Failure of total hip arthroplasty with acetabular deficiency occurred in 55 patients (60 hips) and was treated with acetabular revision using morsellised allograft and a cemented metal-backed component. A total of 50 patients (55 hips) were available for clinical and radiological evaluation at a mean follow-up of 5.8 years (3 to 9.5). No hip required further revision of the acetabular component because of aseptic loosening.

All the hips except one had complete incorporation of the allograft demonstrated on the radiographs. A complete radiolucent line of > 1 mm was noted in two hips post-operatively. A good to excellent result occurred in 50 hips (91%). With radiological evidence of aseptic loosening of the acetabular component as the end-point, the survivorship at a mean of 5.8 years after surgery was 96.4%.

The use of impacted allograft chips in combination with a cemented metal-backed acetabular component and screw fixation can achieve good medium-term results in patients with acetabular bone deficiency.

Clinical experience indicates the beneficial effects of antibiotic-loaded bone cement. Although in vitro studies have shown the formation of a biofilm on its surface they have not considered the gap between the cement and the bone. We have investigated bacterial survival in that gap. Samples with gaps 200 μm wide were made of different bone cements. These were stored dry (‘pre-elution’) or submersed in phosphate-buffered saline to simulate the initial release of gentamicin (‘post-elution’). The gaps were subsequently inoculated with bacteria, which had been isolated from infected orthopaedic prostheses and assessed for their sensitivity to gentamicin. Bacterial survival was measured 24 hours after inoculation. All the strains survived in plain cements. In the pre-elution gentamicin-loaded cements only the most gentamicin-resistant strain, CN5115, survived, but in post-elution samples more strains did so, depending on the cement tested. Although high concentrations of gentamicin were demonstrated in the gaps only the gentamicin-sensitive strains were killed. This could explain the increased prevalence of gentamicin-resistant infections which are seen clinically.