This is a renewal proposal for AR070181. Our long-term goal is to increase total joint arthroplasty (TJA)
longevity by eliminating fretting-corrosion induced adverse local tissue reactions (ALTRs). Lymphocyte
dominated ALTRs—caused by fretting-corrosion debris—remain a frequent cause of catastrophic total hip
arthroplasty (THA) failures with a prevalence of 3 to 5%. The lives of patients suffering an ALTR are changed
forever due to subsequent clinical complications, multiple re-revisions, and systemic toxic effects. Although
surgeons have attempted to mitigate corrosion risk with ceramic heads (with a metal sleeve) and titanium alloy
stems, fretting-corrosion persists, and even worsens due to increased use of modularity in different TJA types.
The initial term of our grant has laid the foundation for unraveling the complicated processes leading to fretting-
corrosion of modular taper junctions in THA and subsequent ALTRs. We found that the primary predictors of
the start of fretting processes are patient femoral off-set, taper surface topography, and surgical assembly
load. At fretting onset, material loss is governed by a mechanical fretting process called “imprinting”. Imprinting
along with insufficient manufacturing tolerances enable joint fluid to enter the confined space (crevice) of the
modular junction. Importantly, the most damaging corrosion process was not crevice corrosion, but rather a so
far little understood process termed cell accelerated corrosion (CAC). CAC appears to be driven by an influx of
macrophages into the modular junction. If activated by fretting debris, macrophages can create a harsh
chemical environment within the crevice that affects preferential corrosion sites within some implant alloy
microstructures. The incidence of ALTR is higher in cases with CAC. Thus, the objective of this study is to
elucidate the mechanism(s) by which synergistically acting implant design, material, patient, and surgical
factors enable ALTR through multiple paths, including imprinting, fretting-corrosion, and CAC. The central
hypothesis is two part: 1) Imprinting and insufficient manufacturing tolerances enable joint fluid to enter the
crevice of modular junctions. 2) Fluid infiltration allows corrosion processes via CAC, under which cells
activated with fretting debris cause a chemical attack and accelerate both material loss and the risk of ALTR.
We will test our hypothesis with three specific aims: 1) Identify factors dictating fretting onset in primary THA
surgery and revision surgical interventions. 2) Determine how implant design, bulk material, and implant alloy
microstructure can enable CAC in THA modular junctions. 3) Determine how implant alloy microstructure can
minimize the risk of material loss and ALTRs under progressing fretting-corrosion in THA modular junctions.
The outcomes of this research will enable a) improved implant geometry tolerances, b) material standards
preventing preferential corrosion sites, and c) preclinical testing strategies that also consider in vivo chemical
conditions. Collectively, this work will provide fretting-corrosion risk management workflows to inform careful
implant design and low-risk choices at primary or revision TJA.
