Understanding Growth Plate Fusion(and growth plate senescence) will help us understand if these processes can be reversed.  And just as a note I am still working on devices and methodology to grow taller.

A Computed Microtomography Method for Understanding Epiphyseal Growth Plate Fusion.

“The epiphyseal growth plate is a developmental region responsible for linear bone growth, in which chondrocytes undertake a tightly regulated series of biological processes. Concomitant with the cessation of growth and sexual maturation, the human growth plate undergoes progressive narrowing, and ultimately disappears. Despite the crucial role of this growth plate fusion “bridging” event, the precise mechanisms by which it is governed are complex and yet to be established. Progress is hindered by the current methods for growth plate visualization; these are invasive and largely rely on histological procedures. Here, we describe our non-invasive method utilizing synchrotron X-ray computed microtomography for the examination of growth plate bridging, which ultimately leads to its closure coincident with termination of further longitudinal bone growth. We then apply this method to a dataset obtained from a benchtop micro computed tomography scanner to highlight its potential for wide usage. Furthermore, we conduct finite element modeling at the micron-scale to reveal the effects of growth plate bridging on local tissue mechanics. Employment of these 3D analyses of growth plate bone bridging is likely to advance our understanding of the physiological mechanisms that control growth plate fusion.”

“It is the terminally differentiated hypertrophic chondrocyte, which mineralizes its surrounding extracellular matrix. This process, thought to involve membrane-limited matrix vesicles, is biphasic and tightly regulated by a number of enzymes and factors including alkaline phosphatase (Alpl), PHOSPHO1, the ankylosis protein (Ank), ecto-nucleotide pyrophosphatase/phosphodiesterase-1 (Enpp1) ”

“as growth slows, the human growth plate undergoes progressive narrowing as bony bridges form and span its width. This ultimately leads to complete growth plate closure and the cessation of human growth. These bone bridges are also known to form upon growth plate injury, thought to be through an intramembranous ossification mechanism”

“in two genetic mutations resulting in estrogen deficiency (in the estrogen-receptor gene, and in the CYP19 gene), the growth plate fails to fuse and growth persists, albeit rather slowly, into adulthood”

“Evidence from studies in both humans and rats revealed the cessation of growth long before any histological evidence of growth plate fusion, suggesting that epiphyseal fusion is a marker of growth cessation and not its cause “<-Thus it may be possible to renew growth plate growth by reversing cessation and not fusion.

“young (8 weeks old) CBA wild-type mice, growth plate bridging is associated with locations that contain high local von Mises stresses. Moreover, we reveal that with aging an increased number and density of growth plate bridges is observed”

” in wild-type mice, increased growth plate bridging translates into increased stresses in the bone directly beneath the growth plate.”<-So maybe these stresses contribute to growth plate closure.

“At 8 weeks, few bridges are detected and overall the growth plate is squeezed in a “sandwich” configuration. This suggests that compressive hydrostatic stresses are engendered across major volumes and that higher shear stresses are generated only at the peripheral edges of the growth plate. Yet, the results of numerous mechanobiological models support that growth and ossification is accelerated by tensile strain (or shear stresses) and that cartilage tends to be maintained by hydrostatic compressive stress“<-so for a longer growth period we need to encourage hydrostatic compressive stress.

A radical switch in clonality reveals a stem cell niche in the epiphyseal growth plate.

“Longitudinal bone growth in children is sustained by growth plates, narrow discs of cartilage that provide a continuous supply of chondrocytes for endochondral ossification. However, it remains unknown how this supply is maintained throughout childhood growth. Chondroprogenitors in the resting zone are thought to be gradually consumed as they supply cells for longitudinal growth, but this model has never been proved. Here, using clonal genetic tracing with multicolour reporters and functional perturbations, we demonstrate that longitudinal growth during the fetal and neonatal periods involves depletion of chondroprogenitors, whereas later in life, coinciding with the formation of the secondary ossification centre, chondroprogenitors acquire the capacity for self-renewal, resulting in the formation of large, stable monoclonal columns of chondrocytes{if these chondroprogenitors never become senescent then we can grow forever}. Simultaneously, chondroprogenitors begin to express stem cell markers and undergo symmetric cell division. Regulation of the pool of self-renewing progenitors involves the hedgehog and mammalian target of rapamycin complex 1 (mTORC1) signalling pathways. Our findings indicate that a stem cell niche develops postnatally in the epiphyseal growth plate, which provides a continuous supply of chondrocytes over a prolonged period.”

“CD73 (encoded by Nt5e) was among the most upregulated stem cell surface markers (4.9 ± 1.2-fold; P28 versus P2; P = 0.018) and immunohistochemical analysis confirmed de novo expression of CD73 at P28 (markers for cell proliferation (Ki67) and differentiation (MEF2C) were controls for developmental changes”

“Cells in the growth plate might also orient as a result of migration or stacking due to tissue polarization, which is reflected by the orientation of primary cilia. Cilia on flat chondrocytes, but not on chondroprogenitors, were polarized (with 61.3 ± 4.8% and 32.8 ± 2.2% of cilia, respectively, oriented longitudinally, P = 0.005, n = 3;”

3j is supposed to summarize it

LSJL is lateral loading of the synovial joints or possible the epiphysis of the bone to stimulate fluid flow to stimulate degradation(remodeling) of the cortical bone and creation of mesenchymal stem cell chondrogenesis through a favorable microenvironment.

Martial arts bone condition is another form of this as impact is a form of loading.  However impact loading would not stimulate the soft tissues surrounding the bone which are all connected to the bone this is an important distinction.  Axial loading does not really drive fluid flow so that elements punching as a studiable stimulus.  However, several martial artists do tapping of the bones of the leg and arm.

The different between this and an LSJL style tapping would be that the tapping would not necessarily be at the longitudinal ends of the bone so the bone would be more innervated and there would be less of a fluid pressure gradient than at the longitudinal ends of the bone.  The goal of martial arts bone conditioning is described as something like calcification or bone thickening which is not exactly what we want.

The other difference between LSJL and martial arts bone conditioning is the intensity of the load.  Short intense bursts is more osteogenic whereas longer less intense bursts of loading are more chondrogenic.  This is primarily because osteocytes respond to sudden changes in fluid flow but osteocytes(probably) cannot make you taller as osteocytes produce bone and bone is what blocks you from growing taller!  Soft tissue is what allows for interstitial growth.  So for LSJL style loading you would tap the longitudinal ends of the bone with more frequency and less intensity.

If the bones weren’t so innervated would you be able to grow via martial arts style loading?  Probably not by rolling a bottle up and down your leg.  But we know that martial artists fracture legs during kicks.

And fractures definitely result in longitudinal bone growth because the bone clot results in a lot of fluid stimulus and it removes the cortical bone impediment.

We also know that there’s a phenomenon known as stress fractures where bones can develop fracture over time to non-overly traumatic loads just as the bone is no longer able to recover.

But we want to know if it’s possible to induce the longitudinal bone growth stimulus without fracturing a bone.  And could it be possible with a tapping stimulus?  The key is to target a less innervated part of the bone which happens to be the epiphysis although there are some epiphysis where regions are fairly innervated.  Tapping the epiphysis also generates a fluid pressure gradient.

With these fluid pressures we want to stimulate bone degradation via osteoclasts(remodeling)[this process could be accelerated via HGH] but we don’t want bone deposition via osteocytes and osteoblasts we want cartilage deposition although it’s feasible that other fibrocartilage tissues could work so that’s why we want sustained loading pressures over time so consistent taps.  The stress fracture phenomenon is also beneficial for our purposes.  Microcracks are good at stimulating fluid forces.

Nerve issues are probably unavoidable but we want to choose the least nerved location.

Does anyone have any anecdotal evidence of martial artist effects on bone?

I know there’s not a lot of solid proof of anything here but basically I’m testing epiphyseal tapping over prolonged periods to generate bone degradation and creating a favorable microenvironment for replacement via soft tissues.  I wanted people to know what I’m working on as I haven’t posted here in a while.  I’m solely dependent on generating proof at this point so if anyone has any evidence of martial artists generating any kind of visible bone adaptation whatsoever that would be extremely helpful.

According to the study it only increases IGF-1, but it may have other effects that are not known about.  Red Clover flowers contain p-Coumaric Acid.  I could only find p-coumaric acid available for scientific use.

p-Coumaric acid stimulates longitudinal bone growth through increasing the serum production and expression levels of insulin-like growth factor 1 in rats.

“The aim of the present study was to examine the effects of p-coumaric acid on the longitudinal growth of the long bone in adolescent male rats. Teatment with p-coumaric acid significantly increased the tibial length and the height of each growth plate zone and the ratio of 5-bromo-2′-deoxyuridine-positive cells relative to total proliferative cells. Expression of insulin-like growth factor 1 and its receptor in the proliferative and hypertrophic zones, and serum levels of growth hormone and insulin-like growth factor 1 were significantly increased as well in the p-coumaric acid-treated group. Via increasing both the serum level of insulin-like growth factor 1 and its expression, p-coumaric acid could promote cell proliferation in growth plate zones. These results suggest that p-coumaric acid has the potential to increase height and may be a feasible alternative to growth hormone therapy.“<-the statement that this may be a feasible alternative to growth hormone therapy makes this seem more powerful than just your typical supplement.

The study also mentions other supplements that have beneficial effects on chondrogenesis.  If you look at figure 1 and 2 you can see that there are differences between p-Coumaric Acid and Growth Hormone growth plates.  The scientists suggest that p-Coumaric acid upregulates IGF-1 and IGF-1R.