A study by Stanford Medicine researchers has revealed that individuals with eczema or asthma have a higher chance of developing osteoarthritis. The findings suggest the presence of an allergic pathway that could be treated with existing drugs.
Scientists have traditionally thought that wear and tear in the cartilage that protects joints and bones are the primary reason behind osteoarthritis. However, the Stanford Medicine study found that inflammation may also play a key role in developing the condition. Researchers from Stanford Medicine teamed up with scientists from the Boston University School of Medicine, the VA Palo Alto Health Care System and Seattle-based Chinook Therapeutics to study risk factors for osteoarthritis.
Osteoarthritis is a type of arthritis that affects more than 50 million people in America. It is more likely to affect older and obese people, has no known cure and often causes disabilities. It is characterized by joint pain, stiffness, swelling, tenderness and loss of flexibility.
Stanford Medicine assistant professor of immunology and rheumatology Matthew Baker, MD, says that the group’s findings pave the way for future studies that could develop ways to halt osteoarthritis progression.
A prior 2019 study by Stanford Medicine clinical and researcher William Robinson, MD, PhD, found that when an antibody called IgE perceives a foreign invader, it activates mast cells that release tryptase and histamine. These two compounds are associated with allergic inflammation, and tryptase especially is key to the progression of osteoarthritis.
Baker has teamed up with other researchers to analyze the association between osteoarthritis, eczema and asthma. The research team found that people who did not have osteoarthritis were likely to develop the condition after being diagnosed with eczema or asthma. Patients with asthma or eczema were 58% more likely to develop osteoarthritis over a decade. The risk of developing osteoarthritis was even higher when patients had both asthma and eczema (115%).
The researchers also compared asthma with chronic obstructive pulmonary disease to see whether the presence of another lung disease that wasn’t associated with allergens increased osteoarthritis risk. Their comparison revealed that patients with asthma were 83% more likely to be diagnosed with osteoarthritis than chronic obstructive pulmonary disease patients. As a result, the researchers concluded that lung disease with no associated allergic response did not increase one’s osteoarthritis risk. Furthermore, they suggested that allergic pathway activation was crucial to the relationship between asthma and osteoarthritis.
Baker explained that existing asthma and mast cell activation syndrome medications could help to treat osteoarthritis symptoms by reducing allergic cytokine and mast cell levels. He said the team now have a “strong basis” to study these medications as a possible treatment against osteoarthritis.
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