BackgroundPrevious studies regarding modular head-neck taper corrosion were largely based on cobalt chrome (CoCr) alloy femoral heads. Less is known about head-neck taper corrosion with ceramic femoral heads.Questions/purposesWe asked (1) whether ceramic heads resulted in less taper corrosion than CoCr heads; (2) what device and patient factors influence taper fretting corrosion; and (3) whether the mechanism of taper fretting corrosion in ceramic heads differs from that in CoCr heads.MethodsOne hundred femoral head-stem pairs were analyzed for evidence of fretting and corrosion using a visual scoring technique based on the severity and extent of fretting and corrosion damage observed at the taper. A matched cohort design was used in which 50 ceramic head-stem pairs were matched with 50 CoCr head-stem pairs based on implantation time, lateral offset, stem design, and flexural rigidity.ResultsFretting and corrosion scores were lower for the stems in the ceramic head cohort (p = 0.03). Stem alloy (p = 0.004) and lower stem flexural rigidity (Spearman’s rho = −0.32, p = 0.02) predicted stem fretting and corrosion damage in the ceramic head cohort but not in the metal head cohort. The mechanism of mechanically assisted crevice corrosion was similar in both cohorts although in the case of ceramic femoral heads, only one of the two surfaces (the male metal taper) engaged in the oxide abrasion and repassivation process.ConclusionsThe results suggest that by using a ceramic femoral head, CoCr fretting and corrosion from the modular head-neck taper may be mitigated but not eliminated.Clinical RelevanceThe findings of this study support further study of the role of ceramic heads in potentially reducing femoral taper corrosion.
The use of multiple-component systems in orthopedic surgery gives the surgeon increased flexibility in choosing the optimal implant, but introduces the possibility of interfacial corrosion. Such corrosion could limit the longevity of prostheses due either to tissue reactions to corrosion products, or to device failure. The incidence and nature of corrosion of modular total hips was evaluated in a consecutive series of 79 retrieved implants from University Hospitals of Cleveland. Surfaces were examined with stereo- and scanning electron microscopy. Several laboratory studies were undertaken to examine mechanisms that might contribute to the initiation of corrosion. The first set of experiments investigated the effect of head neck extension; the second study looked at the effect of material combinations on fretting corrosion and crevice corrosion. Analysis of retrieved implants demonstrated that fretting corrosion played a major role in the initiation of interface corrosion, and that a correlation existed between corrosion and length of neck extensions. Laboratory studies showed that longer head neck extensions may be more susceptible to fretting corrosion because of an instability at the interface. Short-term mixed-metal corrosion studies demonstrated that the coupling of cobalt and titanium alloys did not render the interface more susceptible to corrosion. It is hypothesized that fretting corrosion contributes to the initiation of modular interface corrosion, and that the problem can be reduced by design changes that increase the stability of the interface.
Our research group developed an implant retrieval program to study in vivo degradation of polyethylene. We now have evidence to support our hypothesis that degradation of radiation-sterilized polyethylene occurs in the body for not only historical gamma air sterilized liners, but also for conventional gamma inert sterilized (ArCom) and annealed highly crosslinked polyethylene (Crossfire) liners as well. Our research has also led to the discovery that the most severe manifestations of in vivo oxidation typically occur in regions of the liner experiencing minimal wear, such as the rim of the component, where the body fluids (containing oxidizing species) have access to the polyethylene. Our data from historical, ArCom, and Crossfire retrievals all point to a similar scenario in which the femoral head limits the in vivo oxidation of polyethylene at the bearing surface. Consequently, provided rim impingement does not occur, and the polyethylene locking mechanisms remain relatively isolated from oxidizing fluid, in vivo oxidation does not seem to be clinically important in the first 10 years of implantation for conventional gamma sterilized polyethylene. We conclude that in vivo degradation should be included among the list of potential long-term failure modes for modular polyethylene components for total hip arthroplasty.
Hydrostatic pressure (HP) is thought to increase within cartilage extracellular matrix as a consequence of fluid flow inhibition. The biosynthetic response of human articular chondrocytes to HP in vitro varies with the load magnitude, load frequency, as well as duration of loading. We found that continuous cyclic HP (5 MegaPascals (MPa) for 4 h; 1 Hz frequency) induced apoptosis in human chondrocytes derived from osteoarthritic cartilage in vitro as evidenced by reduced chondrocyte viability which was independent of initial cell densities ranging from 8.1 x 10(4) to 1.3 x 10(6) cells ml(-1). HP resulted in internucleosomal DNA fragmentation, activation of caspase-3, and cleavage of poly-ADP-ribose polymerase (PARP). At the molecular level, induction of apoptosis by HP was characterized by up-regulation of p53, c-myc, and bax-alpha after 4 h with concomitant down-regulation of bcl-2 after 2 h at 5 MPa as measured by RT-PCR. In contrast, beta-actin expression was unchanged. Real-time quantitative RT-PCR confirmed a HP-induced (5 MPa) 1.3-2.6 log-fold decrease in bcl-2 mRNA copy number after 2 and 4 h, respectively, and a significant increase (1.9-2.5 log-fold) in tumor necrosis factor-alpha (TNF-alpha) and inducible nitric oxide synthase (iNOS) mRNA copy number after 2 and 4 h, respectively. The up-regulation of p53 and c-myc, and the down-regulation of bcl-2 caused by HP were confirmed at the protein level by Western blotting. These results indicated that HP is a strong inducer of apoptosis in osteoarthritic human chondrocytes in vitro.
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