Spinal bone spurs form when your body lays down extra bone in response to stress, instability, or damage along the vertebrae. The most common trigger is osteoarthritis, which breaks down the cartilage cushioning your spinal joints and prompts a repair response that overshoots its mark. By age 60, these growths are remarkably common: population surveys have found that 84% of men and 74% of women have at least one detectable bone spur somewhere along their spine.
How Cartilage Loss Triggers Bone Growth
Your spine relies on cartilage to absorb shock between vertebrae and inside the small facet joints that link each vertebra to the next. In a healthy spine, those facet joints carry about 33% of the mechanical load. But as cartilage wears away, the joints can no longer distribute force evenly, and the facet joints end up bearing as much as 70% of the load.
That extra pressure triggers a chain of events. The bone just beneath the damaged cartilage (called subchondral bone) becomes denser and stiffer. Blood flow to the area worsens, starving bone and cartilage cells of oxygen and causing them to die off. In response, your body tries to stabilize the joint by depositing new bone along its edges. These outgrowths are bone spurs, or osteophytes. The process is essentially your skeleton’s attempt to widen the joint surface and spread out the load, but it often creates more problems than it solves by crowding nearby nerves and soft tissue.
The Role of Disc Degeneration
The rubbery discs between your vertebrae lose water content and flatten as you age. When a disc narrows, the two vertebrae on either side sit closer together and shift in ways they weren’t designed for. The altered alignment puts abnormal stress on the facet joints and the edges of the vertebral bodies, both of which respond by growing bone spurs. This is why bone spurs and disc narrowing almost always show up together on imaging. The narrower the disc, the more mechanical stress gets redirected to bone, and the more aggressively the body tries to reinforce the area.
Disc degeneration is most common in the neck (cervical spine) and lower back (lumbar spine) because these regions bear the most weight and allow the most movement. The neck supports the head through a wide range of motion, while the lower back absorbs forces from walking, lifting, and sitting. Both areas are prone to early wear and the bone spur formation that follows.
Genetics and Vitamin D Receptors
Not everyone with the same lifestyle develops bone spurs at the same rate, and genetics explain much of the difference. One of the strongest genetic links involves variation in the vitamin D receptor gene. This receptor is active in both the bone-building cells and cartilage cells found inside bone spurs, suggesting it directly influences how aggressively your body forms new bone. People with one version of this gene variant (the TT genotype) have a 50 to 60% lower risk of developing spinal bone spurs and disc narrowing compared to those with the opposite version.
Other genetic factors play a role too. Variations in genes controlling a growth signal called transforming growth factor beta 1 have been linked to spinal bone spur formation, particularly in women. These genetic differences help explain why some people develop significant spinal changes in their 40s while others reach their 80s with relatively clean imaging.
Inflammatory Arthritis and a Different Type of Growth
Osteoarthritis isn’t the only condition that produces bony growths on the spine. Inflammatory forms of arthritis, particularly ankylosing spondylitis, cause a distinct type of growth called a syndesmophyte. While standard bone spurs grow from the edges of joints, syndesmophytes form within the tough outer ring of the spinal disc itself. They tend to appear first along the back and sides of the vertebral rim rather than randomly around it, which suggests mechanical forces play a role alongside inflammation.
Over time, syndesmophytes can bridge the gap between two vertebrae entirely, and in severe ankylosing spondylitis they may fuse multiple vertebrae together. This creates a rigid segment of spine that limits flexibility and changes how the rest of the spine handles stress. The distinction matters because the underlying cause (an overactive immune system rather than wear and tear) requires a completely different treatment approach.
Ligament Calcification
Bone-like growths on the spine don’t always originate from joints or vertebral edges. The ligaments that run along the inside of the spinal canal can also turn to bone through a process called heterotopic ossification, where bone tissue forms in places it normally shouldn’t exist. One ligament particularly prone to this is the ligamentum flavum, a thick band that connects adjacent vertebrae along the back of the spinal canal.
When this ligament ossifies, its flexible tissue transforms into rigid bone that can press directly into the spinal cord or nerve roots. The process appears to be driven by a combination of mechanical stress, genetic susceptibility, and changes in trace mineral levels. Researchers have found that ossified ligament tissue contains higher concentrations of calcium, fluoride, and copper, and lower levels of zinc and manganese compared to normal tissue. Inflammatory signals also contribute by switching on genes responsible for bone formation in cells that would normally remain fibrous.
Other Contributing Factors
Beyond the primary mechanisms, several factors accelerate bone spur development throughout the spine:
- Poor blood supply: Conditions like atherosclerosis and microvascular disease reduce blood flow to the subchondral bone beneath spinal cartilage. The resulting oxygen deprivation kills off cartilage and bone cells, stiffening the area and making it more vulnerable to mechanical damage.
- Obesity: Extra body weight increases the compressive load on every spinal segment, speeding up disc degeneration and cartilage loss in the facet joints.
- Repetitive stress: Occupations or activities that involve heavy lifting, prolonged sitting, or repeated spinal twisting subject the same joints to cumulative microtrauma over years.
- Previous injury: A herniated disc, vertebral fracture, or spinal surgery can alter the mechanics of a specific segment, concentrating stress and prompting localized bone spur growth years after the original injury.
Why Most Bone Spurs Never Cause Symptoms
Finding bone spurs on an X-ray or MRI doesn’t necessarily mean they’re the source of pain. Given that three-quarters or more of older adults have them, most spinal bone spurs exist silently for years or even an entire lifetime. They only become a clinical problem when they grow into spaces occupied by nerves. In the neck, a bone spur pressing on a nerve root can cause pain, tingling, or weakness radiating into the arm. In the lower back, the same scenario affects the legs. When spurs narrow the central spinal canal itself, the condition is called spinal stenosis, which can cause pain, heaviness, or numbness in both legs during walking.
The severity of symptoms depends far more on location than on size. A small spur growing into a tight nerve passageway (the neural foramen) can cause significant pain, while a large spur on the front of a vertebra may never cause any trouble at all. This is why treatment decisions are based on symptoms and physical findings rather than on what imaging reveals.