Research shows new cause of gout and joint damage

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A recent study by researchers from the University of California San Diego and collaborators has uncovered a new molecular pathway responsible for gout and its progression to joint tissue damage. The findings also suggest a potential target for preventing and treating the disease: a protein called lubricin, found in joint fluid.

Gout is the most common type of inflammatory arthritis. It occurs when urate, a byproduct of breaking down purine-rich foods like red meat and alcohol, accumulates in the body and forms needle-shaped crystals around the joints.

These crystals cause episodes of intense pain, swelling, and tenderness, often beginning in the foot. Over time, if left untreated, gout can lead to chronic joint damage, reducing mobility and quality of life.

For years, high levels of urate in the blood, a condition known as hyperuricemia, have been considered the primary cause of gout. However, most people with elevated urate levels do not develop the disease—only about one in four does. Additionally, gout patients tend to have more urate in their joint fluid than in their blood, a phenomenon that has puzzled scientists.

This study aimed to explore why gout develops in some people but not others, focusing on the genetic and molecular factors involved in urate crystal formation within the joints. The researchers investigated a rare case of gout in a patient who had urate crystal deposits and joint erosion but did not exhibit high blood urate levels.

The team identified a disrupted molecular pathway in the patient, which was linked to significantly reduced levels of lubricin, a protein that protects and lubricates joint tissues. Lubricin also plays a crucial role in regulating white blood cells that promote inflammation in the joints.

Further experiments revealed that lubricin suppresses the production of urate and an enzyme called xanthine oxidase (which creates urate), while also preventing urate from crystallizing in the joint.

When lubricin levels are low, this protective mechanism breaks down, allowing urate crystals to form and trigger inflammation. The researchers confirmed that patients with the common form of gout also had reduced levels of lubricin in their joints.

These findings suggest that genetic variations affecting lubricin production or degradation could explain why some individuals with high blood urate levels develop gout while others do not. The study provides a new perspective on the disease and highlights lubricin as a promising target for therapies aimed at preventing urate crystal formation and joint damage.

Beyond gout, the research underscores the importance of joint health in preventing chronic pain and inflammation.

For those interested in managing pain and inflammation, other studies have found that certain vitamins may help reduce the risk of bone fractures, and some gout medications may even have potential benefits for heart failure. Additionally, adopting a blood-pressure-friendly diet could lower the risk of gout flares.

This groundbreaking study, led by Robert Terkeltaub and published in Arthritis & Rheumatology, opens the door to new treatments for gout that focus on preserving joint health and preventing the disease at its source.

If you care about arthritis, please read studies about extra virgin olive oil for arthritis, and pomegranate: A natural treatment for rheumatoid arthritis.

For more information about arthritis, please see recent studies about how to live pain-free with arthritis, and results showing medical cannabis may help reduce arthritis pain, back pain.

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