Tribocorrosion of a CoCrMo alloy sliding against articular cartilage and the impact of metal ion release on chondrocytes.

Partial knee replacement and hemiarthroplasty are some of the orthopedic procedures resulting in a metal on cartilage interface. As metal implant material, CoCrMo based alloys are commonly used. The aim of the present study is to assess the role of biotribocorrosion on the CoCrMo-cartilage interface with an emphasis on metal release during sliding contact. The biotribocorrosion experiments were performed under controlled electrochemical conditions using a floating cell with a three electrode set up coupled to a microtribometer. Throughout the experiment the coefficient of friction and the open circuit potential were monitored. Analyses of the electrolyte after the experiment show that metal release can occur during sliding contact of CoCrMo alloy against articular cartilage despite the extraordinary low coefficient of friction measured. Metal release is attributed to changes in passive layer caused at the onset of sliding. The released metal was found to be forming compounds with potential cytotoxicity. Since the presence of metal ions in the cartilage matrix can potentially lead to cell apoptosis, the metabolic activity of human osteoarthritic chondrocytes (2D-cultures) was investigated in the presence of phosphate buffered saline containing metal ions using XTT-assay. The experiments indicate that critical concentrations of Co ions lead to a significant decrease in chondrocyte metabolic activity. Therefore, biotribocorrosion is a mechanism that can occur in partial replacements and lead to chondrocyte apoptosis thus playing a role in the observed accelerated degradation of the remaining cartilage tissue after the mentioned orthopedic procedures. STATEMENT OF SIGNIFICANCE: Partial replacements provide an alternative to total joint replacements. This procedure is less invasive, allows a faster rehabilitation and provides a better function of the joint. However, the remaining native cartilage experiences accelerated degradation when in contact with metallic implant components. This work investigates the role of tribocorrosion at the metal-cartilage interface during sliding. Tribocorrosion is a degradation process that can alter significantly the wear rates experienced by metallic implants and lead to the release of metal ions and particles. The released metal can form compounds with potential cytotoxicity on cartilage tissue. The knowledge gained in this work will serve to understand the mechanisms behind the failure of partial replacements and develop future biomaterials with an enhanced lifetime.

Orthopaedic implant related metal toxicity in terms of human lymphocyte reactivity to metal-protein complexes produced from cobalt-base and titanium-base implant alloy degradation.

Metal toxicity from sources such as orthopaedic implants was investigated in terms of immune system hyper-reactivity to metal implant alloy degradation products. Lymphocyte response to serum protein complexed with metal from implant alloy degradation was investigated in this in vitro study using primary human lymphocytes from healthy volunteers (n = 10). Cobalt chromium molybdenum alloy (Co-Cr-Mo, ASTM F-75) and titanium alloy (Ti-6Al-4V, ASTM F-136) beads (70 microm) were incubated in agitated human serum at 37 degrees Celsius to simulate naturally occurring metal implant alloy degradation processes. Particulate free serum samples, which were incubated with metal, were then separated into molecular weight based fractions. The amounts of soluble Cr and Ti within each serum fraction were measured and correlated with lymphocyte proliferation response to the individual serum fractions. Lymphocytes from each subject were cultured with 11 autologous molecular weight based serum fractions either with or without added metal. Two molecular weight ranges of human serum proteins were associated with the binding of Cr and Ti from Co-Cr-Mo and Ti implant alloy degradation (at < 30 and 180-330 kDa). High molecular weight serum proteins (approximately 180 kDa) demonstrated greater lymphocyte reactivity when complexed with metal released from Co-Cr-Mo alloy and Ti alloy than with low (5-30 kDa) and midrange (30-77 kDa) serum proteins. When the amount of lymphocyte stimulation was normalized to both the moles of metal and the moles of protein within each fraction (Metal-Protein Complex Reactivity Index, MPCRI), Cr from Co-Cr-Mo alloy degradation demonstrated approximately 10 fold greater reactivity than Ti in the higher molecular weight serum proteins (approximately 180-250 kDa). This in vitro study demonstrated a lymphocyte proliferative response to both Co-Cr-Mo and Ti alloy metalloprotein degradation products. This response was greatest when the metals were complexed with high molecular weight proteins, and with metal-protein complexes formed from Co-Cr-Mo alloy degradation.