There are limited published data detailing the volumetric material loss from tapers of conventional metal-on-polyethylene (MoP) total hip arthroplasties (THAs). Our aim was to address this by comparing the taper wear rates measured in an explanted cohort of the widely used Exeter THA with those measured in a group of metal-on-metal (MoM) THAs. We examined an existing retrieval database to identify all Exeter V40 and Universal MoP THAs. Volumetric wear analysis of the taper surfaces was conducted using previously validated methodology. These values were compared with those obtained from a series of MoM THAs using non-parametric statistical methodology. A number of patient and device variables were accounted for using multiple regression modelling.Aims
Patients and Methods
We sought to determine whether cobalt-chromium alloy (CoCr) femoral
stem tapers (trunnions) wear more than titanium (Ti) alloy stem
tapers (trunnions) when used in a large diameter (LD) metal-on-metal
(MoM) hip arthroplasty system. We performed explant analysis using validated methodology to
determine the volumetric material loss at the taper surfaces of
explanted LD CoCr MoM hip arthroplasties used with either a Ti alloy
(n = 28) or CoCr femoral stem (n = 21). Only 12/14 taper constructs
with a rough male taper surface and a nominal included angle close
to 5.666° were included. Multiple regression modelling was undertaken
using taper angle, taper roughness, bearing diameter (horizontal
lever arm) as independent variables. Material loss was mapped using
a coordinate measuring machine, profilometry and scanning electron
microscopy.Aims
Patients and Methods
Concerns have been raised that deformation of
acetabular shells may disrupt the assembly process of modular prostheses.
In this study we aimed to examine the effect that the strength of
bone has on the amount of deformation of the acetabular shell. The
hypothesis was that stronger bone would result in greater deformation.
A total of 17 acetabular shells were inserted into the acetabula
of eight cadavers, and deformation was measured using an optical
measuring system. Cores of bone from the femoral head were taken
from each cadaver and compressed using a materials testing machine.
The highest peak modulus and yield stress for each cadaver were used
to represent the strength of the bone and compared with the values
for the deformation and the surgeon’s subjective assessment of the
hardness of the bone. The mean deformation of the shell was 129
µm (3 to 340). No correlation was found between deformation and
either the maximum peak modulus (r² = 0.011, t = 0.426, p = 0.676) or
the yield stress (r² = 0.024, t = 0.614, p = 0.549) of the bone.
Although no correlation was found between the strength of the bone
and deformation, the values for the deformation observed could be
sufficient to disrupt the assembly process of modular acetabular
components. Cite this article:
Abnormal wear of cobalt-containing metal-on-metal
joints is associated with inflammatory pseudotumours. Cobalt ions
activate human toll-like receptor 4 (TLR4), which normally responds
to bacterial lipopolysaccharide (LPS) in sepsis. Activation of TLR4
by LPS increases the expression of chemokines IL-8 and CXCL10, which
recruit leukocytes and activated T-cells, respectively. This study
was designed to determine whether cobalt induces a similar inflammatory
response to LPS by promoting the expression of IL-8 and CXCL10.
A human monocytic cell line, derived from acute monocytic leukaemia,
was treated with cobalt ions and expression of IL-8 and CXCL10 measured at
mRNA and protein levels. Cobalt-treated macrophages showed a 60-fold
increase in IL-8 mRNA, and an eightfold increase in production of
the mature chemokine (both p <
0.001); expression of the CXCL10
gene and protein was also significantly increased by cobalt (both
p <
0.001). Experiments were also performed in the presence of
CLI-095, a TLR4-specific antagonist which abrogated the cobalt-mediated
increase in IL-8 and CXCL10 expression. These findings suggest that cobalt ions induce inflammation similar
to that observed during sepsis by the simultaneous activation of
two TLR4-mediated signalling pathways. These pathways result in
increased production of IL-8 and CXCL10, and may be implicated in
pseudotumour formation following metal-on-metal replacement. Cite this article:
