Diffuse idiopathic skeletal hyperostosis (DISH) has several synonyms, including ankylosing hyperostosis and Forestier's disease [1,2]. It is a noninflammatory disease, with the principal manifestation being calcification and ossification of spinal ligaments and the regions where tendons and ligaments attach to bone (entheses).
Radiographic changes characteristic of DISH may occur in the absence of any musculoskeletal symptoms.
The clinical manifestations, radiographic findings, and treatment of DISH are reviewed here. The clinical features and treatment of another noninflammatory arthritis, osteoarthritis, are presented separately. (See "Clinical manifestations of osteoarthritis" and "Initial pharmacologic therapy of osteoarthritis" and "Surgical therapy of osteoarthritis".)
ETIOLOGY AND PATHOGENESIS
While the cause of diffuse idiopathic skeletal hyperostosis (DISH) remains unknown, mechanical factors, dietary contributions, drugs, environmental exposures, and metabolic conditions have been hypothesized to be important. It is thought that the bone formation that is distinctive of DISH results from abnormal osteoblastic differentiation and activity at the enthesis. An appropriate genetic background, as yet unidentified, external factors, or local or systemic factors may stimulate the abnormal osteoblastic differentiation.
Mechanical factors — Bony bridging is usually more prominent on the right side of the thoracic spine in patients with DISH. By comparison, those with DISH and dextrocardia or situs inversus have more extensive bony bridging on the left side of the thoracic spine. Thus, mechanical factors associated with the change in location of the aorta may affect the development of bony outgrowths . In ossification of the posterior longitudinal ligament of the spine, a condition that can occur with DISH or as an independent entity, ligamentous stretching can increase prostaglandin I2 synthase resulting in stimulation of osteogenic differentiation .