When UA levels rise to pathological ranges (hyperuricemia) or are accompanied by metabolic disturbances, the resulting excess reactive oxygen species and activation of inflammatory pathways—such as NLRP3 inflammasome activation and upregulation of pro-inflammatory cytokines—can enhance pro-resorptive signaling and disrupt the bone microenvironment, thereby increasing bone loss and fracture risk. This evidence concerns the gene NLRP3 and hyperuricemia.