Gout is one of the most painful forms of arthritis.
It happens when needle-like crystals of uric acid collect inside a joint, causing sudden swelling, redness, warmth, and severe pain.
The big toe is a common place for the first attack, but gout can also affect the ankles, knees, wrists, fingers, and other joints. Without good treatment, repeated attacks can eventually damage joints and make everyday movement more difficult.
Uric acid is made when the body breaks down substances called purines, which are found naturally in the body and in some foods. Normally, the kidneys remove much of this uric acid through urine, but levels can rise when the body makes too much or the kidneys remove too little.
For years, high blood uric acid has been seen as the main reason gout develops. But there is a mystery: many people have high uric acid and never get gout, while a smaller number develop gout even without unusually high blood levels.
Researchers from the University of California San Diego and other institutions have found a possible piece of this puzzle. Their study points to an important joint protein called lubricin, which may help stop uric acid crystals from forming.
The research, led by Robert Terkeltaub and colleagues, was published in the journal Arthritis & Rheumatology. The findings suggest that what happens inside the joint itself may be important in deciding whether gout develops.
Lubricin is a protein found in the fluid surrounding joints. As its name suggests, it helps lubricate and protect joint surfaces so that bones can move against each other with less friction.
The researchers became interested in lubricin after studying an unusual woman with gout. She had serious deposits of uric acid crystals and joint damage even though her blood uric acid levels were not high.
By examining cells and joint fluid from this unusual case, the scientists found problems in biological processes linked to lubricin. Most importantly, the patient’s joint fluid had very low levels of the protein.
Further laboratory work suggested that lubricin does much more than simply make joints slippery. It may help prevent uric acid crystals from forming and may also influence inflammation inside the joint.
The researchers also found a connection between lubricin and xanthine oxidase, an enzyme involved in making uric acid. When lubricin is too low, conditions inside the joint may make it easier for uric acid to build up and form painful crystals.
To see whether the finding applied beyond this rare case, the team studied joint fluid from other people with more typical gout. They found that lubricin levels were also lower in these patients than in people without gout.
This could help explain why blood uric acid alone does not tell the whole story. Two people may have similar uric acid levels, but differences inside their joints could affect whether crystals actually begin to form.
Genes may be part of the explanation because genetic differences can influence lubricin and other processes involved in joint health. However, researchers still need more studies to understand exactly how lubricin levels, genes, uric acid, and inflammation work together in gout.
Current gout treatments mainly focus on relieving pain during attacks and lowering uric acid over the long term. These treatments remain important, and the new findings do not mean that people with gout should stop or change their medicines.
Instead, the discovery may point toward another way to fight the disease in the future. If scientists can find safe ways to protect or increase lubricin in joints, it might become possible to make crystal formation less likely and reduce gout attacks.
The research gives scientists a broader view of a disease once explained mainly by high uric acid in the blood. It suggests that the health and chemistry of the joint itself may also determine who develops gout and who does not.
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