At What Age Do Your Growth Plates Close?

Most growth plates close between the ages of about 14 and 19, depending on the bone and the individual, though a few stragglers can remain open into the mid-twenties. The timeline is not a single switch but a rolling sequence: different bones finish growing at different ages, and girls generally complete the process a couple of years before boys. The medial clavicle, at the inner end of the collarbone, is typically the very last growth plate in the human skeleton to fuse, sometimes not fully closing until the early to mid-twenties. That spread of a full decade between the earliest and latest closures reflects how tightly growth plate fusion is tied to hormonal changes during puberty.

The Sequence of Closure

Growth plates do not all shut down at once. They follow a roughly predictable order, starting with the smaller bones and working toward the larger ones. An MRI-based study of adolescents and young adults found that the first site of complete fusion was the calcaneus (heel bone), followed by the lower leg at the ankle end, then the knee area, and finally the wrist region, in ascending order.¹ So if you are a teenager wondering whether you are still growing, the answer depends partly on which bones you are asking about.

The collarbone stands apart from the rest of the skeleton. Analysis of documented skeletal collections and imaging studies shows that the medial clavicle can remain unfused as late as 18 to 24 years, with the youngest age at complete fusion around 18 to 20 and partial fusion visible as late as the early thirties in some imaging studies.² This makes the clavicle especially useful in forensic age estimation, precisely because it is the last bone to finish growing.

Why Girls Finish Growing Earlier Than Boys

The central hormone driving growth plate closure is estrogen. Both boys and girls produce estrogen, though girls produce substantially more of it, and they start producing it earlier during puberty. This is not just a timing issue; estrogen actively speeds up the process that ends bone growth. In animal studies, estrogen treatment caused the rate of chondrocyte proliferation to approach zero earlier than normal, triggering an abrupt fusion event in which the remaining cartilage cells were rapidly replaced by bone.³

This is why girls typically reach their full adult height by about 14 to 16, while boys often keep growing until 16 to 18 or later. In both cases the trigger is the same: once estrogen levels stay high enough for long enough, the cartilage cells in the growth plate run out of the ability to divide. Once that proliferative capacity hits zero, fusion follows quickly. The growth plate does not thin out gradually and fade away; it reaches a tipping point and closes as a relatively sudden event.³

How the Growth Plate Actually Closes

A growth plate is a thin layer of cartilage sandwiched near the ends of long bones. The cartilage cells within it go through a life cycle: they start in a resting state, then begin dividing rapidly, then swell up and mature, and finally die. As they die, blood vessels invade the area and organized bone tissue replaces the cartilage.⁴ Each round of this cycle adds a tiny bit of length to the bone. When the cycle finally stops and the last generation of cartilage cells is replaced by bone, the growth plate is considered fused.⁵

Estrogen is the main hormone that ends this cycle, but it is far from the only player. Thyroid hormones, growth hormone, and a network of local signaling molecules all regulate how fast chondrocytes divide and mature. Thyroid hormone, for instance, directly promotes the maturation step while slowing down cell division, effectively pushing the growth plate through its life cycle faster.⁶ Children with untreated hypothyroidism show severely delayed skeletal development, and restoring thyroid hormone levels brings the growth plate’s structure back toward normal.⁷ Growth hormone works alongside these signals but cannot substitute for thyroid hormone on its own.

How Doctors Measure Skeletal Maturity

If you have ever had your “bone age” checked, the doctor took an X-ray of your left hand and wrist. The standard methods for reading that X-ray, developed decades ago, compare the appearance of the bones in your hand to reference images showing what each bone should look like at a given stage of development.⁸ A bone age that is well ahead of your chronological age suggests your growth plates are closing faster than average, which usually means less remaining growth. A bone age that lags behind suggests you have more growing time left.

The original Greulich-Pyle atlas, which many radiologists still use, is now over 70 years old. Artificial intelligence systems have been developed to automate the assessment, offering faster reads and reducing the variability between different doctors interpreting the same X-ray.⁹ The underlying idea remains the same: how mature your hand bones look gives a good estimate of how mature the rest of your skeleton is and how much growth you have left.

When Puberty Timing Shifts the Schedule

Because estrogen drives fusion, anything that changes when or how fast puberty unfolds also changes when growth plates close. Early puberty is a classic example. A child who enters puberty at age seven or eight will typically shoot up in height faster than peers, but their growth plates will also close sooner, often resulting in a shorter adult height than they would have reached had puberty started at the usual time.¹⁰

The reverse pattern shows up in constitutional delay of growth and puberty, sometimes called being a “late bloomer.” Boys with this pattern have a bone age that lags behind their calendar age, often by a couple of years, meaning their growth plates remain open longer.¹¹ Although these boys get extra time to grow, some studies find they do not always fully reach their predicted adult height, possibly because the growth rate during the extended period is slower than expected.

Childhood Obesity and Bone Age

One of the less intuitive factors that can speed up growth plate closure is excess body weight during childhood. Overweight and obese children tend to have a bone age that runs ahead of their actual age, sometimes substantially. In one study, about two-thirds of obese children had a bone age advanced by a year or more, compared with roughly one in ten normal-weight children. The risk of advanced bone age was about four times higher in overweight kids and nearly thirteen times higher in obese kids.¹²

The mechanism appears to involve higher levels of hormones like leptin, insulin-like growth factor 1, and sex hormones that come along with excess body fat. These hormones push skeletal maturation forward, making the growth plates behave as though the child is older than they are.¹³ The result can be a paradox: an obese child may be tall for their age during childhood but end up shorter as an adult because their growth plates closed earlier than they otherwise would have. This effect is detectable as early as preschool age.

Genetics and Normal Variation

Hundreds of genes contribute to how tall you grow and, by extension, to when your growth plates close. Large-scale genetic studies have identified more than 400 regions in the genome associated with adult height in the general population, and a large portion of these appear to influence growth plate cartilage directly.¹⁴ This means the timing of growth plate closure is not determined by a single gene or a handful of genes but by a huge number of small contributions spread across the genome, layered on top of hormonal and environmental influences.

This genetic complexity is one reason why predicting a child’s exact adult height is so unreliable. Bone age helps, and parental heights help, but there is always a margin of uncertainty because so many variables interact. Two siblings with the same parents and similar nutrition can differ by several inches in final height simply because they inherited different combinations of height-related gene variants.

Growth Plate Injuries in Children

Because growth plates are made of cartilage rather than solid bone, they are among the most vulnerable structures in a child’s skeleton. A fracture that crosses or crushes the growth plate can disrupt normal growth. In a cohort study of children with growth plate fractures in the lower limbs, about one in ten developed a measurable growth disturbance.¹⁵ The risk was dramatically higher when the fracture was displaced by three millimeters or more.

What happens biologically is that the injury triggers abnormal healing within the growth plate. Blood vessels invade the cartilage in places they should not, and bone-forming cells migrate across the plate and lay down a bridge of solid bone connecting the two sides. That bony bridge acts as an anchor, tethering the growth plate and preventing normal elongation on that side.¹⁶ Depending on where the bridge forms, the bone may end up shorter than its counterpart on the other side, or it may grow crooked. The distal femur, just above the knee, is particularly high risk. In one case of a high-energy fracture in a six-year-old, the leg-length difference grew from just over a centimeter at ten months to more than six centimeters over five years, eventually requiring surgery on the opposite leg to even things out.¹⁷

Medical Procedures That Deliberately Close Growth Plates

Growth plate closure is not always something doctors want to prevent. In cases of significant leg-length discrepancy or extreme tall stature, a procedure called epiphysiodesis intentionally stops growth at a specific site. The technique was first introduced in 1933 and works by creating a bony bridge across the growth plate, essentially mimicking what happens in a growth plate injury but in a controlled way.¹⁸ Timing is critical: the surgeon needs to know how much growth remains so that stopping one plate early will produce equal leg lengths by the time the other side finishes growing on its own. If done too early, the discrepancy reverses; if done too late, not enough correction is achieved.

A newer approach uses a tension band plate, a small metal plate screwed across the growth plate, which temporarily halts growth on that side. When the plate is removed, growth can resume. This makes the technique more forgiving, especially for angular deformities where only one side of a growth plate needs to be slowed down rather than permanently stopped.

Does Weight Training Close Growth Plates Early?

This is one of the most persistent myths in youth sports. The concern is that heavy lifting might damage the growth plates and either stunt growth or cause premature closure. Evidence-based reviews have consistently found that supervised resistance training with appropriate technique does not negatively affect growth or skeletal maturation in children and adolescents.¹⁹ The key qualifiers are “supervised” and “appropriate technique.” Unsupervised maximal lifting with poor form could cause an acute injury to any structure, growth plates included, the same way a bad fall or a sports collision could. But the act of progressive resistance training itself does not accelerate growth plate closure.

Environmental Chemicals and Bone Maturation

Emerging research has looked at whether environmental chemicals that mimic or interfere with hormones, known as endocrine-disrupting chemicals, affect the pace of skeletal development. The picture is messy. Some compounds, like certain phthalates, have been associated with advanced bone age in prepubertal girls, while others appear to slow bone maturation. Body weight and pubertal stage appear to mediate these effects, making it hard to tease apart direct chemical influences from indirect ones operating through body composition and hormone levels.²⁰

Animal and observational studies have found that prenatal exposure to endocrine disruptors can affect bone development, potentially leading to delayed bone formation, changes in bone geometry, and altered bone mineral density.²¹ Whether these effects translate into meaningful changes in growth plate closure timing in the general population is still an open question. The exposures studied so far are typically low-level and chronic, and their individual effects on any single child’s height would probably be swamped by genetics and nutrition. Still, it is one of the more active areas of pediatric endocrinology research.

Growth Plate Closure Across the Animal Kingdom

Humans are unusual among mammals in how late their growth plates close relative to sexual maturity and lifespan. A comparative review found that the ratio of age at growth plate closure to average lifespan was substantially higher in humans than in most other species, with some overlap only in the rat.²² In many animals, growth plates close well before midlife, sometimes relatively soon after sexual maturity. Humans, by contrast, keep growing for years after puberty begins and do not complete skeletal maturation until they are roughly a quarter of the way through their expected lifespan.

The sequence of growth plate closure varies across mammals, but a general pattern exists. In a study of 58 mammalian species, researchers found a common overall sequence of which plates close first and last, though it was not universal. Marsupials, interestingly, often maintain many growth plates as unfused throughout life, which appears to be a derived trait rather than a primitive one, since monotremes like the platypus do fully fuse all their growth plates.²³ The closure sequence is driven more by evolutionary lineage than by lifestyle. Whether an animal runs, climbs, or swims does not appear to predict which bones finish growing first.²³

Among primates, the order of growth plate closure is fairly conserved. Work on tamarins and marmosets found a similar sequence of closure across multiple monkey species, supporting the idea of a shared developmental blueprint for primate skeletal development.²⁴ The rates differ, of course. A marmoset completes growth plate fusion in a couple of years, while a human takes about two decades. But the underlying order in which the bones close, from the smaller peripheral sites to the larger central ones, has deep evolutionary roots.