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, involving metabolic, mechanical, and genetic factors. Metabolic factors, such as obesity, type 2 diabetes, hypertension, and dyslipidemia, play a significant role in the development of DISH, with elevated insulin and insulin-like growth factors stimulating osteoblast activity and new bone formation 1. The process begins with calcification of the anterior longitudinal ligament, followed by ossification that creates flowing, candle-wax-like bone bridges across vertebral segments, typically affecting the thoracic spine first.
Key Factors in DISH Pathophysiology
- Metabolic factors: obesity, type 2 diabetes, hypertension, and dyslipidemia
- Mechanical stress: triggering factor, explaining the predilection for the right side of the thoracic spine
- Genetic factors: likely contribute, though specific genes have not been definitively identified
- Elevated insulin and insulin-like growth factors: stimulate osteoblast activity and new bone formation
The distinction between DISH and other conditions, such as ankylosing spondylitis, is crucial, as DISH spares the sacroiliac joints and does not involve inflammation of the intervertebral discs, maintaining disc height even as the surrounding ligaments ossify. While the effects of certain medications, such as acitretin, on the skeletal system have been studied, the primary focus in understanding DISH remains on its underlying pathophysiological mechanisms 1.
From the Research
Pathophysiology of DISH
The pathophysiology of Diffuse Idiopathic Skeletal Hyperostosis (DISH) is not fully understood, but several factors are thought to contribute to its development. These include:
- Genetic factors, as the condition tends to run in families 2, 3
- Vascular factors, such as atherosclerosis, which may play a role in the development of new bone formation 2, 4
- Metabolic factors, such as diabetes mellitus, which is strongly associated with DISH 2, 3, 4
- Mechanical factors, such as the presence of entheseal sites, where new bone forms 2
Clinical Relevance
DISH is often asymptomatic, but it can lead to symptoms such as:
- Back pain and stiffness 4
- Dysphagia (difficulty swallowing) 3, 4
- Functional decline and neurologic deficits 4
- Unstable spinal fractures from low-energy trauma 4
Diagnosis and Management
Diagnosing DISH is important, as it can increase the risk of spinal fractures and is associated with other metabolic and cardiovascular conditions 2, 3, 4. The diagnosis of DISH is typically made using radiographic criteria, such as the presence of flowing ossifications along the anterior spine spanning ≥4 vertebral bodies 4. Management of DISH typically involves careful consideration of the patient's overall health and the use of medications such as non-steroidal anti-inflammatory drugs (NSAIDs) to manage symptoms, although the use of NSAIDs must be carefully weighed against the potential risks of organ damage 5