Monthly Archives: March 2023

Ulnar overgrowth in gymnasts

Some have speculated that ulnar overgrowth in gymnasts is due to premature radial closure like in the paper Gymnast wrist: an epidemiologic survey of ulnar variance and stress changes of the radial physis in elite female gymnasts, but the case of Devon Larratt suggests the possibility of ulnar overgrowth due to dynamic loading methods.

The way the triceps is attached to the olecranon of the ulna suggests that perhaps dynamic muscle pulling of the triceps on the ulna could stimulate growth.

Ulnar variance and skeletal maturity of radius and ulna in female gymnasts

“Ulnar variance and skeletal maturity of radius and ulna in female gymnasts. Med. Sci. Sports Exerc., Vol. 31, No. 5, pp. 653-657, 1999. It is has been suggested that repetitive loading on the distal end of the radius in elite gymnasts may lead to epiphyseal changes, a premature closure (union) of the radius growth plate, and ulnar overgrowth.

It is hypothesized that ulnar overgrowth in female gymnasts is associated with advanced maturity status and early onset of epiphyseal closure of the radius, and later maturity status and later onset of epiphyseal closure of the ulnar.”<-so basically the hypothesis was that gymnastics damaged the growth plate of the radius leading to relative ulnar overgrowth.

“Posterior-anterior radiographs of 201 female gymnasts, participants of the 1987 World Championships Artistic Gymnastics, were used to measure ulnar overgrowth, to determine skeletal maturation of the hand and wrist with the Tanner-Whitehouse technique, and to determine the maturity status of the radius and ulna separately, particularly with regard to the onset of epiphyseal closure. To test the hypothesis, extreme quintiles for ulnar overgrowth were contrasted for skeletal maturation of the hand and wrist and for maturity stages of the radius and ulna as defined by the Tanner-Whitehouse criteria.”

“Female gymnasts who demonstrate ulnar overgrowth are skeletally more advanced in maturity status of the entire hand-wrist compared with gymnasts who did not show ulnar overgrowth. There were, however, no differences between gymnasts in the extreme quintiles of ulnar overgrowth in the maturation of the radius, although gymnasts with ulnar overgrowth show more advanced maturity status of the ulna.

Ulnar overgrowth is thus not apparently associated with advanced maturity of the distal radial epiphysis as defined in protocols for assessing skeletal maturity and does not apparently lead to premature epiphyseal closure of the distal radius.”<-so gymnastics did not cause premature closure of the radius so the overgrowth of the ulna must be due to something else. The hypothesis that they suggest is that the ulna grows faster.

“In gymnastics, the distal radius bears most of the force when the body mass is supported by the upper extremities. As a result, attention is commonly focused on injures of the hand and wrist, given their potential to influence the growth plates of the distal radius and ulna. It has been suggested, for example, that the repetitive loading of the distal end of the radius may lead to epiphyseal changes and premature union, and result in ulnar overgrowth. It has also been hypothesized that “repetitive cyclical injury to the radial epiphysis may cause inhibition of normal growth of the radius and/or stimulation of ulnar growth”, and that the “proposed etiology of wrist pain associated with premature fusion of the distal growth plate of the radius” is chronic overuse”

So this study only suggests that the ulna grows faster due to gymnastics via a growth plate mediated mechanism it does not suggest that mechanical loading is the cause but it does not preclude it either.

An alternative theory as to why torsion can increase height growth

I have previously stated that torsion may increase height growth by dynamically altering the fluid movement of bone and thereby enhancing the longitudinal bone growth of bone including bone which is skeletally mature but these papers offer an alternative theory.

The Phylogeny and Ontogeny of Humeral Torsion

“In a series of specimens extending from fossil material through
recent vertebrates including man there occurs a gradual phylogenetic increase
in the degree of humeral torsion. A further (ontogenetic) torsion is superimposed upon the phylogenetic one in man which increases from birth until the proximal epiphysial cartilage of the humerus disappears and bony fusion occurs.

There is a distinct correlation between the calculated strength of humeral rotator muscles inserting above and below the proximal epiphysis; this suggests that they provide the forces involved in the production of humeral torsion. It is shown that ontogenetic or secondary torsion occurs proximally and not along the shaft of the bone.
Differences in the degree of humeral torsion in either sex of adult Whites and Negroes are given and discussed.”

So this paper is basically saying that it’s the muscular rotator cuffs causing the change in humeral torsion and not the fluid mechanics to bone. However, in practice in contrast to this theory it seems that dynamically loaded bones generate more longitudinal bone growth than just people with muscle imbalances. Ultimately, more experimentation would need to be done to see which theory is correct.

“Our phylogenetic survey shows that the torsion angle increases progressively from crossopterygian fishes through recent mammals to man.”

“Mean torsion values proved to be greater in Whites and more marked on the right side, but bilaterally similar in Negroes.”<-the use of the word Negro shows how old this paper is.

“There are distinct correlations between humeral length and thickness. The longer
bone of a pair usually shows the greater torsion angle. However, in Whites, the
thicker bone is more twisted. while the thinner one has more torsion in Negroes.
The right humerus is usually longer in both groups. The average torsion angle is 74 4″ in
Whites and 72.6″ in American Negroes.

It is suggested that the differences in torsion and thickness of right humeri may be attributable to the predominance of right handedness in the population (about 95% on the right).”

“muscular forces produced humeral torsion at the level of the proximal epiphysial cartilage prior to bony fusion at that level.“

“(a) torsion, indeed, occurs at the proximal epiphysial plate of the humerus, (b) the forces involved are attributable to lateral rotator muscles inserting proximal to the epiphysial line of the humerus and to medial rotators which insert distal to it (I found no evidence that torsion occurs along the humeral shaft); and

(c) my studies of humeri of subjects of known age showed that torsion ceases with the disappearance of the proximal epiphysial cartilage.”<-the problem with this is is that most people do not do dynamic torsional training.

“I found a strong correlation between the degree of torsion and the strength of medial and lateral humeral rotators”

So basically muscular imbalances are what generates torsion in the humerus. So theoretically people who only train bench press pre-skeletal maturity should have more rotated humeri than individuals who engage in more balanced movements. The problem with this theory is that it only looked at small subset of cadavers and most people do not do dynamic torsional activities.

Here’s a more recent study:

Humeral Torsion Revisited: A Functional and Ontogenetic Model for Populational Variation

“Anthropological interest in humeral torsion has a long history, and several functional explanations
for observed variation in the orientation of the humeral head have been proposed. Recent clinical studies have revived this topic by linking patterns of humeral torsion to habitual activities such as overhand throwing. However, the precise functional implications and ontogenetic history of humeral torsion remain unclear. This study examines the ontogeny of humeral torsion in a
large sample of primarily immature remains from six different skeletal collections. The results of this research confirm that humeral torsion displays consistent developmental variation within all populations of growing children; neonates display relatively posteriorly oriented humeral heads, and the level of torsion declines steadily into adulthood. As in adults, variation in the angle of humeral torsion in immature individuals varies by population, and these differences arise early in development. However, when examined in the context of the developing muscles of the shoulder complex, it becomes apparent that variation in the angle of humeral torsion is not necessarily related to specific habitual activities. Variability in this feature is more likely caused by a generalized functional imbalance between muscles of medial and lateral rotation that can be produced by a wide variety of upper limb activity patterns during growth.”

So this more recent paper is saying that torsion is produced by muscular imbalance and not dynamic torsional loads.

“While the association of humeral torsion with a specific habitual activity is suggestive of an underlying functional cause for this morphological pattern, it does not entirely clarify the precise biomechanical and muscular forces acting during ontogeny that produce variation in this feature.”

“humeral torsion was initiated by embryological rotation of the forearm,”

“Several studies have found that, in contrast to nonthrowing control groups, individuals who engage in overhand throwing activity during adolescence and young adulthood display high levels of bilateral asymmetry in their angle of humeral torsion, with the dominant throwing arm possessing a more posteriorly oriented humeral head“

“the difference in humeral torsion between the dominant throwing and contralateral arms in professional handball players averaged 9.48, with a side-to-side difference of up to 298. In contrast, no statistically significant differences were found between right and left arms in the nonthrowing control groups”<-this suggests a functional fluid based mechanism for humeral torsion and therefore the possibility that torsion can induce morphological changes in the bone.

“medieval populations known to be engaging in strenuous weapons training might display similar changes in humeral architecture.”<-but apparently they did not. But that could just mean they did meet the threshold.

“Humeral torsion decreases with age, with infants between birth and 2 years postnatal displaying the highest values”

“While humeral torsion does decrease by 258 from birth to adulthood, it is difficult to determine when adult levels of torsion are attained.”

“Levels of humeral torsion are generally elevated in the populations predicted to be participating in high levels of strenuous activity and lower in less active, more urban groups.”

“In the normal individual, balanced forces of medial and lateral rotators produce a modest degree of humeral torsion. In the individual with a functional imbalance, unopposed forces of medial rotators results in a more posterior orientation of the humeral head.”

“professional throwing athletes experience the same imbalance of medial and lateral
rotators that are characteristic of individuals with obstetric brachial plexus injuries. In this case, however, this imbalance seems to be a product of a slight reduction in the power of the muscles of lateral rotation in combination with a dramatic increase in the power of muscles in medial rotation. In comparison to nonthrowing controls, throwing athletes display relatively stronger muscles of medial rotation”<-I just don’t see throwing creating a sufficient muscle imbalance to cause torsion. I think dynamic loading is more likely.

There’s really not much to say which theory is correct(dynamic torsional loading produces changes in bone architecture versus muscle imbalance produces pull on the growth plate) other than more exprimentation.

Pravilo Training Apparatus may help make you slightly taller

I’ve searched for something akin to bite jumping appliances that can induce articular cartilage endochondral ossification which has been shown to occur in the jaw to other joints of the body that can affect height..

There is a stretching apparatus promoted by Pravilo USA that may potentially work to induce articular cartilage endochondral ossification on height affecting joints.

I have stated in the past that the rack apparatus(and sleep stretching) is not likely to work to make you grow taller. First the load is not really on the bones or the articular cartilage. Second the load is not dynamic which has been to shown to be a key mechanism by which the bite jumping appliance in dentistry serves to induce articular cartilage endochondral ossification. Like dynamic movement is important to the bone(because of bones fluid contents and dynamic movement moves the fluid contents around) to stimulate growth, dynamic movement is important to the cartilage and the cells to stimulate the structure of the cells via fluid forces. Ultimately, a lot of the load is going to be on the tendons and ligaments but just be the constant moving around some of the load is surely going to applied to the articular cartilage.

I do not believe the load is going to be in such a way as to stimulate the bone directly(mostly via the enthesis and the articular cartilage). I do not think that applying load in a tensile fashion is necessary to stimulate the bone via torsional force. Torsion will stimulate the fluid contents of bone regardless of whether the torsion is applied in a compressive or tensile fashion.

I do however think this apparatus has possible potential in which to prove articular cartilage endochondral ossification. However, ACEO(articular cartilage endochondral ossification) is very slow so we’d need actual studies and actual going to the gym here and using the device is cumbersome. If we can prove that ACEO work then we can create easier to use devices.

Here’s an example of how Pravilo training apparatus can induce dynamic loading on the articular cartilage:

The twisting of the body is what makes it dynamic.

At about the one minute mark is where you can see the twisting applied:

In the store on the website there is parts to construct your own apparatus. I’m not sure if it’s worth it as ACEO is very slow. It’d be more for proof of concept. However, it could potentially work for your spine and there is no surgical mechanism that increases spinal height.

Is Scoliosis overgrowth of the spine due to torsion?

With my latest focus on research and experimentation of torsion leading potential bone overgrowth(new longitudinal bone growth). I did some research on scoliosis as in scoliosis there is a lot of research on the spine. Therefore, if torsion could stimulate longitudinal bone growth we’d expect to see overgrowth of the spinal column. It may still be possible however that even if scoliosis did not increase longitudinal bone growth that torsion may still increase longitudinal bone growth as scoliosis may not meet the dynamic threshold over which torsion stimulates longitudinal bone growth. However, I think the papers do suggest that scoliosis causes bone overgrowth.

Three-Dimensional Characterization of Torsion and Asymmetry of the Intervertebral Discs Versus Vertebral Bodies in Adolescent Idiopathic Scoliosis

“High-resolution computed tomographic scans of 77 patients with severe adolescent idiopathic scoliosis were included. Torsion and anterior-posterior and right-left asymmetry of each individual vertebral body and intervertebral disc were studied from T2 to L5, using semiautomatic analysis software. True transverse sections were reconstructed along the anterior-posterior and right-left axis of all endplates. These “endplate-vectors” were calculated semiautomatically, taking rotation and tilt into account. Torsion was defined as the difference in axial rotation between 2 subsequent endplates. Asymmetry was defined as the relative anterior-posterior or right-left height difference of the discs and the vertebrae.”

“There were at least 3 times more torsion, anterior overgrowth, and coronal wedging in the discs than in the vertebrae in the thoracic as well as in the (thoraco) lumbar curves (P < 0.001). These values correlated significantly with the Cobb angle (r ≥ 0.37; P < 0.001). Anterior overgrowth and coronal asymmetry were greater in the apical regions whereas torsion was most pronounced in the transitional segments between the curves.”<-just because torsion is more pronounced in certain segments does not mean that other segments did not undergo torsion overall.

“The discs contribute more to 3-D deformity than the bony structures, and there is significant regional variability. This suggests an adaptive rather than an active phenomenon.”<-the adaptative phenomenon could be torsion.

“On conventional 2-dimensional radiographs, it was observed that the discs were more wedge-shaped than the vertebral bodies in mild scoliotic curves whereas the wedging of the discs and vertebrae became more or less equal in more severe scolioses. These findings suggest that AIS[adolescent idiophatic scoliosisi] is primarily a deformation of the discs and that, according to Hueter-Volkmann’s law[compressed growth plates grow less, stretched growth plates grow more], the deformation of the vertebral bodies is secondary. However, at the same time, others reported increased coronal wedge angles of the vertebral bodies already in mild AIS, indicating abnormal vertebral growth.”

“Torsion per centimeter height: This was defined as the angle between the anterior-posterior axis of the superior endplate and the anterior-posterior axis of the inferior one of the same vertebra or disc in the axial plane divided by the height in centimeters. For example, if we found 3 vertebrae with a total height of 6.0 cm and a total torsion of 15°, torsion was 2.5°/cm.”

“In the thoracic curves, torsion was significantly greater in the IVDs than that in the vertebral bodies (6.2 ± 2.3°/cm height vs. 1.9 ± 0.7°/cm height, respectively; P < 0.001). In the (thoraco) lumbar curves as well, torsion of the IVDs was greater than vertebral torsion: 4.1 ± 2.6°/cm versus 1.2 ± 0.4°/cm; P < 0.001. In the apical as well as transitional levels of the thoracic curves, significantly more torsion was found in the discs than in the vertebral bodies (apex, respectively, 6.0 ± 2.4°/cm vs. 1.8 ± 0.9°/cm; transitional region, 6.3 ± 3.1°/cm vs. 2.1 ± 0.9°/cm; P < 0.001). In addition, a trend was observed that torsion was more pronounced in the transitional levels than around the apex[apex is the peak of the curve]; however, this did not reach statistical significance. In the different regions of the (thoraco) lumbar curves, we also observed that the discs were significantly more affected by torsion than the vertebral bodies: apical region, 3.8 ± 2.5°/cm torsion in the disc versus 0.9 ± 0.4°/cm in the vertebrae; transitional region, 4.7 ± 3.2°/cm versus 1.5 ± 0.8°/cm, respectively (P < 0.001). Again, a trend was observed that torsion was more pronounced in the transitional, nonapical levels of the curvature. In the (thoraco) lumbar curves, this trend became statistically significant (P ≤ 0.001).”
So torsion is correlated with length difference but the degree of torsion does not directly correlate with the difference but there could be different factors than just the degree of torsion like how dynamically the torsion is applied.

” all individual AIS curves were longer anteriorly than posteriorly and rotated both between and within vertebrae in the axial plane. This rotated lordosis has been described by a number of authors, leading to the hypothesis that lordosis is the initiating deformity, and that scoliosis is the result of a disturbed anterior versus posterior growth process”

“anterior “overgrowth” of the discs versus vertebrae in the sagittal plane”

“These findings support that AIS is mainly a 3-D deformity of the discs, suggesting that abnormal vertebral growth is, according to Hueter-Volkmann’s law, rather a consequence than a cause of the deformity”

“scoliosis as a rotatory instability of the spine, and the development of AIS depends on disturbance of the delicate balance between rotational stiffness of the spine on the one hand and rotation-inducing forces on the other. Once the spine decompensates into rotation around the stiff posteriorly located ligamentous axis, the vertebral bodies swing farther away from the midline than the posterior structures. At that point by definition, a lordosis starts to develop, leading to greater anterior length of the spine.”

“In conclusion, the IVDs contribute more to the 3-D deformity in AIS than the vertebral bodies. Because the processes of torsional deformation, anterior overgrowth, and coronal wedging are greater in the discs than in the vertebral bodies and are uniform in primary as well as compensatory AIS curves, it seems more logical that these morphological modifications are rather a consequence (among others through Hueter-Volkmann’s law) than a cause of the deformity.”<-so this suggests that torsion could potentially cause overgrowth.

Since scoliosis can be altered through exercise as suggested by studies such as Scoliosis-Specific exercises can reduce the progression of severe curves in adult idiopathic scoliosis: a long-term cohort study, this suggests that mechanical loading via exercise can alter the discs and vertebral bodies in the same way that scoliosis alters the mechanical loading of discs and vertebral bodies and alters their shape. IN the paper it suggests that the reduction may be due to “concave ligament stretching.” The authors of this study refuse to indulge the possibility that the change may be due to reduction in bon

Relative anterior spinal overgrowth in adolescent idiopathic scoliosis deformity.

“. The differential growth between the anterior and the posterior elements of each thoracic vertebra in the patients with AIS was significantly different from that in the controls (p < 0.01). There was also a significant positive correlation between the scoliosis severity score and the ratio of differential growth between the anterior and posterior columns for each thoracic vertebra (p < 0.01). Compared with age-matched controls, the longitudinal growth of the vertebral bodies in patients with AIS is disproportionate and faster and mainly occurs by endochondral ossification. In contrast, the circumferential growth by membranous ossification is slower in both the vertebral bodies and pedicles”<-the faster growth could be due to mechanical stimulation by torsion.

“Relative anterior spinal overgrowth in AIS has been reported in morphological studies”

Here’s what’s meant by anterior:

“

The longitudinal growth of the anterior column occurs at the growth plates by endochondral ossification and continues until the girl is between 16 and 18 years of age. In contrast, endochondral ossification of the posterior elements is complete by the end of the first decade of life”

“The posterior elements subsequently only grow circumferentially by membranous ossification. We speculated that the pathomechanism of the disproportionate spinal growth in AIS might be a loss of coupling between endochondral and membranous ossification during adolescence.”

“the relatively shorter posterior column acts as a tether which hinders the lengthening of the anterior column during the period of rapid growth, forcing the spine to bend and rotate. Different tissues such as
bone, spinal cord, ligaments, and muscles are included in the posterior column. The issue is which structure in the posterior column causes the tethering.”

“Tethering of the posterior soft tissues such as the posterior ligaments has been presumed to
be the force acting on the spine to create the complicated deformity”<-I have seen other people theorize that the ligaments constrain longitudinal bone growth.

“There is much indirect evidence supporting the hypothesis that uncoupled endochondral-membranous bone formation causes the relative anterior spinal overgrowth in AIS. It is well known that girls with AIS have a tendency to be taller and thinner than their peers.”<-it is also possible that the scoliosis causes the overgrowth itself via torsional mechanical loading.

so this study suggests an alternative mechanism than torsion to cause the overgrowth but it does not rule out the torsion.

Using CRISPR technology to upregulate Chondromodulin could be a possibility in the future

The implication of this study I think is that CRISPR or other gene therapy technology could potentially be used to elevate Chondromodulin levels to either quicken limb lengthening surgery or maybe induce ectopic cartilage formation?

Chondromodulin is necessary for cartilage callus distraction in mice

“Chondromodulin (Cnmd) is a glycoprotein known to stimulate chondrocyte growth. We examined in this study the expression and functional role of Cnmd during distraction osteogenesis that is modulated by mechanical forces. The right tibiae of the mice were separated by osteotomy and subjected to slow progressive distraction using an external fixator. In situ hybridization and immunohistochemical analyses of the lengthened segment revealed that Cnmd mRNA and its protein in wild-type mice were localized in the cartilage callus, which was initially generated in the lag phase and was lengthened gradually during the distraction phase. In Cnmd null (Cnmd−/−) mice, less cartilage callus was observed, and the distraction gap was filled by fibrous tissues. Additionally, radiological and histological investigations demonstrated delayed bone consolidation and remodeling of the lengthened segment in Cnmd−/− mice. Eventually, Cnmd deficiency caused a one-week delay in the peak expression of VEGF, MMP2, and MMP9 genes and the subsequent angiogenesis and osteoclastogenesis. We conclude that Cnmd is necessary for cartilage callus distraction.“

So CNMD gene therapy could potentially be used to treat non-unions in limb lengthening surgery too.

“Cnmd−/− mice did not show abnormalities in cartilage development or endochondral bone formation during embryogenesis or normal growth, and further did not affect natural articular cartilage development. Thus, Cnmd functions as a chondrocyte modulator in specific conditions, causing osteogenesis such as cartilage or bone injury, but not in normal cartilage development and growth.”

“the relationship between mechanical stress and Cnmd in the process of cartilage callus formation during bone repair/regeneration.”<-Perhaps we could induce Cnmd via other mechanical stress mechanisms?

“We focused on distraction osteogenesis, which involves an osteotomy followed by a slow progressive distraction to lengthen congenitally or traumatically shortened extremities”

“Cnmd could directly stimulate chondrocyte proliferation and proteoglycan synthesis in vitro“

“Cnmd is required for cartilage callus formation due to tensile stress on the periosteum and is less involved in it due to hydrostatic pressure between the gaps”<-we can induce hydrostatic pressure and tensile stress via other mechanisms.

” the gap tissue is subject to approximately 15% deformation (compression and tension) during walking in a rabbit tibial lengthening model, indicating that compression as well as tensile forces act on the gap tissue during the distraction phase”

” the fibula spontaneously fractured during the distraction phase and lengthened in the same manner as the tibia.”

“increased expression of Tnmd mRNA in Cnmd−/− mice at the distraction phase. Tnmd is a type II transmembrane protein that shares a cysteine-rich domain with Cnmd at the C-terminus”<-we actually want Tnmd to increase as Tendons are one of the limiting factors in the amount of growth you can get in limb lengthening surgery.

“Tnmd mRNA expression was strongly upregulated by 5% axial cyclic strain in tendon stem/progenitor cells”

“elongation of cartilage callus during distraction osteogenesis was suppressed in Cnmd−/− mice and subsequent bone formation and remodeling slowed and partially failed. The study results indicate that Cnmd-mediated cartilage callus elongation is necessary for distraction osteogenesis and Cnmd could be a mechanical response chondrogenic factor. New insights into the function of Cnmd may establish this molecule as a candidate therapeutic agent for successful bone healing.”