Gout is a form of crystal arthropathy associated with deposition of monosodium urate (MSU) crystals, and is directly related to hyperuricemia arising from abnormal purine metabolism and/or decreased uric acid excretion. Uric acid is the final oxidation product of purine metabolism and plays an important role as an in vivo antioxidant at physiological concentrations. Several case reports have described the presence of tophi in the intervertebral disc (IVD) or endplate of patients with hyperuricemia or gout, and these patients also exhibited severe intervertebral disc degeneration (IDD). We speculated that uric acid may have dual effects on an IVD. On the one hand, physiological concentrations of uric acid have powerful antioxidant activity and can effectively maintain the steady state of the IVD, while on the other hand, high concentrations of uric acid have strong oxidizing activity and the resulting high osmotic pressure can aggravate IDD. Moreover, when MSU crystals accumulate in the endplate and IVD, they lead to a series of mechanical damages and inflammatory reactions that further accelerate IDD. Further basic and clinical studies are needed to clarify the mechanism for the involvement of uric acid in the onset and development of IDD.