Dr. Jay holds two patents related to tribonectins.
Osteoarthritis Basic Science Studies
Association between friction and wear in diarthrodial joints lacking lubricin
Version of Record online: 29 OCT 2007
Copyright © 2007 by the American College of Rheumatology
Arthritis & Rheumatism
Volume 56, Issue 11, pages 3662–3669, November 2007
How to Cite
Jay, G. D., Torres, J. R., Rhee, D. K., Helminen, H. J., Hytinnen, M. M., Cha, C.-J., Elsaid, K., Kim, K.-S., Cui, Y. and Warman, M. L. (2007), Association between friction and wear in diarthrodial joints lacking lubricin. Arthritis & Rheumatism, 56: 3662–3669. doi: 10.1002/art.22974
- Issue online: 29 OCT 2007
- Version of Record online: 29 OCT 2007
- Manuscript Accepted: 20 JUL 2007
- Manuscript Received: 8 FEB 2007
- NIH. Grant Numbers: R01-AR-050180, T32-GM-07250
- Academy of Finland. Grant Numbers: 200970, 110595
- McCutchen Foundation
- University Emergency Medicine Foundation
- Howard Hughes Medical Institute
- Clinical Scientist Award in Translational Research from the Burroughs Wellcome Fund
The glycoprotein lubricin (encoded by the gene Prg4) is secreted by surface chondrocytes and synovial cells, and has been shown to reduce friction in vitro. In contrast to man-made bearings, mammalian diarthrodial joints must endogenously produce friction-reducing agents. This study was undertaken to investigate whether friction is associated with wear.
The lubricating ability of synovial fluid (SF) samples from humans with genetic lubricin deficiency was tested in vitro. The coefficient of friction in the knee joints of normal and lubricin-null mice was measured ex vivo; these joints were also studied by light and electron microscopy. Atomic force microscopy was used to image and measure how lubricin reduces friction in vitro.
SF lacking lubricin failed to reduce friction in the boundary mode. Joints of lubricin-null mice showed early wear and higher friction than joints from their wild-type counterparts. Lubricin self-organized and reduced the work of adhesion between apposing asperities.
These data show that friction is coupled with wear at the cartilage surface in vivo. They imply that acquired lubricin degradation occurring in inflammatory joint diseases predisposes the cartilage to damage. Lastly, they suggest that lubricin, or similar biomolecules, will have applications in man-made devices in which reducing friction is essential.