title: Macrophages-Key cells in the response to wear debris from joint replacements.
abstract: The generation of wear debris is an inevitable result of normal usage of joint replacements. Wear debris particles stimulate local and systemic biological reactions resulting in chronic inflammation, periprosthetic bone destruction, and eventually, implant loosening, and revision surgery. The latter may be indicated in up to 15% patients in the decade following the arthroplasty using conventional polyethylene. Macrophages play multiple roles in both inflammation and in maintaining tissue homeostasis. As sentinels of the innate immune system, they are central to the initiation of this inflammatory cascade, characterized by the release of proinflammatory and pro-osteoclastic factors. Similar to the response to pathogens, wear particles elicit a macrophage response, based on the unique properties of the cells belonging to this lineage, including sensing, chemotaxis, phagocytosis, and adaptive stimulation. The biological processes involved are complex, redundant, both local and systemic, and highly adaptive. Cells of the monocyte/macrophage lineage are implicated in this phenomenon, ultimately resulting in differentiation and activation of bone resorbing osteoclasts. Simultaneously, other distinct macrophage populations inhibit inflammation and protect the bone-implant interface from osteolysis. Here, the current knowledge about the physiology of monocyte/macrophage lineage cells is reviewed. In addition, the pattern and consequences of their interaction with wear debris and the recent developments in this field are presented.
authors.affiliation: Department of Orthopaedic Surgery, Stanford University School of Medicine, Stanford, California; Laboratoire de Biomécanique et Biomatériaux Ostéo-Articulaires-UMR CNRS 7052, Faculté de Médecine-Université Paris 7, Paris, France; Department of Orthopaedic Surgery, European Teaching Hospital, Assistance Publique-Hôpitaux de Paris-Université Paris 5, Paris, France.
authors.forename: Christophe
authors.initials: C
authors.lastname: Nich
authors.forename: Yuya
authors.initials: Y
authors.lastname: Takakubo
authors.forename: Jukka
authors.initials: J
authors.lastname: Pajarinen
authors.forename: Mari
authors.initials: M
authors.lastname: Ainola
authors.forename: Abdelhakim
authors.initials: A
authors.lastname: Salem
authors.forename: Tarvo
authors.initials: T
authors.lastname: Sillat
authors.forename: Allison J
authors.initials: AJ
authors.lastname: Rao
authors.forename: Milan
authors.initials: M
authors.lastname: Raska
authors.forename: Yasunobu
authors.initials: Y
authors.lastname: Tamaki
authors.forename: Michiaki
authors.initials: M
authors.lastname: Takagi
authors.forename: Yrjö T
authors.initials: YT
authors.lastname: Konttinen
authors.forename: Stuart B
authors.initials: SB
authors.lastname: Goodman
authors.forename: Jiri
authors.initials: J
authors.lastname: Gallo
mesh_terms: D000818:Animals; D019643:Arthroplasty, Replacement / Q000009:adverse effects*; D002450:Cell Communication; D006801:Humans; D008264:Macrophages / Q000166:cytology*; D008954:Models, Biological; D009000:Monocytes / Q000166:cytology; D011475:Prosthesis Failure / Q000009:adverse effects*
keywords: aseptic loosening; inflammation; monocyte/macrophage; osteolysis; tissue homeostasis; total joint replacement; wear particles