Growing Taller by Increasing the Periosteal Width

We know that it's possible to increase the size of the periosteum.  Flat bones are not completely covered by periosteum but if the flat bone is in the right location it is people to use an increase in the size of the periosteum to increase height.  Some irregular bones and short bones are also partially covered by periosteum.  For example, the tips of the fingers may have some periosteum allowing you to get some increase in wing span there.

To date most studies have shown increases in periosteal width to be almost insignificant as a result of exercises. And, periosteal width increases tend to need more stimulus to increase than trabecular or cortical bone size. Sprinting increases the size of the periosteum of the tibia by putting lots of shearing and compression forces on the bone(shearing forces in a way cause microfractures on the periosteum).

The most likely way to effectively increase periosteal width is by the usage of heavy weights(such as deadlifts+deadlift variations) which means that growing taller via periosteal width is not the right method if per say a girl wants to maintain her secondary sex characteristics(her femininity).

A workable method to increase torso length can likely be found in some sort of LIPUS method by increasing hydrostatic pressure in a method similar to LSJL.  The vertebral bones do not have periosteum on the top and bottom.

Increases in periosteal width may play a role however by making you taller via the flat bone of the skull and the calcaneus. And, perhaps, if we optimize the exercises we perform we might be able to increase periosteal width by a lot more than 4%. Although, admittedly this is unlikely as sprinting is already incredibly effective at causing shearing forces on the periosteum of the tibia although the calcaneus may benefit from sprinting.

Growth Hormone, however, may be minorly effective on increasing body height via increasing periosteal width(on the flat bone of the skull) even if it cannot increase height on the long bones without a mutation.

This study shows that the periosteum can induce TGF-Beta which is a boon for chondrogenesis so the periosteum may have a secondary effect on height if not a primary one.

Coculture between periosteal explants and articular chondrocytes induces expression of TGF-beta1 and collagen I.

"Micromass pellets of human articular chondrocytes were cocultured for up to 28 days with human periosteal explants either with physical contact or separated by a membrane allowing paracrine interactions only. Quantitative reverse transcription (RT)-PCR, ELISA, immunohistochemistry and collagen isolation were used to analyse the expression and secretion of TGF-beta1, collagens I and II and chondrogenic differentiation markers such as MIA (CD-RAP) and aggrecan.
TGF-beta1 gene expression was induced significantly in paracrine cocultures in periosteum, whereas it was repressed in physical contact cocultures. However, a higher TGF-beta1 secretion rate was observed in physical contact cocultures compared with periosteal monocultures. The expression of COL2A1, melanoma inhibitory activity (cartilage-derived retinoic acid-sensitive protein) [MIA (CD-RAP)] and aggrecan was mainly unaffected by culture conditions, whereas COL1A1 gene expression was increased in periosteal paracrine cocultures. Collagen I staining was induced in micromass pellets from paracrine cocultures, whereas it was repressed in chondrocytes from physical contact cocultures.
We found evidence for a bidirectional regulating system with paracrine signalling pathways between periosteum and articular chondrocytes[extremely likely that this signaling pathway is shared by epiphyseal chondrocytes as well]. Stimulation of TGF-beta1 and COL1A1 gene expression in periosteal paracrine cocultures and the increased release of TGF-beta1 protein in physical contact conditions indicate an anabolic, and not merely chondrogenic micro-environment in this in vitro model for periosteal-based ACI."

"periosteum carries a thin proliferative cambium layer containing mesenchymal cells with chondrogenic and osteogenic potential which contribute to repair tissue formation"<-Periosteum is attached to the bone with sharpey's fibers too so it's possible that the periosteum contributes some mesenchymal cells for usage during LSJL and it's also possible that deformation of the periosteum during LSJL could lead to some of the height growth.

"While BMPs promote hypertrophy, signalling by TGF-βs favours a stable chondrogenic phenotype and inhibits or delays hypertrophy"<-TGF-Beta helps get stem cells to chondrocytes.  Chondrocytes formed in bone make you taller.

Influence of cyclic bending loading on in vivo skeletal tissue regeneration from periosteal origin.

"Periosteum osteogenic and chondrogenic properties stimulate the proliferation then differentiation of mesenchymal precursor cells originating from its deeper layers and from neighboring host tissues[controlling the periosteum is key to controlling the chondrocyte differentiation that we're trying to induce with LSJL]. The local mechanical environment plays a role in regulating this differentiation of cells into lineages involved in the skeletal regeneration process[we can alter this local mechanical environment with stimuli like LSJL].
The aim of this experimental animal study is to explore the influence of cyclic high amplitude bending-loading on skeletal tissue regeneration[LSJL likely applies some degree of bending and bending may generate some hydrostatic pressure so it may have similar effects to LSJL]. The hypothesis is that this mechanical loading modality can orient the skeletogenesis process towards the development of anatomical and histological articular structures.
A vascularised periosteal flap was transferred in close proximity to each knee joint line in 17 rabbits[so they're moving the periosteum to a location not seen in normal development]. On one side, the tibiofemoral joint space was bridged and loading occurred when the animal bent its knee during spontaneous locomotion. On the other side, the flap was placed 12 mm distal to the joint line producing no loading during bending. Tissue regeneration was chronologically analyzed on histologic samples taken from the 4th day to the 6th month.
The structure and mechanical behavior of regenerating tissue evolved over time. As a result of the cyclic bending-loading regimen, cartilage tissue was maintained in specific areas of the regenerating tissue. When loading was discontinued, final osteogenic and fibrogenic differentiation occurred in the neoformed cartilage[the periosteum resulted in new cartilage formation and the cartilage underwent osteogenic differentiation]. Fissures developed in the cartilage aggregates resulting in pseudo-gaps suggesting similar processes to embryonic articular development. Ongoing mesenchymal stem cells stimulation was identified in the host tissues contiguous to the periosteal transfer[the periosteum stimulated MSC development as well]."

Since the periosteum is so important to chondrogenic differentiation and mesenchymal stem cell stimulation, it's likely that increasing periosteal width has benefits as well.

"mechanotransduction modulates the metabolism and synthesis of immature cells as well as their differentiation into different cell lineages."<-LSJL involves mechanotransduction

"High local strain directs precursor cell differentiation into fibrous tissue. On the other hand, mild stress directs precursor cell differentiation into osteochondrogenic cells with direct ossification associated with weak hydrostatic stresses while cartilage growth is favored by higher compressive stresses"<-With LSJL we are going for highly compressive stresses with the clamp.  Direct osteochondrogenic growth likely results in no height growth as there is probably no chondrocyte hypertrophy or apoptosis which is likely what is responsible for the actual change in bone size.

"The mesenchymal precursor cells brought to the surgical bed by the periosteum and the host tissues proliferate before differentiating"<-the wider the periosteum likely the more mesenchymal precursor cells that are available.

"Significant proliferation of precursor cells constituting an undifferentiated blastema in the area of flap, and the first step in cell differentiation was found in both groups on the 4^th day. In the “control” group, the development of neotissue was observed along the medial gastrocnemius. In the “loaded” group, it developed on the medial side of the knee, and remained separate from the intact joint capsule"

"After the 4th day, chondrogenic differentiation of mesenchymal precursor cells, which is a key step in enchondral ossification, was similar in both experimental groups. In the “control” group, a process of ossification of the neotissue matrix gradually replaced all of the cartilage with bone. Between the 15th and 30th day, all the cartilage had disappeared and was replaced either with bone or fibrous tissue. After the 30th day, a segment of long bone, whose mean length was identical to that of the flap (27–32 mm), had formed in the posterior compartment of the muscle[a new segment of long bone formed identical to the length of the periosteum, stretch the periosteum to grow taller?  Limb lengthening surgery does involve stretching the periosteum]. A medullary cavity had developed and usually included bone marrow. Osteoclasts were identified on the surfaces of newly formed bone. At 6 months, the regenerated tissue was composed of 90% bone and 10% fibrous tissue.
In the “loaded” group cartilage and fibrocartilage, differentiation continued until the 3rd month. The presence of cartilage was gradually limited to the ends and to the middle of the newly formed tissue[just like in endochondral ossification with the primary ossification center in the middle and the secondary ossification centers in the end at the epiphysis]. These areas extended to the initial junction with the support bone and to the tibiofemoral joint space, respectively. After the 3rd month, the newly formed skeletal tissue was detached from at least one of its points of attachment to the support bone. Knee bending no longer caused the regenerated tissue to bend. The cartilage had completely disappeared from the newly formed tissues. At 6 months, a bone segment with a medullary cavity had finally developed on the medial side of the knee. It barely interfered with articular range of motion because it was structurally separate from its initial support bone."<-so the formation of skeletal tissue adapts to movement which means that a method like LSJL which alters skeletal formation will not cause problems as the body adapts.  There were no knee bending problems despite the formation of new bone.

" In the earliest stage (4^th day), lytic activity was observed in the tissues in contact with the transfer. This corresponded to necrosis of the superficial layers of muscle in immediate contact with the periosteum. This first stage was followed by a process of muscular regeneration which systematically resulted in complete repair without scar tissue in less than 14 days."<-muscle will adapt to the formation of new bone by remodeling.

"Variations in hydrostatic pressure influence the mechanisms that regulate the proliferation and differentiation of mesenchymal precursor cells. They stimulate proliferation in vitro, while in vivo, they redirect differentiation of precursors of bone tissue towards a cartilage phenotype[<-Why LSJL makes you taller].
Differentiation into chondrogenic cell lines is favored by a local mechanical environment associating high hydrostatic pressures and mild strains[In the LSJL rat study they used relatively low microstrain, maybe it's ideal for LSJL's effectiveness to minimize the microstrain while maximizing the hydrostatic pressure]. High amplitude strain inhibits angiogenesis thus influencing enchondral ossification"

"In our experimental protocol, loading of neotissue by cyclic bending generated a complex mechanical environment which could be described by numerous physical variables such as strain, variations in pressure or fluid as well as shear stress or movements at the cell/matrix and cell/cell interfaces"<-Cyclic bending generated changes in hydrostatic pressure just like LSJL.

"The structure and mechanical response of regenerating tissue evolves over time. As it matures, the regenerating tissue ossifies and mineralisation occurs so that it gradually becomes rigid. This process, which is incompatible with high amplitude knee movements, caused the regenerating tissue to break off from the anchor points of its support bone so that bending-loading no longer occurred[this shouldn't be a problem for us as we are striving for new cartilage formation in the epiphysis not the knee]. We then observed the disappearance of neocartilage, although it had been maintained until this event at the 3^rd month. Thus, the process of enchondral ossification was interrupted, and the cells did not finish their differentiation into cartilage. Nevertheless the deep layer of the periosteum contains cell precursors which are engaged in chondrogenic differentiation, and which form cartilage during monoclonal cell cultures"


"the segments of new cartilage sandwiched between two ossifying structures were not in a physiochemical environment that favored the stability of the cartilage phenotype. The molecular constituents of the extracellular matrix send signals of differentiation to its mesenchymal precursor cells. Thus, although the environment of the articular cavity and the new cartilaginous tissue are chondrogenic, contact with the extracellular bone matrix directs precursors towards osteogenic differentiation"<-This is a problem with LSJL as the stem cells are in an extracellular bone matrix.

" the maintenance of the cartilage phenotype became dependent upon continued cyclic mechanical loading"<-so the frequency of LSJL may have to increase to maintain cartilage phenotype.

Conclusion:  The periosteum is a key source of mesenchymal precursor cells thus increasing periosteal width may help you indirectly grow taller.  The stem cells being activated in LSJL are in an extracellular bone matrix thus it may be necessary to load more frequently to maintain a cartilage phenotype.

Here's an article about direct hypertrophy of periosteal cells which would likely increase both periosteal width and length:

Remodeling of Actin Cytoskeleton in Mouse Periosteal Cells under Mechanical Loading Induces Periosteal Cell Proliferation during Bone Formation.

"The adaptive nature of bone formation under mechanical loading is well known; however, the molecular and cellular mechanisms in vivo of mechanical loading in bone formation are not fully understood. To investigate both mechanisms at the early response against mechanotransduction in vivo, we employed a noninvasive 3-point bone bending method for mouse tibiae. It is important to investigate periosteal woven bone formation to elucidate the adaptive nature against mechanical stress. We hypothesize that cell morphological alteration at the early stage of mechanical loading is essential for bone formation in vivo.
We found the significant bone formation on the bone surface subjected to change of the stress toward compression by this method. The histological analysis revealed the proliferation of periosteal cells, and we successively observed the appearance of ALP-positive osteoblasts and increase of mature BMP-2[remember BMP-2 can help with chondrogenic differentiation as well], resulting in woven bone formation in the hypertrophic area. To investigate the mechanism underlying the response to mechanical loading at the molecular level, we established an in-situ immunofluorescence imaging method to visualize molecules in these periosteal cells, and with it examined their cytoskeletal actin and nuclei and the extracellular matrix proteins produced by them. The results demonstrated that the actin cytoskeleton of the periosteal cells was disorganized, and the shapes of their nuclei were drastically changed, under the mechanical loading. Moreover, the disorganized actin cytoskeleton was reorganized after release from the load. Further, inhibition of onset of the actin remodeling blocked the proliferation of the periosteal cells[so altering the actin cytoskeleton of the periosteum affects the hypertrophy of the periosteum].
These results suggest that the structural change in cell shape via disorganization and remodeling of the actin cytoskeleton played an important role in the mechanical loading-dependent proliferation of cells in the periosteum during bone formation."

"The periosteum is a membrane that lines the outer surface of all bones, except at the joints of long bones. This membrane, which consists of dense irregular connective tissue, is divided into an outer fibrous layer and an inner osteogenic layer. The fibrous layer contains fibroblasts, whereas the osteogenic layer contains the progenitor cells that develop into osteoblasts. In the observation of molecular and cellular phenomena acted by mechanical stress in vitro, the mechanical stress causes remodeling of cell-matrix adhesions, in which the cytoskeleton rapidly responds to external force by actin assembly"

" Upon detailed analysis, we observed that the mechanical loading rapidly decreased the quantity of stress fibers of the actin cytoskeleton and changed the nuclear shapes in the periosteal cells, and then disorganized actin cytoskeleton was remodeled in a time-dependent manner."<-Since mechanical loading decreases the number of stress fibers this could indicate a need for a deconditioning period to allow for new stress fibers to form.

"In addition, to identify the character of the hypertrophic periosteum, we performed anti-periostin antibody staining, since periostin is a typical marker of periosteum"

"At day 3, we found periostin to be expressed throughout the side opposite to the loading point in hypertrophic periosteum"<-So periosteum hypertrophies at the side opposite of the loading point.  So if we want periosteum to increase in length we need to load the ends of the periosteum.

"and this signal had decreased in intensity at day 7 because of the reduced area of periosteum by woven bone formation"<-Periosteum reduces itself when it forms new woven bone, this could explain why adults stop growing taller.  Periosteum reduces it's own area when it secretes new woven bone eventually periosteum is no longer next to the growth plate and growth plates need to be next to periosteum thus growth stops.

"The nucleus itself has been proposed to act a cellular mechanosensor, with alterations in nuclear shape causing conformational changes in chromatin structure and organization and directly affecting transcriptional regulation. By this machinery, extracellular forces can be transmitted across the cytoskeleton to the nucleus, resulting in intranuclear deformations; and the actin cytoskeleton is thought to provide protrusive and contractile forces and compressive bearing microtubules to from a polarized network allowing organelle and protein movement throughout the cell. In fact, compressive stress induces shape changes in chondrocyte nuclei; and collagen synthesis is strongly correlated with nuclear shape"<-So if we induce stress in a certain way we can change nuclei to be more chondrogenic.  This is done by causing hydrostatic pressure like with LSJL.



Direct transformation from quiescence to bone formation in the adult periosteum following a single brief period of bone loading.

"This experiment documents the direct transformation of the normal, quiescent, adult periosteum to active bone formation. The osteogenic stimulus was provided by a single short period of dynamic loading. Periosteal activation and the production of new bone within 5 days of loading was unaccompanied by resorption or the presence of osteoclasts. We therefore conclude that an adult resting periosteum can become directly converted to formation as a physiologic response to an appropriate osteogenic stimulus without the need for resorption. To distinguish this process from remodeling we suggest it be called renewed modeling. It is notable that a single short exposure to an "osteogenic" loading regime can influence the full cascade of cellular events between quiescence and active bone formation."

Aging changes mechanical loading thresholds for bone formation in rats

"The effect of aging on the mechanical loading thresholds for osteogenesis was investigated in rats. We applied mechanical loads varying from 30 to 64 N to the tibiae of 43 19-month-old rats using a four-point bending apparatus. Bone formation rates were measured on the periosteal and endocortical surfaces of the tibial midshaft using double-label histomorphometry. Bone formation rates from the old rats were compared with results from adult (9-month-old) rats that we reported earlier. Bone formation on the periosteal surface of the old rats was predominantly woven-fibered. Periosteal bone formation was observed in a lower percentage of the old rats compared with the younger adult rats for applied loads of 40 N and greater (59% old, 100% adult). However, in the old rats that formed woven bone there were no significant differences in woven bone area (p = 0.1) or surface (p = 0.24) compared with younger adult rats. Therefore, the periosteum of old rats had a higher threshold for activation by mechanical loading, but after activation occurred, the cells had the same capacity to form woven bone as younger adult animals. On the endocortical surface, relative bone formation rates in old rats showed a marginal (p = 0.06) increase in response to an applied load of 64 N but was not increased at lower loads. The relative bone formation rate in the old rats was over 16-fold less than that reported for the younger adult rats at an applied load of 64 N and the relative bone forming surface in old rats in this study was 5-fold less than it was in younger rats under similar loading conditions. In the younger adult rats, a mechanical threshold for lamellar bone formation of 1050 μstrain was calculated for the endocortical bone surface. The old rats required over 1700 μstrain on the endocortical surface before bone formation was increased. The data suggest that both the periosteal and endocortical surfaces of the tibiae of older rats are less responsive to mechanical stimuli."