Bipolar Radiofrequency Plasma Ablation Induces Proliferation and Alters Cytokine Expression in Human Articular Cartilage Chondrocytes

Abstract

The aim of the study was to determine the in vitro effects of plasma-mediated bipolar radiofrequency ablation on human chondrocyte compensatory proliferation and inflammatory mediator expression. Human articular cartilage biopsy specimens, from total knee replacement, and human chondrocytes in alginate culture, from patients undergoing autologous chondrocyte implantation, were exposed to plasma ablation with a Paragon T2 probe (ArthroCare, Austin, TX). Instantaneous chondrocyte death was investigated with live/dead assays of biopsy specimens and cell cultures. Chondrocyte proliferation was determined by Hoechst staining of DNA on days 3 and 6. Messenger RNA expression of IL-1β, IL-6, IL-8, tumor necrosis factor α, high-mobility group protein B1, matrix metalloproteinase 13, type IIA collagen, and versican was determined on days 3 and 6. Live/dead imaging showed a well-defined local margin of cell death ranging from 150 to 200 μm deep, both in the alginate gel and in the biopsy specimens exposed to plasma ablation. The ablation-exposed group showed a significant proliferation increase compared with control on day 3 (P < .043). There were significant increases compared with control in IL-6 expression on day 3 (P < .020) and day 6 (P < .045) and in IL-8 expression on day 3 (P < .048). No differences were seen for IL-1β, tumor necrosis factor α, high-mobility group protein B1, matrix metalloproteinase 13, type II collagen, or versican. This study has shown that exposure to plasma-mediated ablation induces a well-defined area of immediate cell death and a short-term increase in proliferation with human articular chondrocytes in vitro. The exposure also alters cytokine expression for the same period, causing upregulation of IL-6 and IL-8. The results show the potential of plasma-mediated ablation to cause the onset of a tissue regeneration response with human articular cartilage.