The differential diagnosis of subchondral cysts in the carpal bones and associated joint space narrowing might include:
- post-traumatic osteoarthritis (especially with an appropriate history of prior trauma)
- calcium pyrophosphate deposition disease
- inflammatory arthritis
- rheumatoid arthritis
- particle disease
- neuropathic joint (unusual site, especially without involvement of hand proper)
- infection (possible, but unlikely to affect carpal bones as a group).
This differential diagnosis is moderately long -- the key finding that allows us to arrive at the correct answer is correct identification of the lunate prosthesis. It is fairly obvious that the lunate is denser than the other carpals -- however, it may not be immediately obvious that there are no trabeculae in the lunate! One might therefore consider this lunate to be merely sclerotic, and mistakenly make a diagnosis of osteonecrosis.
The etiology in this case is actually inflammatory. Particulate silicone abraded from the prosthesis has caused a hypertrophic villous synovitis with a chronic foreign-body type inflammatory reaction. This "pannus" has eroded articular cartilage and formed intraosseous "cysts", which are not fluid-filled, but instead are actually intraosseous synovium. Clinically, patients may present with pain, swelling and loss of function of the affected joint. Synovitis may occur as soon as 3 months after insertion of the implant, or up to several years later. The characteristic circumscribed erosions may occur even in bones not directly adjacent to the implant. Distortion or breakage of the implant may occur. Regional soft tissue calcification has been reported.
Definitive diagnosis can frequently be made by microscopic examination of synovial fluid aspirate: both intra- and extracellular silicone particles may be identified. Particle disease due to silicone synovitis occurs most frequently in sites where implants are subject to severe compression and shearing forces, such as the wrist and hallux.
Carter and associates found radiographic evidence of silicon synovitis in 75 % of scaphoid implants, 55 % of lunate implants, and 75 % of scapholunate implants. Since patients who have these implants are often otherwise normal, healthy and young, it is especially important to recognize this entity in order that the appropriate therapy be instituted to avoid further joint destruction and resultant disability; recommended treatment is removal of the implant, aggressive synovectomy and curettage of the lytic lesions.
Silicon is not, by any means, the only material that can lead to particle synovitis. This process can also be caused by fragments of polymethylmethacrylate cement, polyethylene, metal, latex, carbon, Dacron, and even bone itself. Although the actual chemical composition of the intraarticular fragments may influence the amount of inflammatory response, particle size may play a more important role. Some studies suggest that the most intense inflammatory response occurs when the particles are small enough (1 - 12 microns) to be engulfed by the macrophages in the joint space. Phagocytosis leads to cell death, leading to the release of bone-resorbing mediators.