Clinical studies, as well as in vitro and in vivo experiments have demonstrated that byproducts from joint replacements induce an inflammatory reaction that can result in periprosthetic osteolysis (PPOL) and aseptic loosening (AL). Particle-stimulated macrophages and other cells release cytokines, chemokines, and other pro-inflammatory substances that perpetuate chronic inflammation, induce osteoclastic bone resorption and suppress bone formation. Differentiation, maturation, activation, and survival of osteoclasts at the bone-implant interface are under the control of the receptor activator of nuclear factor kappa-Β ligand (RANKL)-dependent pathways, and the transcription factors like nuclear factor κB (NF-κB) and activator protein-1 (AP-1). Mechanical factors such as prosthetic micromotion and oscillations in fluid pressures also contribute to PPOL. The treatment for progressive PPOL is only surgical. In order to mitigate ongoing loss of host bone, a number of non-operative approaches have been proposed. However, except for the use of bisphosphonates in selected cases, none are evidence based. To date, the most successful and effective approach to preventing PPOL is usage of wear-resistant bearing couples in combination with advanced implant designs, reducing the load of metallic and polymer particles. These innovations have significantly decreased the revision rate due to AL and PPOL in the last decade.

• Klíčová slova
• RANKL-RANK, Total joint replacement, aseptic loosening, bisphosphonates, debris-induced inflammation, macrophages, osteoclasts, periprosthetic osteolysis, total hip arthroplasty, total knee arthroplasty,
• 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

Numerous studies provide detailed insight into the triggering and amplification mechanisms of the inflammatory response associated with prosthetic wear particles, promoting final dominance of bone resorption over bone formation in multiple bone multicellular units around an implant. In fact, inflammation is a highly regulated process tightly linked to simultaneous stimulation of tissue protective and regenerative mechanisms in order to prevent collateral damage of periprosthetic tissues. A variety of cytokines, chemokines, hormones and specific cell populations, including macrophages, dendritic and stem cells, attempt to balance tissue architecture and minimize inflammation. Based on this fact, we postulate that the local tissue homeostatic mechanisms more effectively regulate the pro-inflammatory/pro-osteolytic cells/pathways in patients with none/mild periprosthetic osteolysis (PPOL) than in patients with severe PPOL. In this line of thinking, 'particle disease theory' can be understood, at least partially, in terms of the failure of local tissue homeostatic mechanisms. As a result, we envision focusing current research on homeostatic mechanisms in addition to traditional efforts to elucidate details of pro-inflammatory/pro-osteolytic pathways. We believe this approach could open new avenues for research and potential therapeutic strategies.

• MeSH
• buněčné mikroprostředí imunologie   MeSH
• Hajdu-Cheney syndrom etiologie   imunologie   prevence a kontrola   MeSH
• lidé MeSH
• mediátory zánětu imunologie   MeSH
• náhrada kyčelního kloubu * MeSH
• osteogeneze MeSH
• protézy kloubů MeSH
• selhání protézy etiologie   MeSH
• zánět etiologie   prevence a kontrola   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH
• Názvy látek
• mediátory zánětu MeSH