Deer antlers are a mammalian appendage capable of regeneration. I don’t believe that eating deer antlers could induce growth plate regeneration but possibly the study of deer antlers could help enable growth plate regeneration. And perhaps studying deer antlers could enable the growth plates to be open for longer. One of the problems with limb lengthening surgery remains muscle and other soft tissue tightness. The growth plate is connected to these soft tissues via the enthesis so it is logical to think that perhaps the enthesis can help provide the cellular ingredients for those soft tissues to grow as needed via the enthesis.
<-perhaps for example there could be an osteotomy and an injection of these stem cells in a region near the enthesis to form new growth plates.
“The annual regrowth of deer antlers provides a valuable model for studying organ regeneration in mammals. We describe a single-cell atlas of antler regrowth. The earliest-stage antler initiators were mesenchymal cells that express the paired related homeobox 1 gene (PRRX1+ mesenchymal cells). We also identified a population of “antler blastema progenitor cells” (ABPCs) that developed from the PRRX1+ mesenchymal cells and directed the antler regeneration process.{could we use similar cells to form new growth plates?} Cross-species comparisons identified ABPCs in several mammalian blastema. In vivo and in vitro ABPCs displayed strong self-renewal ability and could generate osteochondral lineage cells. Last, we observed a spatially well-structured pattern of cellular and gene expression in antler growth center during the peak growth stage, revealing the cellular mechanisms involved in rapid antler elongation.”
“Lower vertebrates have a remarkable capacity to heal in a scar-free manner and regenerate lost appendages, even at the adult stage”
“deer antler offers a singular model to study spontaneous regeneration in mammals because its regeneration is similar and clinically relevant to mammalian long-bone development”
“hard antlers are cast from their pedicles, then both antler bone and cartilage are regenerated from the pedicle periosteum located in the pedicle stumps”
“We further identified a population of regenerative progenitor cells, ABPCs, in the antler blastema, with impressive capacities for self-renewal, osteogenic–chondrogenic differentiation, and bone-tissue repair.”<-in the paper it goes over more what the cell characteristics of the progenitor cells might be. The question is: How do we translate what’s going on in the deer antlers to bone?
If vibration increases cartilage thickness. It is possible too that vibration could induce articular cartilage endochondral and stimulate growth plate growth. There are studies that show that vibration may be do this but the results have been non-overwhelming and mixed. It is possible however that it may be that the vibration stimulus needs to be improved. For example, laterally applying the vibration to the epiphysis and applying the vibration directly to the bone may improve the stimulus. But there are still several studies that show vibration is promising. It’s just the lack of a “smoking gun” study.
“1) 14-days of immobilization of young healthy subjects using a 6°-“head-down-tilt-bed-rest”-model (6°-HDT) would reduce cartilage thickness in the knee and serum Cartilage oligometric matrix protein (COMP) concentration and 2) isolated whole body vibration training would counteract the bed rest effects.”
“While the control intervention resulted in an overall loss in average cartilage thickness of −8% (pre: 3.08 mm±0.6 mm post: 2.82 mm±0.6 mm) in the weight-bearing regions of the tibia, average cartilage thickness increased by 21.9% (pre: 2.66 mm±0.45 mm post: 3.24 mm±0.63 mm) with the vibration intervention. No significant differences were found in the weight-bearing regions of the femur. During both interventions, reduced serum COMP concentrations were observed (control intervention: −13.6±8.4%; vibration intervention: −9.9±3.3%).”<-it is possible that a thickness in cartilage could increase height and induce articular cartilage endochondral ossification it could also stimulate growth plate growth. The thickness of the cartilage was increased versus control which is good but COMP is reduced compared to control which is bad.
“Cartilage presumably maintains and responds to the loads placed on joints during activities of daily living. For instance, the loads generated at the knee during walking correlate with cartilage thickness in the weight-bearing regions of the knee”<-so we could potentially change the way we load to alter cartilage thickness.
“COMP plays a major role in stabilizing the extracellular matrix through its interaction with collagen fibrils and other matrix components. Serum COMP concentrations are elevated in patients with knee osteoarthritis and rheumatoid arthritis but also after a moderate walking exercise in healthy adults and after intense running exercise in athletes. Thus, serum COMP concentration appears to be sensitive to physiological loading.”
“Vibration frequencies between 15 Hz and 90 Hz have been used to achieve adaptations in muscle and bone”
“Training sessions were scheduled at least 30 min after breakfast and lunch. Subjects walked the distance between their room and the training room each session (∼25 steps). Each vibration training unit was composed of five times 60 s of isometric exercise bouts on a vibration platform (Galileo 900, Novotec Medical GmbH, Pforzheim, Germany) in an upright standing position with a knee flexion angle of 30°. Subjects carried an additional load of 15% of their body mass on a diving belt around their pelvis. Between exercise bouts subjects rested for 60 s while sitting on a chair. The vibration platform vibrated at 20 Hz with approximately 3 mm amplitude at the centre of the foot.”<-the vibration in this study could be improved.
“Average and maximum thicknesses in the tibial cartilage increased significantly by 21.9% and 26.6%, respectively[due to vibration]. The percentage change in average and maximum cartilage thicknesses did not differ between the medial and the lateral compartments of the tibia for both study phases. Cartilage thickness in the lateral and the medial compartments of the femoral cartilage did not show significant changes due to the bed rest or to the training intervention”<-maybe the way we as humans typically load does not adequate load the lateral and medial compartments of the femoral cartilage and that’s why we don’t typically gain height there. It’s possible that if all parts of the femoral cartilage was engaged we would gain height and therefore if we change our loading we could stimulate all components of the femoral cartilage and thereby gain height.
“the increased cartilage thickness after the vibration training if the mechanical stimulus increases proteoglycan content of cartilage.”
“Proteoglycans are negatively charged and thus exert a large swelling pressure that causes tensile stress on the surrounding collagen network”
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 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.
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:
“[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”
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.
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.
“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)”
