What are the local and systemic biologic reactions and mediators to wear debris, and what host factors determine or modulate the biologic response to wear particles?

• Published in: Journal of the American Academy of Orthopaedic Surgeons Vol. 16 Suppl 1; p. S42
• Main Authors: Tuan, Rocky S, Lee, Francis Young-In, T Konttinen, Yrjö, Wilkinson, J Mark, Smith, Robert Lane
• Format: Journal Article
• Language: English
• Published: United States 2008
• Subjects: Basic Helix-Loop-Helix Transcription Factors - metabolism; Biocompatible Materials - adverse effects; Bone Resorption - immunology; Dinoprostone - metabolism; Endothelial Cells - immunology; Fibroblasts - immunology; Foreign-Body Reaction - immunology; Humans; Interleukin-1 - metabolism; Interleukin-6 - metabolism; Interleukin-8 - metabolism; Joint Prosthesis; Macrophage Colony-Stimulating Factor - metabolism; Osteoclasts - immunology; Osteogenesis - immunology; Prosthesis Failure; RANK Ligand - metabolism; Stem Cells - immunology; T-Lymphocytes - immunology; Tumor Necrosis Factor-alpha - metabolism
• ISSN: 1067-151X
• DOI: 10.5435/00124635-200800001-00010

New clinical and basic science data on the cellular and molecular mechanisms by which wear particles stimulate the host inflammatory response have provided deeper insight into the pathophysiology of periprosthetic bone loss. Interactions among wear particles, macrophages, osteoblasts, bone marrow-derived mesenchymal stem cells, fibroblasts, endothelial cells, and T cells contribute to the production of pro-inflammatory and pro-osteoclastogenic cytokines such as TNF-alpha, RANKL, M-SCF, PGE2, IL-1, IL-6, and IL-8. These cytokines not only promote osteoclastogenesis but interfere with osteogenesis led by osteoprogenitor cells. Recent studies indicate that genetic variations in TNF-alpha, IL-1, and FRZB can result in subtle changes in gene function, giving rise to altered susceptibility or severity for periprosthetic inflammation and bone loss. Continuing research on the biologic effects and mechanisms of action of wear particles will provide a rational basis for the development of novel and effective ways of diagnosis, prevention, and treatment of periprosthetic inflammatory bone loss.