Diffuse Idiopathic Skeletal Hyperostosis (DISH)

Diffuse idiopathic skeletal hyperostosis, commonly called DISH or Forestier’s disease, is a condition in which the body lays down excess bone along the spine and sometimes at other skeletal attachment points. It is far more common than most people realize, affecting roughly one in ten adults overall and as many as one in five men past age 70, yet it often goes undiagnosed because its stiffness and aching are chalked up to “just getting older.” DISH is not a form of arthritis, and understanding what drives it, how it is spotted, and what complications it can cause gives a much clearer picture of an underappreciated condition.

How Common DISH Actually Is

A 2025 systematic review pooling data from studies worldwide found that the overall prevalence of DISH was about 18% in men and roughly 6–10% in women, depending on whether the studies classified participants by biological sex or broader gender categories.¹ That same review showed a clear age gradient: prevalence sat below 3% in people under 50, climbed to about 12% in the 60–69 age bracket, and reached roughly 20% in those over 80.² A Japanese population study found men were more than five times as likely to have DISH as women after adjusting for age.³

Most published data come from populations in Japan, Europe, and North America. A study of over 3,200 Black patients in the United States found an overall thoracic DISH prevalence of about 8%, with no significant difference between men and women in that cohort, which contrasts with the strong male predominance seen in most other populations.⁴ Whether that reflects genuine biological differences, differences in diagnostic criteria, or selection effects is still debated.

What Causes It

The name says “idiopathic,” meaning no single established cause, and that label still holds. But decades of clinical observation have converged on a strong metabolic theme. Obesity, especially abdominal obesity, type 2 diabetes, high insulin levels, and glucose intolerance all appear more frequently in people with DISH than in matched controls.⁵ A Japanese study found that metabolic syndrome was about twice as common among people with DISH compared to those without it, even after accounting for age, sex, smoking, and drinking.⁶

Of all the growth factors examined in DISH research, insulin stands out. The thinking is that persistently elevated insulin levels stimulate bone-forming cells at points where tendons and ligaments attach to bone. Researchers have identified mesenchymal stem cells in the outer part of the enthesis (the tissue where a tendon or ligament meets bone) as likely targets for these growth signals, along with similar undifferentiated cells in the outer ring of spinal discs and on the bony prominences of vertebral bodies.⁷ In essence, the body’s bone-building machinery appears to be overactive at these attachment sites, and metabolic conditions seem to fuel that overactivity.

A common misconception is that the new bone in DISH grows out of the anterior longitudinal ligament, the tough band running along the front of the spine. Imaging work has shown that at locations of heavy new bone formation, this ligament is actually pushed aside by the growing bone rather than replaced by it, suggesting the bone originates from nearby tissue rather than from the ligament itself.⁸

How DISH Is Diagnosed

The standard diagnostic tool is plain X-ray or fluoroscopy, using a set of criteria established decades ago by Donald Resnick. The classic hallmarks are flowing calcification and ossification along the front and sides of at least four contiguous vertebral bodies, relatively preserved disc height in the involved areas (the discs themselves do not degenerate the way they do in ordinary spondylosis), and the absence of fusion in the sacroiliac joints or the small facet joints of the spine.⁹ The thoracic spine is by far the most common site; one Japanese cohort found nearly 90% of DISH cases involved the thoracic spine.¹⁰

A limitation of Resnick’s criteria is that they capture DISH only after it has become fairly advanced. Researchers have proposed CT-based criteria for an “early” phase of DISH, defined by the presence of near-complete or newly forming bone bridges across fewer vertebral segments than the classic four. In a large validation cohort, these early-phase criteria picked up developing DISH with a sensitivity of 96% and a specificity of 83%.¹¹ Earlier identification matters because it opens a window for monitoring and managing metabolic risk factors before the condition progresses.

Telling DISH Apart from Ankylosing Spondylitis

One of the trickiest clinical questions is distinguishing DISH from ankylosing spondylitis (AS), another condition that stiffens the spine. Both can produce bony bridges between vertebrae, and both reduce spinal mobility. But the two diseases differ in fundamental ways. AS is an inflammatory autoimmune condition that typically strikes younger people, causes erosion of the sacroiliac joints, and is strongly linked to the HLA-B27 genetic marker. DISH is non-inflammatory, peaks in older adults, and is tied to metabolic rather than immune factors.

On imaging, complete fusion of both sacroiliac joints was found in 63% of AS patients but under 2% of DISH patients in one multicenter comparison. Meanwhile, anterior bony bridging along the spine was far more common in DISH (both-sides bridging in about 42%) than in AS (about 7%).¹² The pattern of where bony bridging and joint fusion show up is the strongest imaging clue. Still, overlap exists: about 63% of DISH patients in that study had at least partial sacroiliac fusion, which can trip up radiologists who associate any sacroiliac changes with AS.

When the Neck Is Involved

DISH in the cervical spine can cause a symptom that surprises many patients and even some clinicians: difficulty swallowing. Large bony spurs growing off the front of the cervical vertebrae can press against the esophagus and pharynx. Several mechanisms have been proposed for this dysphagia, including direct physical obstruction of the esophageal passage, inflammation and muscle spasm caused by friction between bone spurs and soft tissue, and restriction of the normal movement of the epiglottis and larynx. The problem is most often linked to osteophyte formation around the C3–C5 vertebral levels, where the epiglottis naturally tilts over the airway.¹³

For patients whose swallowing problems are severe or do not respond to dietary modification, surgical removal of the osteophytes is effective. A systematic review of surgical cases found that anterior cervical osteophytectomy resulted in significant improvement across essentially all reported cases, with only one case of postoperative complications and follow-up ranging from a few months to nearly six years.¹⁴ A multicenter study found that about two-thirds of patients who underwent early decompression reported complete disappearance of swallowing symptoms within a week, though occasional recurrence was noted at follow-up of 18 to 30 months.¹⁵

Airway Problems During Anesthesia

A less obvious but potentially serious consequence of cervical DISH is difficulty with intubation during surgery. Bone spurs protruding into the back of the throat can obstruct a clinician’s view of the vocal cords and block the path for an endotracheal tube. In one documented case, video laryngoscopy revealed a large, rigid bulge from the posterior pharyngeal wall that prevented identification of the epiglottis entirely; multiple alternative intubation techniques also failed before the situation was resolved.¹⁶ In addition to the physical obstruction, the stiffened cervical spine in DISH limits the neck extension that airway management normally relies on, adding a second layer of difficulty and raising the risk of spinal cord injury during positioning.¹⁷ For people with known DISH, anesthesiologists may opt for awake fiberoptic intubation and a smaller-than-standard endotracheal tube.¹⁸

Fracture Risk in a Stiffened Spine

Perhaps the most dangerous clinical consequence of DISH is the dramatically increased vulnerability to spinal fractures, particularly from seemingly minor trauma. When multiple vertebral segments are fused into a single rigid column, a fall that would produce only a bruise in a flexible spine can generate enormous lever-arm forces concentrated at one point. The resulting fracture patterns tend to be severe, often involving all three columns of the spine and carrying a high risk of neurological injury including paralysis.¹⁹

German orthopedic and trauma guidelines recommend against non-operative management for the most common fracture types seen in DISH patients, given the inherent mechanical instability and the risk of the neurological picture worsening over time. For cervical spine fractures in DISH, a combined front-and-back surgical stabilization is recommended.²⁰ Conservative treatment with bracing may be considered in patients whose comorbidities make surgery too risky, but close monitoring for signs of developing nerve damage is critical.²¹

This fracture vulnerability is one reason people with DISH should be especially cautious about falls. It is also why emergency departments need a high index of suspicion when an older patient with a stiff spine presents after a low-energy fall. Standard X-rays can miss these fractures because the existing bone overgrowth obscures normal anatomy; CT scanning is often needed.

The Link to Ossification of the Posterior Longitudinal Ligament

DISH frequently coexists with another ossification condition called OPLL, or ossification of the posterior longitudinal ligament, which runs along the back surface of the vertebral bodies inside the spinal canal. A large multicenter Japanese study found that nearly half of patients with cervical OPLL also had DISH, with older age as a strong correlating factor.²² When both conditions are present together, the spinal canal can be narrowed from both front and back, raising the stakes for any trauma and sometimes producing myelopathy (spinal cord compression symptoms like leg weakness and coordination problems) even without injury.²³ Genetic work has identified a shared susceptibility gene, COL6A1, associated with both OPLL and DISH in Japanese populations, hinting that the two conditions may share part of their biological underpinning.²⁴

Heart Disease and Metabolic Consequences

Because DISH clusters so tightly with obesity, diabetes, and metabolic syndrome, it is natural to wonder whether people with DISH face higher cardiovascular risk. The answer is nuanced. One 10-year follow-up study found that the rate of heart attack was significantly higher in the DISH group than in controls, and that nearly 39% of DISH patients developed cardiovascular disease during the follow-up period, somewhat exceeding what the standard Framingham risk score had predicted.²⁵ A separate study confirmed that the calculated 10-year coronary heart disease risk was significantly higher in DISH patients.²⁶

However, a more recent retrospective study of patients who already had a heavy burden of cardiovascular risk factors found that the presence of DISH itself was not independently associated with death from any cause, cardiovascular death, stroke, or major adverse cardiac events.²⁷ The takeaway is that DISH travels alongside cardiovascular risk, but whether it adds independent danger beyond its metabolic companions remains unclear. Either way, a DISH diagnosis is a reasonable prompt to look carefully at blood sugar, cholesterol, blood pressure, and waist circumference.

Living with DISH and Managing Symptoms

Many people with DISH have no symptoms at all and discover the condition incidentally on an imaging study done for something else. When symptoms do occur, the most common complaints are spinal stiffness, back pain, and reduced range of motion. A community-based study found that people with DISH had roughly 70% higher odds of reporting difficulty bending, and men with DISH were more than twice as likely to be unable to complete a basic chair-stand test without using their arms.²⁸ Grip strength was also slightly lower. Walking and stair climbing, however, were not measurably affected.

There is no drug that has been shown to reverse or halt bone formation in DISH. Management is focused on maintaining mobility and reducing discomfort. A small trial of a 24-week exercise program involving daily stretching, mobility, and strengthening exercises for the spine found a significant improvement in lower-back flexion and a trend toward reduced stiffness, with about half the participants reporting that their condition had improved.²⁹ The overall evidence base for rehabilitation in DISH is thin, but published recommendations center on stretching and mobility exercises, manual therapy, and postural education.³⁰ The practical message is straightforward: keep moving. Regular, gentle spinal exercise will not dissolve the bone bridges that are already there, but it can help preserve whatever range of motion remains and reduce stiffness-related discomfort.

DISH in Ancient Bones and Modern Dogs

DISH is not a product of modern diets or sedentary living, though those factors probably make it more common. Paleopathological surveys have identified DISH in hominin populations spanning millions of years, across diverse geographies and time periods. Where dietary data have been available, ancient individuals with DISH tended to show signs of richer food intake than those without it, reinforcing the metabolic connection.³¹ Even in pre-Columbian North American populations, where DISH was rare, researchers have documented cases among adult skeletal remains in the eastern Tennessee River Valley.³²

An unexpected research angle comes from veterinary medicine. DISH has been identified in dogs, and one breed stands out dramatically: the Boxer, with a prevalence of about 41% compared to roughly 4% across purebred dogs generally.³³ Because dog breeds are essentially closed gene pools with high degrees of relatedness, this extreme concentration in one breed strongly suggests a genetic component. As in humans, canine DISH increases with age and is more common in males. Researchers have proposed the Boxer as an animal model for studying DISH’s genetic basis and progression. Interestingly, Boxer dogs with DISH were found to have significantly lower bone mineral density in their vertebrae than those without it, which runs counter to the intuitive assumption that a bone-forming disease should produce denser bones.³⁴ DISH has also likely been underdiagnosed in dogs, often mistaken for ordinary spondylosis.³⁵

Emerging Biomarker Research

One of the frustrations with DISH has been the lack of a blood test or other simple marker to track it. Diagnosis has relied entirely on imaging, and by the time imaging criteria are met, extensive bone formation has already occurred. Early-stage proteomic research has begun to change that picture. A recent study examining proteins carried in tiny blood-borne particles called extracellular vesicles found that a protein known as AHSG (also called fetuin-A) was significantly elevated in people with DISH. The protein’s level correlated with the number of ossified spinal segments, meaning higher levels corresponded to more extensive disease.³⁶ This is still early-stage work, and no validated clinical blood test exists yet. But if a reliable biomarker can be confirmed, it could open the door to monitoring disease activity and potentially identifying people at risk before the characteristic bone bridges form on X-ray.