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The Bone & Joint Journal
Vol. 100-B, Issue 6 | Pages 725 - 732
1 Jun 2018
Gibon E Barut N Courpied J Hamadouche M

Aims

The purpose of this retrospective study was to evaluate the minimum five-year outcome of revision total hip arthroplasty (THA) using the Kerboull acetabular reinforcement device (KARD) in patients with Paprosky type III acetabular defects and destruction of the inferior margin of the acetabulum.

Patients and Methods

We identified 36 patients (37 hips) who underwent revision THA under these circumstances using the KARD, fresh frozen allograft femoral heads, and reconstruction of the inferior margin of the acetabulum. The Merle d’Aubigné system was used for clinical assessment. Serial anteroposterior pelvic radiographs were used to assess migration of the acetabular component.


Orthopaedic Proceedings
Vol. 96-B, Issue SUPP_11 | Pages 42 - 42
1 Jul 2014
Goodman S Yao Z Ren P Gibon E Rao A Pajarinen J Antonios J Lin T Smith R Egashira K Keeney M Yang F Konttinen Y
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Summary

Wear particles from joint replacements may result in loosening and periprosthetic osteolysis. Interference with systemic macrophage trafficking to the implant, modulation of macrophage phenotype from M1 to M2, and inhibition of NFκB may mitigate these adverse effects.

Introduction

Joint replacement of the lower extremity is highly successful in alleviating pain, and improving ambulation and function. However, prosthetic byproducts of different materials, in sufficient amounts, may lead to loosening and periprosthetic osteolysis. Debris from polymers (such as polyethylene and PMMA), metals and ceramics are capable of inciting an adverse tissue reaction, which is orchestrated by cells of the monocyte/macrophage lineage. Three experimental approaches have been taken by our group to potentially mitigate the adverse biological sequela of particle disease. These include: 1) interfering with ongoing migration of monocyte/macrophages to the implant site by inhibiting the chemokine system 2) altering the functional activities of local macrophages by converting pro-inflammatory M1 macrophages to an anti-inflammatory pro-tissue healing M2 phenotype and 3) modulating the production and release of pro-inflammatory cytokines, chemokines and other potentially harmful factors by inhibiting the key transcription factor NFκB.