Iatrogenic Electrocautery Damage and Cellular-Based Corrosion of Total Joint Arthroplasty Biomaterials

Abstract

Introduction. The number of patients undergoing a Primary Total Knee Arthroplasty (PTKA) has been increasing steadily each year. Of those PTKA patients, 20% report long-term pain and/or some functional deficit. Cobalt-Chromium-Molybdenum (CoCrMo) alloy is one of the most used materials in Total Joint Arthroplasty (TJA) implants due the material’s high strength, high corrosion resistance, and biocompatibility. The release of metal ions and potential occurrence of metallosis in TJA has been shown to be detrimental to the longevity of the implant. The mechanisms leading to this increase in metal ion concentrations have been up for debate, with some believing it is caused by Electrocautery (EC) damage at the time of surgery and others believing it is caused by inflammatory cells attacking the implant surface. The purpose of this thesis is to identify to what degree Electrocautery damage can alter the implant surface and if inflammatory cells are able to alter the implant surface and ingest metal particles. Methodology. To better understand how EC damage can alter implant surfaces, three different types of femoral component bearing surfaces were selected and intentionally damaged in the operating room using the plasma arc from both monopolar (MP) (Bovie) and Bipolar (BP) (Aquamantys) sources. MP and BP EC damage was done at varying power levels using a 3-second hover method 3 mm from the implant surface. Scanning electron microscopy (SEM) (Zeiss, Oberkochen, Germany) was used to obtain a detailed microscopic analysis of the damaged areas. Energy-dispersive X-ray spectrometry (EDS) (Oxford, High Wycombe, UK) was utilized to assess the elements present in pits found in the corroded areas. Surface Topography was analyzed using a profilometer (DektakXT; Bruker, Tucson, AZ) in the central portion of the damaged area for each MP and BP energy setting. Each damaged area was evaluated with the aid of TalyMap (Mountains software; Digital Surf, Besançon, France) using ISO 4287 measurements for Arithmetic Average height (Ra), Kurtosis (Rk), Heighest Peak to Lowest Valley (Rz), and Skewness (Rsk). SEM, EDS, and Surface Topography were also used to look at undamaged areas of the implants. In a separate experiment, IC-21 ATCC murine peritoneal macrophages were cultured with RPMI 1640 growth medium of supplemented with 10% fetal bovine serum (FBS), L-glutamine, and gentamicin. Select groups of cells were then activated using Interferon Gamma (IFNγ) and Lipopolysaccharide (LPS). CoCrMo alloy disks were cut, polished, passivated, and placed into 96 well plates and a select number intentionally damaged in the operating room with a MP EC device. After the cells were allowed to attach to the surface for 24 hours, culture medium was replaced every 12 hours and supernatant fluid was collected every 4 days starting on the second day of the experiment. After 30 days, cells were removed from the surface, counted and digested. The metal concentrations found in the supernatant and digested cell mixture were assessed using inductively coupled plasma spectrometry (ICP-MS), conducted at Brooks Applied Labs (Bothwell, WA). Statistical analysis was conducted using SigmaPlot (Systat Software, Chicago, IL) and Microsoft Excel (Microsoft, Redmond, WA). Results. Surface Profilometry quantified the topographical changes due to the damage form the MP and BP EC devices. The median Ra and Rz measurements were larger for the BP damaged areas compared to the MP for all bearing surfaces. The Oxinium surface displayed the greatest increase in roughness parameters compared to the undamaged regions. The CoCr surface displayed the greatest Rsk for the BP damaged areas. The ZrN had the smallest differences in Rz and Ra for both MP and BP damage areas compared to undamaged areas. SEM imaging displayed pitting in the regions intentionally damage with a MP or BP EC device. Backscatter EDS analysis found significant changes in the elemental profile for the BP damage compared to the MP damage. Cellular corrosion of the CoCr disks was quantified by measuring the concentration of Co, Cr, and Mo in the supernatant fluid collected off of the culture over the course of the 30-day experiment. The Co supernatant concentration was higher in the Undamaged Disks with Activated Cells versus its control which contained medium with no cells. The Cr concentration was higher in the supernatant fluid of the EC Damaged Disks with Standard Cells versus its control which contained medium with no cells. Between experimental groups, higher concentrations of Co and Mo was found in the supernatant of the Undamaged Disks with Standard Cells versus the EC Damaged Disks with Standard Cells. There was also a higher Co supernatant metal concentration when comparing the Undamaged Disks with Activated Cells versus the EC Damaged Disks with Activated Cells. A higher Cr supernatant metal concentration was found in the EC Damaged Disks with Activated Cells versus the EC Damaged Disks with Standard Cells. Following the end of the 30-day experiment, cells were digested to determine their inner metal ion concentration. There was a significantly higher intracellular Co and Mo concentration in the Undamaged Disks with Activated Cells versus the Undamaged Disks with Standard Cells. As well as a higher intracellular Co concentration in the EC Damaged Disks with Activated Cells versus the EC Damaged Disks with Standard Cells. SEM imaging displayed microscopic pitting on the surface exposed to macrophages and EC damage. Backscatter EDS analysis found significant differences in the elemental concentration of Carbon, Oxygen, Iron and Nickel between the experimental groups. From the EDS Backscatter analysis, the disks with EC damage displayed a higher Fe/C ratio compared to the undamaged disks. Showing evidence that EC damage alters the chemical profile of the CoCr disk surface.