Millions of total joint replacements are performed annually worldwide, and the number is increasing every year. The overall proportion of patients achieving a successful outcome is about 80-90% in a 10-20-years time horizon postoperatively, periprosthetic osteolysis (PPOL) and aseptic loosening (AL) being the most frequent reasons for knee and hip implant failure and reoperations. The chemokine system (chemokine receptors and chemokines) is crucially involved in the inflammatory and osteolytic processes leading to PPOL/AL. Thus, the modulation of the interactions within the chemokine system may influence the extent of PPOL. Indeed, recent studies in murine models reported that (i) blocking the CCR2-CCL2 or CXCR2-CXCL2 axis or (ii) activation of the CXCR4-CXCL12 axis attenuate the osteolysis of artificial joints. Importantly, chemokines, inhibitory mutant chemokines, antagonists of chemokine receptors, or neutralizing antibodies to the chemokine system attached to or incorporated into the implant surface may influence the tissue responses and mitigate PPOL, thus increasing prosthesis longevity. This review summarizes the current state of the art of the knowledge of the chemokine system in human PPOL/AL. Furthermore, the potential for attenuating cell trafficking to the bone-implant interface and influencing tissue responses through modulation of the chemokine system is delineated. Additionally, the prospects of using immunoregenerative biomaterials (including chemokines) for the prevention of failed implants are discussed. Finally, this review highlights the need for a more sophisticated understanding of implant debris-induced changes in the chemokine system to mitigate this response effectively.

• Klíčová slova
• aseptic loosening, chemokine receptors, immunoregenerative implant, osteolysis, therapeutics, tissue homeostasis, wear particles,
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH

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.

• MeSH
• lektiny typu C metabolismus   MeSH
• lidé MeSH
• osteoartróza imunologie   patofyziologie   MeSH
• osteolýza patofyziologie   MeSH
• přirozená imunita fyziologie   MeSH
• protézy kloubů škodlivé účinky   MeSH
• receptor pro konečné produkty pokročilé glykace MeSH
• receptory cytoplazmatické a nukleární metabolismus   MeSH
• receptory imunologické metabolismus   MeSH
• revmatoidní artritida imunologie   patofyziologie   MeSH
• signální adaptorové proteiny Nod metabolismus   MeSH
• toll-like receptory metabolismus   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• lektiny typu C MeSH
• receptor pro konečné produkty pokročilé glykace MeSH
• receptory cytoplazmatické a nukleární MeSH
• receptory imunologické MeSH
• signální adaptorové proteiny Nod MeSH
• toll-like receptory MeSH