I am studying vibration due to some anecdotal success using the massage gun on fingers. Looking at vibration results I am seeing mixed results. Sometimes it results in degenerative changes but it is likely that vibration needs to be applied correctly to see results. I believe that like Lateral Synovial joint Loading, vibration would be more effective when applied laterally as that would be more effective in driving fluid flow within the bone. I have written about vibration in the past and in one study I saw that when vibration was applied growth plate parameters increased in the vibrated growth but bone length was about the same so it is possible that bone length at skeletal maturity could be longer in the vibrated group.

Attempt to stimulate longitudinal growth in the dog by mechanical vibration

“In animals, right- and left-handedness leads to larger bones on the dominant side.”

“six miniature partly threaded and self-tapping stainless-steel pins 3 mm in diameter (similar to Denham pins used in orthopaedic surgery) were inserted and allowed to penetrate the skin of the medial sides of the forelegs. The incision was loosely sutured between the pins. Stainless-steel bars were fixed to the ends of the protruding pins. These were grooved and cut to match the yokes on the vibrating rig described below.”<it’s possible these surgical incisions are a confounding factor to longitudinal bone growth.

“The amplitude of vibration was not markedly reduced; this was achieved by incorporating a stiff spring web in the system”

Here’s some images of the vibration mechanism:

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“The vibrator enabled the foreleg to be vibrated longitudinally with respect to the radius and ulna”<-so there’s some lateral and torsional loading here.

“In all, seven animals were experimented upon. The first (Dog 1) was experimented upon alone to see if
the study was humane and feasible. Subsequently, and after an encouraging result, four dogs were used
(Dogs 2A-D). In all of these the vibration was sinusoidal, the frequency 20 Hz and the peak-topeak amplitude 4 mm. Finally, in two more dogs (Dogs 3A and B) the same frequency was used but
the amplitude increased to 6 mm”

“As stated above, Dog 1 was used to test the feasibility of the experimental protocol. The result from this single test was an obvious lengthening of the vibrated side{!!!!!} and it indicated to us that
the study should be expanded. Therefore in Group 2, four animals were used, the experimental procedure
being similar except that the daily average vibration period was increased from 1-7h to 2.1h{so it’s possible that these animals did not increase in bone length due to “overtraining”}. The results of Group 2 were disappointing in that, in two dogs, there was actually a small reduction in growth in length on the vibrated side. Group 3 was a more vigorous test in which the amplitude of vibration was increased to 6-8 mm (peak-to-peak). The dogs tolerated this well but, again, no increase occurred. (In one other animal, pins were inserted on one side only and here there was a slight increase in length of both radius and ulna compared with the undisturbed side{so yes this means that the pins are a confounding variable}.)”

Here’s the exciting increase in bone length:

That is frigging massive. The bone looks a lot different in the length increased bone.

“The arteriograms obtained from Dog 1 before sacrifice showed a slight real increase in calibre of the digital vessels on the vibrated side. The difference did not warrant further arteriograms.”<-So vascularity could contribute to part of the increase?

“Histological examination of the growth plates and of the cortical bone at the site of the pins was unremarkable.”<-this is huge as it means that the increase in size could be unrelated to the growth plate i.e. meaning that it could work post skeletal maturity!!!!!

“The forces were transferred from the radius through the elbow and wrist joints to the arm and paw
respectively. In order to reach these joints, the forces must have passed through the upper and lower
growth plate respectively of the radius, and these will have been subjected to alternating compressive
and distracting forces.”<-one possibility is that the vibration may have induced longitudinal bone growth on the bone but damaged the growth plates. In skeletally mature individuals this would not be an issue as they do not have growth plates. Thus, it would be worthwhile to repeat the experiment on skeletally mature animals.

Here’s the study that was cited in the paper as being about vibration:

The effects of mechanical vibration on bone development in the rat

The study found bone decreased calcium content. This could play a role as the hardness of bone impedes intersititial(longitudinal) bone growth.

And this study too finds slight increase in longitudinal growth!:

“In one series of experiments. lasting for 5 weeks. 20 and 25 Hz was applied for 2.5 hr twice daily with 6
hr of rest intervening. In another series, which lasted for 4 months. the animals received 25 Hz for 12 hr each day without interruption”

So another result that indicates that perhaps by optimizing the vibration stimulus longitudinal bone growth is possible. Also interesting to note that in this study the non vibrated groups grow faster at first. I don’t know what conclusion to draw from that but it is something to explore.

So overall there is not a smoking gun to vibration and longitudinal bone growth but there is some smoke. So it is worth it to keep testing the massage gun method to see if the anecdotal reports continue to have promise. And it is entirely possible that once the method is optimized the results will be stronger than what is reported here.

If migration of stem cells can occur it means that potentially stem cells could migrate to form new growth plates and that cartilage could regenerate at articular cartilage sites potentially leading to height increase via articular cartilage endochondral ossification.

Mechanical Loading Promotes the Migration of Endogenous Stem Cells and Chondrogenic Differentiation in a Mouse Model of Osteoarthritis

“This study evaluated whether mechanical loading can enhance anabolic activities by facilitating the recruitment of stem cells for chondrogenesis{anabolic effects could potentially be used for non-osteoarthritic ie normal cartilage}. We evaluated cartilage degradation in a mouse model of OA through histology with H&E and safranin O staining. We also evaluated the migration and chondrogenic ability of stem cells using in vitro assays, including immunohistochemistry, immunofuorescence, and Western blot analysis. The result showed that the OA mice that received mechanical loading exhibited resilience to cartilage damage. Compared to the OA group, mechanical loading promoted the expression of Piezo1 and the migration of stem cells was promoted via the SDF-1/CXCR4 axis. Also, the chondrogenic diferentiation was enhanced by the upregulation of SOX9, a transcription factor important for chondrogenesis. Collectively, the results revealed that mechanical loading facilitated cartilage repair by promoting the migration and chondrogenic diferentiation of endogenous stem cells. This study provided new insights into the loading-driven engagement of endogenous stem cells and the enhancement of anabolic responses for the treatment of OA.”

A vacuole is a space within a cell that is empty of cytoplasm, lined with a membrane, and filled with fluid. Reduction in vacuoles could potentially that new bone is being formed.

“Mechanical stimulation affects the migration and differentiation of MSCs”

“We developed joint loading modalities in which dynamic lateral loads are applied to synovial joints”

“mechanical loading caused cyclic alteration of the intramedullary pressure, driving oscillatory
fluid flow and molecular transport in the lacunocanalicular network in the bone matrix and the medullary cavity”

“female C57BL/6 mice (~ 14 weeks of age, Animal Center of Academy of Military Medical Sciences, China) were used.”

Piezo1 is greater in loading groups even than non ostearthritic controls meaning LSJL(lateral synovial joint loading) meaning that joint loading should enhance stem cell migration in healthy controls.

joint loading promotes adhesion and migration compounds even above controls. These compounds could potentially help induce new cartilage and bone formation.

“Dynamic loads were sinusoidal at 1 N (peak-to-peak) and the frequency was 5 Hz for 6 min/day (each knee, 3 min).”

“After 2 weeks of mechanical loading, the level of Piezo1 in OA mice was significantly increased”

“knee loading contributed to repairing damaged cartilage by recruiting endogenous stem cells and stimulating chondrogenic differentiation.”

Here’s a diagram which explains how loading could be anabolic to cartilage and bone and potentially non osteoarthritic cartilage and bone as well.

The below study suggests that growth is manituable not only be nutrition but also by mechanical loading(tool use). It states that growth of some elements of the body is prioritized over others in times of nutrient restriction(“the thrity phenotype” hypothesis). Although this study is more geared to that nutrition can alter body height and skeletal length growth. Proving the plasticity(ability of bone to change in length) of bone is essential in proving that bone can change in response to mechanical loading.

Plasticity in the growth of body segments in relation to height-for-age and maternal education in Guatemala

“Plasticity in the growth of body segments between populations has been researched in relation to migration, temporal change and high-altitude studies{height seekers could potentially manipulate altitude or temperature}. We study the within population variation in body segments, thus controlling for some of the environmental and genetic differences that could be at play in between populations studies. We test a version of the thrifty phenotype hypothesis, where the growth of head-trunk and hand are prioritized due to their functional significance over height and leg growth.

A total of 3913 Guatemalan, rural, semi-urban and urban, Maya and Ladino children 6 to 15 years old were studied. Height, sitting height, leg length, and metacarpal length were studied in relation to three proxies for living conditions: height- and leg length-for-age, and maternal education. Estimation statistics and null hypothesis significance testing were used to analyze the data.

Metatarsal length and sitting height values were higher than height and leg length respectively. Relative metacarpal length was conserved across height-for-age groups. Females were less affected than males for metacarpal length and sitting height, but more affected for leg length.

Our results agree with the thrifty phenotype hypothesis, where metacarpal and sitting height growth would be prioritized over height and leg length due to greater functional significance.“

“Plasticity refers to the ability of an organism to modify its biology to respond to changes in the environment, particularly when these changes are physiologically stressful”<-plasticity in height is a very promising idea for height as it means height and bone length can be manipulated.

“in conditions of environmental stress, leg length is often more sensitive than is the head-trunk segment, and that tibia and ulna lengths are also more sensitive than humerus, hand and foot lengths. A proximate reason for this sensitivity is due to the allometry of skeletal growth, where the more proximal body segments grow fastest prenatally and are less exposed to extra-uterine environmental stress, but more distal segments grow most rapidly after birth and are more exposed to environmental stress. The thrifty phenotype hypothesis offers an ultimate evolutionary explanation; the growth of human body segments with greater functional significance, such as “head-brain,” “trunk-major organs,” and “hands-tools” will be prioritized over forearms and legs.”

“the thrifty phenotype hypothesis over the predictions of the distal blood flow and cold adaptation models in the growth of different body segments in living populations “

“According to this hypothesis, the growth of the head-trunk segment would be prioritized due to the important organs that it houses (brain, heart, lungs), and the growth of the hand would be prioritized due to its manipulative function in human tool technology, thus offering an ultimate evolutionary explanation for the differential plasticity in the growth of body segments under different conditions of stress.”

the thrifty phenotype hypothesis is basically that growth is conserved based on nutrients with some bones being prioritized over others in times of nutrient restriction.

I’ve written about heat being used to grow taller before. Heat also increases the rate at which chemical reactions occur which could be part of it. Here’s more on heat to grow taller. Heat could potentially increase solute uptake of the growth plate cartilage. Such things wouldn’t be really helpful to those who are skeletally mature although there is the possibility that heat could provide some kind of stimulus to the bone in which case it would help skeletally mature individuals.

Heat-Induced Limb Length Asymmetry Has Functional Impact on Weight Bearing in Mouse Hindlimbs

“As a noninvasive alternative, we previously developed a once daily limb-heating model using targeted heat on one side of the body for 2 weeks to unilaterally increase bone length by up to 1.5% in growing mice. In this study, we applied heat for 1 week to determine whether these small differences in limb length are functionally significant, assessed by changes in hindlimb weight bearing. We tested the hypothesis that heat-induced limb length asymmetry has a functional impact on weight bearing in mouse hindlimbs. Female 3-week-old C57BL/6 mice (N = 12 total) were treated with targeted intermittent heat for 7 days (40 C for 40 min/day){most humans have intermittent heat exposure though}. High-resolution x-ray (N = 6) and hindlimb weight bearing data (N = 8) were acquired at the start and end of the experiments. There were no significant left-right differences in starting tibial length or hindlimb weight bearing. After 1-week heat exposure, tibiae and femora were ~1 and 1.4% longer, respectively, on the heat-treated sides (40 C) compared to the non-treated contralateral sides (30 C). Tibial elongation rate was over 6% greater. “

“warm-reared mice had consistently longer ears, limbs, and tails when compared to littermates raised at cooler temperatures”<-studies have found however that humans raised at cooler environments tend to be taller. This finding though also means that it’s possibly that not only is growth rate increased but also height at skeletal maturity.

Here’s the heating device:

“heat-induced limb length differences do persist at skeletal maturity in 12-week-old mice that were examined 7 weeks after a juvenile heat-treatment”

” heat-based methods for treating minor limb length discrepancies may ultimately provide alternatives to traditional surgical approaches that can be painful and invasive.”<-so they do think that the method could be applied to humans.

“The increase in bone elongation rate generated by localized heat could help equalize minor limb length and weight bearing asymmetry in children”<-although we’d want something that works in older individuals.

There was a follow up paper:

Heat-Induced Limb Length Asymmetry Has Functional Impact on Weight Bearing in Mouse Hindlimbs

“Limb length inequality results from many types of musculoskeletal disorders. Asymmetric weight bearing from a limb length discrepancy of less than 2% can have debilitating consequences such as back problems and early-onset osteoarthritis. Existing treatments include invasive surgeries and/or drug regimens that are often only partially effective. As a noninvasive alternative, we previously developed a once daily limb-heating model using targeted heat on one side of the body for 2 weeks to unilaterally increase bone length by up to 1.5% in growing mice{1.5% is huge. That’s the difference between 5’9″ and 5’10”}. In this study, we applied heat for 1 week to determine whether these small differences in limb length are functionally significant, assessed by changes in hindlimb weight bearing. We tested the hypothesis that heat-induced limb length asymmetry has a functional impact on weight bearing in mouse hindlimbs. Female 3-week-old C57BL/6 mice (N = 12 total) were treated with targeted intermittent heat for 7 days (40 C for 40 min/day). High-resolution x-ray (N = 6) and hindlimb weight bearing data (N = 8) were acquired at the start and end of the experiments. There were no significant left-right differences in starting tibial length or hindlimb weight bearing. After 1-week heat exposure, tibiae (t = 7.7, p < 0.001) and femora (t = 11.5, p < 0.001) were ~1 and 1.4% longer, respectively, on the heat-treated sides (40 C) compared to the non-treated contralateral sides (30 C). Tibial elongation rate was over 6% greater (t = 5.19, p < 0.001). Hindlimb weight bearing was nearly 20% greater (t = 11.9, p < 0.001) and significantly correlated with the increase in tibial elongation rate on the heat-treated side (R² = 0.82, p < 0.01). These results support the hypothesis that even a small limb length discrepancy can cause imbalanced weight distribution in healthy mice. The increase in bone elongation rate generated by localized heat could be a way to equalize limb length and weight bearing asymmetry caused by disease or trauma, leading to new approaches with better outcomes by using heat to lengthen limbs and reduce costly side effects of more invasive interventions.”

“warm-reared mice had consistently longer ears, limbs, and tails when compared to littermates raised at cooler temperatures”

Here is the skeletal effects:

This next paper is a review paper that covers everything more thoroughly:

Temperature, heat shock proteins and growth regulation of the bone tissue

“Ambient heat modulates the elongation of bones in mammals, and the mechanism of such a plasticity has not been studied completely. The influence of heat on growth and development of bone depends on its values. Five zones of temperature influence on the bone tissue with different biological effects have been distinguished : a) under-threshold thermal zone < 36.6 ºС, insufficient amount of heat is a limiting factor for osteogenesis; b) normal temperature zone 36.6‒37.5 ºС, the processes of breakdown and development of bone in this temperature range is balanced; b) zone of mild thermal shock 39‒41 ºС, the processes of functioning of osteoblasts, osteocytes and formation of the bone tissue intensify; d) the zone of sublethal thermal shock > 42 ºС, growth of bone slows; e) zone of non-critical shock > 50 ºС, bone tissue cells die.{so seems like heat as a stimulus is biphasic where there’s an optimal zone, but heat can be combined with other stimuli}. We propose a model of the mechanism of influence of heat shock on bone growth. Mild heat shock is a type of stress to which membrane enzymes adenylyl cyclase and cAMP-protein kinase react. Protein kinase A phosphorylates the gene factors of thermal shock proteins, stress proteins and enzymes of energy-generating processes – glycolysis and lipolysis. Heat shock protein HSP70 activates alkaline phosphatase and promotes the process of mineralization of the bone tissue. In the cells, there is intensification in syntheses of insulin-like growth factor-I, factors of mitogenic action, signals of intensification of blood circulation (NO) and synthesis of somatotropin. The affinity between insulin-like growth factor I and its acid-labile subunit decreases, leading to increased free and active insulin-like growth factor I. Against the background of acceleration of the capillarization process, energy generation and the level of stimulators of growth of bone tissue, mitotic and functional activities of producer cells of the bone – osteoblasts and osteocytes – activate{would be interesting to see how osteoclasts are affected as they alter growth}. The generally known Allen’s rule has been developed and expanded: “Warm-blooded animals of different species have longer distal body parts (tails) if after birth the young have developed in the conditions of higher temperature”. The indicated tendency is realized through increased biosynthesis of heat shock proteins and other stimulators of growth processes in the bone tissue.”

“In one experiment, two month-old male mice C57BL/6J were exposed to cold (4 °C) and normal (23 °C) temperatures for 28 days. Cold increased the apoptosis of osteocytes and decreased the length of the canals. Those changes were accompanied by decrease in the number of osteocytes that were positive to Е11 (transmembrane glycoprotein, important for differentiation of osteocytes, first of all prolonging dendrites) and ММР13 (matrix metallopeptidase that breaks down the collagen I in extracellular matrix and potentially plays a role in rotating the articular cartilage) after 14 days. The indicated parameters returned to the initial levels after 28 days. The study revealed that after 14 days of influence of
low temperatures the volumetric bone fraction significantly decreased, but recovered after 28 days. Brown adipose tissue affected remodeling of the bone by increasing thermogenesis”

“Mild thermal stress increases the processes of regeneration of blood vessels and bones”

“A study reported that heat stress effectively induced the development of new bone tissue in an experimental model with 58 rats and 10 rabbits. The experimental animals underwent hyperthermia in 45 °С for 15 min once and three times a week, the changes in their bone tissue being determined by x-ray and histological evaluation. After the procedure of thermotherapy (1 time/week over 4 weeks), the experimental groups of rats and rabbits were observed to have a heightened level of osteogenesis compared with the control. The researchers inferred that thermal stimuli with heated materials enhance osteogenesis and increase the area of the development of bones and would be useful in treatment of bone defects in cases of skeletal diseases”<-this could potentially impact height.

Note that just because the muscles are stimulated by exercise to increase temperature does not mean bones do in the same way.

“Heat influence induces HSP expression. They stabilize proteins that strengthen the transmission of the signals of nitrogen oxide (NO), decrease oxidative stress and inflammation of the vessels and improve their function. During passive heat stress, blood circulation in the legs increased ~ 3–4-fold”

“The cartilage has no blood vessels and its nutrition is performed by diffusion of substances. The semi-penetrable “barrier at the border of vessel-cartilage surface” obstructs the molecular transport. To study the peculiarities of overcoming this obstacle, a model of heating the hind legs was used for manipulating the blood circulation in bones in 5-week-old female mice. In the experiment, dextrans were used weighing 10, 40 and 70 kDa, which are close in size to physiological regulators. Increase in the temperature in hind legs from 22 to 34 °C led to increase in vascular access of the abovementioned molecules. In 34 °C, penetration of dextrans 10 kDa into the growth plate increased by > 150%, and 40 and 70 kDa increased only by < 50%“<-so temperature managed to increase nutrient delivery into the growth plate by a significant amount.

“at HSP70 (200 ng/mL) increases the activity of alkaline phosphatase and promotes the mineralization of the bone tissue. In the conditions of osteogenic induction, this heat shock protein increased the expression of osteospecific genes such as transcriptional factors of family runt Runx2 and osterix (OSX). HSP70 promotes osteogenesis and may be a therapeutic mean for treating uncoalesced bones”

“Osteochondral interface between the bone and the cartilage allows these tissues to “communicate” with one another and exchange signal and plastic molecules, thereby providing integrated response to mechanical and thermal irritators”