Grow taller by Gap Repair

Sky's Limbcenter.org operates on the bone stretching principle.  If bone is stretched, tiny gaps are formed within the cortical bone that eventually heal resulting in a taller, longer bone.  Unfortunately, Sky seems to have fallen off the face of the earth and we don't know how Limbcenter is doing.  Here's an example of gap repair taken from an article about Bone Development and fracture repair:


In this article about the periosteum, the author explains about gap repair: "When no gap at all is present between the fractured cortical ends primary bone repair occurs by dint of osteoprogenitor cells derived directly from the Haversian systems within the cortex. This repair mechanism is also termed contact repair and produces lamellar bone already oriented correctly along the long axis of the bone. Gap repair or direct transformational bone repair comes into play when a small gap is present between the fractured ends. In this form, lamellar bone is formed initially at right angles to the bone and is then remodeled to the correct orientation. In wider gaps, woven bone is first produced and transformed to lamellar bone. In neither case is there a cartilage intermediary model."  You create more and more of these gaps by stretching the bone gradually resulting in a taller self.  So, even in cortical bone with no access to the periosteum you can grow taller.  You can grow taller with microfractures.  You can grow taller with the haversian canal.

Sky's method should work.  He just needs to provide photographic evidence.

Does LSJL induce more woven or lamellar bone formation?

Differential gene expression from microarray analysis distinguishes woven and lamellar bone formation in the rat ulna following mechanical loading.

"Formation of woven and lamellar bone in the adult skeleton can be induced through mechanical loading.  [We] distinguish the molecular responses between woven and lamellar bone formation induced through mechanical loading. Rat forelimb loading was completed in a single bout to induce the formation of woven bone (WBF loading) or lamellar bone (LBF loading). A set of normal (non-loaded) rats were used as controls. Microarrays were performed at three timepoints after loading: 1 hr, 1 day and 3 days. The micorarray identified numerous genes and pathways that were differentially regulated for woven, but not lamellar bone formation. Few changes in gene expression were evident comparing lamellar bone formation to normal controls. A total of 395 genes were differentially expressed between formation of woven and lamellar bone 1 hr after loading, while 5883 and 5974 genes were differentially expressed on days 1 and 3, respectively. A strong early inflammatory response preceded an increase in angiogenic and osteogenic gene expression for woven bone formation.  At later timepoints there was evidence of bone resorption after WBF loading."

Woven bone is typically associated with fractures so by analyzing gene expression data we can see if LSJL induces microfractures and if that plays a role in LSJL height increase.

"LBF loading did not increase cell proliferation, vessel volume or expression of angiogenic genes"

"The right forelimbs of adult male rats (Fischer F344, 5 mo., 337±24 g; Harlan) were loaded in axial compression"

"WBF loading applies a cyclic, haversine (2 Hz) waveform to the right forelimbs in a single bout (18 N peak force) until a prescribed increase in displacement (1.3 mm, 65% of fracture). "

"LBF loading applies a trapezoidal waveform to the right forelimb in a single bout (0.5 s triangle load-unload to 15 N, followed by 9.5 s rest; 100 cycles). Both WBF and LBF loading waveforms have a load/unload period of 0.5 s per cycle."

"Two transverse cuts were made to isolate the central 5 mm of the ulna and surrounding periosteum"<-whereas with LSJL the whole bone gene expression was analyzed.

Genes upregulated in Woven Bone:

IL6(up in LSJL)
IL8rb
TLR2
Nfkb1
Nfkbia
Sele
Ptgs2(up 7 fold in LSJL)
Cxcl1(up 6.431 fold in LSJL)
Cxcl2
Cxcl6
Cxcl10
Cxcl13
Cxcr3
MMP13
Ctsk(downregulated initially in woven bone then upregulated)
Ngf
Rel
Hif-1a
Creb1
Nos3
Cebpb
Fzd1
Csnk1a1
Tgfb1
Tgfb3(initially downregulated than upregulated)
BMP2
Smad1(down in LSJL)
Smad5
Csf1
Myc
Ctsk
Ccnd1
Cdk4
Cdc2
e2f1(down in LSJL)
Junb(up in LSJL)

Genes downregulated:

Sost
Egln1(Hif-1a inhibitor)
Ppbp
LRP5
Fzd8
Dkk1
Sfrp4
Dvl1(down in LSJL)
Tgfb2
BMP3
BMP3B
BMP6
BMP7
Acvr2b
Acvr1
Smad6
Smad7
Bambi
Fst
Grem1
Etv4

There is remarkable dissimilarity between woven bone formation and LSJL gene regulation.  The genes in woven bone formation were upregulated much higher than any gene in LSJL(sometimes up to 500 fold).  As noted earlier though gap repair can occur via lamellar and not woven bone formation.

Thus, LSJL is much more likely to induce new formation via lamellar bone formation(okay for height increase via gap repair) or endochondral ossification(great for height increase).

Distal radial fractures heal by direct woven bone formation.

"Descriptions of fracture healing almost exclusively deal with shaft fractures and they often emphasize endochondral bone formation. In reality, most fractures occur in metaphyseal[the area of the bone between the epiphysis and diaphysis] cancellous bone. We studied histological biopsies from the central part of 12 distal radial fractures obtained during surgery 6-28 days after the injury, using routine hematoxylin and eosin staining. New bone formation was seen in 6 cases. It was always in the form of fetal-like, disorganized woven bone. It seldom had contact with old trabeculae and appeared to have formed directly in the marrow. Cartilage was scarce or absent. The samples without bone formation showed only necrosis, scar, or old cancellous bone. The histology suggests that cells in the midst of the marrow respond to the trauma by direct formation of bone, independently of trabecular surfaces."<-If Cartilage was even there at all it's a good sign.

Men were ages 22-77.  Cartilage was found in 3 of the 12 fractures.  One of the individuals with cartilage had woven bone formation but no necrosis or soft tissue on day 28.  Another had necrosis and woven bone formation without soft tissue on day 14.  A third has necrosis and soft tissue but no woven bone formation.

What the three individuals who formed cartilage had in common was they had no bleeding, no trabeculae, and no old osteocytes.

"Cartilage was seen in scant amounts in 3 cases, all dominated by new woven bone formation. The cartilage mainly occurred in relation to necrotic areas{is bone necrosis important to induce cartilage differentiation?}. A gradual transition from cartilage to woven bone could be seen, suggesting that a gradient in local conditions had governed tissue differentiation. Endochondral ossification was never seen, but the small amounts of cartilage observed are most likely prone to undergo this process in due time."

 
"The most prominent occurrence of cartilage (C) in the study. It is located between woven bone and a necrotic hematoma[blood clot]. There appears to be a gradual transition from woven bone, via fibrocartilage, to hyaline cartilage."

"Platelet activation and danger-associated molecular patterns (DAMPs) activate the inflammatory response that is thought to start healing in general"