Research Article

Acetabular Debonding: An Investigation of Porous Coating Delamination in Hip Resurfacing Arthroplasty

Table 4

Acetabular failure descriptions.

Failure CategoryDescription

1. Late acetabular looseningThought to represent initial implant integration with subsequent failure of attachment. We divide late loosening into three subtypes for more detailed analysis

1a. Debonding of the porous coatingThe main mode of interest in the current study. In these cases, initial fixation is achieved through bone ingrowth. At some point beyond 2 years, the well-fixed, porous layer from the component substrate “debonds”, causing subsequent implant loosening. The patients typically have excellent function prior to loosening with no change in acetabular component position on radiographs. They will then present with a 2-3-month prodrome of mild symptoms without radiographic findings before a sudden acute worsening of symptoms and an inability to bear weight on the affected leg. Loosening is then obvious radiographically with shifting of the acetabular component into a markedly steeper position. Intraoperative findings include a grossly loose acetabular component with a section of porous coating debonded from the implant substrate. This contiguous “sheet” of plasma spray coating, usually 20 to 30% of the total surface, is seen to be well fixed to the surrounding bone. The remainder of the porous coating remains attached to the implant and has no apparent bone ingrowth. There is a mild amount of metallosis and reactive fluid with no soft tissue mass. There is no fibrous pseudomembrane.

2b. Loosening with intact porous coatingRarely occurs after 2 years without debonding. These cases may represent cases of initial fibrous ingrowth with radiographically stable implants for at least 2 years and subsequent loss of fibrous fixation. They present with late onset of chronic pain and late change in radiographic AIA. They have acceptable metal ion levels (<10 µm/L) and small collections of serosanguinous fluid, with no significant metallosis, soft tissue masses, or muscle destruction. We exclude cases of AWRF (described below) from this group. Intraoperatively, the acetabular component is either grossly loose or easily detached with a tamp. There is a thin 2-3 mm fibrous membrane present, and the adjacent bone is typically quite hard.

3c. Status of porous coating unknownCases that have failed beyond 2 years and were revised elsewhere; therefore, we cannot categorize the mode of failure or status of the implant coating.

2. Early acetabular looseningOccurs before 2 years and is thought to be due to failure of bone ingrowth into the acetabular component, which can present with an acute cup spinout or a gradual symptomatic shift. In both types, the component usually shifts into a more steeply inclined position. The porous coating is found intact, and in early cases, blood may be encountered where the soft tissue dissection from the original operation has not yet completely healed. In the later cases of gradual shift, there is usually a fibrous layer with serous fluid. Black Ti metallosis is rarely seen. We have not observed AWRF before 2 years.

3.Adverse wear-related failure (AWRF)Caused by inadequate coverage arc [15, 31]. The relationship of AWRF to component bearing size, coverage arc, and implant AIA on standing radiographs was elucidated in our 2013 RAIL paper [31], which describes a safe zone for placing all cup sizes with a 99% confidence level. When these current study cases were performed, the importance of cup position was not yet appreciated. Therefore, a small percentage of AWRF occurred due to acetabular component malposition. These failures present with progressive chronic pain, usually after 5 years postoperatively. If routine blood metal ion testing at 2 years is undertaken, as recommended by DeSmet [15], these cases can be discovered before the patients become symptomatic and when soft tissue damage is minimal. Initially, radiographs are unremarkable except for unacceptably steep AIA (according to RAIL). Progressive femoral neck narrowing and lysis can occur in late cases. 3D studies show large fluid collections and soft tissue masses. Extensive grey tissue staining, milky tan fluid, and inflammatory soft tissue masses are encountered at revision. Usually, some metallic filled lysis is present. Bone loss is typically much less prominent than soft tissue inflammation. Component loosening is rare. We have never seen significant muscle destruction in HRA AWRF. In our experience, tissue inflammation in THA due to trunnion corrosion may be more severe with low ion levels and should be considered separately from HRA pure bearing wear. We emphasize that the tissue destruction seen in MoM THA cases cannot be considered equivalent to AWRF in HRA.