Any loading study with pictures can provide insight on the possibility of ectopic chondrogenesis/endochondral ossification even if they do not directly study longitudinal bone growth as long as there are images.

One method to grow taller as adult:

1)Induce bone degradation allowing space for new growth plates to form(one way this could be induced is by inducing fluid flow flow in the bone via joint loading)

2) stimulate new growth plate formation via mesenchymal condensation(this would be induced by hyrostatic pressure via joint loading)

3) induce endochondral ossification of the ectopic cartilage.  This would happen naturally due to the bone microenvironment.

Knee loading repairs osteoporotic osteoarthritis by relieving abnormal remodeling of subchondral bone via Wnt/β‐catenin signaling

“Osteoporotic osteoarthritis (OPOA) is a common bone disease mostly in the elderly, but the relationship between Osteoporotic (OP) and osteoarthritis (OA) is complex. It has been shown that knee loading can mitigate OA symptoms. However, its effects on OPOA remain unclear. In this study, we characterized pathological linkage of OP to OA, and evaluated the effect of knee loading on OPOA. We employed two mouse models (OA and OPOA), and conducted histology, cytology, and molecular analyses. In the OA and OPOA groups, articular cartilage was degenerated and Osteoarthritis Research Society International score was increased. Subchondral bone underwent abnormal remodeling, the differentiation of bone marrow mesenchymal stem cells (BMSCs) to osteoblasts and chondrocytes was reduced, and migration and adhesion of pre‐osteoclasts were enhanced. Compared to the OA group, the pathological changes of OA in the OPOA group were considerably aggravated. After knee loading, however, cartilage degradation was effectively prevented, and the abnormal remodeling of subchondral bone was significantly inhibited. The differentiation of BMSCs was also improved{this is the kind of thing we would be looking for}, and the expression of Wnt/β‐catenin was elevated. Collectively, this study demonstrates that osteoporosis aggravates OA symptoms. Knee loading restores OPOA by regulating subchondral bone remodeling{subchondral bone remodeling could potentially increase height by increasing bone deposition at the longitudinal ends of bone}, and may provide an effective method for repairing OPOA.”

“Since bone is a mechano‐sensitive organ, moderate pulsating loading, oscillatory compressive loads, can be applied to various synovial joints in a form of elbow loading, knee loading and ankle loading. Joint loading can change intramedullary pressure of bone cavities. The moderately changing pressure may generate fluid flow in a lacuna canalicular network in bone cortex, and activate anabolic genes in bone{the goal would that a change in hydrostatic pressure in the bone would stimulate ectopic chondrogenesis/endochondral ossification}. In our previous studies, we have shown that knee loading is effective in …promoting longitudinal bone growth…”

“Dynamic loads were sinusoidal at 1 N (peak‐to‐peak) and the frequency was 5 Hz for 6 min/day (each knee, 3 min).”

It’s here that we’d look for signs for ectopic chondrogenesis.  It’s hard to tell for sure as there’s no loading group for normal bone.  In the the loading groups(OAL, OPOAL) there are clear differences in the subchondral bone plate.  Although the loading groups, all seem to have differences in the bone but the differences seem stronger in the trabecular bone.  The growth plate is different in the loaded groups but that’s not going to make a difference to adults.

In this it looks like there may be more cellular condensation in the OAL group and the OPOAL group(there are more cells and they’re closer together).  This is a precursor to mesenchymal chondrogenesis.  We’d need signs of bone degradation as well to prove that growing taller as an adult is possible.  And it’s hard to say that without seeing a normal bone.

Note:  I am still working on a new method to increase height.

Sometimes things that are good for bone development are bad for longitudinal bone growth.  Fluoride could be such a case.  We can’t say definitively that fluoride stunts growth but it’s definitely something to watch out for.  Apparently, there is some concern that babies can have too much fluoride which makes sense given their small body size.

It should be noted also that sometimes things that inhibit longitudinal bone growth in one bone can stimulate in another.  This can occur in the spine for example.

Fluoride Inhibits Longitudinal Bone Growth by Acting Directly at the Growth Plate in Cultured Neonatal Rat Metatarsal Bones

“Excessive intake of fluoride inhibits bone growth in both humans and animals. It is unknown whether fluoride acts directly on the growth plate to inhibit longitudinal bone growth, and its mechanism of action has not been elucidated. In this study, we used an organ culture system and SW1353 cells to evaluate the effects of fluoride on endochondral ossification. Neonatal rat metatarsal bones were dissected and cultured with or without fluoride for 7 days. The total length and width of the metatarsal rudiments and the length of the calcification zone were measured. Chondrocyte proliferation, differentiation, and apoptosis were analyzed by immunohistochemistry and TUNEL assay in sectioned bones. The apoptosis was detected by flow cytometry, and the expression of apoptosis-related proteins Bax, Bcl-2, and Caspase-3 were detected by western blotting in SW1353 cells. Linear measurements demonstrated that fluoride induced a biphasic effect on longitudinal bone growth in organ culture, with a significant growth inhibition at a high concentration (10⁻⁴ M) and a stimulatory action at low concentration (10⁻⁶ M) of fluoride{that’s a pretty significant difference between high and low concentration so you can pretty safely take fluoride}. Histomorphometrical analysis of growth plate from fluoride-exposed metatarsal rudiments showed a significant reduction in the height of the proliferative and hypertrophic chondrocyte zones. Analysis of the Col2α1 and Col10α1 expression by immunohistochemistry revealed fluoride-suppressed metatarsal growth plate chondrocyte proliferation and differentiation. In addition, fluoride increased the number of apoptotic chondrocytes in the metatarsal growth plate. Western blotting showed an up-regulated expression of Caspase-3 and Bax and down-regulated expression of anti-apoptotic protein Bcl-2 after treatment with 5 × 10⁻⁴ M fluoride in SW1353 cells. Our findings indicated that fluoride inhibited longitudinal bone growth by acting directly at the growth plate in cultured neonatal rat metatarsal bones. Such growth inhibition was mediated by suppressing proliferation and differentiation, increasing apoptosis of resting chondrocytes and causing premature cell senescence in the growth plate.”

If you read the paper it says that high doses of fluoride can enlarge the growth plate which indicates that an enlarged growth plate is not always beneficial for longitudinal bone growth.

In the paper it says 10 -6 M of fluoride increased Longitudinal bone growth but it was not statistically significant but any longitudinal bone growth is good.

The question is can fluoride in toothpaste, drinking water, and other dental sources reach high concentration and stunt growth?

This is a Hiroki Yokota study who along with Ping Zhang is one of the prime developers of lateral loading modalities.

Generation of the Chondroprotective Proteomes by Activating PI3K and TNFα Signaling

“Chondrosarcoma and inflammatory arthritis are two joint-damaging diseases. Here, we examined whether a counterintuitive approach of activating tumorigenic and inflammatory signaling may generate joint-protective proteomes in mesenchymal stem cells and chondrocytes for the treatment of chondrosarcoma and inflammatory arthritis{we already kind of know that low levels of inflammatory signaling is beneficial, it’s too much that’s the problem}. While activating PI3K signaling and the administration of TNFα to chondrosarcoma cells and chondrocytes promoted tumor progression and inflammatory responses, those cells paradoxically generated a chondroprotective conditioned medium. Notably, the chondroprotective conditioned medium was enriched with Hsp90ab1 that interacted with GAPDH. Extracellular GAPDH interacted with L1CAM, an oncogenic transmembrane protein, and inhibited tumorigenic behaviors, whereas intracellular GAPDH downregulated p38 in chondrocytes and exerted anti-inflammatory effects. The result supports the unconventional approach of generating chondroprotective proteomes.”

“We employed mesenchymal stem cells and chondrocytes to generate chondroprotective proteomes{proteomes are essentially a collection of proteins} by activating PI3K signaling and the administration of TNFα.”

“In response to chemotherapeutic agents, the reverse behavior of resilient cancer cells is frequently observed. While their tumorigenic action may initially be suppressed, cells tend to develop drug resistance and gradually strengthen their progression”

“Chronic inflammation is reported to facilitate tumor progression, while the induction of inflammation may contribute to suppressing tumorigenesis by stimulating immune responses”

“Besides chondrocyte-derived CM, MSC-derived CM, as well as MH7a synovial cell-derived CM, were converted to tumor suppressive by the treatment with YS49, an activator of PI3K signaling. Their application reduced the level of TNFα and MMP13 in C28/I2 chondrocytes”

“Hsp90ab1, a heat shock protein acting as a molecular chaperon, showed the most pronounced anti-inflammatory effect in C28 chondrocytes by downregulating TNFα and MMP13”

” the chondroprotective proteome can be generated from MSCs and chondrocytes by activating PI3K signaling with YS49 and treating them with TNFα. When switched on, both PI3K and TNFα signalings acted tumorigenic in CS cells and inflammatory in chondrocytes. However, YS49 and TNFα converted skeletal host cells such as MSCs and chondrocytes into iTSCs and iISCs, and they generated tumor-suppressive and inflammation-suppressive CMs. We observed that YS49 and TNFα-treated CMs inhibited the proliferation, migration, and invasion of CS cells. Those CMs downregulated Runx2 and MMP9 in CS cells, as well as NFATc1 and cathepsin K in osteoclasts, whereas they decreased TNFα and MMP13 in chondrocytes”

Natural Height Growth has written about Ginza Kojima’s devices before.  The device appeared to be some kind of traction device with a rotational force applied.  The centripetal force could potentially stretch the body.  But all these forces ultimately have to lead to some kind of plastic deformation(permanent stretch of the bone or cartilage).  I speculated previously that the green light may be some kind of radiation that weakens the bone which allows it to be permanently stretched.

Here’s Ginza Kojima’s new website: http://www.shincho-nobashi.jp/

It looks like it applies a rotational/twisting force on the leg combined with some kind of pressure.

It looks like it’s mainly for small amounts of height as taken by this excerpt below.

”

In the case of the whole body course (guarantee course), it is 500,000 yen up to 1 cm, 1,300,000 yen up to 2 cm, and 2,300,000 yen up to 3 cm. (Excluding tax ※ Consumption tax will apply separately)

In the case of the knee and foot bone course (guarantee course), it is 1 million yen to 1 cm, 2 million yen to 2 cm and 3 million yen to 3 cm. (Excluding tax ※ Consumption tax will apply separately)

Please inquire for detailed charges for 3 cm and beyond.”

One limb length testimonial though advertised in the site is for 5 cm which you cannot realistically achieve without actual major bone growth.

”

The effects of the treatment are very individual differences and it is not known how long it will take without actually starting the treatment.

In our hospital, we guide you to receive the treatment once a week 24 times (about 6 months) as a rough guide. In addition, we offer a course that you can receive intensive treatment for a week as a short-term intensive course, so please consult with distant people.”

<-so looks like once a week for 6 months.

The current treatment schedule at our hospital is as follows.

• 1st time 10:00 to 12:00 (30 minutes set time)
• Second time 12:30-14:00
• Third time 14:30-16:00

As mentioned above, an average of 3 sets is given daily. The second and subsequent treatments are basically the same, but we will make adjustments to suit your convenience as much as possible, so please contact us.”<-and 3 sessions of 30 minutes.

This machine advertised elsewhere on the site looks like a traction machine

Gina kojima explains the science behind his thinking here:

“First of all, I thought it would be good to pull. When I grabbed the bones of the foot from both sides and pulled it with a slight force according to the tug of war and the principle of childhood, I thought that it would be fine because the blood vessels became thinner and blood flow would improve. The heart is pumping 6 liters of blood a minute, so the blood vessels become thin if you pull a round blood vessel, and it is the theory that so much pressure will be applied to improve blood flow. It has been 40 years since I started making machines. To be honest, it will be dozens already. Anyway, it is said that if you look at it, why do you spend so much money to make stupid tools, and it keeps making it anyway.”

So this quote makes it seem like a traction device but a lot of traction devices don’t necessarily pull the bone to induce plastic deformation.

As far as traction devices go, you have to either induce plastic deformation in the bone or you have to stimulate the body to grow.

I think the whole body course is the traction machine and the knee course is the elevated height speed machine 2 device.

I think elevated height speed machine 2 device may just be another traction device but specifically for the knee.  Any japenese translators?

I am still working on finding a method to grow taller.  A lot of it is self testing as not a lot of the published papers published lately show promise of non surgical longitudinal bone growth that I could see.

Mechanisms of synovial joint and articular cartilage development

“Articular cartilage is formed at the end of epiphyses in the synovial joint cavity and permanently contributes to the smooth movement of synovial joints. Most skeletal elements develop from transient cartilage by a biological process known as endochondral ossification. Accumulating evidence indicates that articular and growth plate cartilage are derived from different cell sources and that different molecules and signaling pathways regulate these two kinds of cartilage{Could we inject these cell sources into the articular cartilage?  Could we mimic the molecules and signaling pathways with various stimuli?}. As the first sign of joint development, the interzone emerges at the presumptive joint site within a pre-cartilage tissue. After that, joint cavitation occurs in the center of the interzone, and the cells in the interzone and its surroundings gradually form articular cartilage and the synovial joint. During joint development, the interzone cells continuously migrate out to the epiphyseal cartilage and the surrounding cells influx into the joint region. These complicated phenomena are regulated by various molecules and signaling pathways, including GDF5, Wnt, IHH, PTHrP, BMP, TGF-β, and FGF. .”

“Matured articular cartilage is also referred to as hyaline cartilage because of its translucent appearance that reflects its unique constituents, such as type II collagen, glycosaminoglycans (GAGs), and low cellularity. In addition, articular cartilage does not have blood vessels, lymphatic vessels, or nerves. Articular chondrocytes produce extracellular matrices and maintain their environment with very little or no cell turnover{we want cell turnover, HGH increases cell turnover and HGH can make you very tall in certain circumstances}”

” most parts of articular cartilage derive from different lineages from the growth plate cartilage. The first signs of joint development are presented by the appearance of condensed flattened cells at the presumptive joint site within a pre-cartilage tissue known as the interzone, the origin of the joint. Removal of the interzone from a chick embryo leads to an uninterrupted long bone lacking joints, indicating that the interzone provides segmentation of skeletal elements in limbs. The interzone arises from mesenchymal/pre-cartilaginous tissue in which the cells initially express chondrocyte marker genes such as type II collagen, aggrecan, and matrillin-1 ”

“Instead of the decreased expression of these chondrogenic markers, the interzone cells acquire the expression of growth differentiation factor 5 (Gdf5), formerly known as bone morphogenetic protein 14 (BMP14), or cartilage derived morphogenetic protein 1 (CDMP1). Gdf5 is a representative marker for the interzone during early joint development. In addition to Gdf5, Wnt4, Wnt9a (formerly known as Wnt14), Wnt16, Erg, doublecortin, and Gli are also expressed in the interzone”

“Gdf5-expressing cell lineage gives rise to all mature joint structures including articular cartilage, meniscus, ligaments, and synovium ”

” joint components are formed by the integration of peripheral cells in joint development. Epiphyseal chondrocytes migrate into the interzone at early stages, and the external regions of joints such as the synovium/joint capsule and outer parts of the meniscus are mainly composed of lately integrated cells. Thus, the fate of embryonic interzone cells, the surrounding cells, and their progeny cells may be determined by their spatiotemporally environment. “<-so growth plate cells become integrated into the articular cartilage interzone cells but these cells are affected by the articular cartilage cells and microenvironment so that the articular cartilage overall environment is unaltered.  Maybe we can do the reverse and make the articular cartilage more growth plate like…

“IHH is produced from pre-hypertrophic chondrocytes and up-regulates PTHrP expression in peri-articular chondrocytes. PTHrP inhibits the differentiation of proliferating chondrocytes into pre-hypertrophic chondrocytes. This feedback loop determines the length of long bones. Before the feedback loop, pre-hypertrophic chondrocytes around the center of anlagen are associated with interzone generation through the secretion of IHH. The loss of IHH causes not only dwarfism but also joint fusion in distal limb joints ”

“excessive IHH signaling activity in the interzone progeny induces ectopic cartilage formation in the knee ”

“Unlike in endochondral ossification, IHH and PTHrP seem to be independent in interzone generation and joint development. The genetic alteration of PTHrP causes the impairment of endochondral ossification, but no severe changes in joints. Even after IHH signaling becomes silent, PTHrP-expressing cells exist in articular cartilage over a lifetime. Recombinant human PTH (1–34) suppresses osteoarthritis development, and PTH/PTHrP signaling induces lubricin”<-Can we use this fact to become taller?

Those who say that weightlifting stunts growth will have a field day with this one.  Small animals were used and if the loads mentioned in the study caused as much apoptosis then growth would be severly stunted by weight loading.  But if it indicated some cellular regeneration in regards to unplanned apoptosis due to mechanical that would be an amazing breakthrough.  We could trick the cells into thinking there was more apoptosis than there was and that would lead to overgrowth.

Secondary ossification centers evolved to make endochondral bone growth possible under the weight-bearing demands of a terrestrial environment

“The growth of long bones occurs in narrow discs of cartilage, called growth plates that provide a continuous supply of chondrocytes subsequently replaced by newly formed bone tissue. These growth plates are sandwiched between the bone shaft and a more distal bone structure called the secondary ossification center (SOC). We have recently shown that the SOC provides a stem cell niche that facilitates renewal of chondro-progenitrors and bone elongation. However, a number of vertebrate taxa, do not have SOCs, which poses intriguing questions about the evolution and primary function of this structure. Evolutionary analysis revealed that SOCs first appeared in amniotes[essentially egg laying reptiles, birds, and mammals] and we hypothesized that this might have been required to meet the novel mechanical demands placed on bones growing under weight-bearing conditions. Comparison of the limbs of mammals subjected to greater or lesser mechanical demands revealed that the presence of a SOC is associated with the extent of these demands. Mathematical modelling with experimental validation showed that the SOC reduces shear and normal stresses within the growth plate; while relevant biological tests revealed that the SOC allows growth plate chondrocytes to withstand a six-fold higher load before undergoing apoptosis{this provides evidence that too high a load could stunt growth}. Hypertrophic chondrocytes, the cells primarily responsible for bone elongation, were the most sensitive to loading, probably due to their low Young’s modulus (as determined by atomic force microscopy). Our present findings indicate that the primary function of the evolutionary delineation of epiphyseal cartilage into spatially separated growth plates was to protect hypertrophic chondrocytes from the pronounced mechanical stress associated with weight-bearing in a terrestrial environment.”

“hypertrophic chondrocytes undergo apoptosis or trans-differentiation, leaving their calcified extracellular matrix as a scaffold on which invading blood vessels and osteoblasts form new bone tissue.”<-interesting that the acknowledge the transdifferentiation theory.

“commonly to study bone growth (i.e., mice, rats and rabbits), the growth plate is separated from the articular cartilage by a bony fragment, the secondary ossification center (SOC). This skeletal element, formed during early postnatal development, splits the initially contiguous cartilaginous element into two independent structures, the growth plate and articular cartilage ”

“Growth plate chondrocytes appeared to be highly sensitive to load, with 40% dying upon application of a 1N load (as revealed by propidium iodide (PI) staining). At the same time, the SOC clearly protected these cells, allowing them to withstand a load an order of magnitude higher ”  An order of magnitude would be 10N

“directional compressive stress appears to be harmful to chondrocytes, especially hypertrophic chondrocytes”