Researchers identify ways of protecting joint tissue in arthritis
Aberdeen researchers have identified a novel factor that may protect joint tissue when it is under physical stress – which could offer new possibilities for effective treatment to limit joint damage in osteoarthritis (OA).
A team at the University of Aberdeen, funded by a three-year grant of more than £96,000 from the Arthritis Research Campaign (arc), have identified a molecule that stimulates cell metabolism and survival when the tissue is put under stress by physical trauma, a potentially significant factor in the development of OA.
Although it is well recognised that staying active is beneficial for maintaining healthy joints, overuse or physical trauma (typically accidents, sports injuries, and repetitive or strenuous occupational or lifestyle activities) are known to contribute to the development and progression of osteoarthritis.
“The cartilage tissue lining the joints is sensitive to mechanical loads, and protects the joint by distributing the load to prevent stressful conditions,” explained Dr Richard Aspen, Professor in Orthopaedic Science.
“In OA, cartilage function is disturbed and the tissue begins to degenerate. Mechanical loading causes cell death; the tissue has limited capacity for repair and there are currently no means of halting the damage. Understanding how physical strain translates into joint damage is the focus of our research project.”
Professor Aspden and his team are investigating the biochemistry underlying the actions of a protein molecule, known as FGF18, which appears to regulate the formation and breakdown of cartilage cells when they are physically stressed.
Mimicking physical stress at the cellular level requires extremely sensitive measuring equipment and the research team has developed a sophisticated precision system designed to apply mechanical loads to cell culture samples. By measuring the corresponding intracellular metabolic changes using advanced analytical techniques, physical loading can be correlated with biochemical changes in the cells.
Preliminary results show that FGF18 is produced in increased amounts in response to mechanical loading and suggest a possible role for this molecule in regulating the cellular response.
Future research will examine the effects of loading on healthy and osteoarthritic human joint tissue samples to analyse the biochemical changes occurring after mechanical stress.
Understanding the role of FGF18 in the response of articular cartilage to physical trauma may lead to the development of therapies that can delay or prevent cell damage.
