Arthroscopic Surgical Tools: A Source of Metal Particles and Possible Joint Damage

PurposeOur goals were (1) to characterize metal microparticles created by standard arthroscopic instruments and (2) to examine the in vitro cellular responses induced by those particles, including possible synergistic effects with local anesthetic.MethodsWe applied standard surgical tools to 16 foam bone blocks immersed in saline solution (plus 3 non-instrumented controls). Eight specimens underwent 4 minutes of exposure to a 4.0-mm full-radius shaver rotating forward at 6,000 rpm. In the other blocks, 4 holes were created with a 3.0-mm drill through a sleeve. Particles were isolated onto silicon wafers by density gradient ultra-centrifugation, and scanning electron microscopy was used to analyze a minimum of 1,000 particles per wafer. Metal particles were then isolated and purified. Aliquots of sterilized micro-particles were applied to cultured bovine chondrocytes (with or without local anesthetic) and to cultured human or bovine synoviocytes. Chondrocyte viability was assessed with live/dead cell assay by flow cytometry. Synoviocyte responses were assessed with quantitative polymerase chain reaction.ResultsStainless steel or aluminum particles were found in each sample (the same composition as surgical instruments). The mean particle size was 1 to 2 μm (range, 50 nm to 20 μm). Chondrocyte exposure (1 hour) to metal debris induced a small but statistically significant increase in cell death, without any synergistic effect of local anesthetic. Proinflammatory chemokines were consistently upregulated in both human and bovine synoviocytes exposed to metallic microparticles for 3, 24, and 48 hours.ConclusionsThis study shows that metallic microdebris is liberated by common arthroscopic instruments, at scales much smaller than previously recognized. These particles are bioactive, as shown by the in vitro synoviocyte responses initiated by metallic microparticles.Clinical RelevanceOur findings suggest that metallic microparticles could induce intra-articular damage through a synoviocyte-mediated cytokine response if their concentrations reach clinically significant levels.