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Aseptic loosening is the most common cause of failure of joint arthroplasties. Although the exact pathogenesis of the loosening process is not completely understood, particles of polymethyl methacrylate and polyethylene appear to play a crucial role. This paper summarizes past and current clinical and experimental research on the biology of aseptic loosening of joint arthroplasties and discusses the important role of particulate polymeric debris.

Fourteen mature female New Zealand White rabbits underwent implantation of Simplex polymethylmethacrylate (PMMA) powder or particulate (average 67 microns) ultrahigh-molecular-weight polyethylene (UHMWPE) through a drill hole in the proximal right tibia. The left tibia functioned as a prepared but nonimplanted control. Animals were killed after 16 weeks. Histological examination of the bone-implant interface in the particulate PMMA group disclosed a florid foreign-body reaction with the presence of giant cells and histiocytes. The particulate UHMWPE group demonstrated positively birefringent UHMWPE fragments, rimmed by foreign-body giant cells and histiocytes, embedded in a loose connective tissue stroma. UHMWPE interfaces were thicker and contained more histiocytes and fibrocytes; PMMA interfaces contained more marrow cells and lymphocytes. This study underscores the importance of biomaterial debris in the process of aseptic loosening of cemented joint arthroplasties.

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