Search

Background: Tissue breakdown in periodontitis is initiated by bacteria, such as Porphyromonas gingivalis, and is caused largely by host responses. Resolvins protect the host against acute inflammation by blocking the migration of polymorphonuclear neutrophils to initiate resolution. The effects of resolvins on human gingival fibroblasts (HGFs) are unknown. This study examines the effects of resolvin D1 on HGF survival and cytokine expression when treated with or without P. gingivalis supernatant. Methods: Cytotoxicity of resolvin D1 on HGFs with or without a toxic level of P. gingivualis supernatant was measured with lactate dehydrogenase assays. Cytokine arrays were performed on HGF-conditioned media treated with or without resolvin D1 and with or without P. gingivualis supernatant. Results: Resolvin D1 had no cytotoxic effects on HGFs at concentrations between 1 and 1,000 nM (all P> 0.05). Resolvin D1 (1,000 nM) significantly inhibited the toxic effects of 13.5% (v/v) P. gingivualis supernatant on HGFs (P = 0.002). Resolvin D1 significantly reduced the expression of interleu-kin (IL)-6 (P= 0.010) and monocyte chemoattractant protein (MCP)-1 (P = 0.04) in untreated fibroblasts. P. gingivualis (10%) supernatant significantly increased the expression levels of granulocyte-macrophage colony-stimulating factor (CSF), granulocyte CSF, growth-regulated oncogene (GRO), IL-5, IL-6, IL-7,IL-8, IL-10, MCP-1, MCP-2, MCP-3, and monokine induced by γ-interferon. Resolvin D1 significantly reduced the expression of GRO (P= 0.04), marginally reduced the levels of MCP-1 (P= 0.10), and marginally increased the levels of transforming growth factor (TGF)-β1 (P = 0.07) from HGFs treated with P. gingivualis supernatant. Conclusions: Resolvin D1 altered the cytotoxicity of P. gingivualis supernatant on HGFs. Resolvin D1 significantly reduced GRO, marginally reduced MCP-1, and marginally increased TGF-β1 from P. gingivualis-treated HGFs, which could alter the ability of P. gingivualis to induce inflammation. [ABSTRACT FROM AUTHOR]

Background: Calendula officinalis is commonly called the marigold. It is a staple topical remedy in homeopathic medicine. It is rich in quercetin, carotenoids, lutein, lycopene, rutin, ubiquinone, xanthophylls, and other anti-oxidants. It has anti-inflammatory properties. Quercetin, one of the active components in Calendula, has been shown to inhibit recombinant human matrix metalloproteinase (MMP) activity and decrease the expression of tumor necrosis factor-α, interleukin-1β (IL), IL-6 and IL-8 in phorbol 12-myristate 13-acetate and calcium ionophore-stimulated human mast cells. Objectives: To examine the effects of Calendula on human gingival fibroblast (HGF) mediated collagen degradation and MMP activity. Material and methods: Lactate dehydrogenate assays were performed to determine the non-toxic concentrations of Calendula, doxycycline and quercetin. Cell-mediated collagen degradation assays were performed to examine the inhibitory effect on cell-mediated collagen degradation. Gelatin zymography was performed to examine their effects on MMP-2 activity. The experiments were repeated three times and ANOVA used for statistical analyses. Results: Calendula at 2–3% completely inhibited the MMP-2 activity in the zymograms. Doxycycline inhibited HGF-mediated collagen degradation at 0.005, 0.01, 0.02 and 0.05%, and MMP-2 activity completely at 0.05%. Quercetin inhibited HGF-mediated collagen degradation at 0.005, 0.01 and 0.02%, and MMP-2 activity in a dose-dependent manner. Calendula inhibited HGF-mediated collagen degradation and MMP-2 activity more than the same correlated concentration of pure quercetin. Conclusion: Calendula inhibits HGF-mediated collagen degradation and MMP-2 activity more than the corresponding concentration of quercetin. This may be attributed to additional components in Calendula other than quercetin. [Copyright &y& Elsevier]

Background: Members of the matrix metalloproteinase (MMP) family have been shown to be involved in periodontal disease. Risk factors for periodontal disease include tobacco smoking. Cigarette smoke condensate (CSC) is comprised of thousands of chemicals. Nicotine is one of the active components in tobacco. This study compares the effects of CSC and nicotine at the level in CSC on the collagen-degrading ability of human gingival fibroblasts (HGFs) and the expression of selected MMPs and tissue inhibitors of metalloproteinases (TIMPs). Methods: HGFs were seeded in six-well collagen-coated plates, exposed to 100 µg/mL (2.4 µg/mL nicotine) of CSC or 2.4 µg/mL nicotine for 3 days, and then collagen degradation was analyzed. After 3 days exposure to CSC or nicotine, the conditioned media from HGFs was collected and the membrane proteins were extracted for gelatin zymography and Western blot analyses. The mRNA levels of MMP-2, MMP-14, and TIMP-2 were measured by reverse transcription-polymerase chain reaction. Results: The CSC increased collagen degradation, and increased the levels of TIMP-2, MMP-14, and the active MMP-2 in the membrane extracts, and their mRNA levels. CSC also increased the level of active MMP-2 in the conditioned media. Nicotine at the level in CSC (2.4 µg/mL) had little influence on collagen degradation, as well as on the protein and mRNA levels of MMP-2, MMP-14, and TIMP-2. Conclusions: CSC may increase HGF-mediated collagen degradation by affecting membrane-associated MMPs and TIMPs. [ABSTRACT FROM AUTHOR]

Statement of problem: Several studies have reported that polymerized resin materials may release agents into surrounding tissues. These agents could alter cytokine/growth factor expression. Purpose: The purpose of this study was to determine the effects that provisional acrylic resins have on cell toxicity and the expression of cytokines/growth factors from human gingival fibroblasts (HGFs). Material and methods: The materials used in this study were chemically activated bis-acryl composite (Chem-Bis), chemically activated polyethyl methacrylate (Chem-PEMA), chemically activated polymethyl methacrylate (Chem-PMMA), and heat-activated polymethyl methacrylate (Heat-PMMA) resins. HGFs were incubated for 72 hours in the presence of eluate from each resin and in the absence of any eluate (negative control). The conditioned media were then collected and stored at −70°C. Cell toxicity was determined using a lactate dehydrogenase method. Cytokine/growth factor expression was examined using cytokine antibody arrays. The experiments were repeated 3 times. The data were analyzed with 1-way ANOVA, Mann-Whitney test, and 1-sample t test (α=.05). Results: There was no significant cell toxicity observed from the eluates. The cytokine/growth factor expression induced by Chem-Bis was significantly greater than the control for growth-regulated oncogene (GRO) (P<.001), monocyte chemoattractant protein-1 (MCP-1) (P=.031), and tumor necrosis factor-β (TNF)-β (P=.009). For Chem-PEMA, the cytokine/growth factor expression was significantly greater than the control for GRO-α (P=.022), interleukin (IL)-13 (P=.031), and TNF-α (P=.017). The cytokines/growth factors induced by Chem-PEMA were significantly less than the control (P=.008) and Chem-Bis for IL-8 (P=.042). The expression induced by Chem-PMMA was significantly greater than the control for IL-13 (P=.036), IL-1α (P=.003), IL-2 (P=.020), and IL-5 (P=.045). Finally, Heat-PMMA induced significantly greater levels than the control for GRO (P<.001) and IL-13 (P=.008). Conclusions: This study demonstrated that the resins evaluated were nontoxic to the HGFs. There were changes in the cytokine/growth factor levels that were statistically significant, but may not be clinically significant. (J Prosthet Dent 2008;100:390-397) [Copyright &y& Elsevier]