Chronic hyponatremia is increasingly recognized as a potential contributor to impaired bone health, although the underlying pathophysiological mechanisms have not yet been fully elucidated. Experimental studies have demonstrated that low serum sodium levels affect both osteoclast and osteoblast function, resulting primarily in increased bone resorption and secondarily in reduced bone formation. In humans, however, evidence regarding the effects of hyponatremia on bone remains limited. Emerging data indicate that acute hyponatremia reduces bone formation activity, while normalization of sodium levels promotes bone formation. These human findings therefore partially differ from preclinical studies, and it remains unclear whether such discrepancies arise from variations in the etiology or severity of hyponatremia in clinical cohorts. In this review, we summarize the current evidence linking both acute and chronic hyponatremia to altered bone metabolism, with a specific focus on the underlying pathophysiological mechanisms and their clinical implications.