Uric acid is an end product of purine metabolism and is known for being an important pro-inflammatory agonist in gout. What is not well known is that uric acid is also an antioxidant and anti-inflammatory mediator in the body. Uric acid in the circulatory system exhibits positive antioxidant effects. The antioxidant activity of uric acid is significantly higher than that of other antioxidants including vitamins and antioxidant enzymes, and is responsible for approximately half of the antioxidant activity of human plasma. Studies have found a role for oxidative responses in the pathogenesis of osteoporosis. And uric acid was reported to have anti-osteoporotic properties. Oxidative stress has been shown to reduce osteoblastogenesis, thereby slowing bone formation. Observational studies have found a correlation between oxidative stress or plasma antioxidant concentrations and bone mineral density. Increased production of ROS, a product of oxidative stress, was observed in inflammatory arthropathy in response to antioxidant deficiency, and ROS contribute to the osteoporotic process by inhibiting osteoblastogenesis. The reduction of ROS production in mouse osteoclast precursors by uric acid suggests that high bone mineral density may be associated with the antioxidant effects of uric acid. Several clinical studies have shown that uric acid is beneficial for bone metabolism. Mechanistic studies have found a negative correlation between serum uric acid concentrations and urinary excretion of type I collagen amino-terminal cross-linked peptide, and similarly with the bone resorption marker type I collagen C-terminal peptide. uA is dose-dependently associated with reduced osteoclastogenesis in mouse cells in vitro. However, more studies are needed to elucidate whether uric acid acts directly on osteoclasts or through oxidative stress. Several studies have reported that high uric acid in older men and postmenopausal women is associated with higher bone mineral density and lower fracture incidence. For example, a large population-based study in older men found that higher uric acid concentrations were significantly associated with a lower incidence of osteoporosis and fractures. In addition, a prospective cohort study of fracture cases in older men showed that higher serum uric acid levels were associated with increased bone mineral density and a reduced incidence of non-spinal fractures. Further, a large cross-sectional study of healthy postmenopausal women showed an association between higher uric acid levels and higher BMD and an association between lower uric acid levels and decreased BMD also associated with a higher incidence of vertebral fractures. The relationship between uric acid and BMD may be related to the antioxidant effects of normal serum uric acid concentrations. While hyperuricemia increases the risk of cardiovascular disease due to oxidative reactions, in contrast, normal serum uric acid concentrations may have antioxidant effects. Thus, the level of uric acid may determine whether uric acid is a protective antioxidant or a damaging pro-oxidant. AS is characterized by decreased bone mineral density and bone loss in the spine and hip and begins already in the early stages of the disease. 19%-61% of AS patients develop osteoporosis, and packaged AS disease activity promotes the incidence of bone loss. Osteoporosis is less of a comorbidity and more of a manifestation of the disease itself. The pathological mechanism is that in the setting of chronic inflammation, TNF-α and IL-6 inhibit osteoblasts by upregulating Dickkopf-associated proteins and sclerostin, thereby suppressing the Wnt pathway, and TNF-αand IL-6 enhance osteoclasts by inducing B-binding factor agonist receptors. In short, inflammatory activity inhibits osteoblasts while stimulating osteoclasts. A recent study explored the relationship between uric acid concentration and spine and hip bone density in AS patients. To exclude the effects of age and sex hormones, 150 men under 50 years of age were included and patients with a history of allopurinol, fenofibrate, beta blockers and diuretics were excluded. BMI was higher in AS patients with high uric acid, but the difference was not significant (p=0.266). Blood calcium concentration was higher in the higher uric acid group (p=0.004). Lumbar spine BMD increased with increasing uric acid (p=0.033), but there was no such trend for hip and femoral neck BMD. There was a positive trend of correlation between lumbar spine BMD and serum uric acid, which remained after correction for age, BMI (weight/height squared) and blood sedimentation. The low uric acid group had lower BMD than the high uric acid group. Lumbar spine T and Z values were also significantly higher in the high uric acid group. This is the first study to examine the relationship between uric acid and bone mineral density in patients with ankylosing spondylitis. The results of this study found that high uric acid was associated with high bone density in the lumbar spine, whereas low uric acid was more likely to be associated with low bone density and osteoporosis. In addition, low BMD was associated with BMI and blood sedimentation. Consistent with previous findings, this study found a positive correlation between serum uric acid and blood calcium concentration. Metabolic alterations associated with osteoporosis may affect uric acid clearance. pTH was associated with uric acid clearance, and serum uric acid and parathyroid hormone (PTH) concentrations were positively correlated. Serum uric acid is also associated with 1,25-(OH)2D3 levels through regulation of 1a-hydroxylase activity. Uric acid may affect the excretion of urinary calcium. Patients with ankylosing spondylitis have a higher incidence of renal calculi and hypercalcemia. Although this study did not directly detect urinary calcium excretion, the results showed that blood calcium was higher in the high uric acid group, which could suggest that uric acid may affect urinary calcium excretion.