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1.
Dent Mater ; 29(11): 1158-65, 2013 Nov.
Article in English | MEDLINE | ID: mdl-24054334

ABSTRACT

OBJECTIVE: The aim of this study was to investigate the effect of aluminosilicate clay nanotubes (Halloysite, HNT) incorporated into the adhesive resin of a commercially available three-step etch and rinse bonding system (Adper Scotchbond Multi-Purpose/SBMP) on dentin bond strength, as well as the effect on several key physicochemical properties of the modified adhesive. METHODS: Experimental adhesives were prepared by adding five distinct HNT amounts (5-30 wt.%) into the adhesive resin (w/v) of the SBMP dentin bonding system. Bond strength to human dentin, microhardness, and degree of conversion (DC) of the modified adhesives were assessed. RESULTS: From the shear bond strength data, it was determined that HNT incorporation at a concentration of 30 wt.% resulted in the highest bond strength to dentin that was statistically significant (p=0.025) when compared to the control. Even though a significant increase in microhardness (p<0.001) was seen for the 30 wt.% HNT-incorporated group, a significantly lower DC (p<0.001) was recorded when compared to the control. SIGNIFICANCE: It was concluded that HNT can be incorporated up to 20 wt.% without jeopardizing important physicochemical properties of the adhesive. The modification of the SBMP dentin bonding agent with 20 wt.% HNT appears to hold great potential toward contributing to a durable dentin bond; not only from the possibility of strengthening the bond interface, but also due to HNT intrinsic capability of encapsulating therapeutic agents such as matrix metalloproteinase (MMP) inhibitors.


Subject(s)
Dental Cements , Dentin/chemistry , Nanotubes , Microscopy, Electron, Scanning , Microscopy, Electron, Transmission
2.
J Periodontol ; 84(12): 1838-46, 2013 Dec.
Article in English | MEDLINE | ID: mdl-23398023

ABSTRACT

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. gingivalis 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. gingivalis 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. gingivalis supernatant on HGFs (P = 0.002). Resolvin D1 significantly reduced the expression of interleukin (IL)-6 (P = 0.010) and monocyte chemoattractant protein (MCP)-1 (P = 0.04) in untreated fibroblasts. P. gingivalis (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)-ß1 (P = 0.07) from HGFs treated with P. gingivalis supernatant. CONCLUSIONS: Resolvin D1 altered the cytotoxicity of P. gingivalis supernatant on HGFs. Resolvin D1 significantly reduced GRO, marginally reduced MCP-1, and marginally increased TGF-ß1 from P. gingivalis-treated HGFs, which could alter the ability of P. gingivalis to induce inflammation.


Subject(s)
Anti-Inflammatory Agents/pharmacology , Cytokines/drug effects , Docosahexaenoic Acids/pharmacology , Fibroblasts/drug effects , Gingiva/drug effects , Cell Culture Techniques , Cell Survival/drug effects , Cells, Cultured , Chemokine CCL2/antagonists & inhibitors , Chemokine CCL7/analysis , Chemokine CCL8/analysis , Chemokine CXCL1/analysis , Chemokine CXCL9/analysis , Culture Media, Conditioned , Fibroblasts/cytology , Gingiva/cytology , Granulocyte Colony-Stimulating Factor/analysis , Granulocyte-Macrophage Colony-Stimulating Factor/analysis , Humans , Interleukin-10/analysis , Interleukin-5/analysis , Interleukin-6/antagonists & inhibitors , Interleukin-7/analysis , Interleukin-8/analysis , L-Lactate Dehydrogenase/analysis , Porphyromonas gingivalis/immunology , Transforming Growth Factor beta1/analysis
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