There is still debate on whether high uric acid increases bone mineral density (BMD) against osteoporotic fracture or bone resorption caused by gout inflammation. This study aimed to evaluate whether gout offers a protective effect on bone health or not. We conducted a nationwide population-based retrospective cohort study to evaluate the association between gout history and risk factors of fracture.A retrospective cohort study was designed using the claim data from Longitudinal Health Insurance Database (LHID). A total of 43,647 subjects with gout and a cohort of 87,294 comparison subjects without gout were matched in terms of age and sex between 2001 and 2009, and the data were followed until December 31, 2011. The primary outcome of the study was the fracture incidence, and the impacts of gout on fracture risks were analyzed using the Cox proportional hazards model.After an 11-year follow-up period, 6992 and 11,412 incidents of fracture were reported in gout and comparison cohorts, respectively. The overall incidence rate of fracture in individuals with gout was nearly 23%, which was higher than that in individuals without gout (252 vs 205 per 10,000 person-years) at an adjusted hazard ratio of 1.17 (95% confidence interval = 1.14–1.21). Age, sex, and fracture-associated comorbidities were adjusted accordingly. As for fracture locations, patients with gout were found at significant higher fracture risks for upper/lower limbs and spine fractures. In gout patient, the user of allopurinol or benzbromarone has significantly lower risk of facture than nonusers.Gout history is considered as a risk factor for fractures, particularly in female individuals and fracture sites located at the spine or upper/lower limbs.

Chondrosarcoma is a malignancy of soft tissue and bone that has a high propensity to metastasize to distant organs. Nerve growth factor (NGF) is critical for neuronal cell growth, apoptosis, and differentiation, and also appears to promote the progression and metastasis of several different types of tumors, although the effects of NGF upon chondrosarcoma mechanisms are not very clear. We report that NGF facilitates lysyl oxidase (LOX)-dependent cellular migration and invasion in human chondrosarcoma cells, and that NGF overexpression enhances lung metastasis in a mouse model of chondrosarcoma. NGF-induced stimulation of LOX production and cell motility occurs through the inhibition of miR-149-5p expression, which was reversed by PI3K, Akt, and mTOR inhibitors and their respective short interfering RNAs. Notably, levels of NGF and LOX expression correlated with tumor stage in human chondrosarcoma samples. Thus, NGF appears to be a worthwhile therapeutic target for metastatic chondrosarcoma.