Knowledge about the attachment of ligaments and tendons to bone is important to the new method of LSJL loading.  This method involves clamping regions where two bones are attached to each other via ligaments.

According to Physical Therapies in Sport and Exercise there is no communication between tendons and bone however.  It describes the tendon enthesis as as an unmineralized bundle of rounded cell fibrocartilage wrapped in bundles of type II collagen.  It states though that these cells do not have connective arms to other cells so tendons and bones would have no communication.  We are interested in ligaments rather than tendons, as tendons would get  a lot of load from muscular activity but is still relevant as both tendons and ligaments have entheses.

Enthesis fibrocartilage cells originate from a population of Hedgehog-responsive cells modulated by the loading environment.

“Tendon attaches to bone across a specialized tissue called the enthesis. This tissue modulates the transfer of muscle forces between two materials, i.e. tendon and bone, with vastly different mechanical properties. The enthesis for many tendons consists of a mineralized graded fibrocartilage that develops postnatally, concurrent with epiphyseal mineralization.  By genetically demarcating cells expressing Gli1 in response to Hedgehog (Hh) signaling, we discovered a unique population of Hh-responsive cells in the developing murine enthesis that were distinct from tendon fibroblasts and epiphyseal chondrocytes. Lineage-tracing experiments revealed that the Gli1 lineage cells that originate in utero eventually populate the entire mature enthesis. Muscle paralysis increased the number of Hh-responsive cells in the enthesis, demonstrating that responsiveness to Hh is modulated in part by muscle loading{surprisingly lower muscle loading seems to increase responsiveness}. Ablation of the Hh-responsive cells during the first week of postnatal development resulted in a loss of mineralized fibrocartilage, with very little tissue remodeling 5 weeks after cell ablation. Conditional deletion of smoothened, a molecule necessary for responsiveness to Ihh, from the developing tendon and enthesis altered the differentiation of enthesis progenitor cells, resulting in significantly reduced fibrocartilage mineralization and decreased biomechanical function. Hh signaling within developing enthesis fibrocartilage cells is required for enthesis formation.”

“Fibrous entheses include a periosteal component and typically insert into the metaphyses or diaphyses of long bones. By contrast, fibrocartilagenous attachments typically insert into epiphyses or bone ridges. These attachments are characterized by a partially mineralized region of fibrocartilage at the tendon-bone interface, with a round cell morphology and increased proteoglycan content relative to tendon. Due to these characteristics, mature entheses have been likened to arrested growth plates“

Since tendons at first glance do not have much communication between themselves and bones how about ligaments?

Establishing a Coculture System for Ligament-Bone Interface Tissue Engineering

“Ligament-bone interface (enthesis) is a complex structure which comprises of ligament, fibrocartilage and bone. The fibrocartilage transformation adds significant insertional strength to the interface and makes it highly resistant to avulsion forces. Many ACL grafts cannot generate native interfacial region, leading to their failure. Co-culture has proved to be an effective way to generate new tissues in tissue engineering. Studies have found important signaling molecules in transduction pathway of chondrogenesis to be transmitted via gap junctions. Stem cells cocultured between ligament and bone cells would enable transmission of chondrogenic factors from bone/ligament cells to bone marrow stem cells (BMSCs) via gap junctions, resulting in their differentiation into fibrocartilage.  In this study, two set of co-culture (BMSCs and ligament cells; BMSCs and bone cells) were established. Confocal microscopy showed efficient dye transfer from bone/ligament cells into BMSCs. This was further confirmed and quantified by FACS, which showed a gradual temporal increase in the percentage of BMSCs acquiring Calcein.”

This study also states that there is ligament and bone communication:

In vitro study of stem cell communication via gap junctions for fibrocartilage regeneration at entheses.

“Entheses are fibrocartilaginous organs that bridge ligament with bone at their interface and add significant insertional strength. To replace a severely damaged ligament, a tissue-engineered graft preinstalled with interfacial fibrocartilage, which is being regenerated from stem cells, appears to be more promising than ligament-alone graft. Such a concept can be realized by a biomimetic approach of establishing a dynamic communication of stem cells with bone cells and/or ligament fibroblasts in vitro.

The current study has two objectives. The first objective is to demonstrate functional coculture of bone marrow-derived stem cells (BMSCs) with mature bone cells/ligament fibroblasts as evidenced by gap-junctional communication in vitro. The second objective is to investigate the role of BMSCs in the regeneration of fibrocartilage within the coculture.

Rabbit bone/ligament fibroblasts were dual-stained with DiI-Red and calcein (gap-junction permeable dye), and cocultured with unlabeled BMSCs at fixed ratio (1:10). The functional gap junction was demonstrated by the transfer of calcein from donor to recipient cells that was confirmed and quantified by flow cytometry. Type 2 collagen (cartilage extracellular matrix-specific protein) expressed by the mixed cell lines in the cocultures were estimated and compared with that of the ligament-bone coculture (control).

Significant transfer of calcein into BMSCs was observed and flow cytometry analyses showed a gradual increase in the percentage of BMSCs acquiring calcein with time. Cocultures that included BMSCs expressed significantly more type 2 collagen compared with the control.

The current study reported the expression of gap-junctional communication of BMSCs with two adherent cell lines of musculoskeletal system in vitro and also confirmed that incorporation of stem cells augments fibrocartilage regeneration.”

“Inside the embryo, tendons and ligaments appear as fibrous cellular outgrowths from the perichondrium of cartilaginous precursor to later bone. In the neonates, as the cartilaginous anlage ossifies, fibrocartilaginous elements of the ligament are cemented into the initial calcified cartilage, which is later replaced by mature bone. Only a thin layer of proliferative epiphyseal cartilage remains at the interface{this is a very promising fact as proliferative epiphyseal cartilage is a solid start in term of neo growth plate formation}. The resulting mature tendon or ligament insertion comprises four zones: collagenous ligament or tendon, nonmineralized fibrocartilage, mineralized fibrocartilage and cancellous bone”

The role of muscle loading on bone (Re)modeling at the developing enthesis.

“Muscle forces are necessary for the development and maintenance of a mineralized skeleton. Removal of loads leads to malformed bones and impaired musculoskeletal function due to changes in bone (re)modeling. In the current study, the development of a mineralized junction at the interface between muscle and bone was examined under normal and impaired loading conditions. Unilateral mouse rotator cuff muscles were paralyzed using botulinum toxin A at birth. Control groups consisted of contralateral shoulders injected with saline and a separate group of normal mice. It was hypothesized that muscle unloading would suppress bone formation and enhance bone resorption at the enthesis, and that the unloading-induced bony defects could be rescued by suppressing osteoclast activity. In order to modulate osteoclast activity, mice were injected with the bisphosphonate alendronate. Bone formation was measured at the tendon enthesis using alizarin and calcein fluorescent labeling of bone surfaces followed by quantitative histomorphometry of histologic sections. Bone volume and architecture was measured using micro computed tomography. Osteoclast surface was determined via quantitative histomorphometry of tartrate resistant acid phosphatase stained histologic sections. Muscle unloading resulted in delayed initiation of endochondral ossification at the enthesis, but did not impair bone formation rate. Unloading led to severe defects in bone volume and trabecular bone architecture. These defects were partially rescued by suppression of osteoclast activity through alendronate treatment, and the effect of alendronate was dose dependent. Similarly, bone formation rate was increased with increasing alendronate dose across loading groups. The bony defects caused by unloading were therefore likely due to maintained high osteoclast activity, which normally decreases from neonatal through mature timepoints. These results have important implications for the treatment of muscle unloading conditions such as neonatal brachial plexus palsy, which results in shoulder paralysis at birth and subsequent defects in the rotator cuff enthesis and humeral head. “

This study only studied tendon and not ligament entheses though.

This site has a lot of into about entheses:

“The normal enthesis has a tendency to develop new bone formation with ageing. This manifests as incidental “bony spurs” that are visible on X-rays”

“Joint tissues under tension favours bone development and the outermost part of the enthesis is subject to predominant tension (pulling force).”

Here’s an entheses with neo-bone formation:
Fc stands for fibrocartilage and the arrows are pointing at abnormal bone formation.  Not how the fibrocartilage is shaped into the bone like a zone of ranvier.

This website describes the groove of Ranvier:

“During the first year of life, the zone spreads over the adjacent metaphysis to form a fibrous circumferential ring bridging from the epiphysis to the diaphysis”

“This ring increases the mechanical strength of the physis and is responsible for appositional bone growths.  Supplies chondrocytes to periphery“

The site also says that ligaments have rounder cell morphology than ligaments which is more consistent with a chondrocyte cell.  Interestingly it says that ligaments also do not plastically deform which means that they can not permanently increase in length as a result of pulling force.

Strategies to engineer tendon/ligament-to-bone interface: Biomaterials, cells and growth factors.

“The complex and heterogeneous structure of the enthesis is essential to ensure smooth mechanical stress transfer between bone and soft tissues. Following injury, the interface is not regenerated, resulting in high rupture recurrence rates. “

“entheses exhibit gradients in tissue organization, composition and mechanical properties that serve to (1) effectively transfer stress between mechanically dissimilar materials and (2) sustain the heterotypic cellular communications required for interface function and homeostasis”

“the first part of the enthesis consists of fibrous connective tissue (tendon/ligament) characterized by the presence of parallel collagen fibers with interspaced elongated fibroblasts organized in arrays. The ECM primarily consists of collagen type I and small amounts of proteoglycans. The next zone is non-mineralized fibrocartilage, populated by round fibrochondrocytes arranged in rows. The ECM contains mostly collagen type II (typically characteristic of hyaline cartilage) as well as high levels of pericellular collagen type III, small amounts of collagen types I and X, and proteoglycans (mainly aggrecan) with associated chondroitin 4- and 6-sulfate glycosaminoglycans (GAGs). The third zone is mineralized fibrocartilage. This zone is populated by hypertrophic fibrochondrocytes, which are round and bigger than fibrochondrocytes. The ECM is composed mainly of collagen type II with significant amounts of collagen type X and aggrecan. Finally, the mineralized fibrocartilage merges into bone tissue containing osteoblasts, osteocytes and osteoclasts, together with collagen type I and high mineral content (69%) of which 99% is hydroxyapatite”<-Fibrocartilage may not be cartilage but it should should be capable of interestitial growth like growth plates.

“Enthesis fibrocartilage has been proposed to act as a barrier for cellular communication between tendon/ligament fibroblasts and osteocytes. This is due to the fact that fibrocartilage tissue is poorly vascularized and fibrochondrocytes do not express connexins and do not form gap junctions. Thus, intercellular communication needs to take place indirectly via cell–matrix interactions or soluble factors.”<-This will make getting stem cells from the enthesis into the bone slightly more challenging.

” the similarity in cellular and ECM composition between the fibrocartilage and the hyaline cartilage indicates an adaptation to compression. Consistently, mechanical loading plays an important role during enthesis maturation and contributes to the generation of a structural and cellular gradient at the insertion site. This gradation of structural composition turns into a gradation of mechanical properties that enables load transmission and reduces stress concentration”

Enthesis cells express both Scx+ and Sox9+ progenitor cells.  We have to encourage the enthesis to express more Sox9.

“During murine development, a progenitor cell population expressing both scleraxis (Scx) and Sox9 differentiates into Sox9 + chondrocytes or Scx + tenocytes/ligamentocytes to form the tendon/ligament-to-cartilage junction. Tenocytes are derived from both Scx +/Sox9 − and Scx +/Sox9 + progenitors, while ligamentocytes are derived exclusively from Scx +/Sox9 + progenitors[So ligaments always have chondrocyte differentiation capacity]. The closer the tendon is to the cartilaginous primordium, the more tenocytes arise from Scx +/Sox9 + progenitors. Similarly, enthesal chondrocytes located near the tendon/ligament-to-cartilage junction arise from Scx +/Sox9 + progenitors, while growth plate chondrocytes are derived from Scx −/Sox9 + progenitors. As development proceeds, the Scx +/Sox9 + progenitor cells upregulate either Scx expression, leading to cells of the tendon/ligament lineage, or Sox9 expression, leading to cells of the chondrocyte lineage. It has been proposed that TGF-β is necessary for Scx +/Sox9 + progenitor cell lineage specification, while the BMP-4/Scx axis determines its differentiation.”

“Fibrochondrocyte cells are expected to show a higher expression of collagen type II and lower expression of collagen type I when compared to fibroblasts.

Hypertrophic fibrochondrocytes synthetize higher levels of collagen type X.

Chondrocytes produce more collagen type II and less collagen type I than fibrochondrocytes.”

According to this paper, a crocodile may have a fibrocartilagenous growth plate which means that creating such a growth plate for humans is possible:

Crocodilian bone-tendon and bone-ligament interfaces

“We investigated bone-tendon (27 sites) and bone-ligament (12 sites) interfaces in six pairs of crocodile limbs and girdles under light microscopy. These crocodilian interfaces often included a direct, unmediated insertion in which the tendon or ligament fibers inserted directly into the bone itself without fibrocartilaginous mediation. This was quite different from the usual direct insertion known in mammals and lizards. Fibrocartilaginous tissue at the bone-tendon interface is generally believed to protect tendon fibers against shear stress. Other types of insertions were found in the crocodilian epiphyses, namely, hyaline cartilage and pseudofibrocartilaginous insertions. Notably, a thick periosteum/perichondrium and subchondral layer was involved at both interfaces. The thick periosteum/perichondrium seemed to form along the epiphyseal hyaline cartilage and might function in replacement of fibrocartilaginous tissues. Crocodilian thick periosterum/perichondrium would be expected to reinforce the limb and girdle bones — especially their epiphyses, in which secondary centers of ossification are absent. The subchondral layer — a kind of fibrocartila-ginous tissue — seemed to play the role of the growth plate in compensating for the absence of secondary centers of ossification. Therefore, we hypothesized that the crocodile-specific bone-tendon interfaces were the result of these specializations of bone development and growth. In crocodiles, the disadvantages of the single ossification center are effectively compensated for by specialized morphologies, including these interfaces. Specialized bone growth provides the crocodile with the largest body size of the recent reptiles and an extremely fast method of locomotion.”

Although according to the book Fins into Limbs: Evolution, Development, and Transformation avian growth plates become fibrocartilagenous when they are done growing.

The human tibial tubercle is formed by fibrous growth plates.

Here’s a grant about Scx and enthesis:

THE ROLE OF SCLERAXIS AND MECHANICAL LOADING ON ENTHESIS MATURATION

“The development of a functional attachment between tendon and bone (the “enthesis”) is critical for transmitting muscle forces to bone for joint motion. The formation of this attachment is driven by mechanical and biologic factors. Murine models of have demonstrated that removal of muscle load dramatically impairs the development of the enthesis. Furthermore, deletion of scleraxis (Scx), a transcription factor necessary for the development of force-transmitting tendons, leads to defects in enthesis formation. However, the mechanisms driving the mechanosensitivity of enthesis development are not known. Our global hypothesis is that Scx necessary for enthesis development and is driven by mechanical cues during{Maybe we can alter mechanical cues to alter enthesis development}. The first aim of this study is to determine the temporal influence of Scx on neonatal enthesis maturation using an inducible knockout murine model. Expression of Scx will be limited to development up to embryonic day 15.5, post-natal day 1, or post-natal day 7 and developmental adaptations and maturation of the enthesis will be assessed throughout juvenile development. It is expected that deletion of Scx during embryonic development will have a greater effect on enthesis maturation compared to post-natal deletion, and molecular and functional outcomes will be correlated with duration of Scx expression during maturation. These findings will establish the importance of Scx in enthesis development as well as determine its temporal role in post- natal musculoskeletal development. The second aim of this study is to determine the necessity of mechanical loading on Scx expression during development. Using in vivo and in vitro methods, we plan to mimic unloading and overloading, respectively, as well as assess the mechanosensitivity of Scx and its role in maturation and function of the enthesis. Using previously validated models of in vivo unloading and tissue-engineered methods for in vitro dynamic loading, we will track Scx-expressing cells as well as potential differentiation of ASCs into tenocytes. The effect of perturbed loading on the molecular and morphological response of Scx-expressing cells will be correlated with adaptations in structure and function using mechanical tests. These findings will determine the role of mechanical loading in Scx expression as well as the necessity of Scx in mechanically- induced tenogenesis. Lastly, the potency of Scx in load-induced tenogenesis following modulation with growth factors such as BMP-12 will be confirmed using BMP-12 siRNA. Findings from these studies will establish the importance of Scx on post-natal enthesis development, the mechanoresponsiveness of Scx in multi-tiered experimental models, and ultimately lead to new approaches for investigating musculoskeletal development and tissue engineered strategies for mechanosensitive orthopaedic tissues.”

Functional Attachment of Soft Tissues to Bone: Development, Healing, and Tissue Engineering

“Fibrous insertions typically occur over large areas, presumably to distribute forces and reduce stresses, and are characterized by perforating mineralized collagen fibers”

“The first zone consists of tendon/ligament, is populated by fibroblasts, and has mechanical properties similar to those of the tendon/ligament mid-substance. It is composed of linearly arrayed type I collagen fibers. The second zone consists of fibrocartilage, is populated by fibrochondrocytes, and is composed of types I, II, and III collagen and the proteoglycan aggrecan. The third zone is also populated by fibro-chondrocytes and is composed of mineralized fibrocartilage. Here, type II collagen predominates, and there are significant amounts of type X collagen as well as aggrecan. The fourth zone consists of bone proper, within which osteoblasts, osteocytes, and osteoclasts reside in a matrix of mineralized type I collagen.”

“the stratified tissue regions are compositionally distinct but structurally continuous.”<-thus anything that pulls on the tendon/ligament pulls on the bone.

“Enthesis development is initially driven by endochondral ossification: Cartilage mineralizes to form bone, and a fibrocartilaginous transition then develops at the interfaces between the bone and connective tissues.”

“All of the cell types found along the enthesis are mechanoresponsive; therefore, a role for mechanobiology during the development of this tissue is expected. Studies using genetically modified mice with muscular defects demonstrated that, although muscle loading was not required for initiation of enthesis formation, it was necessary for the subsequent growth and maturation of the enthesis”

“The reduction in muscle loading impaired mineral deposition and fibrocartilage formation and led to disorganized fiber distribution and inferior mechanical properties at the developing tendon enthesis.”

“mineralization at the developing enthesis is sensitive to mechanical loading.”

“when calcium phosphate cement was used to fill the tendon-to-bone junction in a rabbit ACL reconstruction model, the ceramic augmented bone tissue growth and organization”

“After the periosteal flap was sutured to the end of a torn rabbit infraspinatus tendon and then attached to bone, a fibrocartilage-like matrix developed after 12 weeks”

It may be possible to apply tensile strain to articular cartilage to induce endochondral ossification there thereby inducing height growth.

Effects of cyclic tensile strain on chondrocyte metabolism: a systematic review.

“Chondrocytes reorganize the extracellular matrix of articular cartilage in response to externally applied loads. Thereby, different loading characteristics lead to different biological responses. Despite of active research in this area, it is still unclear which parts of the extracellular matrix adapt in what ways, and how specific loading characteristics affect matrix changes. This review focuses on the influence of cyclic tensile strain on chondrocyte metabolism in vitro. It also aimed to identify anabolic or catabolic chondrocyte responses to different loading protocols. The key findings show that loading cells up to 3% strain, 0.17 Hz, and 2 h, resulted in weak or no biological responses. Loading between 3-10% strain, 0.17-0.5 Hz, and 2-12 h led to anabolic responses; and above 10% strain, 0.5 Hz, and 12 h catabolic events predominated{catabolic responses doesn’t necessarily mean bad for height growth}. However, this review also discusses that various other factors are involved in the remodeling of the extracellular matrix in response to loading, and that parameters like an inflammatory environment might influence the biological response.”<-3% strain is quite high but that’s for bone for cartilage it may be different.

“cartilage compression exposes the chondrocyte to compressive forces, to osmotic pressure, to fluid flows and also to tensile forces”<-lateral compression such as via lateral loading of the articular cartilage has potential to induce tensile forces.

“after loading with CTS, cells exhibited a more elongated cell shape and aligned perpendicular to the loading direction”

Collagen Type I was upregulated by CTS which could indicated endochondral ossification.

“Fibronectin connects collagen fibers and other ECM proteins. It is linked to the cell membrane through integrins and might transmit forces from the ECM to the chondrocyte. CTS at 7%, 0.33 Hz and 0.5 Hz, for 4, 12 and 24 h increased the fibronectin mRNA levels in comparison to non-loaded chondrocytes”

“7% CTS for 4 h at 0.33 Hz elevated the expression of IGF-1 and IGF-2. The mRNA expression of TGF-β1 was increased by several loading protocols ranging from strains of 5–12%, from 12–48 h and at frequencies of 0.05 and 0.5 Hz”

According to CYCLIC TENSILE STRAIN AND CYCLIC HYDROSTATIC PRESSURE DIFFERENTIALLY REGULATE EXPRESSION OF HYPERTROPHIC MARKERS IN PRIMARY CHONDROCYTES , tensile strain encourages endochondral ossification whereas hydrostatic pressure encourages chondrogenesis.

This study would only be relevant to people with existing growth plates as it only studies load effects on chondrocytes.  But, regardless, since we are studying mechanical loading methods to study height growth any mechanical loading study may be relevant.

Regional variations in growth plate chondrocyte deformation as predicted by three-dimensional multi-scale simulations.

“The physis, or growth plate, is a complex disc-shaped cartilage structure that is responsible for longitudinal bone growth. In this study, a multi-scale computational approach was undertaken to better understand how physiological loads are experienced by chondrocytes embedded inside chondrons when subjected to moderate strain under instantaneous compressive loading of the growth plate. Models of representative samples of compressed bone/growth-plate/bone from a 0.67 mm thick 4-month old bovine proximal tibial physis were subjected to a prescribed displacement equal to 20% of the growth plate thickness. At the macroscale level, the applied compressive deformation resulted in an overall compressive strain across the proliferative-hypertrophic zone of 17%. The microscale model predicted that chondrocytes sustained compressive height strains of 12% and 6% in the proliferative and hypertrophic zones, respectively, in the interior regions of the plate. This pattern was reversed within the outer 300 μm region at the free surface where cells were compressed by 10% in the proliferative and 26% in the hypertrophic zones, in agreement with experimental observations.  While the current model is relevant to fast dynamic events, such as heel strike in walking, we believe this approach provides new insight into the mechanical factors that regulate bone growth at the cell level and provides a basis for developing models to help interpret experimental results at varying time scales. ”

“The physis, or growth plate, is a complex disc-shaped cartilage structure that is responsible for longitudinal bone growth. This growth is modulated by many systemic and local factors including those arising from mechanical loading”

“Potential tissue level signals for modulating endochondral bone formation [include] hydrostatic and octahedral shear stresses and principal stresses”

“chondrocytes, are the active agents of growth and contribute to bone growth through cell proliferation, hypertrophy and extracellular matrix secretion in highly specialized, highly cellular and organized anatomic structures known as chondrons. It is likely that tissue level strains and stresses are experienced differently by chondrocytes embedded within such structures, possibly providing signals of varying intensity and type depending on location.”

“Mechanotransduction is more readily related to cell deformation than to tissue level stresses. In the context of bone growth, there is evidence that cell proliferation and differentiation can be regulated through activation of stretch-activated ion channels in the cell membrane following changes in cellular shape and size”

“Recent observational studies of physeal samples under compression have revealed regional variations in cellular strains and suggest that global physeal strains may be amplified at the cellular level”<-This statement may be applicable to other cells like the enthesis of ligament attachments or mesenchymal stem cells.

“The prescribed compressive displacement which was equivalent to 20% of the initial uncompressed combined initial thicknesses (0.67 mm) of RZ and P/H zones resulted in a -14.8% growth plate engineering strain across the combined layers of the reserve, proliferative and hypertrophic zones, while the combined proliferative and hypertrophic zone received -17.2% strain. The reserve zone experienced -9.5% and the calcified cartilage zone -3.3% compressive strain.”<-Effects on the reserve zone are interesting to us because those contain stem cells so would show any interesting effects on non-growth plate cells.

“Chondrons, the primary functional and structural units of the growth plate, deformed by buckling near the free surfaces where the cartilage bulged outward while remaining straight in the interior regions”

“chondrocytes in the interior of the growth plate undergo about 50% less strain than the prescribed overall growth plate strain.”

“Younger growth plates that are thicker (3 mm) also had thicker reserve zones, which may affect the transverse outward bulging at the free surface differently.”

“During compression of cells at short times scales (~0.5 s) intracellular water is redistributed within the cell[but not necessarily more compression]”

” At long time scales constant external pressure induces cell shrinkage, but cell shrinkage takes an order of magnitude (~10 s,) longer than the transient impact of heel strike or even the 0.2 s duration of the stance phase of a gait cycle and as long as an hour to reach equilibrium”

“growth plate stresses reached values of 0.1 to 0.6 MPa in compression during activities such as sitting. From the stress relaxation experiments on explants it may be estimated that 0.2 MPa corresponds to the stress levels attained after stress relaxation for displacements of the epiphysis equal to 20% of the initial growth plate thickness (defined as the combined thicknesses of the reserve, proliferative and hypertrophic zones).”

“Chondrons appear to be oriented along the minimum principal strain directions, becoming roughly perpendicular to the epiphyseal bone plate, whereas the hypertrophic portion along with the calcified cartilage bars and primary spongiosa align more with the primary compressive load direction along the tibial long axis”

Some interesting info but the significance is unclear yet.

To focus on the disadvantages of height is an unhealthy psychological pursuit.  To focus on striving to grow taller is a healthy psychological pursuit.

Here’s a typical conversation to someone about height:

A:  Don’t worry about height.  It’s what’s on the inside that counts.

B:  Why is it acceptable for height to be descriminated against?  Why is male height so associated with a male’s value?  Why is it acceptable to laugh at people because of their height?

A: You should accept who you are.  Play with the cards your dealt.

B:  If you have a losing hand, do you accept that or do you throw the cards off the table and start a fist fight?  If you can’t beat the game change the rules.

A: Life isn’t fair.  Sucks for you.

If you try to get into an argument with someone about height it usually begins with a lot of platitudes which are refuted until their opposing argument devolves into “too bad”.

The argument with the best reasoning often isn’t the argument that wins.  Short support sites shouldn’t exist.  Realistically, very little improvements can be made for the average or below against the tall.  And ultimately such sites serve as a means of perseverating on height.

You can try to forget your height.  You can play video games.  You can engage in an activity where height is of less importance such as a musical instrument.  Although even in those activities such as piano or guitar, finger length has an effect on playing.  You can get around it with techniques but it’s still a reminder that you’re just not as good.  Even playing pool, height can be an advantage in performing certain shots.

There’s acceptance but will you ever accept?  Ryan Seacrest complains about his height all the time.  There’s escapism but will you be satisfied with just escape?  Most forms of escapism lack the depth and complexity of real life.

The healthiest way to focus on height is to strive to find a way to grow taller.  Instead of dwelling on it.  Instead of comparing height with your friends.  Instead of realizing that you’re shorter than that other guy that you thought was really short.

The research I’ve done on entheses is intriguing and I’m trying to develop a new routine to explore it. What’s most intriguing about Entheses is that it resembles the Zone of Ranvier which contains the stem cells to contribute to the growth plate.  What if by pushing two bones together such as the fibula and the tibia on the epiphyseal region we can stimulate the entheses to form neo growth plates?

Don’t accept that there’s no way to grow taller.

Your height is mostly based on the length of your bones{The other determinants of height are opportunities to find new ways to grow taller}.  The length of the bones is determined mostly by your growth plate{The rest of the length is determined by other means but are difficult to get to contribute in significant ways but again is another way to pursue the quest for height}.  The growth plate goes away after puberty after the exhaustion of the stem cells that contribute to the growth plate.

To grow taller you could find:

1) Increase other minor determinants of height not involving growth plate growth

2) Induce the formation of neo growth plates

3) Induce plastic(permanent) deformation of the long bones.  Stretch the bones in such a way that they increase in length in a way that is instant and permanent(although this has never bone in done and the mechanisms of measurement are not accurate enough to best gauge the elastic and plastic range of a bone).

4) Other?  For you to determine.

Escapism and acceptance aren’t the only options for dealing with your height.  Don’t let people tell you that you should just accept your height.  Every time you think about dwelling on the negative effects of not being tall, focus instead on finding ways to grow taller.

You can get distraction osteogenesis surgery but it costs a lot of money and ideally you’d have multiple surgeries.

This field of science is entirely under researched(but most areas are due to how slowly science progresses).  And due to the complexity it is difficult for it to be Lorenzo’s Oiled(Homemade scientific discovery).  It’ll be hard to find a more efficient way of performing distraction osteogenesis but you could find a home made way of inducing new growth plate formation.  Cells do respond to mechanical and chemical stimulation after all.  And has every manner of mechanical stimulation already been performed?  No.  Especially methods that would appear counterintuitive like lateral joint loading(now adjusted to focus more on pushing two bones together near the entheses rather than clamping the synovial joint region).  And there are novel apparatus to create to generate forces that we couldn’t using our own muscular force.

Don’t dwell on how Dave France doesn’t get as good a roles as James Franco because he’s shorter.  Don’t dwell on how the third Hemsworth brother doesn’t get as many roles because he’s shorter.

Focus on researching methods to grow taller!  Even when I find a way to grow taller, it’s not going to be perfect right away.  I’m going to need your help.  You’re going to need my help.  The faster people stop dwelling on height and start growing taller the faster we can start getting taller.

I do track the websites which link to this website. Some of the most common sites that come to this website are from some of the most negative areas on the internet. The level of anger, bitterness, and spite on these strange internet discussion boards means that you can’t tell the difference between a genuine poster who just wants to vent and rant onto an internet discussion board and a troll. I’ll just say a few messages for those guys who feel depressed, angry, resentful, or just mentally stuck over their short height. This is directed mainly towards reddit/r/short and places like sluthate.com

Guys, take it down a little. You may be 5’6″ and have some level of asperger’s syndrome but that does not mean that you can’t enjoy your life. If you are thinking of killing yourself or hurting another person Rodger Eliot style, then read the following message.

I would assume that most people believe that they are above average in intelligence. Well, two of the principle traits of people who are truly intelligent exhibit are that 1) they can make decisions based on long term goals and 2) have the ability to control their emotional impulses and states. You can may be really good at mathematics but you still can’t control your own emotional state with the behavior of an immature child. For those of you who read this message, you know who you are. Emotional Intelligence has been shown to be often a much better indicator of eventual success in life than any traditional IQ test.

Start of my message

I don’t do much these days for this website since I run my own business which now takes up so much of my time. However, let me assure the regular readers that based on what I have seen from being on the cutting edge of the tissue engineering & biomedical fields, there will be something that will come out in the coming decades that will be much better than the limb lengthening surgeries you see today, which means less pain, less invasive, and less possibility for surgical complications. I am talking about lab grown growth plate implantations and healing intervertebral discs compression. I personally don’t think it is possible to “reopen the growth plates” which so many people hope for. Some little bit of surgical incision will be needed to cut the bone slightly (osteonomy). I do dare to dream big, but I am also a realist on what is possible, and what is pure science fiction. There are no magic pills or silver bullets.

You guys should not be worrying how tall you are and how much the world discriminate against you. You can’t change the world, unless you feel like it is your life’s mission to combat heightism similar to MLK to black/white conflict and put in maybe 20 years of hard work to make slight social changes. I suggest that you should not waste your time and energy on fighting an uphill battle against this hard-wired instinctual pre-programming which most humans have which creates prejudice towards shorter humans.

It is there, heightism exists, shorter guys get less dating and romantic opportunities (and maybe also less respect from other guys in their work), yada yada yada. You can cry about how unfair people are to you all day but at the end of this year, you would realize that all this venting of frustrating you post onto reddit/other doesn’t improve your life overall by much. You did not move that needle of your life gauge even a little bit. For now, just swallow the hard reality of this unfair world and existence we live in, accept that you did not win the genetic lottery like a channing tatum, and go in a different direction.

If you dwell on this fact, about your short stature and how no matter how much you go the gym you can’t change your height, you are going to get stuck psychologically, and maybe spiral down to a psychological state which you can’t get out of.

A lot of guys might tell you to go to the gym to lift weights, work out, build confidence, dress better, have a great social life, etc. and they are only half right. Improving on the areas of life of what you can control helps somewhat, but it won’t help all the time. Sometimes no matter what you do to try to make up for your short stature, that girl you like still won’t move towards you. The reality is that there is probably over 100 Mil other guys in the world out there. They have their own standards, and if they are not willing to lower their height requirement for you, there is nothing you can do. You already did everything else to improve yourself. You did everything you can to make you have a better advantage in this game we call life for success, and maybe sometimes that is still not good enough. Sometimes the only thing that matters is how long your bones are.

Some of you will be depressed. Go outside to the beach and get some sun. Take up long distance running to get the dopamine receptors firing again. Stay off the computer.

Work on yourself on the cognitive level is the best place to start. Take some nootropics, do tDCS, experiment with sleep cycles, learn acupressure and deep tissue massage for stress relief, yoga, fishing, etc. to get your mind away from this sub-reddit and other negative areas on the internet.

Get an education to increase your level of intelligence first (since being smart and short is much better than being tall and stupid in the long run), go into business for yourself to increase your net worth and build real assets, make your money, enjoy life, and come back when you are maybe 15-20 years older. You will have the funds to then spend on the latest cosmetic biomedical treatments. Most of you I would assume don’t have a lot in the wealth area of life. Money is not the be-all,end-all but it is a tool to help you get what you want out of life.

Treat each dollar you have as your soldiers. Each day you send your soldiers out to capture more soldiers which can work for you. That is called using money to make more money (aka investing)

I lived in Gangnam, Seoul for 2 years so that type of exposure made me very accepting of the idea of cosmetic surgery to improve one’s appearance. It is okay, as long as it is empowering and can really improve your quality of life. Some people are against cosmetic surgery since they think that it will change who they think they are to make other people like them, but this world is a very competitive place. You need every little bit of advantage you can get.

Plus, one’s concept of who they are as a person is fluid. It is not static. As we go through life, our “self” evolves over time. Even our core values and belief system changes over time. Don’t be so stuck in your beliefs/value which cause you to miss out on not taking a chance on something great. It is very rare that we regret later in life for doing something instead of not doing something.

For something besides just a nice pep talk which can hopefully get the regular readers out of their heads and negative emotional states, just see how close we already are with the 3D Printed nose which is made from fibrocartilage, not the hyaline cartilage you would need. (https://www.youtube.com/watch?v=FuGZ-G0UCCY). Implantation, transplantation, vascularization problems, people are working on that.

{Tyler’s Comments:  I tend to avoid looking at the validity of the desire to grow taller.

You may say: “You need to accept your height.”

I say: “You need to accept my desire to increase my height.”

Does climbing mount everest make any sense?  What about getting the high score in a video game?

Human height has value.  We as humans should strive to further our value.

“If you set your mind to it, you can accomplish anything.”

ANYTHING………

ANYTHING……

Including growing taller and we should accept nothing less.}

As I recently got back into playing basketball at the local YMCA which I just gave up, I came to realize just how strange it is that so many basketball players have an unnatural obsession on their height.

Back in my college days, I would sometimes eat in the same dining hall as the college athletes and the one time I ever sat really close to a set of basketball players I could over hear their conversation. What struck me as really odd back then was that half of their conversation revolved around how tall they were, or how tall other people were. One guy would tell the other guy about this player from another school, and they would go into his height by picking at it. The strange thing was they they didn’t mention the skill level of that kid, but just how large the opposing athlete was.

To these guys, it seemed like the height of a person defined who they were as a person. It was not their GPA, or GMAT scores, or what they had done in their lives. It was just their height. Back then, I just didn’t understand.

Now that I have started to watch basketball again, professional basketball, the thing that is always brought up is the players height.

Just watch the old 90’s bulls intro. Why is it that the announcers have to list how tall their players are? How often do I need to be reminded that Michael Jordan is 6′ 6″? The LA Lakers announcers do it too. (refer to this link https://www.youtube.com/watch?v=ojHOO4qbE4s). Being tall is not a skill, but people in the basketball world treat it as a skill. Being bigger does not make the player better.

Here is a sick truth that I would need to reveal about the nature of the game today. For most black american guys who play this game today, like in the streets of the inner city, basketball is actually a game of posturing, and showing off. (Refer to here https://www.youtube.com/watch?v=OJixT7F-Vog) People don’t play the game for the fun, for the team effort, or for the personal skills that they develop. They play the game to exert their masculinity and express their dominance. In the African American community, the young males are told to be ultra-masculine in expression. The easiest way to exhibit their dominance and masculinity is being taller than other men. If they are taller than others, they are told to use their body to push through to the post. I can’t even begin to remember how many times I would be in a game where it felt like it was not 5-on-5 but 1-on-1. The ability to pass seems to have been lost on certain people.I personally love playing the game and hearing that swish as the ball goes through the hoop but I have decided to let go of playing this game, and stop all-together to get away from the game.

As I grow older, I realize just how many psychological hang-ups people have over their height when they are playing basketball.

Sometimes I start to question my own motives for even still watching this game. Do I really find this game where abnormally tall guys running (and jumping) up and down the court that mesmerizing? Could it be that at some level in my mind, I have an unhealthy obsession with height just like the fellow basketball players? How many other people in the world also seem to find their primary source of identity through their height?

I had decided long ago that the sport of American Football is a huge waste of time and resources, but now I am adding the sport of Basketball on that list. No more playing the game, and no more watching the game, either in real life or on the internet. Watching one more sports game or event is not going to improve my overall life in any way. Having the local hometown sports team win a national championship does not make my life better or even bring any real prestige to the city.

(I live in the greater Seattle/Pacific Northwest area and I saw the whole Superbowl phenomena happen two months ago. People would make sure to revolve their jobs and business around the football games. The local Whole Foods would announce over the air whether the Seahawks would win or not, and people would crowd around the TV in the local Costco. I am not sorry that the Seattle located team lost. Imagine the type of pressure the team would have been in if they had won a 2nd year. People would be forcing the guys on the team to win again for a 3-peat. )

When people say things like “We Won!” after the local sports team win, I always want to correct them in saying that it is NOT that ‘we won’ but that the team won, they just watched while sitting on their couches and drinking bear and eating chips. Somehow they are trying to find some way to feel good about themselves from the glory of other people’s accomplishments, through association. Maybe not everyone can have the god-given talent to play at the highest professional level and win in athletics, but in the long term, nobody in a hundred years will care about who won the 2014 American Football Superbowl Championship. I am happy that at least the professional athletes today can make millions of dollars, but in the long term, I pity them since everyone knows that the human body is bound to fail, and father time always wins last.