For example, chronic liver disease can elevate levels of RANKL, which further promotes osteoclastogenesis and bone resorption.[33] The disruption of the OPG/RANKL system is a recurring theme in various osteolytic conditions, underscoring the necessity of maintaining this balance for optimal bone health.[34] Additionally, the systemic effects of liver dysfunction extend beyond OPG levels; the gut–bone axis has also been implicated in bone metabolism. This evidence concerns the gene TNFRSF11B and Decreased liver function.