Hyperuricemia, particularly
gout, and the immune inflammatory response are highly integrated. Both, long standing
hyperuricemia and
monosodium urate (MSU) crystal deposition can challenge tendon homeostasis because of their potential to cause
inflammation to the host. Knowledge is emerging from clinical imaging research depicting where MSU crystals deposit, including patellar tendon, triceps and quadriceps tendons. Remarkably, subclinical tendon
inflammation and damage are also present in asymptomatic
hyperuricemia.
Monosodium urate crystals act as danger activating molecular patterns (DAMPs), activating the
inflammasome and inducing the secretion of IL-1beta, a key mediator of the inflammatory response. The crucial role of IL-1beta in driving the inflammatory events during
gout attacks is supported by the clinical efficacy of IL-1beta blockade. Some data implicating IL-1beta as an initiator of
tendinopathy exist, but the link between
hyperuricemia and the development of
tendinopathy remains to be validated. Further knowledge about the interactions of
uric acid with both innate immune and tendon cells, and their consequences may help to determine if there is a subclass of hyperuricemic-
tendinopathy.