header advert
Orthopaedic Proceedings Logo

Receive monthly Table of Contents alerts from Orthopaedic Proceedings

Comprehensive article alerts can be set up and managed through your account settings

View my account settings

Visit Orthopaedic Proceedings at:

Loading...

Loading...

Full Access

OXIDATIVE STRESS AND EXCESSIVE FIBROSIS INITIATE ASEPTIC LOOSENING OF HIP ARTHROPLASTY

7th Congress of the European Federation of National Associations of Orthopaedics and Traumatology, Lisbon - 4-7 June, 2005



Abstract

Introduction: Despite significant progress at the molecular level the etiology of aseptic loosening is still unclear. Fibrosis of the new capsule is an invariable finding at revision hip arthroplasty. Tissue fibrosis has been demonstrated in varies pathologic conditions due to elevated oxidative stress. The present retrospective study was designed to proof the hypothesis that peri-prosthetic fibrosis in aseptic loosening may be caused by elevated oxidative stress and represent an initial step in the pathomechanism of aseptic loosening.

Material and methods: Levels of malondialdehyde (MDA), oxidized (GSSG) and reduced (GSH) gluthatione were assayed as markers of oxidative stress in retrieved capsules of 28 loose hips (Group I) and 12 hips revised for high rate of wear (Group II). Collagen in the periprosthetic tissues was measured as hydroxiproline content and semiquantitatively by electrophoresis. In four representative cases electron microscopy was performed.

Results: MDA level as well as GSH/GSSG and GSH/ GSSG² ratios showed elevated oxidative stress in group I compared to group II and controls. SDS-PAGE electrophoresis showed higher molecular bands in 20 patients compared to controls. Hydroxiproline level in group II is significantly higher than in group I (p< 0.05). MDA, GSH and GSSG correlate significantly with hydroxiproline. A negative correlation between collagen content and osteolysis was established.

Discussion and conclusion: Higher oxidative stress plays role in aseptic loosening of hip arthroplasty. The present data support the hypothesis that the process is initiated by excessive fibrosis which consequently might lead to increase of intraarticular pressure and to extension of the joint space.

Theses abstracts were prepared by Professor Roger Lemaire. Correspondence should be addressed to EFORT Central Office, Freihofstrasse 22, CH-8700 Küsnacht, Switzerland.