Science

Molecule in joints serves as a marker for joint disease

joint disease
Study shows molecule that indicates joint disease Source: Taokinesis (via Pixabay)
Researchers at Cornell University show that lubricin can be elevated in joints prior to the development of joint disease hence can act as a marker molecule.

By Mili Jayadeep | Science Editor

Weight-bearing joints such as the knee are highly specialised consisting of multiple tissues to produce smooth joint movements during locomotion. Joints are designed to take on the impacts of daily activities and work to dissipate the forces acting on it. Joint injuries and diseases can severely compromise joint function hence negatively affecting joint usage resulting in pain and other symptoms. A new study by Cornell University researchers furthers our understanding on joint injuries. Traumatic insults to a joint such as anterior cruciate ligament (ACL) rupture is known to alter the physiological joint microenvironment predisposing the joint to diseases such as osteoarthritis in both animals and humans. This study suggests that a molecule which is a joint lubricant may be indicative of developing joint diseases such as osteoarthritis in the future. 

This study was published in Scientific reports and is the first of its kind to research the function of a molecule known as lubricin and its role in ACL injuries in dog models. The findings for this study may also help further our knowledge in developing therapeutics for ACL injuries and other similar injuries in humans. This is useful in preventing the progression of joint injury to joint disease. 

Heidi Reesink, the Harry M. Zweig Assistant Professor in Equine Health at the College of Veterinary Medicine (CVM) and senior author on the paper explains,

“Lubricin is crucial for normal joint function and the lubrication of cartilage. We know that if a person or animal doesn’t make that protein, they will develop devastating joint disease affecting all the major weight-bearing joints.”

Lubricin was found to be elevated in the ACL-injury dog model, which was contradictory to previous theories. Reesink says,

“The dogma in this field has been that lubricin decreases in joint disease.”

In three dog-models, increased lubricin concentration was recorded prior to signs of arthritis:

 “We also saw increased lubricin in dogs months to years after they injured their ACLs, suggesting that lubricin might be an indicator of ongoing joint instability.”, according to Reesink.

This finding is useful as it can act as a warning signal for potential joint disease hence indicating the need for a change in the treatment approach. A systematic review following this research highlighted the need for further research efforts in this area, later published in the journal of Osteoarthritis and Cartilage. Reesink explains, 

We can help both animals and humans by potentially coming up with better diagnostics, by more fully understanding how these molecules work and designing therapies beneficial to both, by taking advantage of these naturally occurring cases and improving orthopedic care,”

Future work involves longitudinal studies in the canine model studying the concentration of the molecule at different time points following initial injury, during recovery and treatment. This can either be used in veterinary research and is translatable to human joint disease as the dog model has multiple similarities to human joints hence making it an adequately representative animal model. 

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