When Do Spine Growth Plates Close?

Spine growth plates close in stages over roughly two decades, with some internal plates fusing as early as age five and the outermost ones not fully solidifying until the early-to-mid twenties. Unlike the growth plates in your arms or legs, which are single cartilage zones near each end of the bone, each vertebra has multiple growth centers that mature on different schedules. The result is a surprisingly long and uneven timeline that affects everything from scoliosis treatment decisions to injury risk in young athletes.

Two Main Types of Spinal Growth Plates

To understand the timeline, it helps to know that vertebrae grow from two distinct sets of cartilage structures. The first is the neurocentral synchondrosis, a strip of cartilage inside each vertebra that sits between the body (the front weight-bearing block) and the neural arch (the bony ring that protects the spinal cord). This is the growth center that shapes the spinal canal during childhood. The second is the vertebral ring apophysis, a cartilage ring around the top and bottom rims of each vertebral body. The ring apophysis is responsible for the vertebra’s final height and the bony endplate that interfaces with the discs. These two structures close on very different timelines, which is why “when do spine growth plates close” doesn’t have one clean answer.

The Early Closers: Neurocentral Synchondrosis

The neurocentral synchondrosis is completely open throughout the spine in children under about three or four years old. After that, it begins closing from the top of the spine downward. Cadaver studies show the cervical (neck) region closes first, finishing around age five. The lumbar (lower back) region is nearly fully closed by about age ten or eleven. The thoracic (mid-back) region is the slowest, with some synchondroses remaining open through age seventeen.¹ MRI-based studies in living children broadly confirm this pattern, showing the lumbar region reaching near-complete closure by age ten while the thoracic region is only about halfway closed at the same age.²

This matters clinically because the neurocentral synchondrosis influences the shape of the spinal canal. Surgeons operating on young children’s spines, for example to correct congenital deformities, need to know whether this growth center is still active. If it is, placing hardware across it could restrict canal growth. The left and right sides of the synchondrosis close at the same time within each vertebra, so asymmetric closure is not a normal concern.¹

The Late Closers: Vertebral Ring Apophysis

The ring apophyses are the growth plates most people are thinking about when they ask when spine growth plates close, because these are the structures that control how tall each vertebra gets. They first appear as separate ossification centers around age five, then gradually harden and fuse to the main vertebral body. In most people, this fusion is complete somewhere between ages eighteen and twenty, though in some individuals it can take until twenty-five.³

The fusion process doesn’t happen uniformly across the spine. Ossification tends to start in the mid-thoracic region around age twelve, then spreads to the upper thoracic and lower lumbar regions by about age fifteen.⁴ Research tracking ring apophysis maturation has found it correlates strongly with age, but the mid-thoracic spine can lag behind the rest, particularly in girls around the peak of the pubertal growth spurt.⁵ That delayed mid-thoracic maturation is one reason the thoracic spine is especially vulnerable to scoliosis during adolescence.

Why Girls and Boys Mature on Different Schedules

Across the skeleton, growth plates in girls tend to fuse roughly two years ahead of boys.⁶ The spine follows this general rule, with boys showing a later and longer period of active growth plate function.⁷ The neurocentral synchondrosis also appears to close slightly sooner in males than in females, which is an interesting exception to the broader pattern and may reflect the different mechanical demands on the developing spinal canal between sexes.¹

The practical upshot is that a fourteen-year-old girl may have substantially more mature ring apophyses than a fourteen-year-old boy. Doctors managing scoliosis or other spinal conditions have to account for this, because the amount of remaining growth potential directly affects treatment decisions. A boy who is Risser 3 at fifteen may have years of spinal growth ahead; a girl at the same Risser stage might have much less.

Estrogen Is the Primary Off Switch

The hormone most responsible for telling growth plates to shut down is estrogen, and this is true regardless of sex. Both boys and girls produce estrogen (boys convert testosterone to estrogen via an enzyme called aromatase), and in both cases rising estrogen levels during puberty are what ultimately exhaust the cartilage cells in the growth plate and trigger fusion.

Animal research has shed light on the mechanism. Estrogen doesn’t directly turn cartilage into bone. Instead, it accelerates the natural aging process of the growth plate’s cartilage cells, pushing them toward a state where they can no longer divide. Once proliferation essentially drops to zero, fusion happens rapidly as bone tissue replaces the remaining cartilage.⁸ Studies in mice lacking estrogen receptors show continued bone growth well into old age, resulting in abnormally long bones, which mirrors what happens in the rare humans born without functioning estrogen receptors or aromatase.⁹

This explains the sex difference in timing. Girls experience a sharper rise in estrogen earlier in puberty, so their growth plates exhaust their capacity sooner. Boys get a slower ramp-up, which is partly why they end up taller on average: their growth plates stay open longer before estrogen levels accumulate enough to trigger closure.

How Doctors Gauge How Much Growth Is Left

Physicians rarely image every vertebral growth plate to assess skeletal maturity. Instead, they use proxy indicators that are easier to measure and have been validated against actual growth cessation. The two most common are the Risser sign and cervical vertebral maturation staging.

The Risser sign tracks the ossification of the iliac crest apophysis, the bony cap along the top of the pelvis that is visible on standard spine X-rays. Risser stages range from 0 (no ossification) to 5 (complete fusion). A study tracking spinal growth in scoliosis patients found that the iliac apophysis reached full capping (Risser 4) at an average age of about fifteen for girls and sixteen for boys, but about three-quarters of patients still had measurable growth after that point, averaging nearly two centimeters in girls and about two and a half centimeters in boys. No further growth occurred after full fusion at Risser 5, or after closure of the rib head epiphysis or the proximal humerus growth plate.¹⁰ So Risser 4 is not the finish line; it signals that you are near the end, but not there yet.

Cervical vertebral maturation (CVM) is a newer method that reads the changing shapes of the second, third, and fourth cervical vertebrae on a lateral head X-ray.¹¹ CVM stage 3 corresponds to peak growth velocity for both sitting height and arm span, making it especially useful for identifying when a child is in the fastest phase of spinal growth.¹² CVM correlates strongly with Risser grading and can serve as a reliable alternative for assessing skeletal maturity, particularly when minimizing radiation exposure is a priority, since the lateral head X-ray used for CVM involves less radiation than a full pelvis film.¹³

Scoliosis and the Growth Plate Window

The reason spinal growth plate timing matters so much in clinical practice is scoliosis. Curves progress fastest during the pubertal growth spurt, when vertebral bodies are changing shape most rapidly.¹⁴ A child diagnosed with a moderate curve at Risser 0 or 1 is at much higher risk of progression than one diagnosed at Risser 4, simply because there is more growth left for the asymmetry to compound.

Interestingly, research comparing girls with adolescent idiopathic scoliosis to non-scoliotic controls has found that ring apophysis maturation is delayed in the scoliotic group, with many patients still showing incomplete mid-thoracic fusion at age twenty.⁴ Whether the delayed maturation is a cause or a consequence of scoliosis remains debated, but it means that these patients may have a longer window of vulnerability than their peers.

Growth-Modulation Surgery Depends on Timing

A relatively new category of scoliosis surgery called anterior vertebral body tethering (VBT) tries to harness remaining growth rather than fuse the spine. A flexible cord is attached to screws on the convex side of the curve. As the spine grows, the tethered side grows more slowly than the untethered side, gradually straightening the curve. The underlying principle is that compression slows growth while reduced pressure allows it, a concept known as the Hueter-Volkmann principle.¹⁵

The catch is that this only works if there is enough growth remaining. If the procedure is performed on a patient who is nearly skeletally mature, there won’t be enough differential growth to correct the curve, and the tether may even break under load without achieving much benefit.¹⁶ On the other hand, performing it too early on a very immature spine risks overcorrection or creating a reverse curve. Surgeons typically look for patients who are past the onset of the growth spurt but still have several years of growth ahead, often around Risser 0 to 2 with open triradiate cartilage. Getting this timing right is one of the biggest challenges of the technique.

Ring Apophysis Fractures in Young Adults

The fact that vertebral ring apophyses can remain unfused into the early twenties has a less-discussed consequence: they are vulnerable to fracture. In adolescents and young adults who engage in heavy lifting or high-impact sports, a sudden force can avulse a fragment of the bony ring along with disc material, causing a type of herniation that is distinct from the ordinary disc herniations seen in older adults.

A study of young male military service members (median age twenty-one) diagnosed with lumbar disc herniation found that roughly 30% had an associated posterior apophyseal ring fracture. The most common site was the top of the S1 vertebra, followed by the top and bottom of L5.¹⁷ These fractures happen because the disc’s outer fibers are anchored to the ring apophysis, and when the ring hasn’t fully fused to the vertebral body, a forceful load can tear it free.³

This injury pattern is worth knowing about if you’re a young person with sudden-onset back pain after a specific loading event. Standard disc herniation treatments may not be sufficient if a bony fragment is also compressing the nerve. MRI can identify it, but the fragment is sometimes easier to see on CT. Once the ring apophysis has fully fused, this type of fracture essentially becomes impossible, which is why it is almost exclusively seen in people under twenty-five.

Scheuermann’s Kyphosis and Growth Plate Disruption

Scheuermann’s kyphosis is a rigid rounding of the thoracic spine that develops during adolescence, caused by wedge-shaped deformities of at least three consecutive vertebrae. Though its exact cause remains unclear, it is widely believed to involve disruption of the vertebral body growth plates, leading to uneven growth where the front of each vertebra grows less than the back.¹⁸ The condition has a reported prevalence ranging from less than 1% to over 8%, depending on how strictly it is defined and how the population is screened.

Scheuermann’s is relevant here because it is a concrete example of what can go wrong when growth plates behave abnormally. Unlike scoliosis, where the lateral curve progresses because of asymmetric growth plate activity on opposite sides, Scheuermann’s involves front-to-back asymmetry within individual vertebrae. Bracing during the remaining growth period can sometimes improve or stabilize the deformity, but once the growth plates close, the wedge shape is permanent and can only be addressed surgically if it causes functional problems or severe pain.

How Humans Differ from Other Primates

One curious detail that underscores how unusual human spinal growth plate closure actually is: it doesn’t happen in all primates. Histological analysis of lumbar vertebrae in cynomolgus monkeys, a species commonly used in spinal research, found unclosed growth plate cartilage in every animal examined, even those up to about fifteen years old (a relatively advanced age for the species). Human adults, by contrast, show complete epiphyseal closure.¹⁹ This difference matters for researchers who use monkey models to study spinal disc degeneration or biomechanics, because a spine with persistent growth plate cartilage behaves differently under load than a fully fused human spine. It also raises evolutionary questions about why human vertebral growth plates close so definitively, possibly related to the mechanical demands of upright bipedal walking and the forces transmitted through the lumbar spine.