Copyright ©The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Orthop. Mar 18, 2015; 6(2): 172-189
Published online Mar 18, 2015. doi: 10.5312/wjo.v6.i2.172
Biological response to prosthetic debris
Diana Bitar, Javad Parvizi
Diana Bitar, Javad Parvizi, the Rothman Institute at Thomas Jefferson University, Department of Orthopaedic Surgery, Philadelphia, PA 19107, United States
Author contributions: Both authors were involved in the design, acquisition of data, and analysis of this study; both contributed to the writing of this manuscript.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See:
Correspondence to: Javad Parvizi, MD, FRCS, the Rothman Institute at Thomas Jefferson University, Department of Orthopaedic Surgery, 125 S 9th St. Suite 1000, Philadelphia, PA 19107, United States.
Telephone: +1-267-3397813 Fax: +1-215-5035651
Received: April 12, 2014
Peer-review started: April 12, 2014
First decision: April 28, 2014
Revised: September 24, 2014
Accepted: October 14, 2014
Article in press: October 16, 2014
Published online: March 18, 2015

Joint arthroplasty had revolutionized the outcome of orthopaedic surgery. Extensive and collaborative work of many innovator surgeons had led to the development of durable bearing surfaces, yet no single material is considered absolutely perfect. Generation of wear debris from any part of the prosthesis is unavoidable. Implant loosening secondary to osteolysis is the most common mode of failure of arthroplasty. Osteolysis is the resultant of complex contribution of the generated wear debris and the mechanical instability of the prosthetic components. Roughly speaking, all orthopedic biomaterials may induce a universal biologic host response to generated wear débris with little specific characteristics for each material; but some debris has been shown to be more cytotoxic than others. Prosthetic wear debris induces an extensive biological cascade of adverse cellular responses, where macrophages are the main cellular type involved in this hostile inflammatory process. Macrophages cause osteolysis indirectly by releasing numerous chemotactic inflammatory mediators, and directly by resorbing bone with their membrane microstructures. The bio-reactivity of wear particles depends on two major elements: particle characteristics (size, concentration and composition) and host characteristics. While any particle type may enhance hostile cellular reaction, cytological examination demonstrated that more than 70% of the debris burden is constituted of polyethylene particles. Comprehensive understanding of the intricate process of osteolysis is of utmost importance for future development of therapeutic modalities that may delay or prevent the disease progression.

Keywords: Debris, Adverse reaction, Osteolysis, Macrophages, Cytokines, Chemotaxis, Polyethylene, Phagocytosis

Core tip: After a comprehensive review of joint arthroplasty history, this article outlines the fundamental pathophysiology of the debris-induced biological reaction common to all particles types. Furthermore, specific characteristics of polyethylene, metal, ceramic, and polymethylmethacrylate particles are stated separately with their associated clinical relevance. Lastly, future therapeutic strategies to down-regulate periprosthetic osteolysis are enumerated, including anti-inflammatory agents used to modulate the cytokines release, anti-osteolytic agents used to disintegrate osteoclasts morphology, and antioxidants used to demolish the free oxygen radicals produced by the activated macrophages. The reader will find an extensive literature review encompassing all aspects of the debris-induced hostile cellular reaction.