Growth plates at the heel bone (calcaneus) are typically the first in the lower body to finish fusing, followed by the ankle, knee, and finally the wrist, according to MRI-based research tracking adolescents and young adults. The sequence is not random: it follows a broadly predictable pattern driven by local biology and rising estrogen levels during puberty. But the full picture involves dozens of individual growth plates scattered across the skeleton, each on its own schedule, and some that stay open well into your twenties.
The General Sequence From First to Last
A cross-sectional MRI study of adolescents and young adults found that complete growth plate fusion followed a clear ascending order in the lower limb and wrist: the calcaneus fused first, then the distal tibia (lower shin near the ankle), then the proximal tibia and distal femur (around the knee), and finally the distal radius (wrist).1PubMed Central. A cross-sectional magnetic resonance imaging study of factors influencing growth plate closure in adolescents and young adults That order makes intuitive sense when you think about it: the extremities that bear weight earliest and are farther from the trunk tend to close sooner, while the wrist, which contributes less to stature, closes later.
Within the hand and wrist, there is a further sub-sequence. The distal phalanges (fingertips) fuse before the middle and proximal phalanges, and the distal radius is the last bone in the hand-wrist complex to close.2PubMed Central. Relationship between hand and wrist bone age assessment methods This is exactly why a left-hand X-ray is the standard tool for estimating skeletal maturity: the hand contains many small growth plates that close in a reliable sequence, giving clinicians a snapshot of where the whole skeleton stands.
Around the elbow, fusion follows yet another distinct order. A radiological study found that the trochlea fuses first, then the capitulum, then the lateral epicondyle, medial epicondyle, olecranon, and finally the radial head.3MOJ Orthopedics & Rheumatology. Radiological Assessment of Closure Time of Around Elbow Secondary Ossification Centers These distinctions matter in pediatric orthopedics because a fracture near an unfused growth center behaves very differently from one near a center that has already closed.
The Last Growth Plate to Close
If the calcaneus is at the front of the line, the medial clavicular physis is firmly at the back. The growth plate at the inner end of the collarbone does not fully fuse until roughly age 23 to 25.4PubMed Central. The Clavicle Continues to Grow During Adolescence and Early Adulthood That means the clavicle is still technically growing when most people are finishing college. This late closure has practical implications: it is one reason the clavicle is a common fracture site in young adults, since the junction between growing cartilage and solid bone remains a structural weak point longer than almost anywhere else in the body.
The unusually late schedule of the medial clavicle has also made it valuable in forensic age estimation. A CT-based study of the medial clavicular epiphysis found that partial fusion occurred between 16 and 23 years of age, while complete fusion first appeared at 18 in males and 19 in females.5PubMed Central. CT evaluation of medial clavicular epiphysis as a method of bone age determination in adolescents and young adults A separate study in an Indian population confirmed a strong correlation between the degree of clavicular fusion and chronological age, supporting its use to determine whether someone has reached legally significant age thresholds.6PubMed. Computed tomographic analysis of medial clavicular epiphyseal fusion for age estimation in Indian population Research on a Tunisian population reached similar conclusions, finding a strong positive correlation between fusion stage and age.7Egyptian Journal of Forensic Sciences. Forensic age estimation using computed tomography of the medial clavicular epiphysis in a Tunisian population sample In immigration proceedings, criminal cases, and asylum determinations where birth records are unavailable, a CT scan of the clavicle can help establish whether someone is likely over 18.
Why Growth Plates Close at All
A growth plate is a strip of cartilage sandwiched between the end (epiphysis) and the shaft (diaphysis) of a long bone. The cartilage cells in this strip, called chondrocytes, cycle through stages: they rest, they multiply, they enlarge, and then they die and are replaced by bone tissue.8PubMed Central. The growth plate: a physiologic overview As long as the plate’s reservoir of resting chondrocytes keeps feeding new cells into this cycle, the bone keeps getting longer.
Closure happens when that reservoir is exhausted. Estrogen is the hormone most directly responsible for using up the reservoir. Under the influence of rising estrogen during puberty, the rate of chondrocyte proliferation slows and the pool of resting cells is consumed. Once the cartilage cells are gone, blood vessels invade, bone fills the gap, and the growth plate is permanently sealed.8PubMed Central. The growth plate: a physiologic overview This is why estrogen is critical for epiphyseal fusion in both males and females.9PubMed Central. Effects of estrogen on growth plate senescence and epiphyseal fusion Men produce less estrogen than women, but they still produce enough, primarily through conversion of testosterone, to close their growth plates. In rare cases where men have a genetic inability to produce or respond to estrogen, their growth plates never close and they keep growing into adulthood.
The pace of chondrocyte cycling is also regulated by a local feedback loop involving two signaling molecules, Indian hedgehog (Ihh) and parathyroid hormone-related protein (PTHrP). Ihh signals chondrocytes that are maturing too fast, triggering the release of PTHrP, which slows them down and keeps them in a proliferative state longer. This back-and-forth synchronizes the rate of cartilage-to-bone conversion across the plate.10PubMed Central. Organization of the Indian hedgehog–parathyroid hormone-related protein system in the postnatal growth plate When this loop is disrupted by genetic mutations, growth plates can close too early or remain open too long, depending on which direction the signaling tips.
Why Girls Close Earlier Than Boys
Because estrogen drives closure, and girls reach higher estrogen levels earlier in puberty, their growth plates fuse about one and a half to two years before boys’ do on average. This is the primary reason girls tend to reach their adult height before boys. The longer period of growth in boys before and during puberty produces most of the sex difference in adult bone size and stature observed in male-female twin pairs.11PubMed Central. The age of puberty determines sexual dimorphism in bone structure: a male/female co-twin control study
This means boys are not growing faster per year; they are growing for longer. Before puberty, annual growth in leg length does not differ between boys and girls. During puberty, truncal growth accelerates in both sexes but again does not meaningfully differ. The difference in adult stature comes down to the extra years of prepubertal and early-pubertal growth that boys get before estrogen ramps up enough to close the plates.11PubMed Central. The age of puberty determines sexual dimorphism in bone structure: a male/female co-twin control study
When Puberty Comes Too Early or Too Late
In central precocious puberty, where hormonal signals trigger puberty abnormally early, growth plates begin closing ahead of schedule. A child may shoot up in height initially, but because the plates fuse prematurely, they end up shorter as an adult than they otherwise would have been. Gonadotropin-releasing hormone analogs (GnRHa) are an established treatment for this in young girls, suppressing the premature hormonal surge to buy more time before fusion. A meta-analysis found that GnRHa therapy may have a positive effect on final adult height in girls with early puberty, and combining it with growth hormone may offer additional benefit.12PubMed Central. Gonadotropin releasing hormone agonist treatment to increase final stature in children with precocious puberty: a meta-analysis The tricky part is that GnRHa can slow growth velocity during treatment, partially offsetting the height gain from delaying fusion.
On the opposite end, delayed puberty extends the window of growth plate activity. Conditions like constitutional delay of growth (sometimes called “late bloomers”) leave the plates open longer, and these individuals often catch up in final height once puberty eventually kicks in. Growth hormone deficiency, hypothyroidism, and chronic malnutrition can also delay closure but for less benign reasons, since the underlying condition also suppresses the rate of growth itself.
Bone Age Assessment and What Doctors Look For
When a pediatrician suspects a growth problem, one of the first tests ordered is a bone age X-ray, typically of the left hand and wrist. Two main methods exist: the Greulich-Pyle (GP) atlas method, where the X-ray is compared to a set of reference images, and the Tanner-Whitehouse (TW) method, which scores 13 individual bones including the radius, ulna, metacarpals, and phalanges and converts the total to a bone age.13PubMed Central. Bone age assessment: comparative analysis of Greulich-Pyle and Tanner-Whitehouse by pediatric radiologists and endocrinologists
These two approaches do not always agree. A large comparison found that the difference between the methods could span several years, and the GP method showed more variability when the same reader re-read the same X-ray at a later date.14PubMed Central. Bone age assessment: a large scale comparison of the Greulich and Pyle, and Tanner and Whitehouse (TW2) methods For tracking a single child over time, consistency matters more than which method is “better,” which is why clinicians are advised to stick with one method rather than switching between them.
A bone age that is advanced compared to chronological age suggests the growth plates are closing faster than expected, which can signal precocious puberty, hyperthyroidism, or excess cortisol. A delayed bone age might point to growth hormone deficiency, hypothyroidism, or chronic illness. The gap between bone age and chronological age also helps predict remaining growth potential, which feeds into decisions about whether hormonal treatment is worthwhile.
When Growth Plates Close Too Early From Injury
Growth plates are the weakest structural link in a child’s skeleton. A fracture that crosses through the growth plate, classified under the Salter-Harris system, can damage or destroy the cartilage cells responsible for future growth. Injuries that allow blood vessels to bridge across the plate create a particular risk: the vessels can lay down a bony bridge that tethers the plate and stops growth on one side while the other side continues, leading to angular deformity.15PubMed. Imaging of Pediatric Growth Plate Disturbances Loss of blood supply to the epiphysis (osteonecrosis) can also slow or halt growth at the affected plate.
The distal radius and the distal femur are the growth plates most commonly injured in children. The consequences depend on how much growth remains. A growth plate injury at age 15 in a boy with only a year of growth left is a different clinical problem than the same injury at age 10 with five or more years still to go. In younger children with substantial growth remaining, even small bony bridges can produce significant limb-length discrepancies or angular deformities if not addressed.
Surgical Closure of Growth Plates
Sometimes clinicians deliberately close a growth plate. The procedure, called epiphysiodesis, is the standard treatment for children with predicted leg-length differences of roughly 2 to 5 centimeters, provided the growth plates are still open and enough growth remains. The most common techniques involve either drilling or scraping the growth plate to destroy it, or using metal implants to tether it and prevent further elongation.16PubMed. Closing the growth plate: a review of indications and surgical options
The timing of this surgery is everything. Operate too early and you overcorrect, leaving the treated leg shorter than the untreated one. Operate too late and there is not enough remaining growth to correct the discrepancy. Surgeons rely on bone age assessment and growth prediction charts to hit the window. Tethering with a plate or staple has the advantage of being reversible if the timing turns out to be slightly off: remove the implant and growth can resume, assuming the plate has not already fused.
Genetic Conditions That Alter Closure
Achondroplasia, the most common form of dwarfism, is caused by an overactive mutation in the FGFR3 gene. Paradoxically, increased signaling through this receptor suppresses chondrocyte proliferation and maturation, shrinking the growth plate and reducing bone elongation.17PubMed Central. Achondroplasia: Development, pathogenesis, and therapy In severe forms like thanatophoric dysplasia and homozygous achondroplasia, the same signaling pathway promotes premature closure of synchondroses in the spine and cranial base, with increased bone formation around the closing sites.18PubMed Central. FGFR3 promotes synchondrosis closure and fusion of ossification centers through the MAPK pathway
Nutrition also plays a role in growth plate integrity. Vitamin D deficiency disrupts the organized columnar structure of chondrocytes in the proliferative and hypertrophic zones of the plate, leading to larger variations in cell column size and orientation.19PubMed Central. Spatial periodicity in growth plate shear mechanical properties is disrupted by vitamin D deficiency This disorganization weakens the plate mechanically and can contribute to rickets, the classic childhood bone disease. Correcting the deficiency restores normal growth plate architecture, but prolonged deficiency during critical growth windows can permanently affect stature.
Growth Plate Closure Across Species
Humans are not the only animals with growth plates, but the timing of closure relative to lifespan varies wildly. A review comparing laboratory animals found that rats continue bone growth for a greater proportion of their lifespan than any other species studied: the ratio of age at growth plate closure to average lifespan was 22 to 35 percent in rats, overlapping somewhat with humans at 17 to 25 percent, but far exceeding other laboratory species like rabbits and dogs.20PubMed. Review of growth plate closure compared with age at sexual maturity and lifespan in laboratory animals Rats also continued growing for much longer after sexual maturity than other animals, which matters for researchers using rats as models for human bone growth.
A broader evolutionary study of growth plate closure sequences across 58 mammalian species found a general common pattern but no universal one. The sequence in which plates close is driven more by evolutionary lineage than by how an animal moves. Marsupials, for instance, always fuse their girdle elements (around the hip and shoulder) first, while some placental mammals fuse the distal humerus before the girdle.21PubMed. Heterochrony and post-natal growth in mammals–an examination of growth plates in limbs Marsupials also maintain many growth plates as unfused throughout life, while monotremes like the platypus achieve complete fusion of all epiphyseal plates. The marsupial pattern appears to be the evolutionarily derived state rather than the ancestral one, a reminder that permanent growth plate closure is not a biological inevitability but a strategy that has been gained and lost across evolutionary history.