Finger stretcher

We know that the jaw bone can grow throughout adulthood via endochondral ossification of the articular cartilage. This may be why we see people with acromegaly have very large jaws. The reason that the jaw bone continues to grow at the articulations and the other bones don’t is because the jaw bone is less constrained by ligaments and is very moveable so the stress that the articular cartilage undergoes is enough to induce articular cartilage endochondral ossification and also the lateral pterygoid muscle is attached to the articular cartilage directly so if you stimulate the lateral pterygoid muscle in any way either via forced mouth opening or a bite jumping appliance you get the pull with if it’s sufficient results in articular cartilage endochondral ossification. You can literally see this in the histological slides in the above link. The problem is that this likely occurs very slowly unless cell turnover is highly accelerated like via HGH which occurs in acromegaly.

So there are two problems why we don’t see more development of the jaw in normal individuals:

1) The lateral pterygoid muscle isn’t stimulated enough because they don’t chew strong enough food or they don’t practice “mewing“(which does stimulate the lateral pterygoid muscle by the way and it’s slightly dynamic as while you are moving around your muscles have to adjust to keep your tongue to the roof of the mouth). And it’s possible that normal strength training exercise will also stimulate lateral pterygoid development. An exercise like the deadlift pulls on every muscle in the body but that pull won’t be as strong as if you train the lateral pterygoid muscle directly.

2) articular cartilage endochondral ossification is very slow unless again it’s accelerated by HGH.

One problem with the device is that you can’t really do anything else while using it. You might as well just pull on your fingers directly. The other problem I see is that the device doesn’t really look like it would stretch the articular cartilage directly. It looks like it would mostly stretch the skin.

We’d have to really look at the pull to see if it was pulling directly at the articular cartilage. The best bet in my mind to provide a sufficient stretch on the articular cartilage would be a twisting or bending motion of the joint. This would get around the issue of the ligaments limiting the potential stretch. The issue would be potential cartilage damage from improper joint movement. Also based on joint mechanics it may still not stretch the articular cartilage in a sufficient manner.

Sea cucumber is available for sale but it is very expensive.  I found some sea cucumber tablets that were cheap however it’s not for certain that the tablets have all the benefits of eating sea cucumbers directly.

Novel Peptides from Sea Cucumber Intestine Hydrolysates Promotes Longitudinal Bone Growth in Adolescence Mice through Accelerating cell cycle progress by Regulating Glutamine Metabolism

“Sea cucumber intestines are recognized as a major by-product in sea cucumber processing industry and have been shown to have antioxidant properties. However, whether the sea cucumber intestine is beneficial to osteogenic remains unknown. In this study, low molecular weight rich in glutamate/glutamine peptides were obtained from sea cucumber intestines (SCIP) by enzymatic hydrolysis, and orally administered to adolescent mice to investigate the effects on longitudinal bone growth. The results showed that the SCIP supplement significantly increased the femur length and new bone formation rate by 9.6% and 56.3%, and elevated the serum levels of osteogenic markers ALP, Collagen I and OCN{this is pretty nuts.  I couldn’t find studies directly measuring what effect glutamine has on longitudinal bone growth directly}. Notably, H&E staining showed that SCIP significantly increased the height of the growth plate, in which the height of the proliferation zone was elevated by 97.4%. Glutamine is a major determinant of bone growth. We found that the SCIP supplement significantly increased glutamine levels in the growth plate by 44.2% and elevated the expression of glutamine metabolism-related enzymes Gls1 and GLUD1 in the growth plate{so it’s possible that sea cucumbers could have a benefit on glutamine in the growth plate due to some other ingredient in the cucumber other than the glutamine itself}. Further, SCIP upregulated growth plate acetyl coenzyme A levels to promote histone acetylation and accelerated cell cycle progression by upregulating Sox9 expression, thereby contributing to the rapid chondrocyte proliferation. To our best knowledge, this is the first report that SCIP could enhance longitudinal bone growth via promoting growth plate chondrocyte proliferation. Our present study will provide new ideas and a theoretical basis for high-value utilization of sea cucumber intestine.”

“the peptide from Euphausia superba promoted longitudinal bone growth in adolescent mice.  supplement with enzymatic hydrolysate of Stichopus japonicus could promote bone formation in vivo and in vitro.”

“the avascular nature of the growth plate makes glutamine a potential factor for regulating longitudinal bone growth”

“the SCIP supplement significantly increased femur length by 6.8% (SCIP-L{LOW DOSE}) and 9.6% (SCIP-H{High dose}) compared with the normal group”<-so we don’t know if even more is better than the doses mentioned.  The effect of growth plate height, proliferative height, and hypertrophic chondrocytes was also greater based on dose.

“the serum glutamine levels were gradually increased to a maximum between 0.25 h and 0.5 h and returned to baseline after 2 h. Conversely, as serum glutamine levels fell back, glutamine levels in muscle and femur peaked sequentially at 2 h and 3 h.”<-theoretically it could be worthwhile to take glutamine every 2 hours which would be very difficult to do.

“glutamine metabolism has been shown to upregulate chondrocyte proliferation genes (especially Sox9) by epigenetic modification”<-obviously epigenetic modification is very powerful.

“glutamine promoted the growth plate chondrocyte proliferation during endochondral ossification through acetylation modification of the histone 3K9”

So they did have a glutamine only group.  And the sea cucumber growth increased growth plate height further than that.  Also if you look at the growth plates, it’s a pretty dramatic difference.

Based on the information in this paper, it may be worthwhile for everyone growing to take a low cost sea cucumber supplement(i’d say actual sea cucumber is too expensive).  Not only for the growth plate but also joint cartilage.

This study Stichopus chloronotus aqueous extract as a chondroprotective agent for human chondrocytes isolated from osteoarthitis articular cartilage in vitro finds that sea cucumber has anabolic effects on articular cartilage.

I happened to get x-rays a year ago.  I was performing bone tapping at the time and was unable to get a copy of them because I couldn’t find any computer that would play a CD.  I found something that maybe an abnormality and evidence that bone tapping can induce changes in bone morphology but since I don’t have before and after I can’t be sure.  Like I said I just happened to have had xrays ordered.

Here’s the image of what may be an abnormality(if requested I can post full versions of all three xrays I have):

Here’s another tibia x-ray:

Above is a normal tibial x-ray.  Also here the x-rays of someone who performed LSJL.  Essentially the area circled in red looks clearer(less dense) than normal.  Is that indicative of neo-bone formation?  I can’t be sure.  So if someone could find an expert that would be helpful.  I can also provide copies of all the x-rays.  Please comment or email if you can help.

New study related to lateral synovial joint loading:

Knee Loading Enhances the Migration of Adipose‑Derived Stem Cells to the Osteoarthritic Sites Through the SDF‑1/CXCR4 Regulatory Axis

“Osteoarthritis (OA) is a whole joint disorder that is characterized by cartilage damage and abnormal remodeling of subchondral bone. Injecting adipose-derived stem cells (ASCs) into the knee joint cavity can assist in repairing osteoarthritic joints, but their ability to migrate to the damaged site is limited. Our previous studies have shown that knee loading can improve the symptoms of OA, but the effect and mechanism of knee loading on the migration of ASCs in OA remain unclear. We employed a mouse model of OA in the knee and applied knee loading (1 N at 5 Hz for 6 min/day for 2 weeks) after the intraarticular injection of ASCs. The cartilage and subchondral bone repair were assessed by histopathological analysis. Immunofuorescence assays were also used to analyze the migration of ASCs. Using cell cultures, we evaluated the migration of ASCs using the transwell migration and wound healing assays. In vivo experiments showed that knee loading promoted the migration of ASCs, increased the local SDF-1 level, and accelerated the repair of the OA-damaged sites. Mechanistically, the observed effects were blocked by the SDF-1/CXCR4[SDF-1/CXCR4 promotes neovascularization which is great] inhibitor. The in vitro results further revealed that knee loading promoted the migration of ASCs and the inhibition of SDF-1/CXCR4 significantly suppressed the beneficial loading effect. The results herein suggested that the migration of ASCs was enhanced by knee loading through the SDF-1/CXCR4 regulatory axis, and mechanical loading promoted the joint-protective effect of ASCs”

Now we don’t know how much more lateral knee loading stimulates neo-vascularization etc. than regular exercise.  Nor do we know if knee loading promotes subchondral bone repair independently of adipose derived stem cells.  But neovascularization and new cartilage formation are very important findings that could potentially be linked to what’s needed to grow taller.

“A variety of physical rehabilitation regimens can afect the remodeling process of articular cartilage and subchondral bone and alter the symptoms of OA, such as whole-body vibration, axial loading, and bending loading. The knee loading modality, developed by our laboratory, is a mild non-invasive physical therapy, which applies transverse loading to a synovial joint, such as the elbow, knee, and ankle. Knee loading has been shown as an effective loading option for improving OA symptoms. Previous studies showed that knee loading reduced MMP13 activity and prevented OA-induced cartilage degeneration through cross-talk of the cartilage with subchondral bone. Mechanical loading also mitigated OA symptoms by regulating the stress to the endoplasmic reticulum and autophagy. Further, knee loading facilitated repairing osteoporotic OA by relieving the abnormal remodeling of the subchondral bone via Wnt/β-catenin signaling. It contributed to promoting the diferentiation of MSCs into osteogenic and chondrogenic fates”

“Stromal cell-derived factor 1 (SDF-1), a chemokine of a CXC family, and its receptor CXC chemokine receptor 4 (CXCR4) exist widely in the body, and they regulate a variety of physiological processes, including cell proliferation, migration, adhesion, differentiation, and wound healing ”

“A total of 108 female C57BL/6 mice (14 weeks old, Animal Center of Academy of Military Medical Sciences, China) were used.”<-not quite as old as we would like.

“After the induction of OA, mice were injected with GFP-ASCs, followed by daily knee loading for 2 weeks. The injected ASCs in the knee joints of all groups were identified by immunofuorescence staining with antibodies against GFP. In vivo studies showed that GFP-positive cells were found in the OA cartilage 2 weeks after their injections”

” The number of chondrocytes and vacuolar cells was counted. The number of chondrocytes in the OA group was significantly decreased compared to the sham-treated control group, but the number was restored by knee loading or the injection of ASCs”<-it’s very promising that the chondrocyte number was restored be knee loading independently of stem cell injection but again these mice are not as old as we would like.

” IHC analysis showed that collagen II-positive cells in the OA group were significantly decreased. However, the numbers in the OAL group and OA+ASCs group were increased.”<-again very promising that collagen II positive cells were increasing independently of ASC injection

In the top images you can see that the mice still have their growth plate.  It’d be hard to distinguish between changes in the bone caused by Osteoarthritis and those caused by loading.  But if you look at the loaded groups(Loading with and without ASC) you can see in red cartilage in places that did not have cartilage in either the control or the osteoarthritis group at the longitudinal ends of the bone.  And you don’t really see that in the OA+ASC group.  I could be reading it wrong though.

Again here you see cartilage at the sides of the longtiduinal ends of the bone that you don’t really see in the non-loaded groups.