Introduction: The ideal acetabular component has low wear, permanent fixation and physiological bone loading. Recently trabecular metal has been promoted as reproducing the modulus of trabecular bone with a cementless fixation. The aim of this trial was to see if a monobloc trabecular backed polyethylene acetabular component loaded the pelvis physiologically as a cemented polyethylene component.

Method: Between 2004 and 2006 54 patients were ran-domised to a cemented polyethylene acetabular component versus a monobloc trabecular backed polyethylene acetabular component. The primary outcome measurement was bone density in peri-prosthetic acetabular regions of interest measured preoperatively and post operatively at 6 weeks and 1 year. Secondary outcomes measured were radiographic and functional outcomes (HHS and Oxford score).

Results: Radiographically 8 patients in the trabecular group had a significant gap in zone II which resolved in 6 by 1 year. The cemented group had 3 patients with a radiolucent line (zone 1) at 1 year. HHS and OXFORD scores improved with no significant difference between the groups. Both groups had significant loss of bone density in the ilium and ischium. The trabecular group produced a significant increase in bone density in the superolateral region. The cemented group produced increased bone density in the superomedial region.

Discussions and Conclusions: There is a significant reduction in BMD for both groups in the upper pelvis and ischium in keeping with finite element modelling predictions. The press-fit group relative to the cemented group resulted in decreased BMD in the superomedial peri-prosthetic region. The trabecular monobloc cup therefore behaves more like a rigid cementless shell despite the properties of trabecular metal.

Aseptic loosening has become the single most important long-term complication of total joint replacements. The pathophysiology of this loosening is multifactorial in origin ranging from mechanical wear, poor surgical technique, thermal damage and the inflammatory response to particulate wear debris. Cytokines are released in response to macrophage activation by particulate wear debris (PWD), the resultant inflammatory cascade stimulates osteoclastic resorption of bone. The failure of remodelling and repair mechanisms may be as a result of Osteonecrosis from cement (PMMA).

Hypothesis: That PMMA increases Osteoblast susceptibility to necrosis and apoptosis following inflammatory challenge.

Materials and Methods: Osteoblast cell cultures were grown on PMMA cement plates and assessed for apoptosis and necrosis by PI exclusion staining, morphological changes on light and electron microscopy and flow cytometry.

Results: PMMA induced osteonecrosis is highest at 1 hour (34.45) in comparison to control levels (4.55). There is no significant change in Apoptosis at 24 hours. Culture of the Osteoblasts on cement and delayed stimulation with TNF-α causes increased Apoptosis and Necrosis.

Conclusion: PMMA cement causes Osteoblast necrosis in the early stages of polymerisation, after 24 hours there is little increase in apoptosis/necrosis. However Osteoblasts that grow in contact with cement are more susceptible to apoptosis and necrosis following TNFα challenge. This may prove to be an important step in the pathogenesis of Aseptic loosening.

Aseptic loosening is currently the leading cause of failure of total hip arthroplasty. The aetiology of periprosthetic bone resorption is currently under intense investigation. Wear particles are produced from the articulating surface of the femoral and acetabular components. These particles gain access to the bone-cement interface where they are phagocytosed by macrophages. Particle stimulated macrophages differentiate into bone resorping osteoclasts. This leads to periprosthetic bone resorption and subsequent implant loosening.

Nuclear factor kappa B (NFκB) is a transcription factor known to be activated by pathogenic stimuli in a variety of cells. The activation of NFkB would appear to be the primary event in the activation of particle stimulated macrophages in the periprosthetic membrane. NFκB subsequently causes a cascade of events leading to the release of bone resorbing cytokines, namely interleukin-6 (IL-6) and tumour necrosis factor α (TNFα).

The aim of our study was to ascertain if bone resorption could be prevented in vitro by the addition of PDTC, an NFkB inhibitor to particle stimulated macrophages.

Human monocytes were isolated and cultured from healthy volunteers. The monocyte/macrophage cell line was differentiated into osteoclasts by the addition of alumina particles and allowed to adhere onto bone slices. The NFkB inhibitor, PDTC, has added to the cultured osteoclasts. Bone resorption was analysed by counting the number of resorption pits in each bone slice.

The addition of PDTC to stimulated macrophages reduced the number of resorption pits by greater than 40% compared to control.

This is a unique and promising finding that may offer a future therapeutic strategy for the prevention of periprosthetic bone resorption and therefore aseptic loosening in total hip arthoplasty.