Association between friction and wear in diarthrodial joints lacking lubricin
GD Jay, JR Torres, DK Rhee… - … : Official Journal of …, 2007 - Wiley Online Library
Arthritis & Rheumatism: Official Journal of the American College …, 2007•Wiley Online Library
Objective 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. Methods 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 …
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. Methods 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 …
Objective
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.
Methods
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.
Results
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.
Conclusion
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.
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