Innate immunity sensors participating in pathophysiology of joint diseases: a brief overview

. 2014 ; 24 (4) : 297-317.

Jazyk angličtina Země Spojené státy americké Médium print

Typ dokumentu časopisecké články, práce podpořená grantem

Perzistentní odkaz   https://www.medvik.cz/link/pmid25747032

Grantová podpora
R01 AR055650 NIAMS NIH HHS - United States
R01 AR063717 NIAMS NIH HHS - United States

Odkazy

PubMed 25747032
PubMed Central PMC4369672
DOI 10.1615/jlongtermeffmedimplants.2014010825
PII: 1bc2ffc717f40755,473c0e86746a33d5
Knihovny.cz E-zdroje

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.

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Periprosthetic Osteolysis: Mechanisms, Prevention and Treatment

. 2019 Dec 01 ; 8 (12) : . [epub] 20191201

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