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Potentiodynamic Corrosion Testing
Published on: September 4, 2016
Acrylic fragmentation in total hip replacements and its biological consequences
M Jasty1, W Jiranek, W H Harris
1Orthopaedic Biomechanics Laboratory, Massachusetts General Hospital, Boston 02114.
Clinical Orthopaedics and Related Research
|December 1, 1992
Summary
Fragmentation of acrylic cement in joint prostheses causes a foreign-body reaction. This reaction, driven by macrophages and giant cells, leads to bone resorption and implant loosening, independent of the immune system.
Area of Science:
- Biomaterials Science
- Orthopedic Surgery
- Immunology
Background:
- Total joint prostheses loosening is often linked to acrylic cement fragmentation.
- Particulate acrylic debris triggers adverse biologic responses at the bone-cement interface.
Purpose of the Study:
- To investigate the fractographic features of retrieved femoral cement mantles.
- To characterize the biologic response to particulate acrylic debris.
- To determine the role of the immune system in this reaction.
Main Methods:
- Fractographic analysis of explanted cement mantles.
- Histologic and immunohistochemical examination of human and animal tissues.
- Organ culture studies of bone resorption.
- In vivo studies using immunocompetent and immunodeficient mice.
Main Results:
- Cement fractures and wear were common, releasing particulate acrylic debris.
- A macrophage and giant-cell foreign-body granulomatous reaction occurred in response to particulate, not bulk, cement.
- This reaction, capable of bone resorption, was induced by particulate polymethylmethacrylate (PMMA) in all tested mouse strains, regardless of immune status.
- The reaction was sustained by nonimmune phagocytosis and macrophage activation, not classic immune mechanisms.
Conclusions:
- Acrylic cement fragmentation is a key factor in joint prosthesis loosening.
- The biologic response to particulate cement is a nonimmune, macrophage-mediated foreign-body reaction.
- This reaction contributes to bone resorption and implant failure independently of the host's immune system.

