Innate immunity sensors participating in pathophysiology of joint diseases: a brief overview.
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.
Department of Orthopedics, University Hospital and Faculty of Medicine and Dentistry, Palacky University, Olomouc 775 20, Czech Republic.
Jiri
J
Gallo
Department of Immunology, Faculty of Medicine & Dentistry, Palacky University, Hnevotinska 3, 775 15 Olomouc, Czech Republic.
Milan
M
Raska
Department of Clinical Medicine, University of Helsinki and ORTON Orthopaedic Hospital of the Invalid Foundation, Helsinki, Finland.
Yrjo T
YT
Konttinen
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 Stanford University Medical Center Redwood City, CA.
Stuart B
SB
Goodman
D001172:Arthritis, Rheumatoid / Q000276:immunology / Q000503:physiopathology*; D006801:Humans; D007113:Immunity, Innate / Q000502:physiology*; D007595:Joint Prosthesis / Q000009:adverse effects; D037181:Lectins, C-Type / Q000378:metabolism; D053472:Nod Signaling Adaptor Proteins / Q000378:metabolism; D010003:Osteoarthritis / Q000276:immunology / Q000503:physiopathology*; D010014:Osteolysis / Q000503:physiopathology; D000067759:Receptor for Advanced Glycation End Products; D018160:Receptors, Cytoplasmic and Nuclear / Q000378:metabolism; D011971:Receptors, Immunologic / Q000378:metabolism; D051193:Toll-Like Receptors / Q000378:metabolism
D037181:Lectins, C-Type; D053472:Nod Signaling Adaptor Proteins; D000067759:Receptor for Advanced Glycation End Products; D018160:Receptors, Cytoplasmic and Nuclear; D011971:Receptors, Immunologic; D051193:Toll-Like Receptors