This is the first study of arthroscopic descriptions of what happens inside the wrist affected by gout. Some interesting, new findings are reported.
Gout is an inflammatory process that is known to affect the articular cartilage and subchondral bone. The articular cartilage is the thick, fibrous covering or lining of the joint. Subchondral bone is the first layer of bone just under the cartilage.
Gout is considered a metabolic form of arthritis. The body produces too much uric acid (a condition called hyperuricemia). Hyperuricemia causes urate crystals to form and get dumped in the bloodstream. The crystals of monosodium urate (MSU) or uric acid are then deposited on the articular cartilage of joints, tendons and nearby tissues.
People with gout experience painful attacks of arthritis when these crystal deposits build up forming pockets of crystals or nodules called tophi (singular form: tophus). The body sets up an inflammatory response to these crystals. The big toe is affected most often, but other joints such as the wrist (which is the focus of this study) can become swollen and painful.
Over time, the acute inflammatory response turns into a chronic condition. The articular cartilage is worn away right down to the bone. Bone loss can also occur. Until now, it was always thought that the joint was the main area affected. But this study of seven patients examined arthroscopically offers some new insight into the damage that can occur in the other soft tissue structures.
Seven men with previously diagnosed gout came to the physician with new onset of wrist pain on one side. There was pinpoint pain and tenderness over the scapholunate ligament. Testing the integrity of that particular ligament, the surgeons found a positive scapholunate ligament shift test. This indicates wrist instability because the ligament isn’t holding the bones steady. The two bones shift or move more than they should.
Everyone in the study was treated conservatively at first. Care consisted of activity modification, splinting, antiinflammatory medications, and steroid injections. When all of those attempts failed, X-rays and MRIs were ordered. X-rays showed that five of the seven patients had scapholunate advanced collapse (SLAC). That is to say, the cartilage of the two wrist bones (the scaphoid and the lunate) had worn away. The bones started to deteriorate and collapse.
Arthroscopic surgery was scheduled to find out what was causing the problem. Inserting a long, thin probe with a tiny TV camera on the end into the wrist gave the surgeons a clear view of what was going on. They could clearly see urate crystals deposited on and around the scapholunate ligament. The ligament was disrupted (torn). In some cases, the tear was mild. In other patients, the tear was large enough that the surgeon could pass the scope through the gap.
Other ligaments such as the lunotriquetral ligament, and the triangular fibrocartilage complex were also damaged. There were no crystal deposits seen in the triangular fibrocartilage complex (TFCC) of patients– even though there were tears of this soft tissue structure. The TFCC is an important stabilizing structure in the wrist.
They took tiny snips of the synovium and scraped crystal deposits off the ligaments and sent them to the lab for analysis.
From this study, it looks like urate crystals can and do attach to the scapholunate ligament of the wrist. Damage of the tissue leads to disruption of the ligament under less than normal loads. Collapse of the scapholunate bones develops — not from erosion of the cartilage, which is the typical effect of gout — but from damage to the ligaments. That’s the new and surprising information gleaned from this study.
What does this really mean? In the clinic, when a physician sees a patient with known gout now presenting with wrist pain, a diagnosis of ligament instability (not just erosion of the joint) should be considered. The cause is crystalline deposition associated with the underlying condition of gout.
One other finding from this study that was new involved the laboratory preparation of the tissue samples. Tissue removed from the joint at the time of the arthroscopic exam were put either in sterile saline, alcohol, or formalin (liquid formaldehyde, a preservative).
The samples transported to the lab in formalin showed no crystal deposits under the microscope — despite the fact that the surgeons clearly saw them during arthroscopic exam. They concluded that formalin destroys these deposits, whereas saline and alcohol preserve them. The authors suggest transporting future specimens in alcohol to prevent loss of the crystals needed for confirmation of the diagnosis.