Mechanisms of monosodium urate crystal-induced bone destruction in gouty arthritis (Review).

Abstract

The deformities and disabilities resulting from bone destruction in gouty arthritis impose substantial physical and psychological burdens on patients, underscoring the urgent need to elucidate the mechanisms underlying gout-induced osteolysis. Monosodium urate (MSU) crystals play a central role in the pathogenesis of bone destruction in gouty arthritis, significantly disrupting the activity and function of bone-related cells. Mechanistically, MSU induces bone loss by triggering oxidative stress, amplifying inflammatory cascades, and dysregulating bone remodeling pathways. Understanding these pathological mechanisms is essential for early clinical intervention and the development of targeted therapies to prevent disease progression. The present review systematically examines the multifaceted impact of MSU on bone homeostasis and its molecular interactions in gouty arthritis-associated bone destruction, providing insights to refine diagnostic strategies and advance novel therapeutic approaches.