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Journal of Long-Term Effects of Medical Implants
SJR: 0.332 SNIP: 0.491 CiteScore™: 0.89

ISSN Print: 1050-6934
ISSN Online: 1940-4379

Journal of Long-Term Effects of Medical Implants

DOI: 10.1615/JLongTermEffMedImplants.2014010562
pages 259-265

Role of Macrophages in the Biological Reaction to Wear Debris from Joint Replacements

Christophe Nich
Laboratoire de Biomecanique et Biomateriaux Osteo-Articulaires − UMR CNRS 7052, Faculte de Medecine - Universite Paris 7, Paris, France; Department of Orthopaedic Surgery, European Teaching Hospital, Assistance Publique − Hopitaux de Paris
Stuart B. Goodman
Orthopaedic Research Laboratories, Department of Orthopaedic Surgery, Stanford University School of Medicine, Stanford, CA, USA


Normal usage of total joint replacements results in the production of wear debris and other byproducts. In particular, polyethylene particles are heavily involved in the stimulation of local and systemic biological reactions resulting in chronic inflammation, periprosthetic bone resorption (osteolysis), and, eventually, implant loosening. As sentinels of the innate immune system, cells of the monocyte/macrophage lineage initiate the inflammatory cascade that leads to osteolysis. The biological processes involved are complex, based on the unique properties of the monocytes/macrophages, including sensing, chemotaxis, phagocytosis, and adaptive stimulation. The interaction with wear debris triggers the release of pro-inflammatory factors, such as TNF-α, IL-1, and others, pro-osteoclastic factors such as RANKL, and chemokines, such as MCP-1 and MIP-1, all being crucial to the recruitment, migration, differentiation, and ultimately activation of bone resorbing osteoclasts. In parallel, other distinct macrophage populations inhibit inflammation and mitigate its consequences on the bone-implant interface. Here, the role of the monocyte/macrophage cell lineage in the initiation and maintenance of the host inflammatory response to wear debris and subsequent periprosthetic osteolysis is presented.