periprosthetic osteolysis Dotaz Zobrazit nápovědu
Jednou z nejzávažnějších komplikací kloubní náhrady je uvolnění implantátu z kostního lůžka, vedoucí k jeho selhání. Za základní příčinu je považována reakce organismu na otěr. Při funkci kloubní náhrady dochází k tření kontaktních ploch a k produkci otěrových částic – polyetylénu, polymetylmetakrylátu, kovu event. keramiky. Pro organismus nejsou otěrové částice biokompatibilní. Probíhá reakce organismu na cizí těleso. Otěrový materiál je fagocytován makrofágy. Aktivované buňky produkují zánětlivé mediátory, které vyvolávají kaskádu, zatím ne zcela prozkoumaných procesů, jejímž výsledkem je změna poměru novotvorba – resorpce kosti směrem k převaze odbourávání. Klinickým projevem procesu je tvorba otěrového granulomu a periprotetická osteolýza vedoucí k uvolnění a selhání endoprotézy. Detailní pochopení uvedeného mechanismu je nezbytné pro zlepšení dlouhodobých výsledků kloubních náhrad. Možnosti jeho ovlivnění jsou jednak ve změnách konstrukce implantátů, volbě nových mechanicky rezistentních a biologicky inertních materiálů a případném farmakologickém zásahu do procesů vedoucích k osteolýze. Článek je přehledným shrnutím dosud známých skutečností i pracovních teorií o této problematice.
One of the most serious complications of articular prostheses is loosening of the implant from the osseous bed leading to its failure. The assumed basic cause is the reaction of the organism to abrasion. During function of the articular prosthesis the abrasion of the contact surfaces occurs and abrasion particles such as polyethylene, polymethylacrylate, metal and possibly ceramics are produced. The abrased particles are not biocompatible for the organism. A reaction of the organism to the foreign body occurs. The abrasion material is phagocytosed by macrophages. Activated cells produce inflammatory mediators, which cause a cascade of so far not quite elucidated processes the result of which is a change of the ratio: new formation – resorption of bone with a predominance of breakdown. The clinical manifestation of the process is the development of an abrasion granuloma and periprosthetic osteolysis leading to loosening and failure of the endoprosthesis. Detailed understanding of the mentioned mechanism is essential for the improvement of long-term results of articular prostheses. They can be possibly influenced by changes in the construction of implants, the selection of new mechanically resistant and biologically inert materials and possible pharmacological interference with processes leading to osteolysis. The article is a review of hitherto known processes leading to osteolysis and working theories on this problem.
Aseptic loosening and osteolysis are the most frequent causes of total hip or total knee arthroplasty failure. Osteolysis is induced predominantly by polyethylene particles that are produced by adhesive wear of the prosthesis. The particles trigger a complex host's reaction varying in intensity even in response to the same number of particles. These differences indicate that individual predisposition may have an important role in the pathogenesis of osteolysis. The major key mediators of wear-induced osteolysis include the cytokines RANKL, TNF-a, IL-1, IL-6 and IL-8. The inter-individual differences in the extent of bone destruction may therefore be related to variation in the amount and/or activity of these cytokines based on their gene polymorphism. Our pilot study suggests an association of some variants of the cytokine genes (e.g., IL1A-889) with a predisposition to development of severe osteolysis. If this assumption is confirmed by future investigations, this approach can facilitate the pre-operative identification of patients at risk of the development of severe periprosthetic osteolysis and premature failure of the implant.
PURPOSE OF REVIEW: Joint replacement has revolutionized the treatment of end-stage arthritis. We highlight the key role of macrophages in the innate immune system in helping to ensure that the prosthesis-host interface remains biologically robust. RECENT FINDINGS: Osteoimmunology is of great interest to researchers investigating the fundamental biological and material aspects of joint replacement. Constant communication between cells of the monocyte/macrophage/osteoclast lineage and the mesenchymal stem cell-osteoblast lineage determines whether a durable prosthesis-implant interface is obtained, or whether implant loosening occurs. Tissue and circulating monocytes/macrophages provide local surveillance of stimuli such as the presence of byproducts of wear and can quickly polarize to pro- and anti-inflammatory phenotypes to re-establish tissue homeostasis. When these mechanisms fail, periprosthetic osteolysis results in progressive bone loss and painful failure of mechanical fixation. Immune modulation of the periprosthetic microenvironment is a potential intervention to facilitate long-term durability of prosthetic interfaces.
Extensive osteolysis adjacent to orthopedic implants is often associated with wear particles of prosthetic material. The activation of the RANKL/RANK/OPG system is considered to be a likely cause of periprosthetic osteolysis leading to implant failure. The aim of this study was to examine the possible correlation between the clinical extent of osteolysis, the number of wear particles and expression of the osteoclastic mediator RANKL (receptor activator of nuclear factor kappa B ligand) in the tissues around aseptically loosened cemented and non-cemented total hip replacements. Periprosthetic tissues were harvested from 59 patients undergoing revision of hip replacement for aseptic loosening. We observed RANKL-positive cells in 23 of our 59 patients, their presence was noted predominantly in tissues with a loosened cemented endoprosthesis. We have found that RANKL is present only in tissues with a large amount of wear debris and predominantly in cases involving loosened cemented implants.
- MeSH
- imunohistochemie metody využití MeSH
- interpretace statistických dat MeSH
- leptin izolace a purifikace škodlivé účinky MeSH
- ligand RANK izolace a purifikace škodlivé účinky MeSH
- náhrada kyčelního kloubu škodlivé účinky MeSH
- osteolýza etiologie MeSH
- protézy kloubů škodlivé účinky MeSH
- selhání protézy MeSH
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.
- Publikační typ
- časopisecké články MeSH
- přehledy 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
Background: Among patients with hip joint endoprosthesis, periprosthetic osteolysis is the most common complication following primary arthroplasty, and subsequent implant loosening is the leading cause of arthroplasty revision. Causes of stability loss, though not always evident, can be mechanical, allergic, or infectious (bacterial and fungal agents) in nature. Microsporidia, widespread opportunistic fungal pathogens that infect most human tissues, are a potential infectious cause of stability loss. Infections caused by Encephalitozoon species-one of the most common microsporidial pathogens in humans-primarily localize to intestinal and respiratory tracts, but can disseminate to tissues throughout the body. Methods: We examined 53 immunocompetent patients, 23 after revision and 30 after primary hip arthroplasty, for infection by Encephalitozoon species. Periprosthetic tissue, urine sediments, and stool samples were tested by microscopic examination and genus-specific nested polymerase chain reaction followed by genotyping. Results: Ten patients had Encephalitozoon-positive periprosthetic tissues, 9 (39%) after revision and 1 (3.3%) after primary hip arthroplasty. Among the tissue-positive postrevision patients, 7 had a positive urine sample and 1 had a positive stool sample. Encephalitozoon cuniculi genotype II was identified in 88.8% (16/18) of samples. Two urine samples were positive for a novel Encephalitozoon species. Conclusions: Encephalitozoon cuniculi should be considered as a cause of osteolysis in hip periprosthetic tissue, leading to a loss of implant stability.
- MeSH
- Encephalitozoon cuniculi genetika izolace a purifikace MeSH
- encephalitozoonóza komplikace MeSH
- feces mikrobiologie MeSH
- imunokompetence MeSH
- infekce spojené s protézou mikrobiologie moč MeSH
- kyčelní kloub mikrobiologie chirurgie MeSH
- lidé středního věku MeSH
- lidé MeSH
- náhrada kyčelního kloubu * MeSH
- osteolýza mikrobiologie MeSH
- polymerázová řetězová reakce MeSH
- senioři nad 80 let MeSH
- senioři MeSH
- Check Tag
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- senioři nad 80 let MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- MeSH
- artroplastiky kloubů škodlivé účinky MeSH
- kyčelní protézy škodlivé účinky MeSH
- osteolýza MeSH
- Publikační typ
- přehledy MeSH
Bone remodeling is a tightly coupled process consisting of repetitive cycles of bone resorption and formation. Both processes are governed by mechanical signals, which operate in conjunction with local and systemic factors in a discrete anatomic structure designated a basic multicellular unit (BMU). The microenvironment around total joint arthroplasty is a dynamic and complex milieu influenced by the chemical and physical stimuli associated with servicing the prosthesis. A key factor limiting the longevity of the prosthesis is polyethylene wear, which induces particle disease, and this may lead to increased and prolonged activity of BMUs resulting in periprosthetic osteolysis. Several pathways regulating BMU function have been reported in the past, including RANKL/RANK/OPG/TRAF6, TNF-alpha/TNFR/TRAF1, and IL-6/CD126/JAK/STAT. Moreover, the expression and functional activity of all these molecules can be affected by variations in their genes. These may explain the differences in severity of bone defects or prosthetic failure between patients with similar wear rates and the same prosthesis. Simultaneously, this data strongly support the theory of individual susceptibility to prosthetic failure.
- MeSH
- artroplastiky kloubů přístrojové vybavení škodlivé účinky MeSH
- fibroblasty metabolismus MeSH
- financování organizované MeSH
- hodnocení rizik MeSH
- lidé MeSH
- lymfocyty mikrobiologie MeSH
- mechanický stres MeSH
- náchylnost k nemoci MeSH
- osteoklasty metabolismus MeSH
- protézy kloubů MeSH
- remodelace kosti MeSH
- rizikové faktory MeSH
- selhání protézy MeSH
- signální transdukce MeSH
- Check Tag
- lidé MeSH
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.
- Publikační typ
- časopisecké články MeSH
- přehledy MeSH
