Diffuse idiopathic skeletal hyperostosis (DISH), also known as Forestier-Rotes-Querol disease, is characterized by the ossification of the entheses (i.e., enthesopathy). The diagnosis of DISH requires at least two (according to Forestier) or three (according to Resnick) contiguous intervertebral bridges, without severe disk alterations (in contrast to degenerative spinal disease) or ankylosis of the sacroiliac or facet joints (in contrast to spondylarthritis). Although prevalence estimates vary with the number of bridges used to define the disease, the prevalence of DISH is consistently high and increases with age and obesity. Peripheral involvement is common but difficult to ascribe to DISH in the absence of typical spinal changes. Cervical spine ossification is the most extensively studied manifestation, as dysphagia due to esophageal compression may require surgery. As with spondylarthritis, vertebral fractures on a hyperostotic fused spine may escape recognition, placing the patient at risk for complications in the event of subsequent displacement. These fractures are particularly severe, as they often involve the cervical spine and can therefore, cause major neurological impairments. DISH is associated with an increased risk of metabolic syndrome (odds ratio, 3.88). Research into the pathophysiology of DISH has established that serum levels of the natural osteogenesis inhibitor Dickkopf-1 (DKK-1) are low in patients with DISH or spondylarthritis. Although this abnormality might contribute to the entheseal ossification, it has not been found consistently.