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?

Overview

Journal J Am Acad Orthop Surg

Publisher Wolters Kluwer

Specialties General Surgery
Orthopedics

Date 2008 Aug 12

PMID 18612013

Citations 50

Authors

Rocky S Tuan

Francis Young-In Lee

Yrjo T Konttinen

J Mark Wilkinson

Robert Lane Smith

Affiliations

Soon will be listed here.

Abstract

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.

Citing Articles

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