ISSN:
0021-9304
Keywords:
total joint replacement
;
animal model
;
particles
;
polyethylene
;
interface
;
Chemistry
;
Polymer and Materials Science
Source:
Wiley InterScience Backfile Collection 1832-2000
Topics:
Medicine
,
Technology
Notes:
Clinical studies suggest a role for polyethylene (PE) wear debris in the pathogenesis of osteolysis and loosening of total joint replacements. In this study, submicron particles of ultrahigh molecular weight PE (UHMWPE) were placed around pressfit tibial hemiarthroplasties in rabbits to determine the biological reaction. After 6 months the periprosthetic tissue was harvested and characterized biochemically by measuring the extracellular matrix macromolecules, collagen, and glycosaminoglycan (GAG) and quantifying the expression of inflammatory/osteolytic mediators [prostaglandin E2 (PGE2), hexosaminidase, transforming growth factor β (TGFβ), and interleukins-6 and -1 (IL-6, IL-1)]. Particle exposure resulted in a decrease in levels of total extracellular matrix molecules including a 53% decrease in total GAG (p 〈 0.05) and a 74% decrease in total collagen (p 〈 0.005). Collagen content remained significantly decreased when normalized for cellularity (DNA content). Total TGFβ release exhibited a downward trend (p = 0.06) in the particle exposed group. Hexosaminidase and PGE2 levels did not show a difference between groups; however, when normalized for cellularity, PGE2 values exhibited an upward trend in the particle exposed group (p = 0.1). IL-6 was undetected by bioassay and ELISA. Previous studies emphasized that PE debris enhances the degradation of bone. The data from this in vivo model suggest that submicron UHMWPE particles may also act to inhibit biosynthetic pathways of bone and mesenchymal tissue. Decreased levels of collagen, GAG, and TGFβ expression may indicate suppression of bone formation, possibly through a downregulation of osteoblast activity. © 1998 John Wiley & Sons, Inc. J Biomed Mater Res (Appl Biomater) 43: 123-130, 1998
Additional Material:
4 Ill.
Type of Medium:
Electronic Resource
Permalink