Ankylosing spondylitis (AS) does cause bone spurs, and they are one of the hallmark features of the disease. These bony growths form along the spine and at other sites where tendons and ligaments attach to bone. Over time, they can bridge the gaps between vertebrae and progressively limit spinal mobility. About one in three AS patients develops new bone spurs within two years, and nearly half do so within four years.
How AS Bone Spurs Differ From Typical Bone Spurs
The bone spurs caused by AS are technically called syndesmophytes, and they look and behave differently from the osteophytes you’d see with ordinary wear-and-tear arthritis. Osteophytes grow outward from the cartilage-covered edge of a vertebra in a horizontal direction, often alongside disc narrowing. Syndesmophytes grow vertically, parallel to the front edge of the spine, starting where ligaments insert into bone. On an X-ray, radiologists use a 45-degree angle as the dividing line: growths angled closer to vertical are syndesmophytes (AS-related), while those angled more horizontally are degenerative osteophytes.
This distinction matters because the vertical growth pattern of syndesmophytes is what eventually allows them to bridge the space between one vertebra and the next, something horizontal osteophytes rarely do. That bridging is what makes AS uniquely damaging to spinal flexibility.
Why Inflammation Triggers Bone Growth
AS starts with chronic inflammation at the entheses, the spots where ligaments and the outer fibers of spinal discs attach to bone. The vertebral corners and sacroiliac joints are the earliest targets. What makes AS unusual among inflammatory diseases is that the body’s repair response overshoots: instead of simply healing damaged tissue, it lays down entirely new bone where none should exist.
This excess bone formation happens through multiple pathways. Some new bone forms directly from connective tissue turning into bone. In other cases, the body first builds cartilage at the inflamed site, then converts that cartilage into bone, a process driven in part by specific growth-factor signaling in the enthesis and spinal growth plates. The result is progressive bony overgrowth at each vertebral corner, first causing the vertebrae to lose their normal concave shape (called “squaring”), then producing syndesmophytes that extend upward and downward toward neighboring vertebrae.
Where Bone Spurs Form
The spine is the primary site, but not the only one. Along the spine, syndesmophytes typically appear first at the thoracolumbar and lumbosacral junctions. They grow at the anterior (front) vertebral corners, following the path of the spinal ligaments. The sacroiliac joints also undergo bony changes early in the disease.
Outside the spine, AS commonly causes bone spurs at the heels. Inflammation at the Achilles tendon insertion and the plantar fascia attachment on the calcaneus (heel bone) can produce calcaneal spurs. Research shows that people in the early stages of AS tend to have smaller heel spurs, while those with chronic disease develop larger ones. Other peripheral sites where tendons attach to bone, such as the knees, pelvis, and ribs, can also be affected.
How Bone Spurs Affect Mobility
The number and size of syndesmophytes directly correlate with how much spinal movement you lose. Studies measuring the relationship between bone spur scores and physical function show strong correlations with reduced lateral spinal flexion (the ability to bend sideways), cervical rotation (turning your head), and increased thoracic kyphosis (forward rounding of the upper back). Chest expansion, which depends on rib-joint flexibility, also decreases as syndesmophytes accumulate, though the relationship is moderate.
In advanced cases, syndesmophytes completely bridge the disc spaces between vertebrae, fusing them into a single rigid column. When this happens across the facet joints and sacroiliac joints as well, it produces the characteristic “bamboo spine” appearance on X-rays. At this stage, the spine has essentially no segmental movement. This fusion also makes the spine more brittle and vulnerable to fractures from even minor trauma.
How Quickly Do They Progress?
A longitudinal study tracking AS patients found that 33% developed new syndesmophytes within two years and 48% within four years. The single strongest predictor of new bone spur formation is already having existing ones. Patients who start with syndesmophytes at baseline are far more likely to develop additional ones compared to patients whose spines are still clear on imaging.
Doctors track progression using a scoring system that rates 24 vertebral corners in the cervical and lumbar spine on a scale from 0 to 3: zero for normal, 1 for erosion or squaring, 2 for a non-bridging syndesmophyte, and 3 for complete bony bridging between vertebrae. The total score ranges from 0 to 72, and changes over time indicate how fast the disease is advancing structurally.
Can Treatment Slow Bone Spur Growth?
Controlling inflammation is the main strategy for slowing new bone formation, though timing matters enormously. Biologic medications that target a key inflammatory protein (TNF) are associated with a 50% reduction in the odds of spinal progression. Patients who spent more than half their disease duration on these medications had an 80% reduction in odds of new bone spur formation compared to untreated patients. Critically, patients who waited more than 10 years before starting biologic therapy were 2.4 times more likely to show progression than those who started earlier. The protective effect also becomes clearer with longer follow-up, showing significant benefit when tracked over roughly four or more years.
Anti-inflammatory painkillers also play a role, though the evidence is mixed. One randomized trial found that taking celecoxib continuously for two years led to significantly less spinal progression than taking it only as needed for pain. However, a similar trial using diclofenac found no significant difference between continuous and on-demand use. An older retrospective study of a different anti-inflammatory also showed that continuous use delayed or arrested progression compared to intermittent use. The inconsistency between trials means continuous use of these medications isn’t a guaranteed strategy, but the celecoxib data suggests it may help in some patients.
What Drives Individual Differences
Not everyone with AS develops severe bone spurs. Several factors influence who progresses faster. Having a higher baseline level of structural damage is the most reliable predictor. Male sex, smoking, and elevated inflammatory markers in blood tests are also associated with faster progression. The presence of the HLA-B27 gene, which is found in the vast majority of AS patients, is linked to disease susceptibility but does not reliably predict the rate of bone spur formation on its own.
Because the bone formation process can continue even after inflammation is controlled, there is a window of opportunity in early disease when stopping the inflammatory cascade has the greatest chance of preventing structural damage. Once syndesmophytes are established, they don’t reverse. Treatment at that point focuses on preventing new ones from forming and maintaining whatever flexibility remains through exercise and physical therapy.