Researchers have uncovered evidence that cellular senescence – whereby cells stop dividing – is a cause of osteoarthritis, and they suggest targeting these cells could offer a promising way to prevent or treat the condition.
Study co-author Dr. James Kirkland, director of the Robert and Arlene Kogod Center on Aging at Mayo Clinic in Rochester, MN, and colleagues publish their findings in The Journals of Gerontology, Series A: Biological Sciences and Medical Sciences.
Osteoarthritis (OA), also known as degenerative joint disease, is a condition in which cartilage – the tissue that protects the end of each bone in a joint – wears away, causing the underlying bones to rub together. This can cause pain, swelling, and poor joint movement.
As the condition worsens, the bones may lose shape. Additionally, growths called bone spurs may arise, and bits of bone and cartilage can break off and float around the space in the joint. This can trigger an inflammatory response that exacerbates pain, as well as cartilage and bone damage.
OA is the most common form of arthritis in the United States, affecting around 27 million American adults. While the condition can arise in all age groups, it is most common among people aged 65 and older.
There is no cure for OA, only therapies that can help manage symptoms. These include pain and anti-inflammatory medications, such as nonsteroidal anti-inflammatory drugs (NSAIDs) and corticosteroids. In some cases, joint surgery may be required.
Now, Dr. Kirkland and colleagues say their findings may bring us closer to much-needed prevention and treatment strategies for OA.
The precise causes of OA are unclear, though previous studies have suggested cellular senescence might be involved.
Cellular senescence is the process by which cells stop dividing. Senescent cells accumulate with age and can cause severe damage to tissues and organs, contributing to a number of age-related diseases.
For their study, Dr. Kirkland and colleagues set out to determine whether cellular senescence has a causal link with OA – an association they say previous studies have yet to establish.
To reach their findings, the team used a senescent cell transplantation model. This involved taking both senescent and non-senescent cells from the ear cartilage of mice, before injecting these cells into the rodents’ knee joints.
Over a 10-day period, the researchers tracked the injected cells using bioluminescence and fluorodeoxyglucose (FDG)-positron emission tomography (PET) imaging.
The researchers found that the buildup of senescent cells around the knee joints of mice caused them to experience a number of symptoms and characteristics of OA, including leg pain, cartilage damage, and impaired mobility.
No such outcomes occurred as a result of injection with non-senescent cells, the researchers report.
These findings, say the authors, provide evidence of a causal link between cellular senescence and OA, and they also open the door to new ways to delay, prevent, or treat OA.
“Osteoarthritis has previously been associated with the accumulation of senescent cells in or near the joints, however, this is the first time there has been evidence of a causal link.
We believe that targeting senescent cells could be a promising way to prevent or alleviate age-related osteoarthritis. While there is more work to be done, these findings are a critical step toward that goal.”
Dr. James Kirkland