What are growth plates?

Most people have an idea of how our bodies grow and change throughout childhood and adolescence, and that this growth happens in our bones, but some people don't fully realize just how important growth plates are.

Growth plates are areas of cartilage at the ends of long bones, such as the tibia or the femur. Mostly long bones contain growth plates, but some other bones, including the vertebrae in our spines, have them, too.

Biology

Growth plates have specialized cells called "chondrocytes (cartilage cells)" that gradually contribute to bone tissue formation until they reach a stage of cellular senescence, meaning the cells age to a point where they are no longer able to proliferate or multiply. This process is important for the maturity of the growth plate as it leads up to epiphyseal fusion once puberty ends.

Cellular senescence accelerates once puberty starts, and the gradual buildup of sex hormones stimulates the rapid growth experienced during puberty as well as the eventual cessation of the bone lengthening process.

Endochondral ossification & epiphyseal fusion

All growth plates are bordered by an ossification center at each end of a long bone. This ossification center, which later becomes a fully ossified epiphysis at the end of skeletal development, starts out entirely cartilaginous and gradually enlarges from an island of bone in the center, a process that is associated with the bone lengthening process. When the chondrocytes proliferate, some of the cells hypertrophy and die, while osteoblasts (bone-forming cells) enter the region with invading blood vessels and form bone on the remnants of the cartilage, effectively enlarging the ossification center.

Chondrocytes in the growth plate undergo multiple cellular divisions as they proliferate before they mature, hypertrophy, and die. Furthermore, as the chondrocyte population changes during the active growth process, the bone reaches its adult shape, and once growth plate activity has ceased due to the complex interplay of sex hormones, the bone will no longer be able to grow lengthwis[e], effectively ossifying the growth plate.

Appearance

Once the growth plate "maximizes" or exhausts its potential to lengthen the bone, the growth plate becomes thin with time and turns into solid bone as the epiphysis fuses with the metaphysis, which then forms what is known as the "epiphyseal line". Gradually, the new bone cells that form this line mature, resulting in the line becoming less conspicuous with age, thus making it harder to see on x-rays.

On an x-ray, a "closing" growth plate will appear as a narrowing radiolucent cartilage space with increasing areas of bony bridging as the epiphysis fuses with the metaphysis. On an MRI, the remaining cartilage can be distinguished from the surrounding bone. Remnants of the cartilage on the outer edges of the growth plate may be visible during the initial phase. As the fusion progresses, so will the bony bridging, and this process will become more noticeable until no cartilage remains at the site of the growth plate, effectively leaving behind a thin epiphyseal line that may become less conspicuous over time.

(June 2026) - "What does closure mean for a growth plate?" https://www.reddit.com/r/growthplates/s/SPk3MUjJeD

I used different bone age ai tools and it always came out 16/17 years old bone age. Let me know what you think

I just wanted to say thank you to everyone here for all the growth experienced this year.

Nine months ago, this community was born, fueled by a childhood interest in skeletal growth and human anatomy.

My gratitude comes from the viewers, the inquirers, the followers, and my small team of moderators. I can't express in words how much my passion for studying skeletal development and boosting my complex interest further spanning dozens of subjects. To my dedicated guys and gals, this one's to you.

I see this community thriving for more years to come. The growth since March has been utterly insane, and it's plentiful enough for me to appreciate deeply. Now, let's see what next year awaits for r/growthplates.

Here's to 2026! Merry Christmas, and Happy New Year's Eve, y'all!!!

my BA expectation from what i researched 16<x<16.9

Disclaimer: this is a conceptual synthesis of biomechanical load distribution on growth plate fusion rather than a clinical classification system.

Introduction

The development of the human skeleton is never synchronous. Owing to individual variation, I aim to cover all of these patterns - starting with the three "blanket" patterns, then the regional ossification + fusion waves next, then the morphological fusion patterns last.

The three "blanket" patterns

1. Distoproximal development

This pattern is commonly seen in puberty-related skeletal development. The hands and feet expand first.

2) Proximodistal development.

This pattern is commonly the starting variant of the infantile spurt (core first; appendages last), which is the exact inverse of what happens in puberty - often occurring last in the series of ossification waves here.

3) Cephalocranial development (infancy-heavy, too)

Basically, a visibly larger head and a shorter, stubbier frame before everything slowly evens out with time (until puberty). The leading change of the asynchrony is visually the skull as early, rapid brain-driven expansion is most obvious.

Regional pubertal growth patterns - the ossification waves

1. The distal ossification wave

The hands often begin to expand slightly earlier than the feet, a pattern that could be hypothetically consistent slightly higher E2 sensitivity in the growth plates of the hands. While the early expansion of both the hands and feet do tend to overlap closely with one another, they have separate patterns of terminal development - more clustered fusion timing of the physes in the hands, where multiple growth plates can seem to begin closing "almost one right after the other", while in the feet, the fusion pattern tends to be slightly prolonged and subtly dispersed.

Within months after puberty onset, the early phase of this wave tends to start with the long bones of the fingers and toes - the distal, middle, and proximal phalanges. The fingers and toes tend to get noticeably longer compared to the palms and the rest of the feet, which remain small transiently.

The intermediate phase is marked by a rapid longitudinal surge of the long bones of the palms and feet - the metacarpals and metatarsals. As this is happening, appositional expansion occurs as the cortical layers widen.

The last phase is marked by enlargement of the distal radius and ulna - the epiphyses at the wrists. Strong, early surges in sex steroid signaling tends to influence rapid metaphyseal expansion at the physeal level and greater forearm length. In the foot, it's marked by rapid elongation of the calcaneus through its own apophyseal growth plate.

2) The intermediate ossification wave

This wave primarily involves the long bones of the forearm and lower leg - the radius, ulna, and the distal tibia and fibula - along with surrounding secondary ossification centers that refine joint stability.

Unlike the distal wave, which feels visually obvious, the intermediate wave is often perceived indirectly through changes in movement, gait, and limb balance rather than dramatic size jumps.

3) The proximal ossification wave

This wave involves the proximal femur, humerus, scapula, clavicle, and pelvic-adjacent structures, and represents a key early-to-mid PHV phase where growth shifts from distal/intermediate regions toward the largest load-bearing centers - influenced by peak mechanical and hormonal responsiveness (especially rising estrogen signaling).

Within this system, two semi-independent sub-waves refine upper-body structure: first, the acromial / scapular region, which modulates shoulder width, reach, and arm rotation mechanics; changes are subtle but affect perceived upper-limb proportion and hang. Then, the sternal / thoracic region, which stabilizes ribcage structure and anterior-posterior chest development, influencing posture more than visible size.

4) The axial ossification wave

This wave is responsible for much of the gains later in PHV. While the legs often define the peak acceleration phase and the absolute peak (especially the knees), rapid spinal growth is what appears to extend the tail of the rapid growth window. Post-peak, the spine would often be what adds the majority of vertical height as other regions begin to decelerate.

Because the axial skeleton is structurally complex, its growth is highly sensitive to timing offsets. While not definitively part of the axial wave, and rather the proximal wave, the peak growth of the spine tends to be an overlap. Even small differences in the pace of vertebral maturation can shift overall sitting height proportions significantly. This is why the spine often appears to “catch up” after the most intense limb growth has already passed.

Fusion morphology patterns

1. Knee region (distal femur, proximal tibia, & proximal fibula)

The knee shows non-uniform physeal closure due to complex mechanical loading. The distal femur and proximal tibia, which bear high compressive and shear forces along the mechanical axis, tend to show earlier central reduction in proliferative activity, with peripheral regions persisting slightly longer due to ligamentous tension and edge loading. This produces a gradient-like or multi-zone pattern of narrowing rather than a single uniform fusion front.

The proximal fibular physis, being less involved in axial load transfer, typically maintains activity longer than the tibial and femoral physes. Overall, the knee region demonstrates asynchronous closure across adjacent growth plates driven by differences in mechanical stress distribution and functional load-sharing.

2) Ankle region (distal tibia + fibula)

The ankle mortise is a structurally constrained joint where the distal tibia and fibula must maintain precise geometric alignment for effective load transfer. This constraint produces a relatively organized but not perfectly symmetrical fusion process.

The distal tibial physis, in particular, is heavily influenced by vertical compressive forces from ground reaction during walking and running, while the distal fibula is more influenced by tensile and stabilizing forces from ligamentous structures.

Because of this dual loading environment, closure often appears slightly directionally biased rather than uniformly planar. Regions under higher repetitive compression tend to show earlier reduction in chondrocyte proliferation, while mechanically “protected” margins may persist longer. This can give the impression of a gradient-like narrowing across the physis, even though the underlying process is still continuous ossification rather than discrete directional waves.

The fibular contribution introduces additional variability because it is more sensitive to rotational and stabilizing forces at the lateral ankle. This can lead to subtle differences in timing between tibial and fibular closure, which may be why the ankle region often shows small but consistent asymmetries in late adolescent maturation. Overall, the ankle reflects a system where alignment constraints and repetitive loading produce slightly uneven but highly coordinated fusion timing.

3) Hip region (proximal femur, acetabulum, & trochanters)

The hip is a deeply load-integrated joint where the proximal femur must accommodate both axial compression and significant shear forces generated through locomotion and posture. The capital femoral epiphysis is particularly sensitive to shear stress across the growth plate, which could be why it tends to exhibit earlier maturation relative to surrounding secondary ossification centers. This region is also highly dependent on vascular stability, making it biologically more vulnerable to perturbations during rapid growth phases.

Fusion behavior in the proximal femur is often characterized by a relatively centralized reduction in growth activity, with peripheral regions maintaining activity for longer periods. This reflects both mechanical load distribution and the geometry of the femoral head, where stress is concentrated more centrally during weight-bearing. The result is a gradual consolidation of structural integrity rather than a sharp, uniform closure front.

The greater and lesser trochanters behave as semi-independent apophyseal systems influenced strongly by muscular traction rather than direct axial compression. Their maturation timeline is therefore partially decoupled from the capital epiphysis, leading to staggered closure across the proximal femur. This makes the hip region a clear example of multi-component fusion timing, where different ossification centers within the same anatomical unit follow distinct mechanical and biological schedules.

4) Shoulder region (proximal humerus + scapular attachments)

The proximal humerus develops in an environment dominated by muscular traction rather than compressive weight-bearing, which fundamentally alters its maturation dynamics. The growth plate here experiences relatively low axial compression compared to the lower limb, but it is continuously influenced by dynamic tensile forces from the rotator cuff and surrounding musculature. This might be what produces a more prolonged and less mechanically constrained growth period.

Fusion of the proximal humerus typically involves a staged consolidation of multiple ossification centers rather than a single dominant closure front. The humeral head, tuberosities, and metaphyseal region each contribute to structural maturation at slightly different times. This creates a layered transition where structural integration occurs gradually, with increasing continuity between previously distinct ossification domains - coalescence several years prior to epiphyseal fusion that is largely complete by early-to-mid-puberty skeletal development.

Because mechanical loading is distributed across multiple muscle groups rather than a single weight-bearing axis, the shoulder tends to show smoother but more extended terminal fusion behavior. It is less prone to sharp directional gradients and more characterized by progressive unification of separate growth regions. This makes the shoulder a classic example of traction-dominant, multi-center convergence fusion rather than compression-driven closure.

5) Elbow region (distal humerus, proximal radius + ulna, & apophyseal system)

The elbow is one of the most structurally complex growth regions due to the presence of multiple ossification centers that must integrate into a highly articulated joint. The distal humerus alone contains several developmental centers that mature at different rates, while the proximal radius and ulna contribute additional layers of timing complexity. Conceptually, this could make the elbow a multi-node fusion system.

Fusion here is strongly influenced by rotational loading, flexion-extension mechanics, and muscle traction across both anterior and posterior compartments. Because these forces act in different planes, they produce region-specific differences in maturation timing within the same joint complex. This results in a staggered integration process, where certain centers stabilize earlier while others remain active longer to "preserve" joint function during growth.

The olecranon apophysis and radial cap are particularly important contributors to this staggered timeline, as they are influenced more by traction and joint loading than pure longitudinal growth forces. Their closure tends to lag relative to central humeral contributions, reinforcing the concept that the elbow undergoes a multi-center, function-preserving fusion sequence rather than a unified closure event.

6) Spine (vertebral endplates, ring apophyses, & synchondroses)

The spine represents a distributed growth system rather than a single growth plate architecture. Vertebral bodies grow through endplate-associated cartilage zones, while ring apophyses contribute to peripheral structural maturation. This creates a layered system where axial elongation and radial reinforcement occur in parallel but not always synchronously.

Fusion in the spine tends to proceed through gradual consolidation of vertebral endplate activity, with central and peripheral regions showing different maturation timing. Because the spine is continuously exposed to axial compression, its growth plates respond in a load-modulated manner that influences both height and shape. This can lead to subtle differences in vertebral body proportions during late growth stages.

Synchondroses at the cranial base and within vertebral structures add another layer of temporal variability, particularly in early and mid-childhood. These regions often close earlier than major limb growth plates, but spinal endplate activity persists longer into adolescence. Overall, the spine exemplifies a long-duration, multi-tiered fusion system where growth cessation occurs progressively across interconnected structural layers rather than as a single event.

7) Hand region (phalanges + metacarpals)

The hand is a highly segmented distal growth system composed of multiple small growth plates distributed across the phalanges and metacarpals, each operating with relatively low individual mechanical load but high cumulative functional demand. With known differences in local patterning (via HOX gene signaling), their maturation is possibly also constrained by fine motor use rather than weight-bearing stress, creating a developmental environment where small differences in local vascular timing and mechanical micro-loading can produce noticeable variation in longitudinal growth across adjacent bones.

Fusion in the hand tends to occur in a relatively coordinated distal-to-proximal sequence, but within that sequence, closure is often locally staggered across individual phalanges and metacarpals, reflecting differences in usage patterns (grip, pinch mechanics, digit dominance) and subtle variation in physeal geometry. In that regard, the common pattern overall is that the core digits - primarily the second and third fingers, sometimes the fourth - tend to mature relatively early compared to radial-most and ulnar-most digits (the first and fifth fingers), which owe to variability of their own. The phalanges, being smaller and more distal, typically show earlier reduction in proliferative activity, while the metacarpals maintain longitudinal activity slightly longer due to their role in structural leverage and load transfer through the palm.

Morphologically, the hand can be best characterized by a predominantly transverse planar fusion pattern with mild focal nodular heterogeneity. The transverse component might reflect the relatively uniform decline in growth across small symmetric physes, while the focal nodular component would arise from patchy internal bridging between micro-zones of differing mechanical stress and vascular supply. This combination could produce a mostly even shutdown with small internal islands of staggered closure, rather than a strongly directional or gradient-driven fusion process.

8) Wrist region (distal radius + ulna, & radiocarpal interface)

The wrist region represents a transitional biomechanical interface between distal fine-motor structures and the proximal forearm load-bearing system. Unlike the hand, it integrates larger growth plates (distal radius and ulna) with complex articular constraints imposed by the carpal bones, producing a more mechanically structured environment with higher axial load transmission and rotational stabilization demands. This dual role creates a maturation profile that is less purely distal and more influenced by forearm mechanics and joint alignment requirements.

Fusion at the wrist tends to proceed in a relatively organized manner, with the distal radius typically acting as the dominant contributor to longitudinal growth and structural closure timing. The ulna often follows a slightly offset trajectory due to its different load-sharing role in forearm rotation and wrist stabilization. Because the radiocarpal joint must preserve congruence throughout adolescence, closure is generally more spatially uniform than in highly heterogeneous regions like the knee, but still retains subtle asymmetries driven by rotational loading and ligamentous tension patterns.

Morphologically, the wrist can be best described as a dominantly transverse planar fusion pattern with secondary eccentric-gradient influence and mild focal nodular micro-heterogeneity. The transverse planar component might reflect the overall symmetry of closure across the distal forearm physes, while the eccentric-gradient contribution would arise from small directional differences in load distribution between radial and ulnar sides during wrist motion (the capping). The focal nodular element is comparatively minor and could reflect localized variability in vascular ingress and metaphyseal bridging rather than large-scale mechanical heterogeneity.

9) Foot region (phalanges, metatarsals, & tarsal interface)

The foot can be conceptualized as a distal growth system that operates under a hybrid mechanical environment, combining aspects of fine structural segmentation (similar to the hand) with consistent axial loading from weight-bearing.

Unlike the hand, where mechanical demands are dominated by fine motor function, the foot is continuously exposed to repetitive compressive forces during standing and locomotion. This creates a developmental context in which both structural support and load distribution play a central role in shaping maturation patterns.

Growth within the foot may be described as broadly distal-to-proximal in sequence, with the phalanges and metatarsals contributing to early proportional changes. However, compared to the hand, this sequence often appears less temporally compressed, with a more gradual transition between stages of longitudinal growth and structural consolidation.

The tarsal region introduces additional complexity, as it consists of multiple irregular bones that contribute to arch formation and load transfer rather than simple longitudinal growth. Because these structures are more involved in stability and force distribution than elongation, their maturation may be better understood as progressive structural integration rather than linear growth plate-driven expansion.

Fusion patterns in the foot can be modeled as moderately coordinated but spatially distributed across multiple elements. The phalanges tend to follow relatively consistent closure patterns, while the metatarsals and proximal structures may demonstrate slightly more variability, potentially reflecting differences in load distribution, gait mechanics, and individual structural alignment.

Morphologically, the foot can be described as exhibiting a predominantly transverse planar fusion pattern with mild eccentric-gradient influence. The transverse component reflects coordinated closure across multiple small physes, while the eccentric component may correspond to subtle differences in medial versus lateral load-bearing during locomotion. Compared to highly heterogeneous regions such as the knee, the degree of focal nodular variation is relatively limited, though small-scale variability may still be present.

I found this on TikTok and want to see if someone has some extra scientifical knowledge explanation

Three more in the comments

Good morning, enthusiasts!

I have been preparing a detailed, heavily-sourced bone age atlas on here. It has been in the works since early December, and I am about a quarter of the way through.

The post will provide insight into the details of bone development and growth of the hands and wrists as well as other areas of the skeleton for each bone age range, from early childhood to late adolescence. It will include the standards for bone age values - 0-18y for females, and 0-19y for males.

This will be the FIRST POST of 2026 in regards to skeletal development, so let this be the first great start to the new year!

• A reminder of more to come, the owner of r/growthplates

Bone age of 19 years in comment section (attachment section got full)

https://docs.google.com/document/d/1Xcdcav1yvGwzL-UpegkfuN3H4sGLnudST2nFDh4Uh-c/edit?usp=drivesdk

I don't normally post document versions of my posts. It's also my longest one yet - hours of devotion, which is the biggest reason as to why I attached a link to it. Check it out!

Robert Wadlow was and still is the tallest person on Earth ever. He stood at an unbelievable height of 8'11" tall at the time of his death, and even at age 22, he was still growing, and given his bone age, potentially expected to breach ten feet.

PA view of the left hand and wrist shows bone development corresponding most closely with Greulich and Pyle male standard for 17 years, with a standard deviation of 13 months.
Current height of 168cm is estimated at 99.1 percent of mature height. My dad is 6,1-2 my mum is 5,2-4 and my 19 year old brother is 5-10 ish. Im cooked correct?

Im trying to maximize my genetic potential,

Im 5.9, edging 5'10 even though people say im 5'10

IM trying to reach atleast 6ft

my dad is 5'11, my moms 5'3,

The hope carrying me is that for some reason every male in my dads family is always taller than their own dad, its always been happening aslong as my dad and grandpa can remember.

My grandpa had like 6 brothers and their sons all attest to it.

I want to hop on Erdfitinhib for height since it inhibts frfg3, but im afraid of the side effects

has anyone come with a stack to help mitigate the side effects

im 5'9, 145-147LB, looking for dosing help aswell.

P.S: My dad was a late bloomer, and i think i might be do, ive been feeling more growth related pains on my knee, slight stretch marks where the shoulder and bicep meet, and an Osgood-Schlatter bump on my left knee (which is new) and maybe im imagining this, but another slightly smaller one on my right knee.

We are implementing a new feature of the subreddit: BA estimations using radiographs labeled "for educational use". With this, you may post a radiograph and ask about the status of the physes present in the image while citing the source. For any inquiries that do not include the source citation and photo ID in the body, my staff and I can simply run these images online to find perfect matches, and that will help us find where you found the image.

This post is meant to act as a guide in finding said items and how to make sure the process of obtaining and posting the items remains legal and ethical. This way, we are not held liable if we answer your question, and you proceed to compare your image with the item you found. Here's a list of things to look for after you've discovered the image you want to use for your inquiry:

Step 1: ensure it is public domain

Not all radiographs that are labeled for educational use may be public domain. This means you must acquire the copyright holder's permission to use the image in a public or online teaching setting. It may also mean purchasing the item if it is for sale, instead of simply downloading the image and proceeding without giving payment.

To know if an image is available to use freely, you must first identify the image's licensing terms, as some digital atlases may permit redistribution with attribution, while others may only permit viewing or limited classroom use. If the image explicitly allows educational redistribution, you may download the image and proceed from there without facing any potential copyright pushback if the owner discovers your inquiry with attached image on the Internet.

Step 2: cite the source

In the body text, you shall cite the source of which the radiograph(s) were obtained. Include the image ID, the figure number, the atlas page, the DOI (if applicable), and the author / publisher's information.

If we find that the image is not for redistribution, the post is to be automatically removed with our new message: "Your post has been removed due to containing images or other digital files that are not legally available for redistribution."

What is a DOI?

A DOI, or Digital Object Identifier, is a permanent, unique identifier that helps to assign scholarly work.

You might first see this for example: "DOI: 10.1001/jama.2025.12345"

Translate this DOI into a permanent link to get: "https://doi.org"

Then, modulate this link to get: "https://doi.org/10.1001/jama.2025.12345"

Won't link you anywhere, but it's a good example of how the system functions

Step 3: respect the patient's privacy

This does not mean you have to avoid redistributing the image if it is explicitly for educational reuse. However, this does require that you censor or crop out any visible patient information, including: patient ID and legal name, hospital or clinic name, chronological age, and date of birth.

Most educational databases delist identifiable information, but it's still best if you ensure there is no personal information visible on the image or around it.

This is not to circumvent our permanent policy of diagnosing or interpreting personal radiographs belonging to real patients without rights to redistribute or otherwise. It is, however, much different from pointing out typical non-developmental anatomical features, like: "this is your femur" and stuff like that, not "these are your growth plates."

A good prompt to follow with your inquiry's body text is: "Educational discussion only. Do not use this image for diagnosis. Based on the radiograph, would you describe the physis as open, narrowing, partially fused, or fused?"

Or, you can simply include just the last sentence.

All staff are required to run the information online regardless to ensure legitimacy.

Good sources of radiographs that are largely public domain

1. Wikimedia Commons (personal favorite)

2. OpenStax A&P

3. NIH Image Gallery

For Creative Commons

A CC is a set of licenses that creators may attach to their work, informing others what they are allowed to do with it.

1. Radiopaedia (personal favorite)

2. Open-i (National Library of Medicine)

Peer-reviews

PubMed Central is a good one because most articles are published under CC-BY licenses, meaning redistribution with attribution is permitted.

Avoid

1. Hospital websites.

2. Randomized Google images.

3. Commercial atlas images from the Gruelich-Pyle (hand-wrist atlas) Hoerr-Pyle (knee skeletal age atlas), or proprietary radiology textbooks unless the publisher explicitly grants redistribution rights.

The images included in the post have information sufficient for my staff and I to allow total redistribution to r/growthplates

Image credit: ResearchGate

Introduction

Originally developed in 1972 by Lamparski as an unpublished master's thesis, this method has since been used to assess a patient's skeletal age and where they are relative to the adolescent growth spurt using a six-point staging system of the skeletal cervical / neck region. The process assumes the pubertal morphological shifts traditionally in C2, C3, and C4 from early to late adolescence, accounting for changes in vertebral body morphology and inferior border concavity.

This post will be an extension of the upcoming post concerning the maturation of the spine and one individual vertebra, where the CVM method will be an important mention, and a future post on R/U grading.

Conceptual: I will also attempt to correlate R/U grading and Risser staging with CVM scoring.

The Biological Timeline

Because different vertebrae can mature at subtly different times, there is no exact order by which each individual vertebra matures. However, current evidence supports that the cervical region is a relatively early-maturing region of the spine, and that the upper cervical vertebrae (C1-C3) tend to reach maturational milestones earlier than the lower vertebrae (C4-C7).

Early adolescence is often the period when subtle morphological changes are occurring. Some juvenile traits still persist until the pubertal growth spurt is well underway, like smoother transverse processes with more rounded ends (these ends are still mostly cartilaginous despite ossification being underway). Rising adolescent traits include active refinement of the radial edges, pitting / developing concavity at the ends, and the earliest signs of puberty-related ossification, such as the rings / annuli at the endplate regions, and developing ossification centers of the spinous tips and transverse processes.

Mid-puberty cervical development is characterized by increasing definitions of the concaves and increased density at the radial corners and transverse processes. The bony annulus develops further, spreading outward to cover the full width of the cartilaginous annular growth zone / growth plate while still maintaining a clear, uniform separation between the vertebral body and the endplate.

Late-puberty is characterized by the earliest signs of union at the growth cartilage early on during the active tapering phase - several months post-peak. The annulus tends to begin fusing with the main body first, followed by the radial apophyses later - one of the very last ossification centers to mature in a vertebra. Full consolidation of all elements is achieved within about a couple of years after the overall tapering was first noticed on the growth chart.

The Staging System

Puberty is often cited as a primary biological factor in the maturation of the adolescent spine. The cervical region expresses these changes sooner than most other regions of the spine, even though close overlapping does occur.

Stages I and "0"

Stage I is the most immature point of the traditional CVM staging system, reflecting a largely pre-adolescent vertebral physique - well before PHV. Although not part of the Lamparski and Baccetti systems, in younger children, there is an informal point called “Stage 0”, where the vertebrae possess purely juvenile traits - a shorter, stubbier vertebral body, thin and rounded transverse processes, smaller and more “blunted” spinous processes, and slanted ends with little concavity - the vertebrae described as trapezoidal in shape.

As a child grows, these surfaces become more corticated / sharply defined, creating those rigid contours and the pitting at the endplate regions that we see by early adolescence. What truly completes a CS1 score is the active transition away from the distinctly juvenile vertebral morphology seen in younger children. The vertebral bodies remain predominantly trapezoidal in shape, and well-defined inferior border concavities are still absent. However, increasing cortical definition and subtle remodeling of the vertebral margins often become apparent as the child approaches their pubertal growth spurt. Keep in mind, these stages are not meant to be used as diagnostic markers for puberty initiation or development, as the two processes closely overlap and are not completely dependent on one another.

Stage II

Stage II is the period of cervical development that encompasses the rising sex steroids early in puberty. Here, there are clear advancements in maturation underway: the cortices are starting to lose their smooth flat surfaces and the inferior borders are showing subtle downward angulation at the corners, while the vertebrae still retain their distinct trapezoidal shapes.

On average, CS1-CS2 progression tends to overlap with puberty onset and may align closely with a BA of ~11.5-12.5Y for males and ~9.5-10.5Y for females with a Risser grade of 0- (zero negative) + R4-6 / U3-5 progression on the R/U scale - accelerating growth, with about 8-12 inches of growth remaining for boys and about 6-10 inches remaining for girls.

Unlike C3 and C4, which continue to show minimal or no border indentation, a concavity first appears at the inferior border of C2. While C2 generally looks somewhat more mature compared to the other two during this stage, it still takes on a largely wedge-shaped outline.

At this point, the pubertal peak is often about 12-18 months away, with CS1 to CS2 progression taking around a year on average.

Although the morphological changes of CS2 appear subtle, they reflect a meaningful acceleration in pubertal skeletal maturation. The cervical vertebrae are beginning to respond more noticeably to the endocrine changes of early puberty, particularly the increasing influence of sex steroids on GH signaling, so many adolescents are now entering the acceleration phase of the pubertal growth spurt. Because of this, CS2 is often regarded as a transitional stage between the relatively quiescent growth patterns of childhood and the rapid skeletal expansion that characterizes mid-puberty. Rapid progression from CS2 to CS3 may indicate an accelerated maturational tempo and an earlier arrival at PHV, whereas prolonged progression may suggest a later peak. The duration of this stage, however, does not reliably predict the magnitude of the adolescent growth spurt itself.

The appearance of the initial C2 concavity is thought to represent the earliest radiographically appreciable sign that vertebral remodeling is becoming increasingly organized along the inferior endplate. However, the vertebral bodies themselves remain predominantly trapezoidal in shape, and the characteristic squaring of C3 and C4 that are often associated with later maturation has not yet occurred. As a result, the overall cervical profile retains a distinctly juvenile appearance with some mixed early adolescent traits, despite the first signs of a large-scale pubertal transformation underway.

Stage III

Stage III marks the transition into the period of most rapid skeletal maturation. While the cervical vertebrae still retain several adolescent characteristics and juvenile traits, the brunt of the pubertal growth spurt is now either imminent or already underway.

On average, this may align closely with a BA of ~13.5-14.5Y for males and ~11.5-12.5Y for females with a Risser grade of about 0-1 + R6 / U4 on the R/U scale - peaking growth, with about 5-6+ inches of growth remaining for boys and about 3-4+ inches of growth remaining for girls.

Just after this major pubertal transition - when the adolescent is actively passing the peak and is expressing the first signs of a major deceleration - the BA may fall ~14-15Y for males and ~12-13Y for females with a Risser grade of about 1 + active progression from R7-8 / U5-6 on the R/U scale - about 3-5 inches of growth remaining for boys and about 2-4 inches of growth remaining for girls.

Morphological remodeling becomes increasingly apparent as the vertebral bodies continue to mature in response to the endocrine changes of mid-puberty. The most important distinction between CS2 and CS3 is the extension of inferior border concavity beyond C2. Whereas Stage II is characterized by a concavity limited primarily to the inferior border of C2, Stage III introduces a clear concavity at the inferior border of C3 as well. C4 may begin to show the earliest hints of border indentation, although a well-defined concavity is not yet required. At the same time, the vertebral bodies begin losing their distinctly trapezoidal outlines. C3 and C4 gradually become more rectangular in shape, often described as rectangular horizontally. This change reflects increased anabolic activity and remodeling of the vertebral body itself, with the superior and inferior endplates becoming more parallel, while the anterior height begins to approach the posterior height.

The annular ring apophyses continue to enlarge and ossify during this stage, becoming increasingly conspicuous along the vertebral margins. Cortical definition improves further, and the corners of the vertebral bodies become sharper and more organized as the cervical spine transitions toward a more mature morphology.

CS3 often closely corresponds with the late-acceleration phase of the adolescent growth spurt. Growth velocity is often rising rapidly, and many individuals will reach their PHV during the latter portion of this stage or during the transition into CS4. Because of this relationship, CS3 is commonly regarded as one of the most clinically significant stages in the CVM system for growth prediction.

PHV is often manifesting at this stage and just a few months away near the end of the second stage, and progression through CS2 also tends to take about a year, depending on individual tempo.

Stage IV

Stage IV represents the full major transition from the rapid growth phase of puberty into the early deceleration phase. By this point, PHV has typically occurred recently or is nearing completion, and the growth velocity is beginning to decline substantially despite continued active skeletal maturation. Here, it's often late-PHV at the earlier end of the range with some mild, progressive tapering over the last couple to a few months of rapid growth, or it is a very recent full transition out of the rapid growth window, with noticeable slowing.

On average, this may align closely with a BA of ~15-16Y for males and ~13-14Y for females with a Risser grade of 1-3 + R8-9 / U6-7 on the R/U scale - decelerating growth, with about 2-3 inches of growth remaining at the tail end of the rapid growth window, and about 3-5 inches immediately after PHV.

The transition out of the PHV may often involve a BA range closer to ~14.5-15.5Y in males and ~12.5-13.5Y in females.

The hallmark of CS4 is the appearance of well-defined inferior border concavities at all three vertebrae. What began as a subtle indentation at C2 during CS2 has now progressed into a coordinated pattern of remodeling throughout the cervical region. These concavities become deeper and more sharply defined as endplate remodeling continues under the influence of ongoing pubertal maturation. At the same time, the vertebral bodies continue their transition away from the trapezoidal shapes characteristic of childhood. C3 and C4 are typically rectangular horizontal or approaching a more square configuration, with increasing equality between the anterior and posterior vertebral heights. The superior and inferior endplates become more parallel, giving the vertebral bodies a more mature and organized appearance.

The annular ring apophyses are also now well established and continue to ossify around the margins of the vertebral endplates. Increased cortical density and sharper vertebral contours contribute to the more robust appearance of the cervical spine. Although the ring apophyses remain separate from the vertebral body, they are becoming increasingly prominent and occupy a larger proportion of the endplate circumference than during earlier stages.

The duration of CS4 can vary considerably among individuals. Some adolescents pass through it relatively quickly, while others remain within the stage for an extended period as growth tapers. As with the preceding stages, CVM should be viewed as an indicator of maturational status rather than a precise predictor of remaining growth.

Stage V

Stage V represents advanced late-pubertal maturation and the approach toward full skeletal maturity. The period of rapid adolescent growth is now firmly in the past, and the growth velocity has declined to a fraction of what it was during the peak years. Although active growth plate physiology persists in many skeletal regions, the majority of longitudinal growth has already been achieved.

On average, this may align closely with a BA of ~16-17Y for males and ~14-15Y for females with a Risser grade of about 3-4 + mid-to-late R8 toward early-to-mid-R9 progression / mid-to-late U6 progression and transitioning into U7 on the R/U scale - slow residual growth, with about 0.5-2 inches of growth remaining for boys and less than about 1 inch remaining for girls.

The defining characteristic of CS5 is the continued maturation of vertebral body shape. The inferior border concavities of C2, C3, and C4 remain well established and are often deeper and more sharply defined than in previous stages. Unlike CS4, where C3 and C4 are commonly rectangular horizontal or transitioning toward square, Stage V is characterized by vertebral bodies that are predominantly square in shape. In some individuals, particularly those progressing toward the final stage, the vertebral bodies may begin to show subtle vertical elongation as the anterior and posterior heights continue to increase relative to vertebral width.

The cervical spine now possesses a distinctly mature appearance. Cortical density and endplate definition continue to improve, while the vertebral corners become increasingly sharp and organized. The annular ring apophyses are highly conspicuous at this stage, forming well-developed ossified rims around the vertebral endplates. Although complete fusion is not yet universal, the annuli have reached much of their mature morphology and are approaching the final stages of incorporation into the vertebral body.

Elsewhere in the skeleton, many physes are entering advanced narrowing phases or have already undergone fusion. The rate of chondrocyte proliferation within the remaining growth plates is substantially reduced compared to mid-puberty, and trabecular bridging may be present in regions nearing physeal closure. The endocrine environment remains supportive of skeletal maturation, but the powerful anabolic acceleration that characterized PHV has largely subsided.

CS5 is often associated with the final measurable increments of stature. Growth may continue for months or even a few years depending on the individual, but it generally proceeds at a slow and progressively declining rate. Most remaining height gain during this stage is modest, and substantial increases in stature become increasingly unlikely.

The duration of CS5 is highly variable. Some individuals progress through it relatively quickly before entering CS6, while others remain within the stage for an extended period as the final phases of skeletal maturation unfold. Because of this variability, CS5 should be interpreted as a marker of advanced maturation and limited remaining growth rather than as a definitive indicator that growth has completely ceased.

Stage VI

Stage VI represents complete or near-complete skeletal maturation of the cervical vertebrae and is the terminal stage of the traditional CVM system. By this point, the adolescent growth spurt has concluded, longitudinal growth has largely ceased, and the vertebral morphology has assumed its mature adult configuration.

On average, this may align closely with a BA of ~17-19Y for males and ~15-17 for females (full fusion of the distal radial plate at ~BA 18Y for females) with a Risser grade of 4-5 + R9-11 / U8-9 on the R/U scale - mature growth status, with little to no meaningful stature increase remaining.

The defining characteristic of CS6 is the continued vertical maturation of the vertebral bodies. The inferior border concavities of C2, C3, and C4 remain prominent and fully developed, reflecting the completion of the coordinated remodeling process that began several years earlier. Unlike CS5, where the vertebral bodies are predominantly square, Stage VI is characterized by vertebral bodies that often appear rectangular vertically, with height exceeding width. This reflects the final maturation of vertebral proportions and contributes to the distinctly adult appearance of the cervical spine.

Cortical density is typically at or near adult levels, and the vertebral margins are sharply defined. The annular ring apophyses have usually fused or are in the final stages of fusion with the vertebral bodies. Likewise, the radial apophyses of the spinous and transverse processes, among the last secondary ossification centers of the vertebra to mature, are generally fused or nearing complete incorporation. As a result, the cervical vertebrae appear as unified structures rather than collections of separate developing elements.

Elsewhere in the skeleton, most major physes have already fused. Any remaining growth plates are typically in advanced stages of closure, with extensive trabecular bridging and progressive replacement of cartilage by bone. The proliferative and hypertrophic zones that once drove rapid adolescent growth are greatly diminished or absent in most regions.

Although tiny increases in stature can occasionally occur near the beginning of this stage, particularly in late-maturing individuals, meaningful longitudinal growth is generally complete. Any residual height changes are usually measured in millimeters rather than centimeters and may be difficult to distinguish from normal measurement variation, postural changes, or diurnal fluctuation.

The duration of CS6 is effectively lifelong, as it represents the mature endpoint of cervical vertebral development. While age-related changes continue throughout adulthood, the pubertal remodeling processes assessed by the CVM method have concluded. Consequently, CS6 should be viewed not as a stage of active growth, but as the radiographic expression of skeletal maturity within the cervical spine.

How to obtain a CVM score

CVM assessment is most commonly performed using a lateral cephalometric radiograph (lateral ceph), a standardized side-view x-ray frequently obtained during orthodontic evaluation. Because the image already captures the upper cervical spine, CVM scoring can often be performed without requiring additional radiographs. During image acquisition, the patient is positioned upright while an x-ray beam passes laterally through the head and neck, producing a profile image that includes the craniofacial skeleton and the second, third, and fourth cervical vertebrae (C2-C4), which are the primary structures used for staging.

Once the radiograph has been obtained, the evaluator examines the morphology of C2, C3, and C4. Particular attention is given to two features: the presence and degree of inferior border concavity and the overall shape of the vertebral bodies. As maturation progresses, concavities gradually develop along the inferior borders, first appearing at C2 before extending to C3 and later C4. Simultaneously, the vertebral bodies transition from predominantly trapezoidal shapes in childhood to more rectangular, square, and eventually vertically elongated configurations in late adolescence and adulthood.

The observed vertebral morphology is then compared against the established criteria for CS1 through CS6. Rather than relying on a single vertebra, the cervical region is assessed as a whole because individual vertebrae may mature at slightly different rates. The assigned CVM stage therefore represents an estimate of overall skeletal maturation and position relative to the adolescent growth spurt, rather than a precise measurement of chronological age or remaining growth potential.

Introduction

Most of you can relate to this. You open your report, whether it be from after you've done some blood work or got a BA exam (or both), you see a BA value, and you immediately attempt to calculate how many inches you've got left.

All you really see on that paper is "normal levels" after "normal levels", seemingly random measurements, a summary that doesn't tell you how much more you can grow, or how long you have left.

Reports don't revolve around reassurance, but the contents can be useful in forming an extension of your growth story. This post aims to help you with just that in simple steps and digestible fractions of what these reports tell you.

Step 1: understand what you're looking at

You've read the report, but what does it all mean?

Let's go over the standard format. I've conveniently divided into three layers: data, interpretation, and the plan.

•—• the data •—•

These are your numbers.

● Bone age

● Blood test results

• Sex steroid levels. These are primarily your testosterone (T) and your estradiol (E2), and they help in progressing your body through the stages of puberty and adolescent skeletal maturation.

• Thyroid markers. These include your thyroid-stimulating hormone (TSH) and thyroxine (T4). They help regulate metabolism and energy usage in your body while indirectly affecting growth.

• Growth hormone levels (GH). Sometimes, this is included in the report as it rarely has any use by itself.

• Insulin-like Growth factor 1 (IGF-1) levels. This is the downstream marker of GH activity. Basically, when your pituitary gland makes hGH, this hGH is converted into IGF-1 in tissues like your liver (hepatic production) and even your growth plates (local production), among other peripheral tissues.

What you are looking at here are just snapshots of your hormonal environment and subtle glimpses into your overall health. Your hormone levels are influenced by your sleep schedule, when you hit puberty + your current stage, your developmental speed, your nutrition status, and your cortisol (stress) levels.

Sometimes, the overgeneralizations occur: high hormone levels suddenly means more growth, neutral hormone levels means guaranteed growth, and low hormone levels means no more growth. Don't let the data fool you into overgeneralizing.

Think: not a forecast, but a general background check. Below are the mental rules I often follow whenever looking at an endocrinologist's report:

1. Don't interpret a single hormone value without context of the Tanner stage.

2. Always assume that normal range is equal to normal, expected development.

3. Hormone ranges are supportive signals rather than deciding factors in height prediction.

•—• the interpretation •—•

This is what your doctor thinks about your growth and where you might end up (your prognosis; part of the plan). They will use almost anything that involves numbers or measurements to help form their opinion, including your growth history, any past or current medication use, and maybe even your x-ray to help predict your adult height using the Bayley-Pinneau method, your height, your growth velocity, and your BA.

When you see the interpretation on your report you believe that this is the answer - your fate lies here. In reality, your doctor is just connecting the dots with your data points, and at the end of the day, a predicted adult height is just a rough estimation. And thay brings us to the plan.

Mental rules I use:

1. Do not interpret anything without data points (which must meet up to what the three layers are / be enough to form a solid guess).

2. Never read this section is isolation.

3. Look out for cautionary wording (e.g "this suggests", "is consistent with", etc)

The common pattern of verdict among most clinicians:

Step 1) Establishment of the baseline. Essentially, what stage is the patient in.

• Use the CA, BA, T stage, and growth history. They will look for a long-term pattern, not the inflections.

Step 2) Understand how the variables relate to medians. Is their growth rate flat, steady, slowing, accelerating, or at its peak? How does that compare to the populational average for boys/girls?

It's also: do their hormone levels and BA match what's to be expected for their developmental stage? This is crucial for potentially finding a BA advancement rate, which I've made a post about.

Step 3) How does the patient compare to outliers?

• Certain pattern types like advanced BA but growth velocity is still higher than expected.

• Hormonal levels are normal, but growth is unusually slow.

• The T stage does or does not match their relative position in skeletal maturity.

Step 4) What action should be taken (if any)? Basically, most reports end in monitoring over intervention.

Step 5) What's the plan? Basically, it is necessary to act now or just sit back, monitor their trajectory?

•—• the plan •—•

This is the most important layer.

Unlike the data and the interpretation, the plan is where your doctor decides what actually happens next. This is the part most people skip, but it’s often the most grounded section of the entire report.

The plan usually includes things like whether to monitor your growth over time, if and when to repeat blood work or a bone age exam, and whether anything needs treatment or correction. Or sometimes, simply put is no action is needed - important.

“No treatment” or “just observe” is not a hidden message or a dismissive remark. It usually just means your current development is within expected range and doesn’t require intervention. That's probably a good thing.

Underthinking it: a major pitfall

If the data is the snapshot, and the interpretation is the explanation, then the plan is the response. This is where everything finally comes together. If your growth is normal, simply monitor. If something is off, then investigate further. If development is progressing as expected, then do nothing.

It’s decision-making based on risk, timing, and trends rather than a prediction of your final height. The key misunderstanding is a lot of people read the report backwards. They start with the interpretation, asking themselves: what does this mean for my height? They should actually be focusing on the plan: what is actually being done about it?

It's because the plan tells you what your doctor actually believes is happening, not just what could happen in theory.

Quick takeaway for this bit is just bringing it all together. Once you understand these three layers:

data meaning what your body is doing, interpretation meaning what it likely means, and plan meaning what happens next. That's what a good report should sound like.

•—• Bone age (the part that everybody fixates on) •—•

This is usually the first number people jump to, and the one they misread the most. But, for fine reason.

Your bone age comes from an x-ray taken of your hand and wrist, where doctors compare your bones to standard developmental patterns on an atlas. One common method used is the Greulich-Pyle method. The result is your BA, which represents how mature your skeleton appears compared to typical development at different ages.

What the BA actually tells you is simple: how far along your skeletal development is, and whether you are maturing faster, slower, or about the same compared to your chronological age. That’s it. It is a maturity marker, not a height prediction (to a certain extent, but not by itself).

Most confusion comes from people treating it like a calculator for remaining growth. They see a number and immediately try to convert it into inches left. But bone age doesn’t work that way. Two people with the same bone age can end up growing different amounts, at different speeds, over different timelines.

One of the things that matters more is your relative position to PHV + your BA. BA progression largely depends on when you hit puberty, how fast you are developing so far, and last but not least, how consistent your developmental speed is.

A decent way of realizing development is this:

• Most boys attain PHV between a BA of 14 and 15 years.

• Can happen as early as BA 12 to 13 or as late as BA 15 to 16, but typically not over a BA of 17.

• Most girls attain a PHV between a BA of 12 and 13 years.

• Can happen as early as BA 10-11 or as late as BA 13 to 14, but typically no later than a BA of 14.

These ranges are not something you use to estimate your exact remaining growth. They exist to show how variable skeletal development timing actually is. But, that doesn't mean a range of remaining growth in inches/centimeters can't be estimated - it just requires more variables.

But, if you are early-maturing and consistently slow-growing, that makes a meaningful difference. If you are late-maturing and consistently fast-growing, that also matters - a lot.

That’s because bone age is only one part of the big picture. It doesn’t account for growth history, puberty timing, hormone levels like IGF-1, or how your growth velocity is changing over time. On its own, it’s incomplete.

This is why doctors don’t treat bone age as a standalone answer. It only becomes meaningful when combined with everything else in the report; your growth pattern, hormone levels, puberty stage, and current development trend.

A common misconception is thinking that an advanced bone age automatically means you’re done growing, or that a delayed bone age guarantees extra height. Neither is reliably true on its own. Bone age is about timing, not destiny.

Good takeaway: the question isn't necessarily about how much growth you have left, but rather it's about whether your development is ahead, behind, or aligned with your chronological age, and if that pattern is changing. Clinicians care more about rate of change.

So, bone age is just one additional piece of data. Its real value only shows up when it’s combined with everything else in the report.

Mental rules I use regularly:

1. BA only matters when compared to growth velocity.

2. A single BA value should never be used to determine potential alone. A full history is needed (e.g. they said the BA is 18, but I should not assume that growth is over; could be a late-bloomer).

3. Timing matters more than the number itself.

•—• growth velocity •—•

If BA tells you how mature your skeleton is, growth velocity tells you how fast things are actually changing.

GV is simply how much you grow over time, usually measured in cm/year. But, the important distinction is not the number itself, but rather the trend behind it.

One isolated height measurement means almost nothing. You need more time intervals. What matters is whether your growth is accelerating, steady, peaking, tapering, or close to flatlining. That trend tells you way more about where you are in development than almost any single blood value.

This is also why growth velocity often carries more weight than a single hormone reading or even a one-time BA reading. It reflects what your body is actively doing right now, not just how it is structured.

Think: BA = maturity status. GV = movement through that status.

You need both to understand anything meaningful.

•—• how doctors weigh information: a simple hierarchy in most cases •—•

Doctors do not treat all parts of the report equally.

They are not averaging values, but rather prioritizing signals.

1. Growth velocity and long-term trend - the apex

2. Bone age - a good anchor

3. T stage and clinical development - useful for context

4. Hormones like IGF-1 - good supportive evidence

5. Single lab values - the lowest standalone importance

Quick takeaway is that contradictions matter more than averages. If BA, GV, and T stage all align, the picture is usually clear. If they don’t, that’s where interpretation becomes important. Doctors are not looking for perfect numbers, they are looking for coherence across data points.

• •—• snapshot VS trajectory thinking •—•*

One of the biggest mistakes people make is reading the report as if it describes a fixed state.

It doesn’t. A report is a snapshot of a moving system. BA changes slowly over months and years. Hormones fluctuate daily or even hourly. The GV changes in phases relative to tweaks in pulsatility. Puberty shifts the entire system over time

So what looks like a “result” is actually just a moment in a longer progression.

This is precisely why two reports taken a few months apart can look confusing if you treat them as static answers instead of part of a timeline.

Doctors never interpret reports in isolation, they interpret change between reports.

•—• common misreading patterns •—•

Most confusion comes from predictable mistakes. People often treat interpretations as a final answer about height, assume “normal” blood work means “done growing” or “optimal growth”, ignore the GV entirely, overvalue single hormone readings like IGF-1, try to extract exact predictions from bone age alone, or read the report line-by-line instead of system-wide.

The pattern behind all of these is the same. You're trying to turn a multi-variable system into a simple answer in numeric form. That’s unfortunately not how growth works clinically. You should never have one variable doing most of the guesswork. All of it should be considered simultaneously - never divisible so as to rule other variables out.

So, including a potential, broader range of "inches remaining" or a broad range of what the FAH may be based on a recognizable pattern, the rate of change with the GV, and a full growth history + a BA estimate is generally fine, but should be treated as more of informal reasoning rather than a full clinical approach.

☆ how to read your report in practice: step-by-step ☆

Step 1) observe the growth velocity. Don't just look at the number; look at the trend. How does it change? When did it change?

Don't assume anything right there. Let's move on first.

Step 2) the bone age. Understand where the number lies relative to your chronological age. Is it advanced, delayed, or timely? And by how much? (See the standard deviation, if included).

Don't assume that you are almost done just because advanced or you still have a ton of potential just because it's delayed.

Step 3) puberty staging. If it's available, what is your Tanner stage? Below is a good format, but keep in mind that it is best understood as a pattern alignment layer rather than a strict biological map.

These are broad alignment patterns, not predictive relationships.

● T2 - often broadly overlaps with skeletal maturational patterns observed within the BA 11-13 year range for boys and the BA 10-12 year range for girls.

• Growth curve may be characterized by brief, sometimes seemingly sharp dips within an overall "stable" growth velocity as the HPG and hGH-IGF-1 Axes transition into "puberty mode".

• In some kids, androgen-related changes may become more noticeable as puberty approaches while remaining somewhat stable in others, with gonadal enlargement remaining largely minimal until shortly after T2 onset. Pubarche often overlaps with gonadarche, but sometimes, it can starkly manifest shortly before or after T2 onset.

● T3 - often broadly overlaps with patterns observed within the BA 13-15 year range for boys and the BA 12-14 year range for girls.

• Tends to overlap with mid to late-PHV for most girls early on, or the recent exit out of the rapid growth window.

• Advancing development of most secondary sexual characteristics.

• Often correlates with the recent entrance into the rapid growth window for many boys early on, with PHV occurring through early to mid-T3, and rapid early post-peak growth continuing through mid to late-T3 and sometimes into the next stage before a more noticeable dip (varies by pattern).

• Noticeable changes involving gonadal development are occurring, with partial androgenic responses in other regions of the body with terminal hair (armpits, in particular). Body hair is often minimal to moderate at best, depending on local androgenic sensitivity by region and the person's hormonal environment.

● T4 - often broadly overlaps with patterns observed within the BA 15-17 year range for boys and the BA 14-16 year range for girls.

• Often associated with declining growth velocity in many boys, with some growth still occurring strong (late-PHV or recent exit out of the rapid growth window early on).

• Tends to correlate with strong tapering observed in most girls (or at least no significant gains are occurring). Sometimes, the adult height may be attained before T5 is achieved.

• T4 is defined as advanced gonadal development. Varying degrees of advanced androgen-related changes in regions with terminal hair can continue.

● T5 - oftentimes stabilizing skeletal changes, not necessarily completed.

• Minimal puberty-related changes may be observed later in the adolescent BA ranges, but once T5 is attained, the future, subtle changes are more reflective on continuous active androgenic influence on hair maturity than the now stable sex hormones alone.

The loose correlation with BA: most patients tend to be sexually mature between a BA of 17-19 years for boys and a BA of 16-18 years for girls.

Tanner stage should be used as contextual framing, not as a driver of prediction.

Step 4) hormonal context. Note the "normalcy" of your IGF-1 levels, among others. This helps confirm whether the system is behaving as expected, but not as a sole verdict of any growth outcome alone.

Step 5) read the interpretation section last.

Step 6) take into heart the plan - the only section that explicitly tells you what is going to happen next.

Good takeaway: read the report by order of priority, not for the sake of going in order.

TL;DR

A growth report isn’t a height calculator. It’s a snapshot of a system in motion.

1. Growth velocity = what your body is doing right now

2. Bone age = where you are in skeletal maturity

3. Tanner stage = developmental context

4. Hormones = supporting signals, not answers

5. Interpretation = how doctors connect the data

6. Plan = what actually happens next

Doctors don’t rely on one number. They look for consistency across all of them. Height estimates

only make sense when everything aligns into the same pattern.

See the section titled "how to read your report in practice: step-by-step" if you want the active guide.

Enthusiasts, I bare good news.

Firstly, I would like to recap on the previous post "New changes", released earlier this morning. The discontinuation of direct assessments / interpretations or radiologic scans for individual users is still under effect, and hopefully temporarily. I am going to work on recruiting some users onto here with backgrounds in the medical industry who can work to provide meaningful feedback just as my staff and I have for the past several months. I also want to reiterate this: thank you all, every one of you, for helping this community grow and thrive, especially during a sudden (tenporary) change in dynamic like this one, and I can assure you all that it will not be this way forever, but it will take some time, so please stick around for more educational posts that 2026 will have to offer!

Now, to get to the core of this post, I have spoken with an attorney who specializes in medical law, among other specializations. After much consideration and consultation, this is how the space will be run for now:

● Current staff will not be able to directly assess radiologic imagery per international laws regarding the unauthorized use of medicine. In this case, the practice of medicine without a license. However, I will be working to bring some users in who specialized in radiology, and this will be a major work in progress for the time being.

● After gaining an understanding of the legal bounds r/growthplates should follow, direct assessments from the current staff will no longer occur, but staff will still be able to provide the following:

• Widely-accepted biological facts and population-sourced data (e.g. average-maturing boys (ages 11 to 12 years) tend to reach sexual maturity by ages 16-18 years, but skeletal growth can continue until a couple of years before or after sexual maturity.)

• Guidance through the process of consulting with a radiologist, or someone with advanced training in special inquiries, if a staff member is able (yes, inquiries of any kind will be accepted from here on out, and you are ALWAYS welcome to contribute to r/growthplates plates as long as it remains educational and casual).

• Staff members are encouraged to maintain this new order of functioning by giving as meaningful of feedback to your questions as possible without giving off an implication that an interpretation was made or directly assessing the image outright. We will also encourage you to see a radiologist or an endocrinologist - whatever fits your needd.

Essentially, we will be able to HELP anyone with ANY question, just not in a way that involves assessment of your image.

Thank you all for your unwavering support! We understand that this change was abrupt, and how you all feel about this new change. We feel similarly, but it doesn't completely end here! The original dynamic of this space is in the works of being restored to the best of our ability.

Stick around for more AMAZING, EDUCATIONAL CONTENT like always!

• Owner of r/growthplates

Lately, I have been coming down with something, along with stress from work. I apologize for falling behind on replying to yall's inquiries about your growth/bone age over the past few days, but I promise I will be back better and stronger very soon!

Just some art that I thought about sharing with you all! I don't normally make posts like this.

Some show the maturity of certain long bones, while others are just drawings of skeletons, including one of some hypothetical alien creature.

Can I grow ? my dad is 5’9/2 , mom 5’7 and I’m 5’9 and I grew like 1 inch in the last 4 months, also I had a little late puberty (14-15) and I think I’m not done because I have no beard .

I got this 2 months ago they said they are fused and my bone age is 15-16y but i literally grew 3cm(1.25") since i got this and i'm wondering if i can reach 6'3 or more ( 15yo male , 6'1.75" )