From the Guidelines
Diffuse idiopathic skeletal hyperostosis (DISH) is characterized by abnormal calcification and ossification of ligaments and entheses, particularly along the anterolateral aspect of the spine, involving excessive bone formation without preceding inflammation. The pathophysiology of DISH is complex and multifactorial, with metabolic factors playing a central role, as evidenced by the association between DISH and metabolic disorders like type 2 diabetes, obesity, and dyslipidemia 1.
Key Features of DISH
- Excessive bone formation without preceding inflammation, distinguishing it from inflammatory arthropathies
- Metabolic factors, such as insulin and insulin-like growth factors, promoting osteoblast proliferation and bone formation
- Strong association with metabolic disorders like type 2 diabetes, obesity, and dyslipidemia
- Typical involvement of the thoracic spine first, with flowing ossification of the anterior longitudinal ligament creating a "candle wax" appearance on imaging
- Preservation of intervertebral disc spaces and facet joints, unlike ankylosing spondylitis
Pathophysiological Process
The ossification process in DISH gradually progresses over years, often remaining asymptomatic until significant bone formation causes stiffness, pain, or neurological complications from nerve compression. Mechanical factors and repetitive microtrauma may contribute to the predilection for certain anatomical sites. While no specific genetic marker has been identified, familial clustering suggests genetic predisposition may influence susceptibility to this disorder.
Clinical Implications
Understanding the pathophysiology of DISH is crucial for the diagnosis and management of this condition, as it can help identify individuals at risk and inform treatment strategies to prevent or slow disease progression. Although the study by the British Association of Dermatologists 1 focused on the effects of acitretin on the skeletal system, it highlights the importance of considering the potential for skeletal abnormalities, including DISH-like involvement, in patients undergoing long-term treatment with systemic retinoids.
From the Research
Pathophysiology of DISH
The pathophysiology of Diffuse Idiopathic Skeletal Hyperostosis (DISH) is characterized by the ossification and calcification of ligaments and entheses, leading to the formation of new bone tissue [(2,3,4,5)]. This process can result in the fusion of vertebrae and the formation of bridging ossifications, which can lead to a range of clinical symptoms, including pain, stiffness, and reduced mobility [(2,3,5)].
Key Features of DISH
- Ossification and calcification of ligaments and entheses [(2,3,4,5)]
- Formation of new bone tissue [(2,3,4,5)]
- Fusion of vertebrae and formation of bridging ossifications [(2,3,5)]
- Association with metabolic disorders, such as diabetes mellitus and hyperinsulinemia [(2,3,5)]
Clinical Presentations of DISH
- Asymptomatic in most individuals [(2,3,5)]
- Pain, stiffness, and reduced mobility [(2,3,5)]
- Dysphagia and airway obstruction 3
- Unstable spinal fractures [(2,5)]
Note: The study 6 is not directly relevant to the pathophysiology of DISH, as it focuses on the cardiovascular safety and fracture prevention effectiveness of denosumab versus oral bisphosphonates in patients receiving dialysis.