Basic calcium phosphate injections into joints have been shown to increase serum levels of the alarmin S100a8, for example, which can stimulate the activation of toll-like receptors in response. This process can in turn lead to the production of IL-1, Dr. McCarthy noted. “BCP plays an important role in the pathogenesis of OA,” she said, and in turn, the associated synovial inflammation may lead to more crystal formation.
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More accurate tests for BCP crystals in synovial fluid are needed, Dr. McCarthy said, and “we need to understand that the complexity of OA requires heterogeneity of treatment.” Colchicine may be used to help control crystal-induced flares, but neuromuscular complications are a concern, she said, and colchicine trials in OA have shown limited benefit. The current evidence suggests a connection between OA severity and crystal activity in the joints, she added, but future research may lead to therapies to break that vicious crystal–inflammation cycle.
Susan Bernstein is a writer based in Atlanta.