Tuesday, November 8, 2011

Does the structure of bone provide insight into growing taller?

Stuart J Warden was a friend of CH Turner who developed part of LSJL.  SJ Warden published a new paper and it provides some insight into bone and possibly insights into height growth.

Specialized Connective Tissue: Bone, the Structural Framework of the Upper Extremity
"Bone is a connective tissue containing cells, fibers, and ground substance. There are many functions in the body in which the bone participates, such as storing minerals[bone is not hydrophillic like cartilage, so if there are high quantities of water it makes sense for stem cells to differentiate into chondrocytes to store water, although water is not a mineral], providing internal support, protecting vital organs, enabling movement, and providing attachment sites for muscles and tendons. Bone is unique because its collagen framework absorbs energy, whereas the mineral encased within the matrix allows bone to resist deformation."<-In biology, structure correlates with function.  Can there be any instances where a longer bone would improve bones function?  Yes, if bone were longer it would serve better at enabling movement in some cases.  But, playing basketball doesn't make people taller.  Neither do bigger muscles or tendons.  Only storing water requires the formation of cartilage which is what enables growing taller via endochondral ossification.
"Cortical bone thins toward the expanded ends (epiphyses) and interposed developing region (metaphysis) of long bones where it plays a lesser, yet clinically significant mechanical role"<-Maybe thicker cortical bone is a blocker of endochondral ossification?
"The periosteum covers external surfaces of most bones and is divided into two distinct layers—an outer fibrous and inner cellular layer. The cellular or “cambium” layer is positioned in direct contact with the bone surface and is of particular interest as it contains mesenchymal stem cells (MSCs), which have the potential to differentiate into osteoblasts and chondrocytes, and differentiated osteogenic progenitor cells. The localization of these cell types has made the cellular layer a target for drug therapies and cell harvesting for tissue engineering purposes."<-Since periosteal stem cells are right there next to the bone, they are a good target for chondrogenic differentiation.  Unfortunately, they are oriented on a longitudinal axis rather than a horizontal(except for the flat bone of the skull).
"The endocortical surface of a bone faces the medullary canal and is lined by the endosteum, a single thin layer of bone lining cells (mature osteoblasts) and osteoblasts, which form a membrane over endocortical and trabecular bone surfaces to enclose the bone marrow. The endosteum contains osteoprogenitor cells, but does not appear to contain either MSCs or hematopoietic stem cells (HSCs). However, a portion of HSCs can be found next to the endosteum suggesting reciprocal communication between cells within the endosteum and multipotent HSCs. The close relationship between the cells forms a so-called stem cell niche, whereby the cells of the endosteum physically support and influence stem cell activity."<-There's no endosteum in the epiphysis of the bone.  Maybe the functions of the endosteum can be mimicked in the epiphysis to help form new cartilagenous growth plates there.
"Lamellae in cortical bone form osteons or bone structural units, which consist of a central canal enveloped in concentric lamellae of bone tissue. Outer lamellae form first along the boundary of the osteon known as the cement line, with each successive lamella being laid concentrically inside the preceding one. In trabecular bone, lamellae are stacked into saucer-shaped bone packets that are separated by cement lines. The first lamellae are formed toward the center of the trabeculae with each successive lamella being stacked in parallel layers toward the bone surface. Uniformly spaced throughout lamellae are lenticular cavities called lacunae from which branching canaliculae radiate in all directions. The canaliculae penetrate the lamellae of the interstitial substance to anastomose with canaliculae of neighboring lacunae to form a continuous network of interconnecting cavities."<-Thus bone has the ability to communicate to other parts of the bone.
"Without the addition of mineral to collagen, bone tissue would have properties similar to a rubber band, whereas without collagen, bone is brittle such as chalk."<-If bone had properties similar to a rubber band it would be much easier to make longer.  Demineralizing the bone is a potential way for height growth to occur.
"Osteoclasts are large, multinucleate cells that exclusively mediate the process of bone resorption. Osteoclastogenesis begins when a HSC is stimulated to generate mononuclear cells, which then become committed preosteoclasts and are introduced into the blood stream[so the bone has a way for stem cells to enter the blood steam we just have to make those cells chondrocytes instead of osteoclasts]. The circulating precursors exit the peripheral circulation at or near the site to be resorbed, and fuse with one another to form a multinucleated immature osteoclast. Mature osteoclasts establish a microenvironment between themselves and the underlying bone by peripherally attaching to the matrix using integrins. The attachment creates a compartment between the ruffled basal border of the osteoclast and the bone surface that is isolated from the general extracellular space. An electrogenic proton pump transports in H+ ions to acidify the compartment, which acts to mobilize the mineralized component of bone. This exposes the organic matrix, which is subsequently degraded using proteases. The end result is the removal of bone matrix and the development of characteristic shallow cavities known as Howship’s lacunae."<-So osteoclasts attach to bone matrix using integrins.  Can we use similar integrins to encourage chondrocytes to attach to the site of a new growth plate?  Osteoclasts acidifing the compartment is also useful in making the collagen more elastic.  Elastic bone is much easier to stretch.  However, once bone is degraded by protease there is none to stretch.
"Osteoblasts are bone-forming cells and develop locally after proliferation of MSCs residing in the bone marrow stroma and periosteum. Mature osteoblasts express the matrix proteins type I collagen and osteocalcin, and alkaline phosphatase—a key enzyme in the mineralization process. Rows of active osteoblasts secrete unmineralized matrix (osteoid) before becoming either bone lining cells or incorporated into the bone matrix. Cells that become incorporated into the matrix gradually develop long cytoplasmic processes to remain in communication with surrounding cells and are considered immature osteocytes. As the matrix matures and mineralizes, and the osteoid seam moves further away, the osteocyte becomes entombed in a bony matrix."<-If we could get osteoblasts to secrete matrix on the longitudinal ends of bones then we could become taller.
"Osteocytes are the most numerous bone cells and are dispersed throughout the matrix where they occupy lacunae[although LSJL is about chondrogenic differentiation of mesenchymal stem cells, osteocytes are likely a part of the process]. Lacunae are interconnected by an elaborate network of thin tunnels called canaliculi through which osteocytes pass cytoplasmic or dendritic processes[we can determine which cytoplasmic and dendritic processes help with height growth and mimic them to grow taller]. These processes connect individual osteocytes with neighboring cells via gap junctions to facilitate both the transport of nutrients for osteocyte viability and the conveying of intercellular messages[so osteocytes have the ability to communicate with other cells including possible communicating with mesenchymal stem cells to differentiate into chondrocytes]. Intercellular communication is also facilitated by the osteocytic release of signaling molecules into the extracellular fluid, which flows through the lacuna-canalicular system[LSJL increases this fluid flow thus possibly amplifying these signaling molecules]. Osteocyte function remains unclear; however, their principal role appears to be the sensing of mechanical stimuli. In addition, recent evidence has also found osteocytes have the capacity to regulate mineral metabolism and alter their surrounding matrix."

"Bones of the upper extremity predominantly develop by endochondral ossification wherein condensations of mesenchymal cells differentiate into chondrocytes to form a cartilaginous template (or “anlage”). Exceptions are parts of the clavicles and scapulae, which form via intramembranous ossification that does not involve a cartilaginous precursor. In the anlage, chondrocytes hypertrophy and an ossification center forms by neovascularization of the initially avascular cartilaginous template. Osteoblasts associated with the newly developed vasculature begin secretion and mineralization of a type-I collagen-containing extracellular matrix. As development continues, the ossification center propagates toward the epiphyseal growth plates."<-This mentions the ossification center propagating toward the epiphyseal growth plates this would of course mean that inhibiting estrogen and bone growth would help height growth by giving more time for chondrocytes to grow.  However, this has been found not to be the case and that only very low or high levels of estrogen are detrimental to growth.  If there is an ossification center, the rate of it's growth does not seem to affect height growth.  In fact, it's likely a byproduct of normal endochondral ossification.  Also, if trying to form a new growth plate with LSJL the region should already be vascularized which may prove problematic with forming a new ossification center.

"[Motor paralysis] interferes with skeletal growth and modeling leading to the development of bones with reduced length, mass, and size"<-So exercise definitely affects growth but there may be diminishing returns as exercise does not seem to positively correlate with height past a point.

This study finds a correlation though between muscle size and bone size(although a shared variable like serum levels of myostatin may be involved):

Mechanical loads and cortical bone geometry in healthy children and young adults
"Muscle torque was positively associated with tibia length and muscle CSA[cross sectional area], independent of age, sex, and race."<-Increasing tibial length increases muscle torque.
"muscle CSA was positively associated with endosteal circumference"<-If the endosteum does help with height growth then this could be a mechanism to how muscle CSA helps with height growth.

"the study had limited power to detect significant differences in musclebone relations in the mature vs. growing skeleton"<-the more mature bone is similar to growing bone the more likely that mature bone is able to grow longer.

"changes in estimated bone strength during growth are highly correlated with changes in lean mass and muscle cross-sectional area (CSA) but not fat mass. When the growing bone is not subject to mechanical loading, muscle size and function are reduced and bone lacks the shape necessary for its function. In a study of arm side-to-side differences in growing tennis players, greater muscle size induced by exercise was positively correlated with changes in bone mass, size, and strength. However, the greater muscle size only accounted for 12%–16% of the side-to-side variance in bone outcomes, suggesting that other mechanical factors may contribute to bone adaptation during growth."<-So muscle size may play a role in up to 12% of bone length increasing.

"Tibia length is highly associated with Zp and with muscle CSA."<-Tibial length is correlated to muscle CSA.

"muscle CSA was positively associated with Zp, explaining 85% of the variance in Zp. Conversely, tibia length alone was significantly associated with greater Zp, explaining 84% of the variance in Zp."<-The fact that percentage of variance explained in bone strength is so similar between muscle and bone means that Bone Length and Muscle CSA are likely connected.

Remember, that muscular activity lowers myostatin levels which could trickle into effecting the bone.

So, potential mechanisms to manipulate height growth are altering osteocyte communication(done by LSJL which increases fluid flow), making the bone more acidic so it's more elastic(but how to do this safely?), and integrin binding(would need to involve cellular engineering).  Also, the endosteum is linked to muscle CSA and the endosteum is involved with bone marrow stem cell differentiation so maybe the endosteum is linked to myostatin which is linked to bone muscle and bone marrow stem cells.


  1. what in your opinion are the biggest problems preventing adult height gain ?

  2. apart from the obvious the reason i ask is that if we can solve every problem in our path we come up against then all that will be left are definite answers and sucess?possibility of height gain is certain in my view if we can identify and solve the most relevant issues of why adults dont grow.every problem potentially has a solution within reason height growth is within reason thats certain.thanks now whats no1 problem we must tackle

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  4. I have a list of supplements that are needed for growth with fused plates.

  5. what about vibration plates?