Diffuse Idiopathic Skeletal Hyperostosis (DISH) — Presentation, Investigations and Treatment

DISH (Forestier–Rotés-Querol disease, originally “senile ankylosing hyperostosis”) is a systemic, non-inflammatory skeletal disorder characterised by ossification and calcification of spinal and extraspinal ligaments and entheses, particularly the anterior longitudinal ligament.

It is a disease of older adults — prevalence rises steeply after 50 and reaches up to 25–40% of men over 70, with a male to female ratio of about 2:1. The majority of cases are asymptomatic and found incidentally.

DISH is a “new bone formation” disorder — it is neither degenerative disc disease nor an inflammatory spondyloarthropathy, though imaging overlap with both is common.

The cause is unknown. The core abnormality is differentiation of enthesial fibroblasts into bone-forming cells, driven by local growth factors — insulin, IGF-1, growth hormone, TGF-β, bone morphogenetic proteins and endothelin-1.

Strong metabolic associations: type 2 diabetes and hyperinsulinaemia, obesity, hypertension, dyslipidaemia and hyperuricaemia. DISH is increasingly regarded as the skeletal manifestation of the metabolic syndrome.

Other associations: male sex, advancing age, long-term retinoid use (isotretinoin, etretinate) and hypervitaminosis A, hypoparathyroidism, acromegaly, and probable genetic contributions (COL6A1).

Paradox worth remembering: patients with DISH have higher bone mineral density than controls, yet fracture easily — the long, rigid, ankylosed spine behaves mechanically like a long bone.

Most patients are asymptomatic; DISH is commonly an incidental finding on a chest radiograph or CT performed for another reason.

Axial symptoms: dull mid-thoracic and lumbar back pain with progressive stiffness, typically mild, worse after inactivity and in cold weather, and without the dramatic NSAID response seen in spondyloarthritis.

Reduced spinal range of movement with preserved sacroiliac joints, progressive thoracic kyphosis and loss of lumbar lordosis, contributing to postural instability and falls.

Cervical DISH and dysphagia — the key geriatric presentation. Large anterior osteophytes at C3–C5 mechanically compress and tether the oesophagus, producing progressive dysphagia to solids and then liquids, with weight loss. This is an under-recognised and reversible cause of dysphagia in older adults, sometimes termed “DISHphagia”.

Other cervical complications: hoarseness, globus sensation, stridor and acute airway obstruction, obstructive sleep apnoea, aspiration pneumonia, and difficult intubation or failed nasogastric tube placement.

Peripheral enthesopathy: calcaneal (heel) spurs, olecranon and patellar spurs, and “whiskering” of the iliac crest, ischial tuberosity and greater trochanter — these can cause local pain and be mistaken for tendinitis or bursitis.

Serious spinal complications: ossification of the posterior longitudinal ligament (OPLL) and ligamentum flavum causing myelopathy or radiculopathy; and — most important — unstable three-column hyperextension fractures of the rigid spine after trivial falls, which carry high rates of delayed diagnosis, neurological injury and mortality.

Diagnosis is radiological, using the Resnick and Niwayama criteria on a lateral thoracic spine radiograph: (i) flowing ossification along the anterolateral aspect of at least four contiguous vertebral bodies; (ii) preserved intervertebral disc height in the involved segments without significant degenerative disc disease; and (iii) absence of apophyseal (facet) joint ankylosis and of sacroiliac erosion, sclerosis or fusion.

The classic radiographic appearance is “flowing” or “dripping candle wax” ossification, most often on the right side of the thoracic spine — the pulsating descending thoracic aorta is thought to protect the left side.

CT is best for defining osteophyte size, oesophageal and airway compression, and — critically — for fracture detection in the rigid spine. Always obtain CT (and MRI if there is any neurology) rather than plain films when a DISH patient falls, because fractures are easily missed.

Barium swallow / videofluoroscopy dynamically demonstrates the level responsible for dysphagia and confirms adequate oesophageal decompression after surgery. Flexible endoscopy excludes malignancy and manometry excludes a motility disorder.

Laboratory tests are normal — ESR and CRP normal or only mildly raised, HLA-B27 negative, calcium, phosphate and alkaline phosphatase normal. Screen every patient for diabetes, lipids, uric acid and blood pressure, since the metabolic comorbidity is the real health burden.

Key differential diagnoses:

There is no disease-modifying therapy; management is symptomatic and complication-focused.

Conservative care: analgesics and NSAIDs for pain, physiotherapy for posture, range of motion and core strength, activity modification, local heat, and weight reduction with tight control of diabetes, lipids and blood pressure — metabolic control is the only intervention likely to influence the underlying process.

Management of dysphagia: diet and texture modification with speech-and-language therapy, anti-reflux measures and proton pump inhibitors, upright positioning and small frequent meals, and muscle relaxants where spasm contributes. Enteral feeding or gastrostomy for refractory dysphagia with weight loss.

Local corticosteroid injection helps symptomatic peripheral enthesopathy; bisphosphonates have been used for painful enthesopathy with limited evidence.

Surgery is reserved for failure of conservative treatment, severe dysphagia with significant weight loss, or airway compromise. The procedure is anterior osteophytectomy through a Smith–Robinson or trans-pharyngeal approach, sometimes combined with cricopharyngeal myotomy. Symptom relief is generally excellent, but counsel about recurrence and complications — recurrent laryngeal nerve palsy, haematoma, oesophageal perforation and dysphonia. Tracheostomy may be needed for acute airway obstruction.

Spinal decompression and stabilisation for myelopathy or fracture. Any DISH patient who falls and has new spinal pain must be assumed to have an unstable fracture until CT proves otherwise — a classic and dangerous geriatric trap.

Anaesthetic and nursing implications: anticipate difficult intubation (fibreoptic technique, cervical rigidity), difficult nasogastric tube insertion, careful positioning of the rigid kyphotic spine, and meticulous pressure-area care.