The study monitored in vitro early response of connective tissue cells and immunocompetent cells to enosseal implant materials coated by different blood components (serum, activated plasma, and plasma/platelets) to evaluate human osteoblast proliferation and synthetic activity and inflammatory response presented as a cytokine profile of peripheral blood mononuclear cells (PBMCs) under conditions imitating the situation upon implantation. The cells were cultivated on coated Ti-plasma-sprayed (Ti-PS), Ti-etched (Ti-Etch), Ti-hydroxyapatite (Ti-HA), and ZrO2 surfaces. The plasma/platelets coating supported osteoblast proliferation only on osteoconductive Ti-HA and Ti-Etch whereas activated plasma enhanced proliferation on all surfaces. Differentiation (BAP) and IL-8 production remained unchanged or decreased irrespective of the coating and surface; only the serum and plasma/platelets-coated ZrO2 exhibited higher BAP and IL-8 expression. RANKL production increased on serum and activated plasma coatings. PBMCs produced especially cytokines playing role in inflammatory phase of wound healing, that is, IL-6, GRO-α, GRO, ENA-78, IL-8, GM-CSF, EGF, and MCP-1. Cytokine profiles were comparable for all tested surfaces; only ENA-78, IL-8, GM-CSF, and MCP-1 expression depended on materials and coatings. The activated plasma coating led to uniformed surfaces and represented a favorable treatment especially for bioinert Ti-PS and ZrO2 whereas all coatings had no distinctive effect on bioactive Ti-HA and Ti-Etch.

• MeSH
• Coated Materials, Biocompatible adverse effects   chemistry   MeSH
• Cell Line MeSH
• Chemokine CCL2 metabolism   MeSH
• Chemokine CXCL1 metabolism   MeSH
• Chemokine CXCL5 metabolism   MeSH
• Cytokines metabolism   MeSH
• Epidermal Growth Factor metabolism   MeSH
• Granulocyte-Macrophage Colony-Stimulating Factor metabolism   MeSH
• Wound Healing drug effects   MeSH
• Interleukin-6 metabolism   MeSH
• Interleukin-8 metabolism   MeSH
• Leukocytes, Mononuclear drug effects   metabolism   MeSH
• Humans MeSH
• Osteoblasts drug effects   metabolism   MeSH
• Cell Proliferation drug effects   MeSH
• Titanium adverse effects   chemistry   MeSH
• Inflammation metabolism   MeSH
• Check Tag
• Humans MeSH
• Publication type
• Journal Article MeSH
• Names of Substances
• Coated Materials, Biocompatible MeSH
• Chemokine CCL2 MeSH
• Chemokine CXCL1 MeSH
• Chemokine CXCL5 MeSH
• CXCL1 protein, human MeSH Browser
• CXCL5 protein, human MeSH Browser
• Cytokines MeSH
• Epidermal Growth Factor MeSH
• Granulocyte-Macrophage Colony-Stimulating Factor MeSH
• Interleukin-6 MeSH
• Interleukin-8 MeSH
• Titanium MeSH

Fibrinogen is one of the plasma proteins most susceptible to oxidative modification. It has been suggested that modification of fibrinogen may cause thrombotic/bleeding complications associated with many pathophysiological states of organism. We exposed fibrinogen molecules to three different modification reagents-malondialdehyde, sodium hypochlorite, and peroxynitrite-that are presented to various degrees in different stages of oxidative stress. We studied the changes in fibrin network formation and platelet interactions with modified fibrinogens under flow conditions. The fastest modification of fibrinogen was caused by hypochlorite. Fibers from fibrinogen modified with either reagent were thinner in comparison with control fibers. We found that platelet dynamic adhesion was significantly lower on fibrinogen modified with malondialdehyde and significantly higher on fibrinogen modified either with hypochlorite or peroxynitrite reflecting different prothrombotic/antithrombotic properties of oxidatively modified fibrinogens. It seems that, in the complex reactions ongoing in living organisms at conditions of oxidation stress, hypochlorite modifies proteins (e.g., fibrinogen) faster and more preferentially than malondialdehyde. It suggests that the prothrombotic effects of prior fibrinogen modifications may outweigh the antithrombotic effect of malondialdehyde-modified fibrinogen in real living systems.

• MeSH
• Platelet Adhesiveness drug effects   physiology   MeSH
• Sodium Hypochlorite pharmacology   MeSH
• Fibrinogen chemistry   metabolism   pharmacology   MeSH
• Indicators and Reagents chemistry   pharmacology   MeSH
• Cells, Cultured MeSH
• Peroxynitrous Acid chemistry   MeSH
• Humans MeSH
• Malondialdehyde chemistry   pharmacology   MeSH
• Oxidative Stress drug effects   physiology   MeSH
• Blood Platelets drug effects   metabolism   MeSH
• Structure-Activity Relationship MeSH
• Check Tag
• Humans MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Names of Substances
• Sodium Hypochlorite MeSH
• Fibrinogen MeSH
• Indicators and Reagents MeSH
• Peroxynitrous Acid MeSH
• Malondialdehyde MeSH

The role of platelets in hemostasis may be influenced by alteration of the platelet redox state-the presence of antioxidants and the formation of reactive oxygen and nitrogen species. We investigated the effects of two antioxidants, resveratrol and trolox, on platelet activation. Trolox and resveratrol inhibited aggregation of washed platelets and platelet-rich plasma activated by ADP, collagen, and thrombin receptor-activating peptide. Resveratrol was a more effective agent in reducing platelet static and dynamic adhesion in comparison with trolox. The antioxidant capacity of resveratrol was, however, the same as that of trolox. After incubation of platelets with antioxidants, the resveratrol intraplatelet concentration was about five times lower than the intracellular concentration of trolox. Although both antioxidants comparably lowered hydroxyl radical and malondialdehyde production in platelets stimulated with collagen, TxB(2) levels were decreased by resveratrol much more effectively than by trolox. Cyclooxygenase 1 was inhibited by resveratrol and not by trolox. Our data indicate that antioxidants, apart from nonspecific redox or radical-quenching mechanisms, inhibit platelet activation also by specific interaction with target proteins. The results also show the importance of studying platelet activation under conditions of real blood flow in contact with reactive surfaces, e.g., using dynamic adhesion experiments.

• MeSH
• Platelet Aggregation drug effects   physiology   MeSH
• Antioxidants pharmacology   MeSH
• Cell Adhesion drug effects   physiology   MeSH
• Chromans pharmacology   MeSH
• Cyclooxygenase 1 metabolism   MeSH
• Hemostasis drug effects   MeSH
• Collagen pharmacology   MeSH
• Cells, Cultured MeSH
• Humans MeSH
• Malondialdehyde metabolism   MeSH
• Resveratrol MeSH
• Stilbenes pharmacology   MeSH
• Thromboxane B2 metabolism   MeSH
• Blood Platelets drug effects   physiology   MeSH
• Check Tag
• Humans MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Research Support, N.I.H., Extramural MeSH
• Names of Substances
• 6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid MeSH Browser
• Antioxidants MeSH
• Chromans MeSH
• Cyclooxygenase 1 MeSH
• Collagen MeSH
• Malondialdehyde MeSH
• Resveratrol MeSH
• Stilbenes MeSH
• Thromboxane B2 MeSH