The effects of displacement rate and proteoglycan digestion on the fracture resistance of tissue grown from chondrocyte culture

Brendan E. Koop, Jack L. Lewis, Michelle M. Fedewa, Theodore R. Oegema

Research output: Contribution to journalArticlepeer-review

2 Scopus citations

Abstract

Fracture toughness of cartilage and cartilage replacement tissues is important in injury and disease. For example, cartilage is thought to weaken before it fibrillates in the disease osteoarthritis. Since both loading rate and proteoglycan content affect viscoelastic properties, they may both affect fracture toughness of cartilage and cartilage analogs. In this study, fracture toughness of tissue grown in chondrocyte culture was measured as a function of loading rate and proteoglycan digestion. Control tissue and tissue digested with chondroitinase ABC (cABC) to remove proteoglycans were tested at displacement rates of 0.1 and 0.5 mm/sec. Displacement rate had no effect on fracture toughness for either control or digested tissue. Proteoglycan digestion reduced tissue thickness by 30% and when evaluated on a material basis increased fracture toughness. There was no interaction between digestion and loading rate. When the fracture toughness was normalized to collagen content, which removed the effect of tissue shrinkage, there was no effect of proteoglycan digestion on fracture toughness. These data suggest that proteoglycans do not contribute to tissue toughness, other than by reducing thickness and increasing collagen density.

Original languageEnglish (US)
Pages (from-to)823-828
Number of pages6
JournalJournal of Materials Science: Materials in Medicine
Volume13
Issue number9
DOIs
StatePublished - Sep 2002

Bibliographical note

Funding Information:
This work was supported by the NSF Materials Research Science and Engineering Center at the University of Minnesota, the Catherine Mills Davis Endowment to the Orthopaedic Surgery Department, and NIH grant AR46577. The authors acknowledge useful discussions with Michelle Oyen -Tiesma an d Robert Cook.

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