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Study provides evidence of microfracutre theory

There are studies that show that periosteal stripping may induce skeletal bone overgrowth pre-skeletal maturity. The below study shows evidence that fracture without periosteal damage may lead to skeletal overgrowth. Microfractures alter the fluid flow within the bone to that may be a mechanism by which microfractures can affect but that also means that it’s possible that fluid flow alone can lead to skeletal overgrowth. It’s important to note that we would need to study what exercises actually cause microfractures. There would need to be actual studies done otherwise it’s just speculation as to whether an exercise causes microfractures and don’t know if the microfractures are created to be sufficient stimulus.

Overgrowth of long bone in rabbits by growth stimulation through metaphyseal hole creation

“Overgrowth of long bones was noted in pediatric patients who underwent anterior cruciate ligament reconstruction. Hyperaemia[blood vessels having more blood than normal] during creating a metaphyseal hole and the microinstability made by the drill hole may induce overgrowth{This is interesting because we could create temporary instabilities in bones and joints via exercise!}. This study aimed to determine whether metaphyseal hole creation accelerates growth and increases bone length and compare the effects of growth stimulation between metaphyseal hole creation and periosteal resection. We selected 7- to 8-week-old male New Zealand white rabbits. Periosteal resection (N = 7) and metaphyseal hole creation (N = 7) were performed on the tibiae of skeletally immature rabbits. Seven additional sham controls were included as age-matched controls. In the metaphyseal hole group, the hole was made using a Steinman pin at the same level of periosteal resection, and the cancellous bone beneath the physis was removed by curettage. The vacant space in the metaphysis below the physis was filled with bone wax. Tibiae were collected 6 weeks after surgery. The operated tibia was longer in the metaphyseal hole group (10.43 ± 0.29 cm vs. 10.65 ± 0.35 cm){about 2%, so if this happened on every bone it would take a 69 inch individual to about 70 1/3}. Overgrowth was higher in the metaphyseal hole group (3.17 ± 1.16 mm) than in the sham group (− 0.17 ± 0.39 mm. The overgrowth in the metaphyseal hole group was comparable to that in the periosteal resection group (2.23 ± 1.52 mm, P = 0.287). In rabbits, metaphyseal hole creation and interposition with bone wax can stimulate long bone overgrowth, and the amount of overgrowth is similar to that seen in periosteal resection.”

“During ACL reconstruction, there was no circumferential periosteal damage; instead, the drill hole was made from the metaphysis to the epiphysis, and the hole was filled with a tendon graft. The overgrowth was also reported in children with proximal metaphyseal fracture as Cozen’s phenomenon, and the overgrowth after proximal cortical breakage without extensive periosteal damage”

“Increased metabolic activity at the physis or bony instability has been suggested to the other possible cause of the overgrowth”

“The cortical hole made by drilling at the metaphysis could increases metabolic activity at the physis through hyperaemia and the large cortical hole would be related to the bony instability. During ACL reconstruction, a cortical hole made at the metaphysis to the phyis and interposition of the vacant space with the tendon may promote hyperaemia and bony microinstability”

The questions is if there is any instances of growth promotion in skeletally mature individuals.

Study finds that vibration can induce articular cartilage endochondral ossification

We’ve studied endochondral ossification of the articular cartilage in the condyle before. If vibration can induce endochondral ossification of the articular cartilage in the jaw it is theoretically possible that it could induce endochondral ossification in any joint unless the jaw cartilage is special. Which I don’t believe it is I believe that the jaw is more mobile than other joints and subjected to superior loading. If other joint regions were subjected to the same kind of loading as the jaw they could grow as well.

Effects of Mechanical Stimuli on Adaptive Remodeling of Condylar Cartilage

“Trabecular bone has been shown to be responsive to low-magnitude, high-frequency mechanical stimuli.
This study aimed to assess the effects of these stimuli on condylar cartilage and its endochondral
bone. Forty female 12-week-old C3H mice{this is pre skeletal maturity unfortunately, howver later in the study they say that the mice are “adult”} were divided into 3 groups: baseline control (killed at day 0), sham (killed at day 28 without exposure to mechanical stimuli), and experimental (killed following 28 days of exposure to mechanical stimuli).

The experimental group was subjected to mechanical vibration of 30 Hz, for 20 minutes per day, 5 days per week, for 28 days. The specimens were analyzed by micro-computed tomography. The experimental group demonstrated a significant decrease in the volume of condylar cartilage and also a significant increase in bone histomorphometric parameters. The results suggest that the low-magnitude, high-frequency mechanical stimuli enhance adaptive remodeling of condylar cartilage, evidenced by the advent of endochondral bone replacing the hypertrophic cartilage{vibration can induce articular cartilage endochondral ossification, if this can occur in other joints with articular cartilage then you can get longer bones by that mechanism!}.”

“there is a linear association between bone-regenerative capacity and bone density”<-So could things that increase bone density increase bone regenerative capacity?

“We achieved mechanical stimulation to the animals by placing them, while still in their cages with bedding removed, directly on a device which generated vertical ground-based vibration. This machine generated 30-Hz pulses, creating peak-to-peak accelerations of 2.9 m/sec2, referred to as a fraction of earth’s gravitational field, 0.3 g (1g = 9.8 m/sec2). Based on Rubin’s previous research, it is believed
that this produces peak strains of approximately 5 μє. Animals in the Experimental group were subjected to 20 minutes’ vibration per day for 5 days per week for a total of 28 days,”<-so the mice were subjected to vibration not specific to the jaw and it still underwent articular cartilage endochondral ossification. It would be interesting if other bones changed as well.

“the LMHF stimuli induced osteogenesis, leading to adaptive growth of the condyle in adult mice.”<interesting that they call these adult mice! But we have to be sure they’re skeletally immature

“the adaptive modeling of condylar cartilage is characterized by enhanced transition from chondrogenesis to osteogenesis. The vibrating mechanical stimulation in the present study was shown as a possible mechanism for the acceleration of the modeling.”

“A questionable aspect of this study design is the degree of transmission of the vertical ground-based oscillation, since it diminishes as the signal travels proximally through the skeleton. In a study measuring transmissibility in the hips and spines of humans standing on the oscillating plate, the authors showed
that approximately 80% of a 30-Hz ground-based signal reached the hip and spine”

This study here suggests that vibration can have benefit on growing bone:

Does Vibrational Loading Modulate the Effects of Radiotherapy on Growing Bone?

“[we evaluate] the possible beneficial effects of low-magnitude high-frequency mechanical vibration (LMHFV) stimuli on growing irradiated bone and the possibility for restoration of function of the epiphyseal plate”

“

ighteen 3-week old weanling male Sprague-Dawley rats were subjected to a standard radiation dose of 17.5 Gray applied to right hind limbs, with the contralateral leg serving as a non-irradiated control. Then, the animals were divided into three groups: A) rats subjected to (LMHFV) only at 45 Hz, 0.3 g for 20 minutes once per day, 7 days/week, for 3 weeks, B) rats subjected the same conditions of LMHFV plus an injection of spermine NONOate, a nitric oxide donor that that has shown weak positive results as post-irradiation recovery agent, and C) rats subjected to sham LMHFV. After euthanizing the animals, skeletal growth was measured by x-ray analysis, marrow mesenchymal stem cell osteoblastic potential was measured by CFU-F analysis, and bone morphology was measured by micro-CT analysis.

X-ray and CFU-F analyses show statistically significant differences between right and left limbs in all groups. No statistical significance was observed between vibration versus control groups, but trends suggest there could be some positive effect of vibration, although not statistically significant. Micro-CT results show a clear difference between right and left limbs in all groups. Regarding vibration versus control groups, micro-CT results are ambiguous, but do suggest that vibration may have altered local growth characteristics and stimulated local shape changes in the 20% region from the distal end of the femur, just above the growth plate.”

“Eighteen 3-week old weanling male Sprague-Dawley rats were obtained from Taconic Farms (Germantown, NY) and randomly divided into three groups: A) rats subjected to low-magnitude high-frequency vibration (LMHFV) only at 45 Hz, 0.3 g for 20 minutes once per day, 7 days/week, for 3 weeks, B) rats subjected to LMHFV with the same conditions as group A plus an injection of spermine
NONOate, a nitric oxide donor , and C) rats subjected to sham LMHFV, placed in cages
used for vibration but with no stimulus applied.”<-so we’re looking at group A versus group C as to whether vibration can increase bone length.

“there was possibly a difference, although not statistically significant, between right femora of different groups (A: 32.6±2.3 vs. B: 31.9±2.2 vs. C: 31.2±1.2, Figure 2), as well as total leg lengths of the femur
plus the tibia between different groups (A: 66.4±2.4 vs. B: 65.3±2.9 vs. C: 64.4±2.1, Figure 4).”<-So vibration group was longer than via group C.

“the ability of physical signals to influence bone morphology is strongly dependent on the signal’s magnitude, frequency and duration”

Study finds vibration increases height

I’ve been getting slow but steady results with the massage gun on my hand on bone length(I haven’t ruled out trying to use two or more massage guns simultaneously) so I did some more research on vibration.

Body height change from motor vehicle vibration

“Seventeen (17) subjects were exposed to tri-axial vehicle whole-body vibration for approximately 3 h, and measured hourly for body height. The control was the same environment, but no vibration. A broad band predominantly z-axis acceleration (1.6—10 Hz), with a mean level of 0.885 m/s2 at the seat, was generated by a semi-truck tractor driven on secondary roads. The dominant one-third octave band of the vibration at the seat was 2 Hz with an acceleration magnitude of 0.521 m/s2. At the end of the first hour, the results indicated a subject growth by 1.14 mm when exposed to vibration and a shrinkage of nearly equal amount without vibration. In the second and third hours, subjects followed the natural tendency to shrink under both conditions. At the end of the third hour, the subject height with vibration was 2.23 mm higher than that without vibration.”

<-interesting that the subjects kept growing. There a couple of possibilities vibration may increase the amount of hydration by the intervertebral discs thus reducing height loss by diurnal variation and/or vibration could stimulate anabolic effects within the bone/cartilage thus resulting in permanent height gain. It’s interesting that the height keep increasing at the third hour. We’d want to know the point at which the height increase stops.

“The spine, specifically the intervertebral disc, has been shown to be a non-rigid system and indeed exhibits a slow deformation or creep response over time when loaded”<-this suggests that just rehydration of the discs occurs but actually deformation of the discs. Which is exciting as it means torso height increase would be possible.

“This creep effect can reduce the overall body height (stature) of an average individual by 1%, approximately 17.5 mm, over the course of the day. The creep
response arises from the gravitational force loading the spine. Once the gravity is removed from loading, the cellular osmotic action within the soft tissues of the intervertebral disc causes the disc to swell, bringing about height recovery in a daily cycle.”<-this alludes to disc hydration. The question is can the discs be positively deformed in such a way as to increase height.

“the upper-body loading during short-term shock events repeated enough could possibly be responsible for generating microfractures in the spine”<-for those who subscribe to microfracture theory.

“With seat inclination of 90°, body height was seen to grow (increase stature) at 4 Hz (1.86 mm), and to shrink at 6 Hz (0.04 mm) and 8 Hz (0.14 mm) for 1 m/s2 after 1 h exposure. Absence of vibration on the same seat produced about 1.1 mm shrinkage for 1 h. Overall, with a 90° seat back, 1.27 mm of shrinkage was seen, while an inclined 110° backrest produced 0.81 mm growth in the subjects.”<-so looks vibration is biphasic with there being an equilibrium range where you get the most height growth

Figure 4. Vibration increased height up to 1 hour and otherwise reduced height loss.

“This study provides evidence that there can be an active mechanism for changing intervertebral disc height and the associated pressure change that occurs with it.”<-the question is, is if any of this is permanent and can it be applied to other joints or the growth plate or other cartilagenous regions.

Studies such as Possible mechanisms of low back pain due to whole-body vibration also state that vibration increased spinal height and that may be responsible for lower back pain. Other studies suggest that vibration increases height loss. This could be again because vibration is biphasic with there being an optimal vibration stimulus for stimulating the IVDs.

There’d have to be a longitudinal study done to see if there’s anyway for vibration to induce permanent beneficial increases in height. There have been studies done on people in construction/etc and they show height loss however since vibration is biphasic(either too much or too little is suboptimal) it is likely that they were overdoing the vibration stimulus and this was the cause for the height loss.

From Exposure to whole-body vibration and hospitalization due to lumbar disc herniation, moderate to high exposure to vibration had slightly less height.

Table 1. This could be correlational though. It’s not a true longitudinal study. White-color workers could be taller due to “tall privilege” getting them better jobs.

So we still need either longitudinal studies on vibration or self testing to see if vibration can positively impact either bone length or the cartilage.

Study finds strong evidence that Ritalin may stunt growth

Methylphenidate is ritalin

Methylphenidate Promotes Premature Growth Plate Closure: In Vitro Evidence

“It is well known that patients with attention deficit hyperactivity disorder treated with stimulants, such as methylphenidate hydrochloride (MPH), have reduced height and weight. Even though MPH has an anorexigenic effect{loss of appetite, some people have said that the loss of height is due to appetite loss and can therefore be recovered by compensatory eating}, an additional impact of this drug on the growth plate cannot be discarded. In this study, we aimed to determine the cellular effect of MPH on an in vitro growth plate model. We tested the effects of MPH on the viability and proliferation of a prechondrogenic cell line via an MTT assay. In vitro differentiation of this cell line was performed, and cell differentiation was evaluated through the expression of cartilage- and bone-related genes as measured via RT-PCR. MPH did not alter the viability or proliferation of prechondrogenic cells. However, it reduced the expression of cartilage extracellular matrix-related genes (type II collagen and aggrecan) and increased the expression of genes involved in growth plate calcification (Runx2, type I collagen, and osteocalcin) at different phases of their differentiation process. Our results evidence that MPH upregulates genes associated with growth plate hypertrophic differentiation. This may induce premature closure of the growth plate, which would contribute to the growth retardation that has been described to be induced by this drug.”

It should be noted that increasing growth plate hypertrophy does not always result in decreased height. But increasing growth plate hyertrophy and growth plate calcification should result in increased height velocity which is not corroborated by the typical reduced height observed of children treated with ritalin. If there was a height conservation and catch up growth involved you’d expect that the reserve zone would have greater gene expression in children treated with ritalin.

“MPH Does Not Affect Chondrocyte Viability and Proliferation”<-This is good.

“MPH treatment provokes faster progress of the endochondral ossification process.”<-again though this doesn’t always result in reduced height at skeletal maturity.

“reduction in COL2 and ACAN expression during the last days of differentiation may also indicate premature termination of the proliferative phase of chondrocyte maturation, and thus, early initiation of the hypertrophy and mineralizing phases.”

“certain drug treatments can impair the regulatory mechanisms of the growth plate and cause its premature closure. Stimulant treatment may have unknown interactions with the biological factors regulating skeletal growth, including signaling proteins, transcription factors, and hormones. These drugs, including MPH, raise the amount of dopamine in the synaptic space by blocking the dopamine transporter (DAT).”

Here’s a study that shows that Ritalin anecdotally reduces height:

Trajectories of Growth Associated With Long-Term Stimulant Medication in the Multimodal Treatment Study of Attention-Deficit/Hyperactivity Disorder

“16 years of consistent stimulant treatment of children with ADHD in the MTA was associated with changes in height trajectory, a reduction in adult height”

“[a study] revealed that the entire ADHD group, including medicated and nonmedicated participants, was 1.29 cm shorter than the LNCG non-ADHD peer group”

“consistent and extended use of stimulant medication may be associated with some suppression of height into the adult years”

“the main finding of this study—that stimulant use over development may be associated with a possible
decrease in adult height in individuals consistently treated—has not been found in all prior growth studies of children with ADHD who were treated chronically with stimulants. However, those studies reported lower cumulative doses and did not use our methodology of determining trajectories of
growth over time”

“the possible changes in adult height (up to 1.5 inches shorter)”

Can bone remodeling contribute to height?

Microfracture theory and bone remodeling theory are two theories floated around that can possibly contribute to height. Here’s a review paper about bone remodeling, is there anything in it related to height?

Toward a Unifying Theory of Bone Remodeling

“remodeling increases both when mechanical loading is excessively low{there’s a training program called Hypertrophy Specific Training or HST that involves using periods of low mechanical loading to make muscle more susceptible to high mechanical loading would it be possible to use the same principles for bone?}, that is, in a disuse state, and when it is excessively high, producing substantial fatigue damage, is contrary to the widely held assumption that a signal generated by osteocytes in proportion to mechanical loading stimulates bone lining cells to activate remodeling. The new theory resolves this disparity by assuming that lining cells are inclined to activate remodeling unless restrained by an inhibitory signal{so if we remove this inhibitory signal we can can have bone remodeling all the time?}, and that the mechanically provoked osteocytic signal serves this inhibitory function.
Consequently, remodeling is elevated when signal generation declines due to reduced loading, or when signal generation or transmission is interrupted by damage due to excessive loading{Thus we could potentially get bone remodeling without mechanical loading}. Otherwise, remodeling is kept at a relatively low level by inhibitory signals produced through physiologic loading.
Furthermore, the inhibitory signal is postulated to be identical to that proposed by Marotti as the mechanism for conversion of osteoblasts to osteocytes, and responsible for the diminishment of apposition rate during refilling of osteonal basic multicellular units. Consequently, a single, mechanically derived signal, produced in the osteocytic syncytium, may control osteoblast and bone lining cell functions, and thereby a variety of important phenomena in bone biology{Thus it would be really easy to produce some sort of pill if there is only one signal}.”

“when an osteocyte becomes buried to a critical depth in the bone matrix, an additional osteocyte is recruited to maintain contact with the bone surface as the BMU wall thickness increases. the osteocyte sends an inhibitory signal through its processes to the osteoblasts forming bone above it. This causes the most affected osteoblast to slow its production of osteoid, and it is buried in the matrix by the adjacent osteoblasts.”

“microcracks and more diffuse disturbances of the calcified matrix structure. It seems clear from observing such damage that it could easily interfere with both the normal flow of fluids over osteocyte processes within canaliculae (signal generation) and with the passage of signals from one cell to another through these processes (signal transmission).“<-this suggests that it is not the microfractures themselves that stimulate growth but rather the fluid flow that is changed by the microfractures. This suggests that it is possible to get bone growth via fluid flow alone and microfractures are not needed.

“diffuse damage to the calcified matrix could release Ca ions or cytokines that could act to reduce
the inhibitory signals produced by the osteocytes, or their transmission from cell-to-cell. microdamage results in osteocyte apoptosis, again interrupting both signal generation and transmission”

“remodeling is known to be activated is local bone matrix necrosis—that is, when osteocytes die. This may occur from microdamage or when the haversian blood supply is interrupted following fracture”<-again fluid flow driven changes not the microfracture itself.

Concluding thoughts: It’s difficult to imagine a possible way in which osteocytes can help you grow taller as bone is a tissue not capable of interstital growth(growth from within) thus needing a cartilage or fibrous intermediate. Unless new bone is deposited at longitudinal ends. But this paper does enforce the idea that it is not microfractures themselves that cause new bone formation but rather the change in fluid flow caused by those microfractures. It is also likely that any soft tissue caused by an exercise routine within the bone would benefit more from changes in fluid flow than the microfractures themselves.

Huge news someone other than Yokota/Zhang use a joint loading device

This is huge that someone else is doing a LSJL like device it means that something could be close to being put into practice.

Micromechanical Loading Studies in Ex Vivo Cultured Embryonic Rat Bones Enabled by a Newly Developed Portable Loading Device

“Mechanical loading has been described as having the potential to affect bone growth{we want it to affect bone growth post skeletal maturity of couse}. In order to experimentally study the potential clinical applications of mechanical loading as a novel treatment to locally modulate bone growth, there is a need to develop a portable mechanical loading device enabling studies in small bones. Existing devices are bulky and challenging to transfer within and between laboratories and animal facilities, and they do not offer user-friendly mechanical testing across both ex vivo cultured small bones and in vivo animal models. To address this, we developed a portable loading device comprised of a linear actuator fixed within a stainless-steel frame equipped with suitable structures and interfaces. The actuator, along with the supplied control system, can achieve high-precision force control within the desired force and frequency range, allowing various load application scenarios{the potential would be to use the device to induce longitudinal bone growth on skeletally mature individuals}. To validate the functionality of this new device, proof-of-concept studies were performed in ex vivo cultured rat bones of varying sizes. First, very small fetal metatarsal bones were microdissected and exposed to 0.4 N loading applied at 0.77 Hz for 30 s. When bone lengths were measured after 5 days in culture, loaded bones had grown less than unloaded controls (p < 0.05). Next, fetal rat femur bones were periodically exposed to 0.4 N loading at 0.77 Hz while being cultured ex vivo for 12 days. Interestingly, this loading regimen had the opposite effect on bone growth, i.e., loaded femur bones grew significantly more than unloaded controls{femurs have different proportions than metarsal bones, one possibility is that femur bones shape makes it more susceptible to fluid based forces and pressure gradients, due to the femurs longer shape it is possibly more susceptible to deforming forces than metatarsals}. These findings suggest that complex relationships between longitudinal bone growth and mechanical loading can be determined using this device. We conclude that our new portable mechanical loading device allows experimental studies in small bones of varying sizes, which may facilitate further preclinical studies exploring the potential clinical applications of mechanical loading.”

“two use-cases were devised: repetitive impact loading of small force (0.05–0.5 N) at a range of  30–180 repetitions and continuous sinusoidal loading of medium force (0.5–5 N) at a frequency range of 5–20 Hz.”<-something like a massage gun does something similar of repetitive impact loading.

Above is the device used.

So unfortunately for metarsals it does look like yes the device suppressed growth. However, initially the 0.1N load enhanced growth. More studies would have to be done.
In contrast femur bones grew pretty uniformly and the difference is pretty significant. Again, I think it is possible that this could be due to the different shape of the femur bones or maybe the load was too strong for the smaller metatarsal bones.

“Its square shape securely covers the entire cartilage area on each side of the embryonic femur bone, allowing the indenter to apply mechanical loading specifically to the growth plate in a stable manner.”<-just because the growth plate was the thing that was loaded does not necessarily mean that the growth plate was solely responsible for the growth there could be effects elsewhere as well including that which induces longitudinal bone growth.

“we identified that the same load applied to bones of different dimensions has opposing effects on bone growth, suggesting that the effects of mechanical loading on growth are dependent on the magnitudes and relative dimensions of the bones.”<-so they too think that the shape of the bone has an impact on whether growth is induced or not. The fact that the shape of the bones matter also suggests that yes it is possible that not all of the growth is due to the growth plate.

“Embryonic metatarsal bones from Day 19.5 of gestation are approximately 1 mm in length, whereas femur bones are approximately 4 mm, indicating that the level of mechanical loading that stimulates or inhibits bone growth is likely dependent on bone size.”

This is the sentence where the cite Yokota/Zhang’s joint loading study: ” The device’s controller enables sinusoidal loading, which has been demonstrated to have a bone growth-promoting effect in mice “