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Review
. 2019 Oct;15(3):286-296.
doi: 10.1007/s11420-018-9641-5. Epub 2018 Nov 9.

Mechanically Induced Periprosthetic Osteolysis: A Systematic Review

Benjamin A McArthur  1 , Ryan Scully  2 , F Patrick Ross  3 , Mathias P G Bostrom  3 , Anna Falghren  4
Affiliations
Review

Mechanically Induced Periprosthetic Osteolysis: A Systematic Review

Benjamin A McArthur et al. HSS J. 2019 Oct.

Erratum in

Abstract

Background: Peri-prosthetic bone loss can result from chemical, biological, and mechanical factors. Mechanical stimulation via fluid pressure and flow at the bone-implant interface may be a significant cause. Evidence supporting mechanically induced osteolysis continues to grow, but there is no synthesis of published clinical and basic science data.

Questions/purposes: We sought to review the literature on two questions: (1) What published evidence supports the concept of mechanically induced osteolysis? (2) What is the proposed mechanism of mechanically induced osteolysis, and does it differ from that of particle-induced osteolysis?

Methods: A systematic review was performed of the PubMed and Web of Science databases. Additional relevant articles were recommended by the senior authors based on their expert opinion. Abstracts were reviewed and the manuscripts pertaining to the study questions were read in full. Studies showing support of mechanically induced osteolysis were quantified and findings summarized.

Results: We identified 49 articles of experimental design supporting the hypothesis that mechanical stimulation of peri-prosthetic bone from fluid pressure and flow can induce osteolysis. While the molecular mechanisms may overlap with those implicated in particle-induced osteolysis, mechanically induced osteolysis appears to be mediated by distinct and parallel pathways.

Conclusions: The role of mechanical stimuli is increasingly recognized in the pathogenesis of peri-prosthetic osteolysis. Current research aims to elucidate the molecular mechanisms to better target therapeutic interventions.

Keywords: aseptic loosening; osteolysis; revision total joint replacement; total hip replacement; total knee replacement.

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Conflict of interest statement

Conflict of InterestRyan Scully, MD, F. Patrick Ross, PhD, and Anna Falghren, PhD, declare that they have no conflicts of interest. Benjamin A McArthur, MD, reports grants from Orthopedic Research and Education Foundation, during the conduct of the study. Mathias P.G. Bostrom, MD, reports being a paid consultant for Smith & Nephew, outside the submitted work.

Figures

Fig. 1
Fig. 1
Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) flow diagram for manuscript inclusion in the systematic review.
Fig. 2
Fig. 2
A rat model for mechanically induced osteolysis. A titanium (Ti) plate is inserted with a central plug protruded into a milled depression in the cortex. After 5 weeks of osseointegration, the plate is replaced by loading piston; after 5 days of fibrous tissue formation, cyclic loading is initiated.
Fig. 3
Fig. 3
Postmortem analysis demonstrates mechanically induced osteolysis. Comparison of an unloaded specimen with fibrous membrane (a) with a specimen after loading (b) demonstrates significant areas of bone resorption adjacent to loading zone.
Fig. 4
Fig. 4
A model for osteoclastogenesis in mechanically induced osteolysis. Osteoclastogenesis is stimulated by macrophage colony-stimulating factor (M-CSF) and receptor activator of nuclear factor κ-B ligand (RANKL) activation of precursor cells, which appears to be mediated by inflammatory cytokines such as interleukins 1β (IL-1β) and 6 (IL-6) and perhaps others. Osteoclast precursor cells are defined by the presence of colony-stimulating factor 1 receptor (c-Fms) and RANK. Osteoprotegerin (OPG), a decoy receptor for RANKL, and denosumab, a monoclonal antibody that binds RANKL, have been shown to block osteoclastogenesis in this setting.
See this image and copyright information in PMC

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