Katharina Buczek
Osteoarthritis, or OA, is the most common type of arthritis. Referred to by some as degenerative joint disease or “wear and tear” arthritis, OA causes joint cartilage to break down and underlying bone structures to change. This most frequently occurs in the knees, hips, and hands.
But, even though OA affects over thirty-two million U.S. adults, there is a lack of treatments that target the onset of the disease rather than the domino effect of pain that occurs afterward.
So, researchers at the University of Florida Scripps Biomedical Research recently set their sights on OA prevention and discovered how one specific protein could be the answer.
“People need an osteoarthritis medication that addresses the root cause of cartilage damage and depletion as there currently are no disease-modifying drugs for what is the number one cause of disability in the United States,” explained Patrick Griffin, a biochemist and one of the study’s authors.
As adults get older and joints undergo more and more stress, chondrocytes– a type of cell that helps upkeep healthy joint cartilage– start to fail. But, the team found that activating one nuclear receptor protein known as RORB could reverse this failure.
RORB is short for “retinoic acid receptor-related orphan receptor beta” and has been linked to many bodily processes in the past– including circadian rhythm and even the development of the retina in the womb.
But, how this nuclear receptor could play a role in OA prevention had been unknown until now.
The team discovered that by activating and increasing RORB activity, chondrocytes formed. In addition, anti-inflammatory effects and decreased cartilage degradation were also observed.
So now, Griffin is confident that RORB activation could be instrumental in preventing or delaying the development of OA.
“While our work is in the early stages, our study suggests that the nuclear receptor RORB could present a novel therapeutic target to protect cartilage damage and perhaps turn on cartilage regeneration,” he said.
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