Monosodium urate (MSU) crystals are the direct cause of gout, a form of inflammatory arthritis. These microscopic, needle-like structures are formed from uric acid, a waste product from the breakdown of purines. When uric acid levels are high, it can solidify into crystals within joints and soft tissues. This accumulation triggers an inflammatory response, leading to the intense pain and swelling of a gout attack.
The Formation Process
The formation of MSU crystals begins with high levels of uric acid in the blood, a condition known as hyperuricemia. Normally, the kidneys filter excess uric acid from the blood for excretion in urine. If the body produces too much uric acid or the kidneys excrete too little, its concentration rises.
This is similar to dissolving sugar in water; there is a limit to how much can dissolve before the liquid becomes saturated. Uric acid has a saturation point in bodily fluids of approximately 6.8 mg/dL. When blood uric acid levels exceed this threshold for extended periods, the synovial fluid that lubricates joints becomes supersaturated.
Once the synovial fluid is saturated, uric acid precipitates out of the solution, forming solid MSU crystals. Local factors can encourage this process. Lower temperatures in peripheral joints like the big toe reduce urate solubility, making crystallization more likely. Dehydration can also contribute by concentrating uric acid in the blood.
Impact on the Body
The body perceives the sharp, needle-shaped MSU crystals in a joint as a foreign threat, initiating an inflammatory response. The crystals’ charged surfaces interact directly with cell membranes, provoking this defensive reaction.
White blood cells called neutrophils are among the first responders to the affected joint. These immune cells attempt to engulf the crystals through phagocytosis. During this process, neutrophils release a cascade of inflammatory chemicals, including cytokines, which amplify the alarm signals.
This chemical and cellular activity is responsible for the symptoms of an acute gout attack. The inflammatory mediators cause blood vessels to widen, leading to redness, heat, and swelling. The combination of physical irritation from the crystals and chemical irritation from the immune response results in severe pain. Over time, crystal deposits can form larger masses called tophi, causing chronic pain and joint damage.
Identifying Crystals in the Body
While blood tests can reveal high uric acid, the standard for diagnosing gout is identifying the crystals within an affected joint. This is done through arthrocentesis, or joint fluid aspiration, where a physician withdraws a small sample of synovial fluid with a needle.
The fluid sample is examined under a polarized light microscope, which uses filters to reveal the specific characteristics of crystalline structures.
Under the polarized light microscope, MSU crystals are seen as thin, sharp, needle-shaped structures. They also exhibit a specific optical property called negative birefringence. This means that when viewed with a red compensator filter, the crystals appear yellow when aligned parallel to the filter’s axis and blue when they are perpendicular, confirming a gout diagnosis.
Managing Crystal Buildup
The management of gout focuses on two distinct goals: long-term control of uric acid levels and short-term relief from acute attacks. The primary long-term strategy is lowering blood uric acid below its saturation point to prevent new crystal formation and allow existing ones to dissolve. This is achieved with urate-lowering therapies like allopurinol and febuxostat, which reduce the body’s uric acid production.
Lifestyle adjustments also support medical treatment. Modifying the diet to reduce high-purine foods like red meat, organ meats, and some seafood can lower uric acid. Maintaining hydration helps the kidneys flush out uric acid and prevents it from becoming too concentrated.
The second goal is managing the pain and inflammation of an acute flare-up. These treatments calm the inflammatory response but do not eliminate the crystals. Nonsteroidal anti-inflammatory drugs (NSAIDs) reduce pain and swelling. Colchicine is also effective, especially at the first sign of an attack, by interfering with neutrophil actions. Corticosteroids, taken orally or injected into the joint, can also suppress severe inflammation.