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Different apoptosis modalities in periprosthetic membranes
Maurizio Sabbatini1, Valentina Piffanelli, Francesca Boccafoschi
1Human Anatomy Laboratory, Research Center for Biocompatibility, Clinical and Experimental Medicine Department,University of Eastern Piedmont A Avogadro, Via Solaroli 17, 28100 Novara, Italy. maurizio.sabbatini@med.unipmn.it
Journal of Biomedical Materials Research. Part A
|January 24, 2009
Summary
Periprosthetic membranes from hip arthroplasty show debris from implants can cause cell death. In septic conditions, caspase-3 may drive tissue proliferation rather than cell death.
Area of Science:
- Biomaterials Science
- Cell Biology
- Orthopedic Surgery
Background:
- Periprosthetic membranes form around implants during revision surgery.
- Understanding cellular responses to implant debris is crucial for addressing implant failure.
Purpose of the Study:
- Investigate apoptotic and proliferation signals in periprosthetic membranes.
- Differentiate cellular responses to debris from cementless (titanium alloy) and cemented (Co-Cr) prostheses under aseptic and septic conditions.
Main Methods:
- Collected periprosthetic membranes during revision hip arthroplasty.
- Utilized fluorescence and colorimetric immunohistochemistry to assess cell death (Bax, caspase-3) and proliferation (Ki-67) signals.
- Analyzed samples from aseptic and septic, cementless and cemented prosthesis.
Main Results:
- Aseptic cementless debris (titanium alloy) induced oxidative cell death in macrophages and fibroblasts.
- Aseptic cemented debris (Co-Cr) induced apoptotic-like cell death in fibroblasts and some leukocytes.
- Septic environments showed reduced leukocyte apoptosis, while fibroblasts exhibited proliferation (Ki-67) and caspase-3 activation, suggesting a role in proliferation.
Conclusions:
- Implant debris composition and prosthetic fixation type influence cellular responses.
- Septic conditions may alter the role of caspase-3 from cell death to tissue proliferation.
- Apoptosis in periprosthetic tissues can signify inflammation resolution, normal turnover, or cell renewal linked to proliferation.
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