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The generation of prosthetic implant wear after total joint arthroplasty is recognized as the major initiating event in development of periprosthetic osteolysis and aseptic loosening, the leading complication of this otherwise successful surgical procedure. We review current concepts of how wear debris causes osteolysis, and report ideas for prevention and treatment. Wear debris primarily targets macrophages and osteoclast precursor cells, although osteoblasts, fibroblasts, and lymphocytes also may be involved. Molecular responses include activation of MAP kinase pathways, transcription factors (including NFkappaB), and suppressors of cytokine signaling. This results in up-regulation of proinflammatory signaling and inhibition of the protective actions of antiosteoclastogenic cytokines such as interferon gamma. Strategies to reduce osteolysis by choosing bearing surface materials with reduced wear properties should be balanced by awareness that reducing particle size may increase biologic activity. There are no approved treatments for osteolysis despite the promise of therapeutic agents against proinflammatory mediators (such as tumor necrosis factor) and osteoclasts (bisphosphonates and molecules blocking receptor activator of NFkappaB ligand [RANKL] signaling) shown in animal models. Considerable efforts are underway to develop such therapies, to identify novel targets for therapeutic intervention, and to develop effective outcome measures.

The low wear rates associated with ceramic hip articulations have made them a popular bearing for younger patients. Although few complications have been observed, one report revealed several instances of incomplete seating of the ceramic liner in the metallic shell. We performed a cohort study of consecutive THAs using a ceramic-ceramic bearing. Radiographic analysis showed 50 (7.2%) of the group of 694 hips had evidence of incomplete seating of the liner in the metallic shell. Although we observed no adverse effects at 6 to 12 weeks, we encourage surgeons to carefully assess liner placement in the metal shell at the time of surgery to avoid this unintended consequence and to assess placement at the time of followup so patients can be properly followed when incomplete seating is identified. Level of Evidence: Level IV, therapeutic study. See the Guidelines for Authors for a complete description of levels of evidence.

The Contour cage introduced in 1999 was designed to improve fixation and provide a surface for bone ongrowth. To determine whether the rates of radiographic loosening and/or revision have been reduced with the Contour design, we retrospectively reviewed the medical records and radiographs of 29 patients (average age, 68.1 years) undergoing 31 acetabular revisions with a Contour cage. The minimum followup was 24 months (mean 30 months, range, 24-58 months). Based on the Paprosky classification, two hips were Type 2B, seven were Type 3A, and 22 were Type 3B. Two hips (7%) were revised for loosening; one of these two was also infected. An additional five hips (16%) had signs of radiographic loosening. The mean Harris hip score improved from 45 to 80; functional scores improved less than the pain scores. Only 14 hips (45%) had an excellent or good clinical result and three of these 14 hips had radiographic signs of loosening; presuming these three hips eventually fail, only 35% of the hips had a good or excellent result. We found an association between number of previous surgeries and radiographic loosening and revision. Our data suggest the Contour cage offers little advantage over other antiprotrusio cages and highlight the substantial limitations of current methods available for treating patients with extensive acetabular bone loss.