Abstract
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.
Highlights
Total joint arthroplasty (TJA) is the only fully effective therapeutic choice for patients suffering from end-stage degenerative arthritis
We have developed nuclear factor κB (NF-κB) sensing and IL-4 over-expressing genetically modified MSCs to treat chronic inflammation [176,180]
Key check points potentially applicable to modification of implant-induced responses are those associated with (i) macrophage polarization; (ii) pro-osteoclastic signaling of periprosthetic cells; (iii) the receptor activator of nuclear factor kappa-B ligand (RANKL)-mediated osteoclastogenesis; (iv) the NF-κB and mitogen-activated protein kinase pathways involved in inflammation/osteoclastogenesis; (v) extension of necrosis vs. apoptosis in the periprosthetic membranes
Summary
Total joint arthroplasty (TJA) is the only fully effective therapeutic choice for patients suffering from end-stage degenerative arthritis. Bone cement particles were examined in relation to debris-induced inflammation [39] and hypersensitivity [40]. There is long-term clinical experience demonstrating that prosthetic joint infection is associated with erosive bone resorption if left undiagnosed and untreated. Along these lines, remnants of bacteria circulating in the blood stream might exacerbate inflammation induced by sterile prosthetic byproducts from TJA, despite the absence of clinical infection [43,44]. Several studies demonstrate that debris-induced inflammation is more rapid when endotoxin or other proteins specific for bacteria were added to the prosthetic particles [10,17,45]. Several studies have examined the role of DAMPs in PPOL [50,51,52]
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