In a recent series of experiments, scientists found that a specific antioxidant helps prevent the damage that osteoarthritis causes to cartilage. This may also have applications for bone and brain disorders.
Osteoarthritis is the most common arthritis type, causing pain and stiffness in the joints as cartilage steadily breaks down.
It is often referred to as “wear and tear” arthritis, as opposed to rheumatoid arthritis, which is caused by an immune response.
Most commonly affecting a person’s hands, knees, hips, feet, and spine, osteoarthritis symptoms tend to get worse over time.
Symptoms of joint swelling and tenderness can come and go over time — or, in some people, they can be constant. The degree of severity varies a great deal between individuals.
As the most common joint disorder in the United States, osteoarthritis affects over 30 million adults.
Several interventions can help manage osteoarthritis, including physical therapy, medications, and surgery. To date, however, nothing halts the progression of this debilitating condition.
It is still not exactly clear why cartilage continues to break down, and what mechanisms underpin the changes.
Risk factors for osteoarthritis include advancing age and obesity, so as the global population becomes older and heavier, the condition is likely to become increasingly prevalent.
Delving deeper into osteoarthritis
Recently, researchers led by Frederique Cornelis — from KU Leuven in Belgium — looked into the cellular changes involved in osteoarthritis and the interactions between certain proteins. Their findings are published in the journal Science Translational Medicine.
Specifically, the team was interested in ANP32A, which is a protein involved in a number of roles within cells, including intracellular transport and cell differentiation.
The researchers noted that levels of ANP32A were significantly lower in tissue samples from both humans and mice with osteoarthritis. This piqued their interest — so, using gene expression profiling, they dug a little deeper into the protein’s function.
They used a mouse model that is incapable of producing ANP32A, which causes them to develop osteoarthritis and osteopenia, or bone loss. They also developed a condition similar to cerebellar ataxia, symptoms of which include stumbling and a lack of coordination.
The study authors summarize their initial findings: