Rheumatoid arthritis causes inflammation that damages the cartilage and erodes the bone of the joints, leading to pain and deformation.
The study, led by Dr. Ahuva Nissim, of Queen Mary University of London, is published in the journal Arthritis Research & Therapy.
Rheumatoid arthritis causes long term inflammation in the synovium - the thin layer of protective tissue that lines the joints and produces fluid that lubricates them. This long-term inflammation eventually damages the cartilage and erodes the bone of the joints, leading to pain and deformation.
Treatments that control rheumatoid arthritis currently involve painkillers, non-steroidal anti-inflammatory drugs (NSAIDs), steroids or another group of small molecule drugs called disease modifying anti-rheumatoid drugs (DMARDs) that suppress inflammation.
Newer biologic drugs that are designed to reduce inflammation by blocking inflammatory signals are effective, but unfortunately, they can cause serious side effects such as infection because they suppress the immune system in the rest of the body as well.
For their study, Dr. Nissim and colleagues developed antibodies that seek out and travel to damaged arthritic cartilage; they then fused a biologic drug to these antibodies and injected them into the body cavity of mice with induced arthritis in their joints.
The results showed the drug could be delivered specifically to the arthritic joints, with much-reduced side effects compared with a systemic approach that allows the drug to circulate in the whole body.
Targeting biologic drugs increases potency while minimizing side effects
Dr. Nissim says they believe their approach to treating rheumatoid arthritis shows promise because:
"Targeting of biologic drugs to the inflamed joint will result in high local concentrations and low systemic concentrations, increasing efficacy while minimizing side effects."
Also, she says, the new approach is likely to be effective with a lower total dose, which reduces the cost of treatment.
The biologic drug they used in their study was the anti-inflammatory cytokine IL-10.
Other studies have shown effective ways of delivering drugs to joints, but these used injections into the joint. The authors wanted to find a different way, that avoids injection into the joint, because - as they explain in their study paper - due to the number and inaccessibility of many affected joints, direct injection "is not a feasible option."
Meanwhile, Medical News Today recently learned how research led by the University of Illinois at Chicago College of Medicine found that deactivating a cell protein may halt progress of rheumatoid arthritis. The study shows for the first time that activation of a single protein on the surface of white blood cells flooding into the fluid around the affected joints is a trigger for the disease.