Hyperostosis is excessive growth of bone tissue, either on the surface of existing bones or into surrounding soft tissues like ligaments and tendons. It’s not a single disease but a feature shared by several conditions, the most common being diffuse idiopathic skeletal hyperostosis (DISH), which affects the spine and joints. Other forms include hyperostosis frontalis interna, which thickens the inner surface of the skull, and Caffey disease, a rare genetic condition in infants. Each type has distinct causes, affected populations, and implications for daily life.
Diffuse Idiopathic Skeletal Hyperostosis (DISH)
DISH is by far the most common form of hyperostosis. It causes the ligaments and tendons that attach to your spine to gradually harden and turn into bone, a process called ossification. The thoracic spine (mid-back) is the primary site, though it can spread to the neck, lower back, and peripheral joints like the knees, elbows, and heels. DISH was first described in 1950 and is sometimes still called Forestier’s disease.
The condition is surprisingly common. Roughly 25% of men and 15% of women over age 50 have it. Many never know, because DISH often produces no symptoms in its early stages. When it does cause problems, the most typical complaints are back stiffness, reduced spinal mobility, and a gradual increase in thoracic kyphosis (a rounded upper back). In the cervical spine, bone growth along the front of the vertebrae can press on the esophagus, causing difficulty swallowing or, less commonly, hoarseness.
DISH is not just a spinal condition. Research shows that the genetic variants linked to DISH also correlate with increased bone mineral density throughout the body, suggesting a systemic tendency toward heightened bone formation. The underlying mechanism involves stem cells in ligament and tendon attachment points that abnormally differentiate into bone-forming cells, driven by an excess of growth factors like insulin and insulin-like growth factor 1. This helps explain why DISH is strongly associated with type 2 diabetes, obesity, and metabolic syndrome.
How DISH Differs From Ankylosing Spondylitis
Because both DISH and ankylosing spondylitis (AS) cause spinal stiffness and show bony changes on imaging, the two are sometimes confused. The differences are significant, though. AS is an inflammatory autoimmune disease that typically strikes younger adults, often before age 45, and is associated with the HLA-B27 gene marker, elevated inflammation markers, and erosion of the sacroiliac joints where the spine meets the pelvis. DISH, by contrast, tends to appear in older adults, shows no sacroiliac joint erosion, and isn’t driven by inflammation. A history of psoriasis, inflammatory bowel disease, or eye inflammation (uveitis) points toward AS rather than DISH.
On X-rays, the distinction is visible. AS produces thin, vertical bony bridges (syndesmophytes) growing from the edges of vertebral discs, eventually creating a “bamboo spine” appearance. DISH produces thick, flowing bone formation along the front and side of the spine that bridges at least four consecutive vertebrae, sometimes described as looking like dripping candle wax or a parrot beak in the cervical spine.
Diagnosing DISH
DISH is diagnosed primarily through imaging. The most widely used criteria, established by Resnick and Niwayama, require three findings on X-ray: flowing bone growth bridging at least four consecutive thoracic vertebrae, preserved disc space height (meaning the discs themselves aren’t degenerating), and no erosion or fusion of the sacroiliac or spinal facet joints. An alternative set of criteria lowers the threshold to three consecutive vertebrae but adds the presence of bony overgrowth at tendon attachment points in the arms or legs.
CT scans provide more detailed views and can reveal early ossification that plain X-rays miss. The condition is often discovered incidentally when imaging is done for another reason, such as a chest X-ray or a CT scan after a fall.
Symptoms and Complications of DISH
Many people with DISH experience only mild stiffness, particularly in the morning or after prolonged sitting. As the condition progresses, the range of motion in the spine gradually decreases. Pain, when present, tends to be a dull ache in the mid or lower back rather than sharp or shooting.
The more serious complications relate to where the extra bone forms. In the cervical spine, large bony projections can compress the esophagus or airway, making swallowing difficult or causing a sensation of something stuck in the throat. In rare cases, this can affect breathing. The stiffened spine also becomes more brittle, and even a minor fall can cause fractures that would be unlikely in a flexible spine. These fractures carry a higher risk of spinal cord injury because the rigid segments concentrate force at the fracture site. Nerve compression in the lower spine can cause pain, numbness, or weakness in the legs.
Managing DISH
There is no treatment that reverses the bone growth already present in DISH, so management focuses on maintaining mobility and controlling discomfort. Physical therapy is the cornerstone, emphasizing stretching and range-of-motion exercises to preserve spinal flexibility for as long as possible. Anti-inflammatory medications help during flare-ups of pain. Some patients are prescribed bisphosphonates, which slow bone remodeling and may reduce further ossification.
Surgery becomes an option when complications are severe. If cervical bone spurs cause significant swallowing difficulty or airway compression, a surgeon can remove the excess bone. Spinal fractures in DISH patients often require stabilization because the rigid spine doesn’t heal well with bracing alone. Early treatment of fractures matters, since delayed intervention increases the risk of neurological damage.
Hyperostosis Frontalis Interna
Hyperostosis frontalis interna (HFI) is a thickening of the inner table of the frontal bone, the part of the skull behind your forehead. It occurs most often in postmenopausal women, with studies reporting prevalence rates as high as 73% in women over 60 in some populations. Among women of reproductive age, the rate drops to around 17%. This pattern strongly suggests a hormonal component, likely related to the estrogen changes that accompany menopause. HFI also occurs at higher rates in people with acromegaly, a condition caused by overproduction of growth hormone.
HFI is usually an incidental finding on a head CT or skull X-ray. Most people with it have no symptoms at all. When symptoms do occur, the most commonly reported are headaches, vertigo, cognitive decline, and depression, though establishing a direct causal link between the skull thickening and these symptoms remains difficult since they’re also common in the same age group for other reasons. Obesity is a frequent comorbidity.
Caffey Disease: Hyperostosis in Infants
Caffey disease, also called infantile cortical hyperostosis, is a rare genetic condition that causes excessive bone growth in infants, typically appearing before five months of age. It results from a specific mutation in the COL1A1 gene, which provides instructions for building type I collagen, a major structural protein in bone. The mutation swaps a single amino acid in the collagen protein, disrupting its normal structure.
The condition follows an autosomal dominant inheritance pattern, meaning a child needs only one copy of the mutated gene to be affected. About 20% of people who carry the mutation never develop symptoms, a phenomenon called incomplete penetrance. Some children inherit the mutation from a parent, while others have a new mutation with no family history. Caffey disease causes swelling of the soft tissue over affected bones (commonly the jaw, collarbones, and long bones of the arms and legs), along with irritability and fever. In most cases, it resolves on its own within the first two years of life.