Macrophage polarization and activation in response to implant debris: influence by "particle disease" and "ion disease".
Macrophages derive from human embryonic and fetal stem cells and from human bone marrow-derived blood monocytes. They play a major homeostatic role in tissue remodeling and maintenance facilitated by apoptotic "eat me" opsonins like CRP, serum amyloid P, C1q, C3b, IgM, ficolin, and surfactant proteins. Three subsets of monocytes, classic, intermediate, and nonclassic, are mobilized and transmigrate to tissues. Implant-derived wear particles opsonized by danger signals regulate macrophage priming, polarization (M1, M2, M17, and Mreg), and activation. CD14(+) monocytes in healthy controls and CD16(+) monocytes in inflammation differentiate/polarize to foreign body giant cells/osteoclasts or inflammatory dendritic cells (infDC). These danger signal opsonins can be pathogen- or microbe-associated molecular patterns (PAMPs/MAMPs), but in aseptic loosening, usually are damage-associated molecular patterns (DAMPs). Danger signal-opsonized particles elicit "particle disease" and aseptic loosening. They provide soluble and cell membrane-bound co-stimulatory signals that can lead to cell-mediated immune reactions to metal ions. Metal-on-metal implant failure has disclosed that quite like Ni(2+), its neighbor in the periodic table Co(2+) can directly activate toll-like receptor 4 (TLR4) as a lipopolysaccharide-mimic. "Ion disease" concept needs to be incorporated into the "particle disease" concept, due to the toxic, immune, and inflammatory potential of metal ions.
Department of Clinical Medicine, University of Helsinki and ORTON Orthopaedic Hospital of the Invalid Foundation, Helsinki, Finland.
Yrjo T
YT
Konttinen
Department of Medicine, Institute of Clinical Medicine, Helsinki University Central Hospital, 00029 HUS, Finland; Department of Orthopaedic Surgery, Stanford Medical Center, Stanford CA 94305-5341 , USA.
Jukka
J
Pajarinen
Department of Orthopaedic Surgery, Yamagata University Faculty of Medicine, Yamagata, Japan.
Yuya
Y
Takakubo
Department of Orthopedics, University Hospital and Faculty of Medicine and Dentistry, Palacky University, Olomouc 775 20, Czech Republic.
Jiri
J
Gallo
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.
Christophe
C
Nich
Department of Orthopaedic Surgery Yamagata University School of Medicine Yamagata, Japan.
Michiaki
M
Takagi
Department of Orthopaedic Surgery Stanford University Medical Center Redwood City, CA.
Stuart B
SB
Goodman
D019643:Arthroplasty, Replacement; D002454:Cell Differentiation; D016764:Cell Polarity; D006801:Humans; D007595:Joint Prosthesis / Q000009:adverse effects*; D008262:Macrophage Activation; D008264:Macrophages / Q000276:immunology* / Q000378:metabolism; D011475:Prosthesis Failure