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Kompendium 2020 Forschung & Klinik

Das Kompendium 2020 der Universitätsklinik für Orthopädie und Unfallchirurgie von MedUni Wien und AKH Wien (o. Univ.-Prof. R. Windhager) stellt einen umfassenden Überblick über die medizinsichen Leistungen und auch die umfangreichen Forschungsfelder dar. Die Veröffentlichungen zeigen die klinische Relevanz und innovative Ansätze der einzelnen Forschungsrichtungen. Herausgeber: Universitätsklinik für Orthopädie und Unfallchirurgie MedUni Wien und AKH Wien Prof. Dr. R. Windhager ISBN 978-3-200-07715-7

Das Kompendium 2020 der Universitätsklinik für Orthopädie und Unfallchirurgie von MedUni Wien und AKH Wien (o. Univ.-Prof. R. Windhager) stellt einen umfassenden Überblick über die medizinsichen Leistungen und auch die umfangreichen Forschungsfelder dar. Die Veröffentlichungen zeigen die klinische Relevanz und innovative Ansätze der einzelnen Forschungsrichtungen.

Herausgeber: Universitätsklinik für Orthopädie und Unfallchirurgie
MedUni Wien und AKH Wien
Prof. Dr. R. Windhager

ISBN 978-3-200-07715-7

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TOP-Studien<br />

32<br />

Figure 1: Time integrated SDAI was significantly<br />

higher in patients with RCL (median; 25th and 75th<br />

percentile: 10.8; 8.6 and 15.8) than in controls<br />

without RCL (7.0; 2.7 and 15.5) (Figure 1; p=0.043).<br />

DMARDs had a protective effect on such risk. This link between inflammation<br />

and RCL was further substantiated in the comparison between RA and OA,<br />

being particularly evident for TKA.<br />

Priv.-Doz. DDr. Christoph Böhler<br />

Author:<br />

Christoph Böhler is a specialist<br />

for Orthopaedics and Traumatology<br />

at the Medical University of<br />

Vienna. His clinical and scientific<br />

focus are on primary and<br />

revision arthroplasty. In August<br />

2021 he will start a clinical<br />

Adult Reconstruction Fellowship<br />

at the University of Toronto,<br />

Canada.<br />

Local inflammation plays a pivotal role in the pathogenesis of aseptic loosening,<br />

by which generation of wear debris between the bearing surfaces<br />

leads to activation of macrophages and immune cells, which then release<br />

pro-inflammatory cytokines like TNF-alpha and IL-6. These induce osteoclast<br />

activation and lead to increased bone resorption, osteolysis and eventually to<br />

aseptic loosening. The systemic inflammation of RA may play a role in enhancing<br />

the local inflammation underlying the described processes leading to<br />

aseptic loosening. The implication of these findings for clinical practice are<br />

potentially substantial, at least for individuals with RA and TJA: no patients<br />

in remission showed RCL. Analogously to the observation that in sustained<br />

remission of RA joint damage does not progress, this makes the case that<br />

in the presence of TJA even stricter disease control should be pursued, with<br />

clinical remission being the clear treatment target. Biological DMARDs had<br />

a protective effect on the risk of RCL. Previously, it has been shown that<br />

TNF-inhibitors are able to stop the progression of joint destruction. The<br />

majority of the patients in the biological DMARDs group were treated with<br />

TNF-inhibitors, potentially also suggesting a role of TNF alpha in the mediation<br />

of the inflammatory process leading to aseptic loosening.<br />

Conclusion<br />

Taken together, inflammation in RA patients, as evidenced by higher levels<br />

of disease activity, increases the risk for radiographic loosening after TJA. In<br />

OA patients, as a control disease without systemic inflammation, the risk is<br />

significantly lower. Biological DMARDs may reduce the risk of RCL, although<br />

this would need prospective evaluation. Our data suggest that RA patients<br />

with TJA should regularly undergo orthopaedic and radiographic evaluation<br />

and, in the context of treating RA to target, might be considered for a more<br />

stringent control of disease activity.

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