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”

Update:  I’m still working on a new non-LSJL method.

I don’t believe that chocolate can make you wildly taller but it tastes good.  I also think the optimal diet for longitudinal bone growth varies on developmental stage.

Chocolate and Chocolate Constituents Influence Bone Health and Osteoporosis Risk

“Bone loss resulting in increased risk of osteoporosis is a major health issue worldwide. Chocolate is a rich source of antioxidant/anti-inflammatory flavonoids as well as dietary minerals with the potential to benefit bone health. However, other chocolate constituents such as cocoa butter, sugar and methylxanthines may be detrimental to bone. Human studies investigating the role of chocolate consumption on serum bone markers and bone mineral density (BMD) have been inconsistent. A contributing factor is likely the different composition and thereby, nutrient and bioactive content amongst chocolate types. White, followed by milk chocolate, are high in sugar and low in flavonoids and most minerals. Dark chocolate (45-85% cocoa solids) is high in flavonoids, most minerals, and low in sugar with ≥70% cocoa solids resulting in higher fat and methylxanthine content. The aim of this review was to examine the relationship between consuming chocolate, its flavonoid content, and other chocolate constituents on bone health and osteoporosis risk. Studies showed postmenopausal women had no bone effects at moderate chocolate intakes; whereas, adolescents consuming chocolate had greater longitudinal bone growth{whether this fact can be used for any purpose though….}. Based on flavonoid and mineral content, unsweetened cocoa powder appeared to be the best option followed by dark chocolate with higher cocoa content in terms of supporting and preserving bone health. Determining dietary recommendations for chocolate consumption regarding bone health is important due to the growing popularity of chocolate, particularly dark chocolate, and an expected increase in consumption due to suggestions of health benefits against various degenerative diseases.”

“Diets that promote bone health have mainly focused on increasing Ca and
vitamin D consumption, but there is growing interest in phytochemicals[chemicals produced by plants]”

“Dietary polyphenols consist of a large group of plant-derived secondary metabolites
divided into four different classes, one of which is the flavonoids (diphenylpropanes C6-C3-C6).
Flavonoids contain several classes of bioactive compounds.  There is evidence
that intake of specific flavonoids may promote bone health including: soybean isoflavones (e.g. genistein{genistein may increase HSP90 levels and HSP90 definitely affects the growth plate but in some instances it stimulated growth and some incidences suppressed it} and daidzein), flavonols (e.g. aglycone quercetin{quercetin definitely impacts factors involved in longitudinal bone growth but the evidence is not that strong}) found in plums, and flavonones (e.g. hesperidin) found in citrus pulp and juice.  Another food source noted for its flavonoid content is chocolate.  Cocoa, a major constituent in chocolate, has the highest flavanol content of all foods on a per-weight basis and contributes to greater total dietary intake of flavonoids than tea, fruits, and vegetables ”

“Both animal models and human clinical trials have reported an inverse association
between reactive oxygen species (ROS) and bone health.  ROS can affect bone cells in
various ways including stimulation of osteoblast apoptosis and senescence and by upregulation of receptor activator of nuclear factor kappa-B ligand (RANKL) to activate osteoclast differentiation and bone resorption”<-I think though there is a role for ROS.  It’s just too many is a bad thing.  And bone can be inhibitory towards longitudinal bone growth but it’s degradation of bone(bone turnover) not degradation of bone building cells that would be beneficial.

“catechins preserved bone-forming osteoblasts by exerting anti-inflammatory actions”

” In a randomized, double-blinded placebo-controlled study, pre-pubertal (n=149, age 6.6-9.4 years) girls consumed two Ca-supplemented food products daily to achieve a Ca dose of 850 mg/d.  Results showed consuming Ca-supplemented chocolate bars, cakes or cocoa beverages for 48 weeks significantly increased height and bone mass acquisition in the radius and femur”

“Feeding murine dams chow diet supplemented with 400 mg unsweetened chocolate during pregnancy and lactation resulted in progeny with significantly shortened forefeet and hindlimbs.  Vascular endothelial growth factor (VEGF), which plays a role in ontogenesis and longitudinal bone growth related to angiogenesis in the epiphyseal growth plate, was significantly reduced in the femora of immature (age 4-weeks old) mice pups exposed perinatally to chocolate.  A follow-up study investigating the relationship of the chocolate constituent, catechins on angiogenesis and bone mineralization in the progeny of murine dams fed chocolate showed a negative correlation between embryo tissue epigallocatechin concentration and mean number of newly-formed blood vessels.  Crystallinity of compact bone of diaphyses was 17% greater and femoral epiphyseal cancellous bone was 30% greater in pups age 4-weeks old exposed perinatally to chocolate compared to pups from control dams.  The authors suggested anti-angiogenic activity of chocolate catechins disturbed the processes of bone elongation and mineralization “<-so chocolate may be better at different stages.

Here’s the study on chocolate(along with other calcium enriched foods) consumption in girls:

Calcium–enriched foods and bone mass growth in prepubertal girls: a randomized, double-blind, placebo-controlled trial.

“High calcium intake during childhood has been suggested to increase bone mass accrual, potentially resulting in a greater peak bone mass. Whether the effects of calcium supplementation on bone mass accrual vary from one skeletal region to another, and to what extent the level of spontaneous calcium intake may affect the magnitude of the response has, however, not yet been clearly established. In a double-blind, placebo–controlled study, 149 healthy prepubertal girls aged 7.9+/-0.1 yr (mean+/-SEM) were either allocated two food products containing 850 mg of calcium (Ca-suppl.) or not (placebo) on a daily basis for 1 yr. Areal bone mineral density (BMD), bone mineral content (BMC), and bone size were determined at six sites by dual-energy x-ray absorptiometry. The difference in BMD gain between calcium-supplemented (Ca-suppl.) and placebo was greater at radial (metaphysis and diaphysis) and femoral (neck, trochanter, and diaphyses) sites (7-12 mg/cm2 per yr) than in the lumbar spine (2 mg/cm2 per yr). The difference in BMD gains between Ca-suppl. and placebo was greatest in girls with a spontaneous calcium intake below the median of 880 mg/d. The increase in mean BMD of the 6 sites in the low-calcium consumers was accompanied by increased gains in mean BMC, bone size, and statural height. These results suggest a possible positive effect of calcium supplementation on skeletal growth at that age. In conclusion, calcium–enriched foods significantly increased bone mass accrual in prepubertal girls, with a preferential effect in the appendicular skeleton, and greater benefit at lower spontaneous calcium intake.”

“Both statural height and body weight, however, were significantly greater among the spontaneously high- versus low-calcium consumers (129.160.7 vs. 126.560.7 cm, P , 0.001; 27.560.5 vs. 25.760.5 kg, P , 0.001, respectively). ”

There were several non calcium enriched foods in the study and not just chocolate so it’s likely the calcium and not the chocolate making the girls taller.

Ischemia is reduced blood supply to an organ(in our case we would be interested in cartilage and bone).

“Ischemic osteonecrosis is a process that involves impaired outflow of blood from the marrow space, increased intramedullary blood pressure, and reduced blood flow circulation in the bone marrow. This results in the death of osteocytes and other marrow tissues.” from Ischemic Osteonecrosis.  Now obviously osteonecrosis is not what we want but there’s a difference between doing cardio to induce an oxygen debt and choking yourself to death.  It’s a matter of severity.  If we can induce healthy, moderate ischemia(“Ischemia is a restriction in blood supply to tissues”) then that may be enough for neo chondrogenesis.  Maybe via something like occlusion bands?  It looks like intramedullar pressure is not what can induce possible chondrogenic adaptation but likely enhanced blood flow as a result of transient ischemia.

They’ve already kind of studied the effects of knee loading on osteonecrosis and found that it protects against it in “Knee loading protects against osteonecrosis of the femoral head by enhancing vessel remodeling and bone healing“

But we know that osteonecrosis increases intramedullary pressure so we can study this to see if it can prove that theory that increase intramedullary pressure can induce neo-chondrogenesis.

“Intramedullary pressures in osteonecrosis can be 5 times greater than normal because of backup pressure.”

“Shock wave therapy is based on the principles of ultrasonic lithotripsy and success in treating orthopedic neuralgias. Inducing micro-trauma by treatment of ischemic jawbones with an extra-oral ultrasonic wand can induce new circulation and bone regrowth”

“Where there is more bleeding, more bone will follow.” <-it’s probably not the ischemia that can induce anabolic effects but the overcompensation that occurs when blood flow returns to normal.  Sort of like the oxygen debt and exercise.  It may be the changes in blood flow that have the beneficial effects rather than the restriction itself.

Femoral Head Deformation and Repair Following Induction of Ischemic Necrosis

“Ischemic necrosis of the femoral head can be induced surgically in the piglet. We used this model to assess femoral head deformation and repair in vivo by sequential magnetic resonance imaging and by correlating end-stage findings with histologic assessments.

Ischemic necrosis of the femoral head was induced in ten three-week-old piglets by tying a silk ligature around the base of the femoral neck (intracapsular) and cutting the ligamentum teres. We used magnetic resonance imaging with the piglets under general anesthesia to study the hips at forty-eight hours and at one, two, four, and eight weeks. Measurements on magnetic resonance images in the midcoronal plane of the involved and control sides at each time documented the femoral head height, femoral head width, superior surface cartilage height, and femoral neck-shaft angle. Histologic assessments were done at the time of killing.

Complete ischemia of the femoral head was identified in all involved femora by magnetic resonance imaging at forty-eight hours. Revascularization began at the periphery of the femoral head as early as one week and was underway in all by two weeks. At eight weeks, magnetic resonance imaging and histologic analysis showed deformation of the femoral head and variable tissue deposition. Tissue responses included (1) vascularized fibroblastic ingrowth with tissue resorption and cartilage, intramembranous bone, and mixed fibro-osseous or fibro-cartilaginous tissue synthesis and (2) resumption of endochondral bone growth{Obviously resumption of endochondral bone growth in adults would be what we want}. At eight weeks, the mean femoral head measurements (and standard error of the mean) for the control compared with the ligated femora were 10.4 ± 0.4 and 4.8 ± 0.4 mm, respectively, for height; 26.7 ± 0.8 and 31.2 ± 0.8 mm for diameter; 1.1 ± 0.1 and 2.3 ± 0.1 mm for cartilage thickness; and 151° ± 2° and 135° ± 2° for the femoral neck-shaft angle. Repeated-measures mixed-model analysis of variance revealed highly significant effects of ligation in each parameter (p < 0.0001).

Magnetic resonance imaging allows for the assessment of individual hips at sequential time periods to follow deformation and repair. There was a variable tissue response, and histologic assessment at the time of killing was shown to correlate with the evolving and varying magnetic resonance imaging signal intensities. Femoral head height on the ischemic side from one week onward was always less than the initial control value and continually decreased with time, indicating collapse as well as slowed growth. Increased femoral head width occurred relatively late (four to eight weeks), indicating cartilage model overgrowth concentrated at the periphery.”

“At higher magnification, the tissue was vascularized fibrocartilage.”<-this is good because fibrocartilage indicates possibly new cartilage(neo growth plates).

“Increased vessels within the lateral epiphyseal cartilage were frequently seen, many of which eventually became associated with ectopic foci of endochondral ossification.”<-ectopic means abnormal which could mean new growth plates.

“Greater cartilage height was observed in the ligated group compared with contralateral, control femoral heads at two weeks (F = 9.6, p = 0.003), four weeks (F = 33.4, p < 0.0001), and eight weeks (F = 55.7, p < 0.0001).”

Quantification of Angiogenesis in Otosclerosis

“The determinants of clinical versus histologic otosclerosis{“Otosclerosis is a condition where one or more foci of irregularly laid spongy bone replace part of normally dense enchondral layer of bony otic capsule in the bony labyrinth.”} are unknown, but angiogenesis is associated with active disease. We hypothesized that quantification of angiogenesis in otosclerotic human temporal bones could reveal significant differences between clinical and histologic cases.

Study Design: We reviewed all otosclerosis specimens meeting criteria from the temporal bone collection of the Massachusetts Eye and Ear Infirmary and 10 normal controls.

Methods: Digital images were taken at predilection sites, followed by computer‐assisted analysis. Canalicular area (CA), the aggregate of vascular spaces within bone, microvessel density (MVD), area, and depth were the main measures. Evidence of a direct connection between local vessels and the vasculature of the otosclerotic focus was also recorded for each specimen.

Results: The average area (mm²) and depth (number of sections containing otosclerosis) of clinical lesions was significantly greater than histologic lesions. Total microvessel counts were significantly greater in clinical versus histologic lesions, and both clinical and histologic lesions contained significantly greater numbers of microvessels than the normal otic capsule. CA was also significantly higher in clinical lesions. MVD was slightly but not significantly higher in clinical lesions. Importantly, a direct connection between named vessels and the otosclerotic vasculature was significantly more frequent in clinical lesions.

Conclusions: Computer‐assisted quantification revealed significantly greater measures of angiogenesis in clinical versus histologic otosclerosis. Direct connection to adjacent vessels may support angiogenesis in this disease. Sustained angiogenesis may be an important determinant of clinical otosclerosis.”

“otosclerosis resulted from instability in embryonic cartilage rests called “globuli interossei.” Because these rests are remnants of incomplete endochondral ossification, one possibility is that otosclerotic bone represents resumption of arrested endochondral ossification in the globuli interossei.”

“Indirect evidence for resumed endochondral ossification within the globuli interossei exists in otosclerotic temporal bones: otosclerotic bone demonstrates a woven pattern on polarized light microscopy identical to immature woven bone formed at sites of endochondral ossification“

“Angiogenesis is critical for the conversion of cartilage to bone to the extent that animal models of endochondral ossification are used to assess candidate angiogenesis inhibitors”

“The development of otosclerosis requires angiogenesis, which may reflect resumed endochondral ossification of the globuli interossei.”

Quantifying the effect of ischemia on epiphyseal growth in an extremity replant model

“Warm ischemia (21°C) of 0, 2, 4, 6, or 8 hours was produced in a modified hindlimb preparation of 35 10-week-old Lewis rats by amputation. Subsequent microvascular anastomoses of each hindlimb to a syngeneic animal was done after which fluorochrome bone labels were administered 5 minutes after operation and on day 14 after operation. Epiphyseal plate growth (that between bone labels) was analyzed histomorphometrically and statistically. Epiphyseal plate growth was found to have a linear inverse relationship to ischemia time. Overgrowth occurred at all ischemic periods except 8 hours, and vascular pedicle patency decreased as ischemia time progressed.”

“Early clinical reports suggested that epiphyseal growth after replantation might be an all-or-none phenomenon, with overgrowth not uncommon”

“warm ischemia in a young rat hindlimb replant model. In general, at time periods of total warm ischemia between 0 and 4 hours, epiphyseal overgrowth (up to three times that of control hindlimbs) and excellent vascular pedicle patency may be expected. At 6 hours of total warm ischemia some minor epiphyseal overgrowth and good to fair vascular patency can be expected. At 8 hours of total warm ischemia and later, normal or retarded epiphyseal growth and poor vascular patency rates are expected.”

That 8 hours did not induce overgrowth likely means that the growth stimulation is not due to the ischemia itself but due to the compensation afterwards.

Ischemia’s effects may be due to hypoxia.

Effect of Hypoxia on Gene Expression of Bone Marrow‐Derived Mesenchymal Stem Cells and Mononuclear Cells

“MSC have self‐renewal and multilineage differentiation potential, including differentiation into endothelial cells and vascular smooth muscle cells. Although bone marrow‐derived mononuclear cells (MNC) have been applied for therapeutic angiogenesis in ischemic tissue, little information is available regarding comparison of the molecular foundation between MNC and their MSC subpopulation, as well as their response to ischemic conditions. Thus, we investigated the gene expression profiles between MSC and MNC of rat bone marrow under normoxia and hypoxia using a microarray containing 31,099 genes. In normoxia, 2,232 (7.2%) and 2,193 genes (7.1%) were preferentially expressed more than threefold in MSC and MNC, respectively, and MSC expressed a number of genes involved in development, morphogenesis, cell adhesion, and proliferation, whereas various genes highly expressed in MNC were involved in inflammatory response and chemotaxis. Under hypoxia, 135 (0.44%) and 49 (0.16%) genes were upregulated (>threefold) in MSC and MNC, respectively, and a large number of those upregulated genes were involved in glycolysis and metabolism. Focusing on genes encoding secretory proteins, the upregulated genes in MSC under hypoxia included several molecules involved in cell proliferation and survival, such as vascular endothelial growth factor‐D, placenta growth factor, pre‐B‐cell colony‐enhancing factor 1, heparin‐binding epidermal growth factor‐like growth factor, and matrix metalloproteinase‐9[extracellular matrix remodeling], whereas the upregulated genes in MNC under hypoxia included proinflammatory cytokines such as chemokine (C‐X‐C motif) ligand 2 and interleukin‐1α. Our results may provide information on the differential molecular mechanisms regulating the properties of MSC and MNC under ischemic conditions.”

There are some anabolic genes in here(table 2).

Anabolic Pathways(table 4).

Spontaneous regeneration can occur after osteonecrosis

Spontaneous regeneration of the mandible following hemimandibulectomy for medication-related osteonecrosis of the jaw

“oral function including mobility of the tongue and buccal mucosa may influence spontaneous regeneration of the mandible”

GIRK3 deletion facilitates kappa opioid signaling in chondrocytes, delays vascularization and promotes bone lengthening in mice

“Activation of G protein-coupled receptor (GPCR) signaling pathways is crucial for skeletal development and long bone growth.  protein-gated inwardly-rectifying K⁺ (GIRK) channel genes are key functional components and effectors of GPCR signaling pathways in excitable cells of the heart and brain, but their roles in non-excitable cells that directly contribute to endochondral bone formation have not been studied. In this study, we analyzed skeletal phenotypes of Girk2^−/−, Girk3^−/− and Girk2/3^−/− mice. Bones from 12-week-old Girk2^−/− mice were normal in length, but femurs and tibiae from Girk3^−/− and Girk2/3^−/− mice were longer than age-matched controls at 12-weeks-old. Epiphyseal chondrocytes from 5-day-old Girk3^−/− mice expressed higher levels of genes involved in collagen chain trimerization and collagen fibril assembly, lower levels of genes encoding VEGF receptors, and produced larger micromasses than wildtype chondrocytes in vitro. Girk3^−/− chondrocytes were also more responsive to the kappa opioid receptor (KOR) ligand dynorphin, as evidenced by greater pCREB expression, greater cAMP and GAG production, and upregulation of Col2a1 and Sox9 transcripts. Imaging studies showed that Kdr (Vegfr2) and endomucin expression was dramatically reduced in bones from young Girk3^−/− mice, supporting a role for delayed vasculogenesis and extended postnatal endochondral bone growth. Together these data indicate that GIRK3 controls several processes involved in bone lengthening.”

“GIRK channels are homo- and hetero-tetramers formed by four mammalian GIRK subunits (GIRK1/Kcnj3, GIRK2/Kcnj6, GIRK3/Kcnj9, and GIRK4/Kcnj5). GIRK channels are activated when GPCR ligands stimulate pertussis toxin-sensitive G_i/o-G proteins; the liberated Gβγ subunit then binds to GIRK channels and increases their gating. The resultant efflux of K⁺ reduces the excitability of neuronsand cardiomyocytes. Knockout studies in mice have shown that GIRK2-containing GIRK channels mediate pain relief evoked by opioids and other analgesics. In chondrocytes, K⁺ efflux reduces swelling during unloading and can affect proteoglycan secretion”<-so maybe GIRK2 and GIRK3 knockouts have more chondrocyte hypertrophy and are more responsive to mechanical loading.

“GIRK2 mutations in patients with Keppen Lubinsky syndrome, which is characterized by growth above the 50th to 75th percentile at birth with subsequent developmental delays and other phenotypes “

“Girk3 deletion increases femur and tibia lengths and augments kappa opioid signaling in chondrocytes. Thus, these data identify GIRK3 as a suppressor of bone lengthening and kappa opioid activity in developing skeletons.”

“Numerous GPCR-signaling pathways, including kappa opioids, influence growth.”

Need to get the full paper and research more on GIRK3.

I’m still working on height increase.  Just doing more independent research and learning more about anatomy and physiology and actions of cells as the research I’m looking at is a lot of the same old, same old.  Maybe the key is to look at older studies before things were set in their ways.  It seems in the old days they were willing to try new risks to get people to grow taller.

Essentially the study found that heat did not increase bone length however there was some promise in that decalcification could be caused by the heat and that could enable longitudinal bone growth.  And the study shows islands of cartilage which could be the creation of new growth plates which is quite promising.  But the heat itself actually didn’t stimulate the growth plate itself.  It was only the heat degeneration the calcified bone matrix and stimulating the creation of growth plate islands that incurred new growth.

The effect of heat upon the growth of bone

“GROWTH in length of long bones consists of two mutually independent processes, the division and palisade arrangement of cartilage cells, and the subsequent calcification of the matrix between these cells and its replacement by bone. It is generally agreed that growth is dominated by the activities of the cells of the reserve zone and those in the adjacent apex of the cartilage columns. The subsequent enmeshment, of hypertrophic cartilage cells within a calcified matrix must prevent elongation at other sites. Recent attempts to stimulate the growth of bone have been based upon the production of an irritative lesion within the metaphysis, stimulating ossification rather than cartilage-cell division. ”

“Chapchal and Zeltienrust (1947-48) reported an inconstant increase in the rate OF growth in the rabbit after the insertion of metal or ivory pins within the metaphysis. Wilson (1952) using copper and constantan wire in the dog produced similar results. The application of these methods to limb inequality in children has been reported by Pease (1962). Metal or ivory screws WPI’P inserted transversely into the metaphysis of the femur and tibia. Each of the seven children subjected to this procedure showed an increase in the rate of growth of the shorter limb, but equalization of length was not attained. ”

“The overgrowth of bone which is constantly seen after fractures, in the presence of arteriovenous aneurysms, and in association with bone and joint infections”

arteriovenous aneurysm an abnormal communication between an artery and a vein in which the blood flows directly into a neighboring vein or is carried into the vein by a connecting sac.<-Lateral loading can increase blood flow.  Though this probably won’t work without existing growth plates.

“increase in the length of a limb following the production of an arteriovenous fistula in the dog”

“One of the clinical features of most cases of limb elongation with an increase in the temperature of the skin, and in the arteriovenous aneurysm this is associated with an increase in the temperature of bone”

“The rate of growth of the ulna was in some animals slightly depressed, in rabbit 480 markedly SO. In this animal there was considerable formation of new bone around tJie resistor, although the epiphyseal cartilage appeared normal. The overgrowth of the ulna noted in rabbit 465 was not associated with any abnormal histological appearance of the epiphyseal cartilage and the radiographs suggest that the discrepancy may have been due to a disturbance of growth in the control limb. The radiographs also show a relative decalcification of the the whole of the treated forelimb and this may have been associated with a generalized hyperemia{excess of blood in the vessels} of this limb.”

“Where the heating level was high, the epiphyseal cartilage is affected. The earliest changes in this region are an irregularity of the cartilage columns and a granularity of the matrix. When cellular destruction occurs it is at first confined to the region of the apex of the cartilage columns and is associated with fibrillation of the cartilage matrix. ”

“In only one animal (465) did an increase in bone length occur. This animal was heated for two days and, the wires having broken, the resistor was left unheated for a further 36 days. Although the increase in length of the limb was considerable, aid was associated with a generalized decalcification of the forelimb, suggesting an increase in the vascularity of this member, the difference in length of the limbs may have been due to some abnormality of growth on the control side. “<-So decalcification is key to growing taller.  High levels of heat can was found to cause necrosis which reduced growth but if decalcification can enhance growth.  Then maybe heat could enhance growth by decalcifying bones.

“heat has been shown to stimulate the production of cartilage around the resistor and to produce islands of endochondral ossification within the bony epiphysis and along the shaft of the radius.”<-islands of endochondral ossification is promising because it shows new induction of bone growth.

“Islands of cartilage were produced within the bony epiphysis close to the resistor, and along the ulnar border of the radial shaft. Some of them islands showed endochondral ossification, but there was no increase of cellular activity in the epiphyseal cartilage. A large cartilaginous mass developed in the region where the resistor was buried, and, in many animals, the transverse diameter of the metaphysis was greatly increased. ”

Figure 8 is an image near the resistor so there should be islands of cartilage visible.  I can’t tell If there are cartilage islands or not and if there are cartilage islands we can’t say for sure whether they are not just broken off cartilage from the growth plate.  Cartilage islands within the diaphysis would be key to seeing if heat can induce new growth plates.

Here’s mentioned overgrowth.

I’m still working on my own device.   I’m not sure if the device listed here is stimulatory enough to induce longitudinal bone growth.  The device may be useful if you have existing growth plates.  But to grow taller you’d need bone breakdown to occur faster than bone buildup{so that cartilage has room to grow} and the device is optimized for bone buildup.

Development of an Artificial Finger-Like Knee Loading Device to Promote Bone Health.

“This study presents the development of an innovative artificial finger-like device that provides position specific mechanical loads at the end of the long bone and induces mechanotransduction in bone{So you could theoretically use your own fingers to see what such an a device would do; use your own fingers to press on the epiphysis of bone}. Bone cells such as osteoblasts are the mechanosensitive cells that regulate bone remodeling{in order to induce height growth you’d need a lot more than bone remodeling, you need to degrade cortical bone and induce MSC differentiation into chondrogenic cells}. When they receive gentle, periodic mechanical loads, new bone formation is promoted{how this bone formation is promoted is of importance of whether such a method can induce height growth}. The proposed device is an under-actuated multi-fingered artificial hand with 4 fingers, each having two phalanges. These fingers are connected by mechanical linkages and operated by a worm gearing mechanism. With the help of 3D printing technology, a prototype device was built mostly using plastic materials. The experimental validation results show that the device is capable of generating necessary forces at the desired frequencies, which are suitable for the stimulation of bone cells and the promotion of bone formation. It is recommended that the device be tested in a clinical study for confirming its safety and efficacy with patients.”

Cortical bone is highly inhibitory towards longitudinal bone growth.  You need to generate sufficient fluid flow to induce degradation of the cortical bone or you likely will not be able to grow taller.  I think it would take a lot of fluid flow for that to happen.  Maybe with very high frequency and duration with this device it would be possible.

” if a small magnitude of mechanical stimuli is applied at a high frequency, an osteogenic response can be stimulated via mechanotransduction in bone cells.”<-we don’t care about stimulating bone cells EXCEPT for osteoclasts.  We need to simulate stem cells to differentiate into chondrocytes.

“Osteocytes are the most abundant type of cells in bone tissue, and they constitute more than 90% of the cells in bone matrix. They are rooted in the calcified bone medium, and communicate with each other and with bone-forming osteoblasts through slender processes and gap junctions. Osteocytes are highly mechanosensitive. Haversian system or osteon, one of the key components of a porous bone matrix, encloses a blood vessel in its center and sets up the canals known as Haversian canals or Volkmann’s canals. Osteogenesis is induced by the process of osteoinduction in which premature cells are recruited, stimulated and developed into pre-osteoblasts{we just need to induce a microenvironment where premature cells are induced into pre-chondrocytes instead and one way to do that is via a high hydrostatic pressure environment which could be induced by manipulating fluid flow}. Osteogenesis can also result from osteoconduction which is the passive process of bone growth on surfaces such as bone-implant surfaces”

“When rapid mechanical loading is applied at the end of long bone (e.g., knee), it is proposed that the interstitial fluid present around the osteocytes in the lacuna-canalicular network induces a pressure gradient and elevates nutrient transport throughout the porous network. “<-interstitial fluid flow could do more than this.  If you have a lot of fluid flow it could induce shear that degrades the cortical bone that prevents longitudinal bone growth.