Periprosthetic Osteolysis: Mechanisms, Prevention and Treatment

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

Status PubMed-not-MEDLINE Jazyk angličtina Země Švýcarsko Médium electronic

Typ dokumentu časopisecké články, přehledy

Perzistentní odkaz   https://www.medvik.cz/link/pmid31805704

Grantová podpora
VES16-31852A Ministry of Health of Czech Republic
R01 AR063717 NIAMS NIH HHS - United States
R01 AR073145 NIAMS NIH HHS - United States
R01AR055650, R01AR063717, R01AR073145, R01AR072613 NIH HHS - United States
R01 AR072613 NIAMS NIH HHS - United States

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.

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Lin T., Kohno Y., Huang J.-F., Romero-Lopez M., Pajarinen J., Maruyama M., Nathan K., Yao Z., Goodman S.B. NFκB sensing IL-4 secreting mesenchymal stem cells mitigate the proinflammatory response of macrophages exposed to polyethylene wear particles. J. Biomed. Mater. Res. Part A. 2018;106:2744–2752. doi: 10.1002/jbm.a.36504. PubMed DOI PMC

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