Browsing by Author "Arancibia, R."

Now showing 1 - 7 of 7
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    Chitosan-triclosan particles modulate inflammatory signaling in gingival fibroblasts
    (2018) Pavez, L.; Tobar, N.; Chacon, C.; Arancibia, R.; Martinez, C.; Tapia, C.; Pastor, A.; Gonzalez, M.; Martinez, J.; Smith, P. C.
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    Diabetes y su impacto en el territorio periodontal
    (2012) Smith, P.; Retamal, I.; Cáceres, M.; Romero, A.; Silva, D.; Arancibia, R.; Martínez, Constanza
    Diabetes y enfermedad periodontal corresponden probablemente al mejor ejemplo de cómo una enfermedad sistémica puede tener un efecto en el territorio periodontal. Si bien esta asociación ha sido extensamente estudiada, muchas de las asociaciones propuestas presentan contradicciones. En la presente revisión de la literatura se analizan los siguientes tópicos relevantes para la práctica clínica en periodoncia e implantología: i) Identificación de enfermedad periodontal severa y su capacidad para diagnosticar casos de diabetes; ii) Efectos de la diabetes sobre la enfermedad periodontal; iii) Efectos de la diabetes sobre la reparación periodontal y periimplantaria; iv) Efecto del tratamiento periodontal sobre el control metabólico de la diabetes.
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    Effects of cigarette smoke and nicotine on cell viability, migration and myofibroblastic differentiation
    (2012) Silva, D.; Cáceres, M.; Arancibia, R.; Martínez, C.; Martínez, J.; Smith, P. C.
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    Involvement of MT1-MMP and TIMP-2 in human periodontal disease
    (WILEY, 2010) Oyarzun, A.; Arancibia, R.; Hidalgo, R.; Penafiel, C.; Caceres, M.; Gonzalez, M J; Martinez, J.; Smith, P. C.
    Objectives:
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    Methylglyoxal and methylglyoxal-modified collagen as inducers of cellular injury in gingival connective tissue cells
    (2016) Retamal, I. N.; Hernández, R.; González-Rivas, C.; Cáceres, M.; Arancibia, R.; Romero, A.; Martínez, Constanza; Tobar, N.; Martínez, J.; Smith, P. C.
    Background and Objectives: Methylglyoxal is a toxic product derived from glucose metabolism that plays a role in inflammation, diabetes and aging. In addition, the periodontal pathogen Tannerella forsythensis may also generate this compound. However, the effects of methylglyoxal on gingival cells are still poorly understood. In the present study, we have explored whether methylglyoxal or methylglyoxal-treated collagen may modulate cell viability, death and proliferation in gingival connective tissue cells. In addition, we have searched for inflammatory mediators secreted by cells upon exposure to these conditions. Material and Methods: Primary cultures of human gingival fibroblasts were stimulated with soluble methylglyoxal or cultured over a collagen matrix glycated by this agent. Cell viability was evaluated through the MTS assay. Cell death was assessed through DAPI nuclear staining, annexin V and propidium iodide assays. Cell proliferation was evaluated through double immunofluorescence for DAPI and Ki67. Protein levels of matrix metalloproteinases and cytokines were assessed through antibody arrays, enzyme-linked immunosorbent assay, real-time reverse transcription polymerase chain reaction and immunofluorescence. Statistical analysis was performed using the Kruskall-Wallis and Mann-Whitney tests. Results: Soluble methylglyoxal, but not culture of gingival fibroblasts over a methylglyoxal-modified collagen matrix, induced a reduction on cell viability. Moreover, soluble methylglyoxal induced apoptotic cell death as indicated by DAPI nuclear staining, annexin V and propidium iodide assays. Neither soluble methylglyoxal, nor methylglyoxal-modified collagen modified cell proliferation. Using an antibody array, enzyme-linked immunosorbent assay and immunofluorescence assays, we determined that both, soluble methylglyoxal and methylglyoxal- modified collagen stimulated an increase in tissue inhibitor of metalloproteinase (TIMP)-1 protein levels. Conclusions: Soluble methylglyoxal is a highly cytotoxic compound that induces cell death through apoptosis in gingival fibroblasts. TIMP-1 is induced in these cells upon direct exposure to methylglyoxal or after culture of gingival fibroblasts over methylglyoxal-treated collagen. As TIMP-1 has been implicated in cell survival and matrix remodeling, we propose that increased TIMP-1 protein levels may be part of a protective response of gingival connective tissue cells upon exposure to methylglyoxal or after the interaction with the collagen matrix that has been modified by this agent.
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    Triclosan inhibits tumor necrosis factor-alpha-stimulated urokinase production in human gingival fibroblasts
    (WILEY, 2009) Arancibia, R.; Caceres, M.; Martinez, J.; Smith, P. C.
    Background and Objectives: Destruction of the supporting periodontal tissues is mediated by the action of several proteolytic enzymes. Urokinase is a serine protease that plays a key role in connective tissue destruction through conversion of plasminogen into plasmin. The present study was conducted to evaluate the effect of triclosan on the production and activity of urokinase in cultured gingival fibroblasts.
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