The Role of TLR and Chemokine in Wear Particle-Induced Aseptic LooseningReport as inadecuate

The Role of TLR and Chemokine in Wear Particle-Induced Aseptic Loosening - Download this document for free, or read online. Document in PDF available to download.

Journal of Biomedicine and BiotechnologyVolume 2012 2012, Article ID 596870, 9 pages

Review ArticleDepartment of Orthopaedic Surgery, The First Affiliated Hospital of Soochow University, Orthopaedic Institute of Soochow University, 188 Shizi Road, Jiangsu, Suzhou 215006, China

Received 31 July 2012; Revised 2 October 2012; Accepted 3 October 2012

Academic Editor: Mouldy Sioud

Copyright © 2012 Qiaoli Gu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Wear particle-induced periprosthetic osteolysis remains the principal cause of aseptic loosening of orthopaedic implants. Monocytes-macrophages phagocytose wear particles and release cytokines that induce inflammatory response. This response promotes osteoclast differentiation and osteolysis. The precise mechanisms by which wear particles are recognized and induce the accumulation of inflammatory cells in the periprosthetic tissue have not been fully elucidated. Recent studies have shown that toll-like receptors TLRs contribute to the cellular interaction with wear particles. Wear particles are recognized by monocytes-macrophages through TLRs coupled with the adaptor protein MyD88. After the initial interaction, wear particles induce both local and systemic migration of monocytes-macrophages to the periprosthetic region. The cellular migration is mediated through chemokines including interleukin-8, macrophage chemotactic protein-1, and macrophage inhibitory protein-1 in the periprosthetic tissues. Interfering with chemokine-receptor axis can inhibit cellular migration and inflammatory response. This paper highlights recent advances in TLR, and chemokine participated in the pathogenesis of aseptic loosening. A comprehensive understanding of the recognition and migration mechanism is critical to the development of measures that prevent wear particle-induced aseptic loosening of orthopaedic implants.

Author: Qiaoli Gu, Qin Shi, and Huilin Yang



Related documents