Published online Mar 18, 2015. doi: 10.5312/wjo.v6.i2.172
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.
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.