title: Surface modification of cyclic olefin copolymers for osteochondral defect repair can increase pro-destructive potential of human chondrocytes in vitro.
abstract: Materials on the basis of cycloolefin copolymers (COC) are suitable for subchondral defect repairs. The objective of this study was to evaluate the influence of surface modification of COC and COC/LLDPE blends on the viability and gene expression of chondrocytes. Human chondrocytes were incubated on the surface of the studied materials. Half of the materials were plasmatically modified with a subsequent type II collagen application. The gene expression of matrix metalloproteinases (MMP-1,-3,-13), pro-inflammatory cytokines (IL-1, TNF-alpha) and apoptotic molecules (BAX, Bcl-2) was evaluated using quantitative Taq-Man PCR after 48 h incubation. Chondrocyte viability was evaluated by the MTT test after 2, 4 and 8 days of incubation. The synthesis of MMPs was measured by ELISA assay in cell culture medium after 48 h of incubation. Chondrocytes incubated on plasmatically modified in contrast to unmodified materials demonstrated significantly increased gene expression of IL-1 (p<0.05), MMP-1 and MMP-3 (p<0.05 for both comparisons) as well as MMP-13 (p<0.001). Increased gene expression was confirmed by significantly increased production of active forms of particular MMPs into the cell culture medium. Unlike surface unmodified polymers, the modified materials showed time-dependent reduction of chondrocyte viability. The gene expression of TNF-alpha and apoptotic molecules by chondrocytes was not significantly changed by different materials. Cycloolefin copolymers and their blends may represent suitable materials for tissue engineering, however, their surface modification followed by collagen type II application may, at least under in vitro conditions, reduce the viability of chondrocytes and induce their pro-destructive behavior. The potential benefit or disadvantage of surface modifications of materials for osteochondral defect repairs needs to be further elucidated.
authors.affiliation: Institute of Rheumatology, First Medical Faculty, Charles University Prague, Prague, Czech Republic. polanska@revma.cz
authors.forename: M
authors.initials: M
authors.lastname: Polanská
authors.forename: H
authors.initials: H
authors.lastname: Hulejová
authors.forename: M
authors.initials: M
authors.lastname: Petrtýl
authors.forename: Z
authors.initials: Z
authors.lastname: Bastl
authors.forename: I
authors.initials: I
authors.lastname: Spirovová
authors.forename: Z
authors.initials: Z
authors.lastname: Krulis
authors.forename: Z
authors.initials: Z
authors.lastname: Horák
authors.forename: D
authors.initials: D
authors.lastname: Veigl
authors.forename: L
authors.initials: L
authors.lastname: Senolt
mesh_terms: D017209:Apoptosis / Q000187:drug effects; D001672:Biocompatible Materials / Q000494:pharmacology*; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects; D019902:Chondrocytes / Q000166:cytology / Q000187:drug effects* / Q000502:physiology; D024043:Collagen Type II / Q000494:pharmacology; D003516:Cycloparaffins / Q000494:pharmacology*; D015870:Gene Expression / Q000187:drug effects; D006801:Humans; D066298:In Vitro Techniques; D007375:Interleukin-1 / Q000235:genetics; D008422:Materials Testing; D020781:Matrix Metalloproteinase 1 / Q000235:genetics / Q000378:metabolism; D053509:Matrix Metalloproteinase 13 / Q000235:genetics / Q000378:metabolism; D019278:Matrix Metalloproteinase 3 / Q000235:genetics / Q000378:metabolism; D010003:Osteoarthritis / Q000188:drug therapy* / Q000473:pathology; D011108:Polymers / Q000494:pharmacology*; D019736:Prostheses and Implants; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics
chemical_list: D001672:Biocompatible Materials; D024043:Collagen Type II; D003516:Cycloparaffins; D007375:Interleukin-1; D011108:Polymers; D014409:Tumor Necrosis Factor-alpha; D053509:Matrix Metalloproteinase 13; D019278:Matrix Metalloproteinase 3; D020781:Matrix Metalloproteinase 1