Recovery of articular cartilage metabolism following thermal stress is facilitated by IGF-1 and JNK inhibitor

Am J Sports Med. 2004 Jan-Feb;32(1):191-6. doi: 10.1177/0363546503260743.

Abstract

Background: The safety of intra-articular use of thermal probes is related to whether chondrocytes can tolerate exposure to high temperatures and whether cytoprotective agents may improve chondrocyte survival after thermal injury.

Purpose: This study was conducted to characterize the metabolic responses of articular cartilage after short-term exposure to temperatures between 50 degrees C and 60 degrees C with and without addition of insulin-like growth factor 1 (IGF-1) and c-Jun N-terminal kinase (JNK) inhibitor.

Methods: Human articular cartilage from osteoarthritic knees was subjected to defined thermal stress.

Results: Although significant reduction of proteoglycan synthesis was observed after 5 seconds of exposure to 55 degrees C and 60 degrees C and after 10- to 30-second exposures to 53 degrees C, recovery of metabolic activity levels was observed after 7 days.

Conclusion: Addition of IGF-1 and JNK inhibitor Sp600125 enabled the cartilage to maintain significantly higher levels of proteoglycan synthesis immediately after thermal stress. IGF-1 also enhanced recovery of metabolic activity after 7 days.

Clinical significance: Results from this study indicate that there may be time and temperature parameters within which thermal chondroplasty can be safely performed. The data additionally suggest that inadvertent chondrocyte injury may be minimized through potential addition of substances like IGF-1 or JNK inhibitor.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Cartilage, Articular / metabolism*
  • Chondrocytes / metabolism*
  • Humans
  • Hyperthermia, Induced*
  • Insulin-Like Growth Factor I / pharmacology*
  • JNK Mitogen-Activated Protein Kinases
  • Mitogen-Activated Protein Kinases / antagonists & inhibitors*
  • Proteoglycans / biosynthesis*

Substances

  • Proteoglycans
  • Insulin-Like Growth Factor I
  • JNK Mitogen-Activated Protein Kinases
  • Mitogen-Activated Protein Kinases