What is Skeletal Hyperostosis?
Skeletal hyperostosis is a condition characterized by abnormal bone overgrowth, most commonly manifesting as diffuse idiopathic skeletal hyperostosis (DISH), which involves calcification and ossification of ligaments and entheses (tendon/ligament insertion sites), particularly along the spine. 1
Key Pathological Features
DISH specifically involves "flowing" ossification along the anterolateral margins of at least four contiguous vertebrae, distinguishing it from degenerative spondylosis or spondyloarthropathy. 2 The condition represents systemic calcification of soft tissues, predominantly affecting:
- Spinal ligaments (especially thoracic spine on the right side)
- Entheses throughout the body
- Intervertebral disc spaces
- Sternocostal articulations 3
The ossification creates bridging bone formations that progressively stiffen the spine and can extend to extraspinal sites. 1
Clinical Presentation and Demographics
DISH most commonly affects men over 50 years of age and is observed across all continents and races. 1 While many patients remain asymptomatic, symptomatic presentations include:
- Back pain and spinal stiffness 2
- Reduced range of articular motion 1
- Dysphagia (difficulty swallowing) from cervical involvement 2
- Cervical myelopathy and lumbar stenosis 2
A critical pitfall: DISH dramatically increases the risk of unstable spinal fractures from even minor trauma (such as ground-level falls), as the rigid, osteoporotic spine becomes vulnerable to injury. 4, 2 Diagnosis of these fractures is often delayed because patients have baseline spinal pain and the inciting trauma may be trivial. 2
Drug-Induced Skeletal Hyperostosis
Long-term systemic retinoid therapy (etretinate, acitretin, isotretinoin) can cause skeletal hyperostosis as an adverse effect, particularly with 2-4 years of treatment. 5 This manifests as:
- Extraspinal tendon and ligament calcification (ankles, pelvis, knees most common) 5
- DISH-like spinal involvement with degenerative spondylosis and syndesmophytes 5
- Bone exostoses 5
In children, retinoid-induced hyperostosis can include premature epiphyseal closure, periosteal thickening, and extraosseous calcification, though this appears dose-dependent and linked to high doses (up to 3.5 mg/kg) used for months to years. 5 Recent British Association of Dermatologists guidelines note that routine radiographic monitoring is not recommended for long-term acitretin therapy, as evidence does not support this practice and exposes patients to unnecessary radiation; targeted X-rays should be reserved for atypical musculoskeletal pain. 5
Pathophysiology
The etiology remains poorly understood, but DISH is often an indicator of underlying metabolic disease, with associations to:
- Hyperinsulinemia with or without hyperglycemia
- Hypertension
- Hyperlipidemia
- Hyperuricemia 6
Recent research implicates disrupted purine metabolism and pyrophosphate homeostasis in the development of ectopic mineralization, with loss of equilibrative nucleoside transporter 1 (ENT1) producing DISH-like lesions in animal models. 3
Distinction from Other Conditions
Skeletal hyperostosis differs from primary osteoarthritis in prevalence patterns, gender distribution, anatomical sites of involvement, and the magnitude and distribution of spinal and peripheral joint changes. 6 The formal diagnosis requires multiple contiguous fully formed bridging ossifications, which likely represent advanced disease stages. 1