Bipolar radiofrequency plasma ablation induces proliferation and alters cytokine expression in human articular cartilage chondrocytes.

Purpose: 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.

Methods: 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.

Results: 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.

Conclusions: 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.

Clinical Relevance: The results show the potential of plasma-mediated ablation to cause the onset of a tissue regeneration response with human articular cartilage.