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General Orthopaedics

METAL RELEASE AND DAMAGE MECHANISMS IN AUTOPSY TOTAL KNEE ARTHROPLASTY FEMORAL COMPONENTS

The International Society for Technology in Arthroplasty (ISTA), 29th Annual Congress, October 2016. PART 1.



Abstract

Introduction

Previous studies of CoCr alloy femoral components for total knee arthroplasty (TKA) have identified 3rd body abrasive wear, and apparent inflammatory cell induced corrosion (ICIC) [1] as potential damage mechanisms. The association between observed surface damage on the femoral condyle and metal ion release into the surrounding tissues is currently unclear. The purpose of this study was to investigate the damage on the bearing surface in TKA femoral components recovered at autopsy and compare the damage to the metal ion concentrations in the synovial fluid.

Methods

12 autopsy TKA CoCr femoral components were collected as part of a multi-institutional orthopedic implant retrieval program. The autopsy components included Depuy Synthes Sigma Mobile Bearing (n=1) and PFC (n=1), Stryker Triathlon (n=1) and Scorpio (n=3), and Zimmer Nexgen (n=4) and Natural Knee (n=2). Fluoro scans of all specimens prior to removal was carried out to assure no signs of osteolysis or aseptic loosening were present.

Third-body abrasive wear of CoCr was evaluated using a semi-quantitative scoring method similar to the Hood method [2]. ICIC damage was reported as location of affected area and confirmed using a digital optical microscope with 4000X magnification.

Synovial fluid was aspirated from the joint capsule prior to removal of the TKA device. The synovial fluid was spun at 1600 rpm for 20 minutes in a centrifuge with the cell pellet removed. The supernatant was analyzed in 1 mL quantities for ICP-MS (inductively coupled plasma mass spectrometry) by Huffman Hazen Laboratories. Data was expressed as ppb.

Results

Mild to severe damage (Damage Score ≥ 2) was observed on 92% of the components in at least one quadrant, with no severe damage (Damage Score = 4) observed. ICIC damage was observed on three components in three different regions (the posterior lateral, anterior, and medial bearing surface). These observations were confirmed with digital optical microscopy, where we observed as interconnecting pits and indentations with a spiraling or trailing region, consistent with prior observation of ICIC in retrievals (Figure 1).

Cobalt was detected in 7 cases, however the metal levels were not as high as levels observed in patients with a failed joint replacement (Table 1). There was no correlation between the metal ion concentration and the damage score on the CoCr femoral condyle.

Discussion

This study documents the damage mechanics and associated metallic release into the synovial fluid of “well-functioning” TKA components retrieved at autopsy. It has been suggested that ICIC damage is actually damage from electrocautery during surgery. However, we observed ICIC damage on autopsy retrievals in which the use of electrocautery is unlikely. The damage mechanisms observed on the autopsy TKA components were similar but less severe compared to mechanisms observed in long-term TKA components from revision surgery [1]. More research is needed to better understand the metal release from CoCr femoral components and periprosthetic tissue reactions in TKA.


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