STP1301

    The Fibrous Tissue Interface Surrounding Well-Fixed, Revised, Cementless Acetabular Components for Hip Replacement

    Published: Jan 1997


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    Abstract

    Ten well-fixed, cementless, metal-backed acetabular components were revised due to recurrent hip dislocation, polyethylene wear or during femoral revision due to aseptic loosening. Eight cups were modular and two cups were nonmodular. Seven of the eight modular cups were fixed with one or more screws; the two nonmodular cups had two pegs but no screws for fixation. The cups were revised after a period of 3.5–72 months. The fibrous tissue surrounding the implant was harvested, and frozen sections were processed using immunohistochemistry and in situ hybridization. The tissue formed a thin, gritty, incomplete fibrous layer that was tightly adherent to the surface of the metal-backed components. Scattered macrophages and lymphocytes were present within the fibrous stroma in all tissues. Gross, black metallic staining of 3 tissues was associated with increased cellularity. Generally, macrophages expressed mRNA for EL-1, IL-6, PDGFa, and TNFa, and fibroblasts were TGFb positive; these factors are known to modulate the remodeling of bone. No relationship was found between the cellular and cytokine profiles and modularity, the type of metal backing, the presence of screws or the time in situ. The fibrous tissue surrounding well-fixed, cementless, metal-backed acetabular cups undergoing revision surgery contained many of the cellular elements and cytokines associated with loosening and osteolysis.

    Keywords:

    total joint replacement, cementless acetabular cups, modularity, well-fixed, immunohistochemistry, in situ hybridization


    Author Information:

    Goodman, SB
    Associate Professor and Chief, Stanford University School of Medicine, Stanford, California

    Huie, P
    Research Associate, Stanford University School of Medicine, Stanford, California

    Song, Y
    Research Assistant, Stanford University School of Medicine, Stanford, California

    O'Connor, M
    Clinical Professor, Stanford University School of Medicine, Stanford, California

    Woolson, ST
    Clinical Associate Professor, Stanford University School of Medicine, Stanford, California

    Maloney, WJ
    Professor, Stanford University School of Medicine, Stanford, California

    Schurman, DJ
    Professor, Stanford University School of Medicine, Stanford, California

    Sibley, R
    Senior Research Associate, Stanford University School of Medicine, Stanford, California


    Paper ID: STP12018S

    Committee/Subcommittee: F04.22

    DOI: 10.1520/STP12018S


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