Abstract
Introduction
The release of metal debris and ions has raised concerns in joint arthroplasty. In THA metal debris and ions can be generated by wear of metal-on-metal bearing surfaces and corrosion at modular taper interfaces, currently understood to be mechanically assisted crevice corrosion (MACC) [1]. More recently, inflammatory-cell induced corrosion (ICIC) has been identified as a possible source of metal debris and/or ions [2]. Although MACC has been shown to occur at modular junctions in TKA, little is known about the prevalence of other sources. The purpose of this study was to determine the sources of metallic debris and ion release in long-term implanted (in vivo > 15y) TKA femoral components. Specific attention was paid to instances of ICIC as well as damage at the implant-bone interface.
Methods
1873 retrieved TKA components were collected from 2002–2013 as part of a multi-center, IRB-approved retrieval program. Of these, 52 CoCr femoral condyles were identified as long term TKA (Average: 17.9±2.8y). These components were predominantly revised for loosening, PE wear and instability. 40/52 of the components were primary surgeries. Components were examined using optical microscopy to confirm the presence of 5 damage mechanisms (polyethylene failure, MACC corrosion of modular tapers, corrosion damage between cement and backside, third-body wear, and ICIC). Third-body wear was evaluated using a semi-quantitative scoring method based on the percentage of damaged area. A score of 1 had minimal damage and a score of 4 corresponded to severe damage. Polyethylene components were scored using the Hood method and CoCr components were scored similarly to quantify metal wear. The total area damaged by ICIC was quantified using photogrammetry. Images were taken using a digital SLR with a calibrated ruler in the same focal plane. Using known pixel dimensions, the ICIC damaged area was calculated.
Results
Surface damage indicative of corrosion and/or CoCr debris release was identified in 92% (n=48) of the components. Third-body wear was the most prevalent damage mechanism identified in 77% (n=40/52; Figure 1) of these components. ICIC was identified in 38% (n=20/52, figure 2) of the components. The polyethylene damage scores were predominantly a score of 4 out of a maximum score of 4 (89%). The corresponding femoral components had moderate to severe damage scores, with 39% with a score of 2, 37% scoring 3 and 22% scoring 4 out of a maximum score of 4. The total ICIC damaged area was an average of 0.11 ± 0.12 mm2 (Range: 0.01–0.46mm2).
Discussion
In this study, we sought to identify mechanisms that could lead to the release of CoCr debris/ions in TKA. Five different mechanisms of potential metal release were observed. The most prevalent were third-body wear and ICIC damage. However the clinical implications remain unclear for several mechanisms because none of the devices were revised due to adverse local tissue reactions or biologic reactions to CoCr. Although we documented the prevalence of each damage mechanism, the quantity of metal removal was not investigated, warranting future studies.
