Effects of polyethylene particles on tissue surrounding knee arthroplasties in rabbits

✍ Scribed by Sacomen, Daemen ;Smith, R. Lane ;Song, Yong ;Fornasier, Victor ;Goodman, Stuart B.

• Publisher: John Wiley and Sons
• Year: 1998
• Tongue: English
• Weight: 305 KB
• Volume: 43
• Category: Article
• ISSN: 0021-9304
• DOI: 10.1002/(sici)1097-4636(199822)43:2<123::aid-jbm6>3.0.co;2-q

✦ Synopsis

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 E 2 ( PGE 2 ) , hexosaminidase, transforming growth factor b ( TGFb ) , 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 õ 0.05 ) and a 74% decrease in total collagen (p õ 0.005 ) . Collagen content remained significantly decreased when normalized for cellularity ( DNA content ) . Total TGFb release exhibited a downward trend ( p Å 0.06 ) in the particle exposed group. Hexosaminidase and PGE 2 levels did not show a difference between groups; however, when normalized for cellularity, PGE 2 values exhibited an upward trend in the particle exposed group ( p Å 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 TGFb expression may indicate suppression of bone formation, possibly through a downregulation of osteoblast activity.