Hyperuricemia and gout: effects on bone and articular cartilage (literature review)

Gout is a disease characterized by deposition of sodium monourate crystals in tissues which is the reason of inflammation among persons with hyperuricemia (HU). The prevalence of HU, which can be considered the first stage of gout formation, varies in different countries. Despite this, only a small number of persons with HU have been shown to develop symptoms of gout. Recent data suggest that HU is an independent risk factor for cartilage and bone damage. UA, both in the form of crystals and in a dissolved form, activates damage and potentiates cell death by releasing reactive oxygen species, activating the necroptosis pathway, neutrophil traps, synthesis of pro-inflammatory cytokines, and other pathogenetic mechanisms that cause the negative effects of HU and gout on articular cartilage and subchondral bone. The association of HU and osteoarthritis (OA) is well known and based on the common pathogenesis, but the direction of this relationship is still a debatable issue. The accumulated data suggest the need for a deeper study of the relationship of gout and asymptomatic HU with pathological processes leading to the development and progression of OA and disorders of bone metabolism.