Abstract
BackgroundThe toxicity of released metallic particles generated in metal-on-metal (MoM) total hip arthroplasty (THA) using cobalt chromium (CoCr) has raised concerns regarding their safety amongst both surgeons and the public. Soft tissue changes such as pseudotumours and metallosis have been widely observed following the use of these implants, which release metallic by-products due to both wear and corrosion. Although activated fibroblasts, the dominant cell type in soft tissues, have been linked to many diseases, the role of synovial fibroblasts in the adverse reactions caused by CoCr implants remains unknown. To investigate the influence of implants manufactured from CoCr, the periprosthetic synovial tissues and synovial fibroblasts from patients with failed MoM THA, undergoing a revision operation, were analysed and compared with samples from patients undergoing a primary hip replacement, in order to elucidate histological and cellular changes.ResultsPeriprosthetic tissue from patients with MoM implants was characterized by marked fibrotic changes, notably an increase in collagen content from less than 20% to 45–55%, an increase in α-smooth muscle actin positive cells from 4 to 9% as well as immune cells infiltration. Primary cell culture results demonstrated that MoM synovial fibroblasts have a decreased apoptosis rate from 14 to 6% compared to control synovial fibroblasts. In addition, synovial fibroblasts from MoM patients retained higher contractility and increased responsiveness to chemotaxis in matrix contraction. Their mechanical properties at a single cell level increased as observed by a 60% increase in contraction force and higher cell stiffness (3.3 kPa in MoM vs 2.18 kPa in control), as measured by traction force microscopy and atomic force microscopy. Further, fibroblasts from MoM patients promoted immune cell invasion by secreting monocyte chemoattractant protein 1 (MCP-1, CCL2) and induced monocyte differentiation, which could also be associated with excess accumulation of synovial macrophages.ConclusionSynovial fibroblasts exposed in vivo to MoM THA implants that release CoCr wear debris displayed dramatic phenotypic alteration and functional changes. These findings unravelled an unexpected effect of the CoCr alloy and demonstrated an important role of synovial fibroblasts in the undesired tissue reactions caused by MoM THAs.
Highlights
The toxicity of released metallic particles generated in metal-on-metal (MoM) total hip arthroplasty (THA) using cobalt chromium (CoCr) has raised concerns regarding their safety amongst both surgeons and the public
While immune cells play a key role in the initiation and progression of the tissue reactions [1, 10], some evidence suggests that chronic inflammation occurs because of the activated fibroblasts, resulting in the inappropriate survival and retention of immune cells within inflamed tissue [11]
To further investigate whether this interaction between fibroblasts and immune cells occurs in vivo following exposure to CoCr particulates and associated ions, we examined ex vivo the properties of fibroblasts isolated from periprosthetic synovial tissues from patients implanted with a MoM THA, retrieved during revision operations
Summary
The toxicity of released metallic particles generated in metal-on-metal (MoM) total hip arthroplasty (THA) using cobalt chromium (CoCr) has raised concerns regarding their safety amongst both surgeons and the public Soft tissue changes such as pseudotumours and metallosis have been widely observed following the use of these implants, which release metallic by-products due to both wear and corrosion. Synovial tissues retrieved at the MoM revision surgery have shown the presence of a large number of amorphous particles predominantly composed of chromium and cobalt [5,6,7] The majority of these particles from the implants are in the nano-sized scale and the severity of the adverse tissue reactions is reported to be related with the complexity of the particles and blood metal ion levels [7]. The role of stromal fibroblasts and tissue/extracellular matrix (ECM) organisation in the inflammatory response following exposure to cobalt metal wear and corrosion products in vivo remains largely unknown
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