PubMed · 11407821
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M Gross. 2001. Electronic data collection at source for a joint replacement registry.. https://pubmed.ncbi.nlm.nih.gov/11407821/
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The interaction of macrophages and ultra-high molecular weight polyethylene (PE) wear plays an important role in perpetuating chronic inflammation at the bone implant interface, leading to peri-implant osteolysis and mechanical failure of the implant. A model to study the interaction of human mature macrophages with orthopaedic biomaterial wear has been previously developed. With the use of the model, in this study, the mature human monocyte-derived macrophages (MDMs) were observed with light, fluorescent, and scanning electron microscopy (SEM), as well as transmission electron microscopy (TEM). The cell viability was investigated using calcein and ethidium staining. Following exposure to PE particulate, the morphology of the human MDMs was heterogeneous: rounded, flattened, and elongated. There was no morphological evidence of cytotoxicity or apoptosis. The MDM viability was not influenced by phagocytosis of PE particulate in a negative fashion. In fact, more prolonged cell viability was observed in the human MDMs exposed to PE particulate when compared to controls.
Orthopedic wear debris has been thought to be an important factor associated with osteolysis and loosening of total joint arthroplasties. Previous in vitro studies have reported that particles of wear debris induce the release of pro-inflammatory cytokines and other inflammatory mediators from macrophages and other cells. Several recent investigations, however, have suggested that the wear particles themselves may not be primarily responsible for the inflammatory cellular responses, but that the observed cytokine release in vitro may be caused by endotoxin adsorbed to commercially available particle preparations. The intracellular pathways involved in macrophage signal transduction also are poorly understood. The purposes of this study are to use isolated orthopedic wear debris particles to evaluate pro-inflammatory cytokine release and nuclear factor kappa B (NFkappaB) activation from macrophages. Cells from human monocyte/macrophage cell line (THP-1) were differentiated and incubated with particles of debris that had been isolated from a failed human total hip arthroplasty. The titanium-alloy particles did not evoke release of TNF-alpha or IL-1beta whereas lipopolysaccharide (LPS) or LPS-treated debris particles induced both TNF-alpha and IL-1beta. LPS-treated particles, but not particles alone, stimulated NFkappaB activation. Our results suggest that at the concentrations tested in this study, endotoxin-free wear debris particles may not themselves initiate inflammatory cellular responses in differentiated THP-1 cells. It is unclear whether adsorbed endotoxin is clinically associated with osteolysis and/or loosening in total joint arthroplasties, but several factors, including adsorbed endotoxin, need to be investigated to explore the cellular responses responsible for osteolysis and/or loosening.
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