epithelial and fibroblastic cells, TGF-β1 closely mimicked EMD in nuclear accumulation of smad2, phosphorylation of MAP kinase family members, and consequent cell type-specific growth modulation. Anti-TGF-β antibody, at levels which completely blocked TGF-β1-induced smad2 translocation, strongly blocked EMD-induced smad2 translocation. This antibody also blocked other actions of EMD in epithelial cells, i.e. p38-MAP kinase (p38-K) phosphorylation, p21WAF1/cip1 expression, and inhibition of DNA synthesis. In support of our previousproposal,thesedatasuggest that TGF-β1 (or a TGF-β-like substance), which is delivered as a principal bio-active factor in EMD, inhibits epithelial cell proliferation probably by a smad2-mediated, p21WAF1/cip1-dependent mechanism. However, the same neutralizing antibody failed to convincingly block EMD-induced fibroblastic proliferation, which suggests that EMD may contain additional unidentified mitogenic factor(s), which act in combination with TGF-β to fully stimulate fibroblastic proliferation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1034/j.1600-0765.2002.01615.x
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