In Vitro Evidence for Cell‐Accelerated Corrosion Within Modular Junctions of Total Hip Replacements

Abstract

Corrosion at modular junctions of total hip replacement (THR) remains a major concern today. Multiple types of damage modes have been identified at modular junctions, correlated with different corrosion characteristics that may eventually lead to implant failure. Recently, within the head-taper region of the CoCrMo retrieval implants, cell-like features and trails of etching patterns were observed that could potentially be linked to the involvement of cells of the periprosthetic region. However, there is no experimental evidence to corroborate this phenomenon. Therefore, we aimed to study the potential role of periprosthetic cell types on corrosion of CoCrMo alloy under different culture conditions, including the presence of CoCrMo wear debris. Cells were incubated with and without CoCrMo wear debris (obtained from a hip simulator) with an average particle size of 119 ± 138 nm. Electrochemical impedance spectroscopy (EIS) was used to evaluate the corrosion tendency, corrosion rate, and corrosion kinetics using the media after 24 h of cell culture as the electrolyte. Results of the study showed that there was lower corrosion resistance (p < 0.02) and higher capacitance (p < 0.05) within cell media from macrophages challenged with particles when compared with the other media conditions studied. The potentiodynamic results were also in agreement with the EIS values, showing significantly higher corrosion tendency (low E corr ) (p < 0.0001) and high I corr (p < 0.05) in media from challenged macrophages compared with media with H 2 O 2 solution. Overall, the study provides in vitro experimental evidence for the possible role of macrophages in altering the chemical environment within the crevice and thereby accelerating corrosion of CoCrMo alloy.

Wear particles induce a new macrophage phenotype with the potential to accelerate material corrosion within total hip replacement interfaces

“…Changes in macrophage dynamics provide insights into the cellular mechanisms of CAC. Previous findings from in vitro experiments 9 suggested that amongst the periprosthetic cell populations, macrophages have a prominent impact, generating a corrosive environment. The results showed an increase in corrosion kinetics and rate of corrosion of CoCrMo alloy when exposed to media produced by macrophages challenged with wear particles.…”

“…THP-1 monocytes were treated with 5 ng/mL PMA (Sigma, P1585) for 24 h. Further, the cells were treated in three different conditions 1) M1 macrophages by incubating with, 20 ng/mL IFN-γ (R&D systems, Cat# 285-IF-100), and 10 pg/mL LPS (Sigma, #8630), 2) M2 polarization by incubating cells with 20 ng/mL IL-4 (R&D Systems, Cat#204-IL-010)), and 20 ng/mL IL-13 (R&D Systems, Cat#213-ILB-005) 49 and, 3) M CA cells were generated by treating CoCr wear particles at a concentration of 1 μg/mL to M0 macrophages for a period of 24 hours (Figure 2a). The concentration of wear particles was chosen based on the dose-dependent toxicity evaluation reported in our previous studies on neuronal cells 47 , monocytes, macrophages and osteoblast cells 9 . The results from the previous study showed that the concentration of wear particles required to challenge the monocytes and macrophages with >88% viability after 24 hours was 1 μg/ml.…”

“…Also, severe corrosion damage such as pitting, intergranular corrosion, and localized etching have been observed, which points to an aggressive chemical attack. In our previous study, we provided substantial in vitro evidence for cell-accelerated corrosion (CAC), highlighting the prominent role of macrophages in producing a corrosive chemical environment 9 . Furthermore, we found that macrophages can alter the chemical environment in the presence of wear debris generated from CoCrMo alloy and compromise the corrosion properties of CoCrMo alloy.…”

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“…These effects can have downstream long-term effects on prosthesis longevity such as ROS generation potentially being linked with endoprosthesis loosening through excessive cell death in the surrounding areas [26]. Similarly, the inflammatory conditions caused by these particles could give way to activate macrophage promoted corrosion, resulting in feedback that drives an accelerated corrosion rate [31]. Ultimately, these effects highlight the importance in analyzing the material to identify ways to strengthen and reduce corrosion or wear products that may become biologically relevant.…”

In vitro testing for hip head-neck taper tribocorrosion: A review of experimental methods

“…More recently, biological factors have also been identified 5 and termed cell-accelerated corrosion (CAC). 6 In vitro studies are challenged by head-neck taper connection tribocorrosion's multifactorial nature and inherently involve simplifications. At their most complex, invitro simulations attempt to replicate the taper connection's failure process.…”