“…Gouty arthropathy occurs secondary to abnormal purine metabolism, the end product of which is uric acid, combined with underexcretion or overproduction of uric acid, resulting in sustained hyperuricemia. Hyperuricemia, above the local solubility, can lead to monosodium urate (MSU) crystal deposition ( Figure 1 ) in joints, on the surface of the hyaline cartilage and within periarticular soft tissues such as tendons, ligaments, retinacula, and bursae, with resulting inflammatory response [ 7 , 13 , 14 , 16 , 17 , 19 , 22 , 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 , 31 , 32 ]. Gout predominantly affects the peripheral joints, but the axial skeleton may also be affected [ 33 ].…”