Here’s the last LSJL update.  Here’s the feet images from the this time which have had the best results out of what I’ve been clamping:

The size increase is not due to flattening of the arches as the arch on the right foot actually looks bigger.  You’ll note that the second and third toe look bigger as well.  My wingpsan has increased from 74.5″ to 74.75″ up from the 72.5″ it was before I started LSJL.  It is very difficult however to take a good wingspan picture.

Part of the trouble with LSJL has been slipping when clamping and a possible solution is that rather than clamping the epiphysis of the bone is to clamp the neck of the bone.

Considering the spillover of the second and third toe growth, I’d say it’s probably more important to generate clamping force than it is to be at the optimal location.  Clamping at the neck of the bone also clamps the muscle as well which result in more fluid flowing into the bone.  Also clamping at the neck of the bone gets closer to the bone marrow and one key conclusion I’ve come to my LSJL research so far is that the cortical bone and the outer periosteum(growth in width is difficult as well as growth in length) inhibit bone growth and inner periosteum and bone marrow stimulate bone growth.  Distraction osteogenesis both gets rid of cortical bone via fracture and stimulates the bone marrow via blood clot.

By continuing to clamp the epiphysis of the bone is likely the reason why my length gains plateaued as whenever I tried to increase the clamping force the clamp would slip off.  By clamping the neck of the bone I can continue to increase the clamping force without having to worry about slippage.  Hopefully, this will allow me to get some leg length increases that I’ll be able to report otherwise I’ll see if I can continue to gain in the feet and that’ll be proof of concept that I can use to gain more resources to establish better clamping technology to gain in the legs.

I bought a new clamp for my fingers as the standard six inch clamp was just too big.

The problem with this is all the holes in the clamp that make clamping uncomfortable.  If neck clamping with the Irwin Quick Grip clamp doesn’t work

 

I can doing the C-class clamp again but I worry even with clamping the neck of the bone rather than the epiphysis there’ll be too much slipping.

We’ll see what happens in one to two weeks.  And if it doesn’t seem to be working I’ll switch it up.  Considering my foot growth if I don’t observe results in a reasonable time frame then it’s time to switch things up

 

I tried hand clamping but I seemed to plateau with it so I’m back to using the C-class but more intensely than before.  Here is me doing some bones with a C-class clamp.  I’ve been getting some progress with my feet at least but that could be because changes in the feet are more noticeable because my shoes feel more snug.  Here’s the last feet images I took for comparison.  The first image there is actually the before picture.  Also the II phalanxes(toe closest to big toe) seems longer as well which makes sense since I’m clamping close by.

But my feet seemed to go up in size very quickly once I change methodology of using the C-class clamp over the hand clamp.  So if there’s no changes in a week then I will try something different.  Michael thought about using two C-class clamps at once.  Ideally, yes you want to gain height but the feet is where I’m getting results and if my right shoe no longer fits that would be hard to deny proof and I could use that proof to acquire more resources to translate to height increase research.

Since the II toe is growing I’m worried less about a precise clamping location and more about clamping force.  Now it is possible that the feet could be flattening but the big toe is already pretty straight.  Well if I can keep getting results than such minutiae won’t matter.

Here’s pictures of my feet:

The right toe is bigger.  I’m not to the point where I need to go up a size for my right foot but I’m closer.

Here’s some unilaterally swollen feet:  The bones don’t physically look longer.  So I don’t think it’s swelling making my feet appear longer.

Here’s another unilaterally swollen foot:

Here’s another:

This study basically explains that macrophages are key to neo-endochondral ossification:

Fracture healing via periosteal callus formation requires macrophages for both initiation and progression of early endochondral ossification.

“The distribution, phenotype, and requirement of macrophages for fracture-associated inflammation and/or early anabolic progression during endochondral callus formation were investigated. A murine femoral fracture model [internally fixed using a flexible plate (MouseFix)] was used to facilitate reproducible fracture reduction. IHC demonstrated that inflammatory macrophages (F4/80(+)Mac-2(+)) were localized with initiating chondrification centers and persisted within granulation tissue at the expanding soft callus front. They were also associated with key events during soft-to-hard callus transition. Resident macrophages (F4/80(+)Mac-2(neg)), including osteal macrophages, predominated in the maturing hard callus. Macrophage Fas-induced apoptosis transgenic mice were used to induce macrophage depletion in vivo in the femoral fracture model. Callus formation was completely abolished when macrophage depletion was initiated at the time of surgery and was significantly reduced when depletion was delayed to coincide with initiation of early anabolic phase. Treatment initiating 5 days after fracture with the pro-macrophage cytokine colony stimulating factor-1 significantly enhanced soft callus formation. The data support that inflammatory macrophages were required for initiation of fracture repair, whereas both inflammatory and resident macrophages promoted anabolic mechanisms during endochondral callus formation. Overall, macrophages make substantive and prolonged contributions to fracture healing and can be targeted as a therapeutic approach for enhancing repair mechanisms. Thus, macrophages represent a viable target for the development of pro-anabolic fracture treatments with a potentially broad therapeutic window.”

“inflammatory macrophages were required for initiation of fracture repair, whereas both inflammatory and resident macrophages promoted anabolic mechanisms during endochondral callus formation.”

“Periosteal endochondral callus formation progresses via four sequential and interdependent phases: inflammation leading to granulation tissue formation, early anabolism (soft cartilaginous callus formation), late anabolism (hard bony callus formation), and remodeling to reinstate the original bone architecture and mechanical strength”

“recruited inflammatory macrophages are derived from blood monocytes and rapidly infiltrate tissues compromised by injury, abnormal function, and/or infection”

“Inflammatory macrophages predominate in fracture granulation tissue and associate with chondrification centers. Representative images of periosteal fracture zone (Supplemental Figure S1A) 7 days after osteotomy and MouseFix plate fixation surgery in 12-week-old C57Bl/6 mice (n = 6 with assessment at multiple sectional depths per sample). All sections were counterstained with hematoxylin. A: Image represents approximately half of the periosteal fracture zone (proximal) with the osteotomy-generated fracture gap (FG) at the bottom left of the image. Granulation tissue predominates at this time point. Tissue section was stained by IHC for the F4/80 pan-macrophage antigen (brown). The black box demarks the region shown in B and C. The blue box demarks the region shown in E and F. B: IHC for F4/80 expression within fracture granulation tissue. The dashed line demarks the interface between the mesenchymal (closest to bone, below dashed line) and inflammatory (above dashed line) stratum. F4/80+ cells with stellate morphological characteristics are evident in both the inflammatory and mesenchymal (arrows) strata. The circle demarks a single osteomac within this field. C: IHC for Mac-2 expression (brown) in a serial section to that shown in B. Arrows point to the same cells indicated in B and highlight the high degree of overlap in F4/80 (B) and Mac-2 (C) staining patterns. The circle indicates the Mac-2neg osteomac identified in B. D: Quantification of the number of F4/80+ and macrophage-like Mac-2+ cells within the mesenchymal stratum of the granulation tissue. An average area of 0.15 mm2 was assessed in six independent samples, and the number of positive cells was not statistically different. E: F4/80+ macrophages (brown, arrows) adjacent to a periosteal chondrification center. F: Mac-2 staining in a serial section to E confirms induction of Mac-2 expression in condensing chondrocyte-like cells within the periosteal chondrification center (blue boxed area). The same F4/80+ macrophages noted in E can be traced and express Mac-2 (arrows). Dashed line in B, C, E, and F demarks the mesenchymal (lower)- inflammation (upper) strata junction within the granulation tissue. Original magnifications: ×10 (A), ×40 (B and C); ×60 (E and F). Scale bars: 100 μm (A); 50 μm (B and C); 37.5 μm (E and F).”

“chondroblasts were identified as F4/80negMac-2+ condensed mesenchymal cells (Figure 1F). F4/80+Mac-2+ (Figure 1, E and F) inflammatory macrophages were observed adjacent to chondrification centers and associated vascular structures.”

” Cartilage and woven bone formations were absent within the periosteal fracture zone [with no macrophages]”

Macrophages are also present in the soft to hard callus transition although this is not as important for purposes as creating the initial growth plate is the limiting factor.

” inflammatory macrophages [were present] in the mesenchymal stratum of the granulation tissue, including some that were associated with developing chondrification centers”

“The developmental vascular canals were broad invaginations with osteoclasts/chondroclasts at the apical tip, presumably excavating the canal path via matrix degradation, followed by a mixture of mesenchymal cells, osteoclasts/chondroclasts, lysosomal cells, macrophages, and endothelial cells.”

“macrophages are pro-mitogenic toward chondrocytes.”<-macrophages undergo chondrocytes to undergo cell division.

Resting and injury-induced inflamed periosteum contain multiple macrophage subsets that are located at sites of bone growth and regeneration.

“Better understanding of bone growth and regeneration mechanisms within periosteal tissues will improve understanding of bone physiology and pathology. Macrophage contributions to bone biology and repair have been established but specific investigation of periosteal macrophages has not been undertaken. We used an immunohistochemistry approach to characterise macrophages in growing murine bone and within activated periosteum induced in a mouse model of bone injury. Osteal tissue macrophages (osteomacs) and resident macrophages were distributed throughout resting periosteum. Tissues were collected from 4 week old mice and osteomacs were observed intimately associated with sites of periosteal diaphyseal and metaphyseal bone dynamics associated with normal growth. This included F4/80+Mac-2-/low osteomac association with extended tracks of bone formation (modeling) on diphyseal periosteal surfaces. While this recapitulated endosteal osteomac characteristics, there was subtle variance in the morphology and spatial organization of modelling-associated osteomacs, which likely reflects the greater structural complexity of periosteum. We also demonstrated that osteomacs, resident macrophages and inflammatory macrophages (F4/80+Mac-2hi) were associated with the complex bone dynamics occurring within the periosteum at the metaphyseal corticalization zone. These 3 macrophage subsets were also present within activated native periosteum after bone injury across a 9 day time course that spanned the inflammatory through remodeling bone healing phases. This included osteomac association with foci of endochondral ossification within the activated native periosteum. These observations confirm that osteomacs are key components of both osteal tissues, in spite of salient differences between endosteal and periosteal structure and that multiple macrophage subsets are involved in periosteal bone dynamics”

“The periosteum is a specialized connective tissue composed of a vascularized and innervated fibrous membrane that encapsulates bone. It has two layers: an outer fibrous capsule layer containing elastic connective tissue (including Sharpey’s fibres), fibroblasts and blood vessels; and, an inner cambium layer containing capillaries, nerves, pre-osteoblasts/bone lining cells, osteoblasts and undifferentiated mesenchymal stromal/stem cells (also referred to as periosteum-derived progenitor cells)”<-these stem cells could potentially be involved in neo growth plate formation.

“Progenitor cells within the endosteum and periosteum have different potential: endosteal progenitors are restricted to osteoblastic differentiation but periosteal progenitors have osteoblastic and chondrocytic bi-potential.”<-It isn’t necessarily true that endosteal progenitors are restricted to osteoblast differentiation it could be influenced by the microenvironment.

Macrophages in bone fracture healing: Their essential role in endochondral ossification.

“In fracture healing, skeletal and immune system are closely interacting through common cell precursors and molecular mediators. It is thought that the initial inflammatory reaction, which involves migration of macrophages into the fracture area, has a major impact on the long term outcome of bone repair. Interestingly, macrophages reside during all stages of fracture healing. Thus, we hypothesized a critical role for macrophages in the subsequent phases of bone regeneration. This study examined the impact of in vivo induced macrophage reduction, using clodronate liposomes, on the different healing phases of bone repair in a murine model of a standard closed femoral fracture. A reduction in macrophages had no obvious effect on the early fracture healing phase, but resulted in a delayed hard callus formation, thus severely altering endochondral ossification. Clodronate treated animals clearly showed delayed bony consolidation of cartilage and enhanced periosteal bone formation. Therefore, we decided to backtrack macrophage distribution during fracture healing in non-treated mice, focusing on the identification of the M1 and M2 subsets. We observed that M2 macrophages were clearly prevalent during the ossification phase. Therefore enhancement of M2 phenotype in macrophages was investigated as a way to further bone healing. Induction of M2 macrophages through interleukin 4 and 13 significantly enhanced bone formation during the 3week investigation period. These cumulative data illustrate their so far unreported highly important role in endochondral ossification and the necessity of a fine balance in M1/M2 macrophage function, which appears mandatory to fracture healing and successful regeneration.”

The failure of endochondral ossification was macrophage specific and not indirectly related to osteoclasts.  Osteoclasts and macrophages come from the same progenitor cell.