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Periprosthetic Osteolysis: Mechanisms, Prevention and Treatment

by 1,2,* and 3
1
Department of Orthopaedic Surgery, Stanford University, 450 Broadway St. M/C 6342, Redwood City, CA 94063, USA
2
Department of Bioengineering, Stanford University, Stanford, CA 94305, USA
3
Department of Orthopaedics, Faculty of Medicine and Dentistry, Palacky University Olomouc and University Hospital Olomouc, I. P. Pavlova 6, 779 00 Olomouc, Czech Republic
*
Author to whom correspondence should be addressed.
J. Clin. Med. 2019, 8(12), 2091; https://doi.org/10.3390/jcm8122091
Received: 27 October 2019 / Revised: 28 November 2019 / Accepted: 29 November 2019 / Published: 1 December 2019
(This article belongs to the Special Issue Orthopaedics: Medicine and Mechanisms)
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. View Full-Text
Keywords: Total joint replacement; total hip arthroplasty; total knee arthroplasty; periprosthetic osteolysis; aseptic loosening; debris-induced inflammation; RANKL-RANK; macrophages; osteoclasts; bisphosphonates Total joint replacement; total hip arthroplasty; total knee arthroplasty; periprosthetic osteolysis; aseptic loosening; debris-induced inflammation; RANKL-RANK; macrophages; osteoclasts; bisphosphonates
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MDPI and ACS Style

Goodman, S.B.; Gallo, J. Periprosthetic Osteolysis: Mechanisms, Prevention and Treatment. J. Clin. Med. 2019, 8, 2091. https://doi.org/10.3390/jcm8122091

AMA Style

Goodman SB, Gallo J. Periprosthetic Osteolysis: Mechanisms, Prevention and Treatment. Journal of Clinical Medicine. 2019; 8(12):2091. https://doi.org/10.3390/jcm8122091

Chicago/Turabian Style

Goodman, Stuart B.; Gallo, Jiri. 2019. "Periprosthetic Osteolysis: Mechanisms, Prevention and Treatment" J. Clin. Med. 8, no. 12: 2091. https://doi.org/10.3390/jcm8122091

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