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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.2014010825
pages 297-317

Innate Immunity Sensors Participating in Pathophysiology of Joint Diseases: A Brief Overview

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
Milan Raska
Department of Immunology, Faculty of Medicine & Dentistry, Palacky University, Hnevotinska 3, 775 15 Olomouc, Czech Republic
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
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

ABSTRACT

The innate immune system consists of functionally specialized "modules" that are activated in response to a particular set of stimuli via sensors located on the surface or inside the tissue cells. These cells screen tissues for a wide range of exogenous and endogenous danger/damage-induced signals with the aim to reject or tolerate them and maintain tissue integrity. In this line of thinking, inflammation evolved as an adaptive tool for restoring tissue homeostasis. A number of diseases are mediated by a maladaptation of the innate immune response, perpetuating chronic inflammation and tissue damage. Here, we review recent evidence on the cross talk between innate immune sensors and development of rheumatoid arthritis, osteoarthritis, and aseptic loosening of total joint replacements. In relation to the latter topic, there is a growing body of evidence that aseptic loosening and periprosthetic osteolysis results from long-term maladaptation of periprosthetic tissues to the presence of by-products continuously released from an artificial joint.