Osteoarthritis affects millions of people and becomes more common with age.
The condition slowly damages cartilage, the smooth and flexible tissue that covers the ends of bones and helps joints move without painful friction.
When healthy cartilage begins to break down, the joint loses some of its natural cushioning. Over time, this can cause pain, swelling and stiffness, making everyday activities such as walking, climbing stairs or getting out of a chair more difficult.
There is currently no cure that can reliably restore cartilage damaged by osteoarthritis. Exercise, physical therapy, weight management and pain medicines can help control symptoms, while people with severe joint damage may eventually need surgery or a joint replacement.
Scientists at the University of Southern California have now identified a biological process that could point toward a very different kind of treatment. Instead of only reducing pain, the approach may eventually help researchers find ways to restore some of the youthful properties of aging cartilage.
The research team, led by Dr. Denis Evseenko, studied a protein called STAT3. This protein helps control many activities inside cells, including signals related to cell growth, survival and repair.
The researchers were particularly interested in chondrocytes, the cells responsible for producing and maintaining cartilage. Like other cells in the body, these cells change as people get older and gradually become less effective at maintaining healthy tissue.
The team found evidence that STAT3 plays an important role in controlling this aging process. When STAT3 activity was increased in cartilage cells, some of the biological signs associated with aging moved in the opposite direction.
In other words, the cells began to show features more commonly associated with younger cartilage. This does not mean the researchers literally turned old cells into young cells, but it suggests that some age-related changes in cartilage may be more reversible than previously believed.
To investigate this, the scientists examined what is sometimes called an epigenetic clock. Epigenetics refers to chemical changes that influence how genes are switched on or off without changing the underlying DNA code.
These chemical patterns change as cells age, allowing researchers to estimate their biological age. The USC researchers developed a way to measure these age-related changes in cartilage and used it to study what happened when STAT3 activity was altered.
Activating STAT3 appeared to reverse some of the aging patterns. In contrast, reducing STAT3 activity accelerated signs of aging and was linked to greater deterioration of cartilage.
The researchers also studied an enzyme called DNMT3B, which helps control chemical markings on DNA. Their experiments suggested that the relationship between STAT3 and DNMT3B may be important in determining whether cartilage maintains healthy characteristics or moves toward damaging age-related changes.
In experiments involving mice with joint injuries, disabling STAT3 was associated with worse osteoarthritis. The findings helped the researchers understand how changes at the cellular level could contribute to damage across an entire joint.
The team also noticed something surprising in damaged cartilage. Some cells appeared to be trying to return to a less mature state as part of an attempted repair process, but the new tissue did not develop into strong, fully functional cartilage.
This suggests that simply making cartilage cells behave younger may not be enough. Any future treatment would probably need to carefully guide those cells so they produce strong tissue capable of handling the pressure and movement of a working joint.
The findings were published in the peer-reviewed journal Aging Cell. The study provides new clues about why cartilage loses its ability to maintain itself with age and identifies STAT3 as a possible target for future osteoarthritis treatments.
However, the research is still at an early stage and does not mean a cartilage-restoring treatment is currently available. STAT3 is involved in several important processes throughout the body, including inflammation, so scientists would need to find a safe and highly controlled way to influence it.
The researchers are now interested in ways to activate the beneficial effects of STAT3 without causing unwanted inflammation or other problems. Much more laboratory research and eventually human studies would be needed before such an approach could become a treatment.
Still, the discovery offers an intriguing new direction. If scientists can learn how to safely restore healthier behavior in aging cartilage cells, future osteoarthritis treatment might move beyond controlling pain and toward repairing the damaged joint itself.
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