Atomic Scale Origin of Metal Ion Release from Hip Implant Taper Junctions

Abstract

Millions worldwide suffer from arthritis of the hips, and total hip replacement is a clinically successful treatment for end‐stage arthritis patients. Typical hip implants incorporate a cobalt alloy (Co–Cr–Mo) femoral head fixed on a titanium alloy (Ti‐6Al‐4V) femoral stem via a Morse taper junction. However, fretting and corrosion at this junction can cause release of wear particles and metal ions from the metallic implant, leading to local and systemic toxicity in patients. This study is a multiscale structural‐chemical investigation, ranging from the micrometer down to the atomic scale, of the underlying mechanisms leading to metal ion release from such taper junctions. Correlative transmission electron microscopy and atom probe tomography reveals microstructural and compositional alterations in the subsurface of the titanium alloy subjected to in vitro gross‐slip fretting against the cobalt alloy. Even though the cobalt alloy is comparatively more wear‐resistant, changes in the titanium alloy promote tribocorrosion and subsequent degradation of the cobalt alloy. These observations regarding the concurrent occurrence of electrochemical and tribological phenomena are vital to further improve the design and performance of taper junctions in similar environments.

Osteoblasts-derived Exosomes as Novel Communicators in Particle Induced Periprosthetic Osteolysis

“…Histopathological examinations reveal that Ti wear debris with a diversity of sizes and crystal structures accumulate in the synovia-like peri-implant membrane, bone marrow as well as periimplant regions that are affected by brotic and in ammatory changes [6]. Due to their high persistency (low solubility), the interaction of wear debris with cells and tissues induce a complex immune response that can lead to periprosthetic osteolysis (degeneration of bone causing aseptic loosening) and implant failure with a consequent need of a revision surgery [3][4][5][7][8][9][10]. Besides the severe consequences for the patients' health conditions (e.g., higher rates of mortality, hospital readmission, dislocation, and infection), revision surgeries pose a high nancial burden on healthcare systems (longer surgery time, expensive prostheses, longer hospitalization periods, and higher rates of health complications) [10][11].…”

“…Background Titanium (Ti) and its alloys are the biomaterials mostly used in joint replacements due to their excellent biocompatibility [1][2]. However, one of the main drawbacks to Ti is its susceptibility to both mechanical wear (due to cyclic loading) and corrosion (due to the contact with biological uids) events resulting in the release of wear debris and corrosion products that give rise to local and systemic complications to patients [3][4][5]. Histopathological examinations reveal that Ti wear debris with a diversity of sizes and crystal structures accumulate in the synovia-like peri-implant membrane, bone marrow as well as periimplant regions that are affected by brotic and in ammatory changes [6].…”

“…The main biological mechanisms underlying the response to Ti wear debris are innate immune response where the phagocytosis of wear particles induces macrophages activation [12]. The reactivity of macrophage results in a pro-in ammatory milieu (up-regulation of pro-in ammatory cytokines, mainly IL-1b, IL-6, and TNF-alfa) in the proximity of bone that perturb its homeostasis (reduced osteoblastogenesis and increased osteoclastogenesis) leading to periprosthetic bone osteolysis [5,[7][8][9][10]12]. Although chronic in ammatory reaction is mostly driven by macrophages, osteolysis is also indirectly caused by the contribution of other cell types such as osteoblasts, dendritic cells, osteoclasts, and synovial broblasts.…”

“…Besides that, chronic in ammation can be maintained by a continuous release and diffusion of soluble mediators that drive progressive bone resorption, but it can also cause severe and extended pathologies such as metallosis or necrotic-appearing soft tissue masses [13]. One red ag is the ability of some debris, especially those at the nanoscale, to cross epithelial barriers and travel through the lymphatic or circulatory system and accumulate far from the site of the implant resulting in systemic toxicity [3][4][5]. Their circulation protected from phagocytosis by patrolling monocytes can be supported by extracellular vesicles (e.g.…”

Peripheral Blood Lymphocyte Subpopulations in Patients Following Small Diameter Metal-On-Metal Total Hip Replacement at Long-Term Follow-Up

“…In a recently published investigation, Balachandran et al described the folding mechanisms that take place during fretting at the taper junction between a co-chromium head and the femoral titanium taper. These folding mechanisms create raised shelves on the titanium surface that micro-plow the oxide film of the cobalt alloy and thereby promote tribocorrosion and metal ion release [4]. Accumulating metal ions are able to influence both bone metabolism and the immune system through different pathways, thereby contributing to the pathomechanisms of implant loosening and ALTR formation.…”