Library Subscription: Guest
Begell Digital Portal Begell Digital Library eBooks Journals References & Proceedings Research Collections
Journal of Long-Term Effects of Medical Implants

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

Journal of Long-Term Effects of Medical Implants

DOI: 10.1615/JLongTermEffMedImplants.2014011355
pages 267-281

Macrophage Polarization and Activation in Response to Implant Debris: Influence by "Particle Disease" and "Ion Disease"

Yrjo T. Konttinen
Department of Orthopaedics, Teaching Hospital, Faculty of Medicine and Dentistry, Palacky University, Olomouc, Czech Republic; Department of Orthopaedics, ORTON Orthopaedic Hospital, 00280 Helsinki, Finland; COXA Hospital for Joint Replacement, 33520 Tampere, Finland
Jukka Pajarinen
Department of Medicine, Institute of Clinical Medicine, Helsinki University Central Hospital, 00029 HUS, Finland; Orthopaedic Research Laboratories, Department of Orthopaedic Surgery, Stanford University School of Medicine, Stanford, CA, USA
Yuya Takakubo
Department of Orthopaedic Surgery, Yamagata University Faculty of Medicine, Iida-Nishi 2-2-2, Yamagata, 990-9585, Japan
Jiri Gallo
Department of Immunology, Faculty of Medicine and Dentistry, Palacky University, Olomouc, Czech Republic; Department of Orthopaedics, Teaching Hospital, Faculty of Medicine and Dentistry, Palacky University, Olomouc, Czech Republic
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
Michiaki Takagi
Department of Orthopaedic Surgery, Yamagata University Faculty of Medicine, Iida-Nishi 2-2-2, Yamagata, 990-9585, Japan
Stuart B. Goodman
Orthopaedic Research Laboratories, Department of Orthopaedic Surgery, Stanford University School of Medicine, Stanford, CA, USA

ABSTRACT

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 Ni2+, its neighbor in the periodic table Co2+ 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.