A1 Vertaisarvioitu alkuperäisartikkeli tieteellisessä lehdessä

Autoinflammation Around AES Total Ankle Replacement Implants




TekijätKoivu H, Takakubo Y, Mackiewicz Z, Al-Samadi A, Soininen A, Peled N, Kukis M, Trokovic N, Konttinen YT

KustantajaSAGE PUBLICATIONS INC

Julkaisuvuosi2015

JournalFoot and Ankle International

Tietokannassa oleva lehden nimiFOOT & ANKLE INTERNATIONAL

Lehden akronyymiFOOT ANKLE INT

Vuosikerta36

Numero12

Aloitussivu1455

Lopetussivu1462

Sivujen määrä8

ISSN1071-1007

DOIhttps://doi.org/10.1177/1071100715596608


Tiivistelmä

Background: Failure of total ankle replacement (TAR) can be characterized by early peri-implant osteolysis even in the presence of very modest numbers of wear particles. The hypothesis of the study was that this reaction is in part mediated by autoinflammatory responses mediated via damage-associated molecular patterns (DAMPs, danger signals) and pattern-recognizing danger signal receptors (PRRs). Methods: Peri-implant tissue and control samples from 10 patients with AES implants were immunostained for hypoxia inducible factor-1 alpha (HIF-1 alpha), activated caspase-3, high-mobility group box 1 (HMGB1), receptor for advanced glycation end product (RAGE), and toll-like receptors TLR2 and TLR4. Results were evaluated on a 0 to 4 scale (from 0% to > 50% stained area). Results: Peri-implant tissue around failed TAR implants had a relatively high mean HIF-1a score of 3 on a scale, which however was similar in control samples. HMGB1 (a DAMP) was seen to be mobilized from nuclei to cellular cytoplasm, and the active caspase-3+ cells were increased. All PRRs were increased in revision samples. Conclusions: Increased expression of HMGB1 and other danger signals together with increased PRR-dependent responsiveness could contribute to autoinflammatory peri-implantitis, multilocular cyst formation, and osteolysis in failed TAR implants. Level of Evidence: Level IV, case series.




Last updated on 2024-26-11 at 20:31