Monthly Archives: September 2012


This page is dedicated to understanding to a very high level the structure and function of the bones, joints, and spine. All of tis stuff is written by me from my studies on orthopedics

Note: All citations, references, links, sources, and used material will be labeled with a specific number i.e. Source 1 = (1)

Sources used: Source 1, Source 2, Source 3, Source 4, Source 5, Source 6, Source 7, Source 8, Source 9, Source 10, Source 11, Source 12, Source 13, Source 14

Orthopaedics is the study of the bones, joints, and spine of the human body. Let’s first focus on the bones first. In a toddler’s body there is about 270 bones. There is 206 bones in the human physically mature adult body. (1)

Bones are classified by their shapes. There are 5 main types of bones,

  • The long bones,
  • The short bones,
  • The flat bones,
  • The irregular bones.
  • The sesamoid bones

An example of a long bone is the femur or humerus. An example of a short bone is the bones of the wrist or ankles. For flat bone, skull bones. For irregular bones, that would be like the vertebrate.


The majority of the bones is a type of bone matrix, which is made of both living and non living tissue.

1. Living tissue in the bones comprise of bone cells, blood vessels, nerves. For the bone cells, there are 3 main types.

  • Osteoblasts – bone cells that build up bone
Osteoblasts – The osteoblasts seem to be able to create hormones themselves, with one example being the prostaglandins, which act on the bone. They also produce at a high rate of alkaline phosphate, a type of enzyme that plays some role in mineralizing the bone and making matrix proteins (2). The osteoblast are immature bone cells and eventually get trapped in the bone matrix and turn into osteocytes.
  • Osteoclasts – bone cells that tear down bone
Osteoclasts – The osteoclasts are responsible for bone resorption. They come from a monocyte stem cell lineage (??) (2). They are large and located in bone surfaces called Howship’s lacunae or resorption pit.
  • Osteocytes – mature bone cells that don’t form bones anymore
Osteocytes – Osteocytes are what the osteoblasts turn into after they get into the bone matrix and get trapped there. The osteoblasts themselves created the bone matrix. The space that they occupy and get trapped in are called lacunae. They seem to be able to regulate the bone’s response to stress and mechanical load (2).

2. Non-living tissue is the bone matrix which is the collagen fibers and crystalline salts.

Crystalline Salts – The crystalline salt are of two elements, Calcium and Phosphates. The Calcium and Phosphates combine to form hydroxyapatite crystals.

Collagen Fibers – The Type I Collagen make up the organic part of of the non living bone matrix.

What gives the bone its strength?

Answer: Two main components, collegan and the calcium salts.

  • Collagen Fibers – gives the bone high tensile strength – is almost as strong as reinforced concrete! (about 150 MPa)
  • Calcium Salts – gives the bone high compression strength – stronger than even reinforced concrete! (about 200 MPa)

This suggest that at least for long bones, the bone is less resilient to torsion forces applied. It seems fractures in long bones occurs most when a torsion force is applied.

  •  The shear stress strength of long bones is low in comparison to its tensile and compressive load strength at around 50 MPa (2)


Let’s only look at the structure of the long bone, like a femur.

The bone is elongated in form. There are two expanded ends of the bone, which are the epiphysis, which forms a joint with another bone. At the very ends of the epiphysis is a layer of cartilage cover called the articular cartilage. For the epiphysis, they are not made of compact bone but of another type of bone called the cancellous or trabecular bone type which is spongy in appearance. The cancellous bone has a high surface area and high porosity, which the cavities being rod and plate like in form.

The shaft in the middle of the bone between the two epiphysis ends is called the diaphysis. Besides the area which the articular cartilage is covering, the rest of the long bone is covered in a layer called the periosteum. Inside the layer of the periosteum is another thicker layer of bone called the compact  bone which is in the diaphysis middle region. This is also very strong, and tough, with a low porosity and make up around 80% of the bone weight of the body.

The cortical bone in the diaphysis forms a inner cavity called the inter medullar cavity in the middle of the bone. This cavity continues on into the spongy bone areas of the epiphysis and is filled with a tissue called marrow. There are two types of marrow, yellow and red. The yellow marrow is found in the inter medullary cavity in the diaphysis region while the red marrow is found in the epiphysis spongy bone area. The yellow marrow is used as fat storage while the red marrow is to create blood cells. The red bone marrow participates in the formation of red blood cells (RBCs) through the process of erythropoiesis

Bone Growth 

Bones, specifically long bones, can grow in three main ways, longitudinally, radially, or by density. This means that the long bone is either going to grow longer, thicker, or stronger.

The type we are trying to achieve is to get the long bones like our femur and tibia to increase longitudinally, especially after the stage of puberty and our epiphyseal growth plates have fused and even the epiphyseal line has disappeared.

First, the formation of bone is called Ossification. There is two types of ossification, Endochondral and Intramembranous

1. Endochondral Ossification:  This type of ossification is the main way for most of the bones in the body to form and grow. There appears to be an initial piece of hyaline cartilage that grows over time. There are 5 main steps in this type of ossification (2)…

  • Development of cartilage model
  • Growth of cartilage model
  • Development of the primary ossification center – It seems the actual endochondral ossification actually starts here.
  • Development of the secondary ossification center
  • Formation of articular cartilage and epiphyseal plate

2. Intramembranous Ossification: This type occurs during the formation of the flat bones of the skull but also in other bones in the skull and clavicle (2). This type of bone is formed from a type of tissue that is not cartilage, one of them called the mesenchyme tissue. There appear to be 4 steps in this type of ossification…

  • Development of ossification center
  • Calcification
  • Formation of trabeculae
  • Development of periosteum
It seems that all newborns have bones that are only of red marrows, but as they grow older the red marrow gets replaced by the yellow marrow which is for fat storage.
For our purposes, we need to know more about the Longitudinal growth of long bones.
First, longitudinal growth (I will call it LG) depends on both the proliferation and hypertrophy of the chondrocytes in the growth plate (3). It is hard for the long bones to grow in LG fashion because they also have to deal with the structure and weight of the bone tissue around it and also serve another function. It requires rapid growth rates, where the rate of osteoblasts producing bones must be more than the rate of osteoclasts taking away bone .
The chondrocyte cells in the growth plate must multiply but also expand in size to push the epiphysis and articular cartilage at the ends away from the metaphysics and diaphysis.
Bone Remodeling
Bone remodeling or turnover is the two simultaneous process of bone breakdown or resorption and the process of bone building which occur at the same time to form the bone which seem to look the same form throughout time. This is accomplished by the osteoblasts and the osteoclasts who seem to work together by signally with each other to keep other in check. The purpose of the remodeling is to regulate calcium homeostasis and to repair any damaged bone parts that result from everyday actions.
It is important to note that when the osteoblasts are forming bone, they are actually removing calcium from the blood and binding the calcium to the inorganic non living bone matrix to make the bone harder and stronger. When the osteoclasts are breaking apart the bone units, they are resorbing the calcium back into the bloodstream and making the inorganic bone matrix less strong. Both of the processes occur at the same time in a  coupled way in site specific locations.
Thus, the size and volume of the bone is determined by the rates of bone formation and bone resorption. There are many growth factors which work in localized bone areas to increase osteoblast activity. These include the TGF-beta, IGFs, FGF, and BMPs. It seems that the bone cells themselves can produce these types of growth factors to be stored in the bone matrix. These factors which are stored can then be released from the matrix leading to osteoblast creation. There is a law known as Wolff’s Law that shows that repeated loads of stress to a bone region leads to that region of bone thickening. the theory behind it is that the bone cells have a piezoelectric effect, which means that mechanical force application causes small electrical potential, which leads back to a mechanical expression.
The action of osteoblasts and osteoclasts are controlled by a number of chemical factors that either promote or inhibit the activity of the bone remodeling cells, controlling the rate at which bone is made, destroyed, or changed in shape. The cells also use paracrine signalling to control the activity of each other. (2)

Disorders & Pathologies

The most common types of disorders that affect the bone and skeletal system is osteoporosis. Osteoporosis is where the bones in the body lose their strength and density from increased bone porosity. This leads to an increase in the likelihood of fracture. It happens most often with women who have reached past menopause but it can also occur within men or women who are suffering from certain kinds of hormone pathologies

What exactly causes height increase?

Height increase is actually caused by at least 4 main processes, . Most people would tell you that height increase only comes about from the longitudinal growth of the long bones like the femur and tibia but they are not taking into consideration the growth of other bones in the body, specifically the short bones, the flat bones, and the irregular bones. The 32 vertebrate in our back are irregular bones and they do increase in size when we were still growing and that did contribute to our height. Our torso makes up about 1/3rd of our total height.

However, most people will only focus on the endochondral ossification in the long bones. It is important to note that the short bones also go through endochondral ossification just like the long bones.

Let’s look closer at the process of endochondral ossification. This type of ossification is the type of process in the first formation of long bone, the growth in length of the long bone, and the natural healing of bone fractures. Cartilage is used in this process.

The cartilage goes through a type of growth called interstitial growth which chondrocytes which are cartilage cells divide and multiple while are the same type excreting waste which is used to make up the cartilage matrix .

Another type of growth that happens is known as appositional growth in the endochondral ossification process. This is where the long bones get thicker so the width increases since the extracellular matrix on the edge of the chondrocyte stacked columns also increases from the excretion of the chondrocytes. This happens at the same time new chondroblasts are made in the perichondrium.

For the long bone, there are actually two main areas that experience endochondral ossification, not one. There is the middle part called the diaphysis but also the outer parts called the epiphysis. The middle part is the primary center while the outer parts is the secondary center.

For Primary Center In Middle Diaphysis Section (taken from Wikipedia)

The first site of ossification occurs in the primary center of ossification, which is in the middle of diaphysis (shaft). Then:

  • Formation of periosteum: The perichondrium becomes the periosteum. The periosteum contains a layer of undifferentiated cells (osteoprogenitor cells) which later become osteoblasts.
  • Formation of bone collar: The osteoblasts secrete osteoid against the shaft of the cartilage model (Appositional Growth). This serves as support for the new bone.
  • Calcification of matrix: Chondrocytes in the primary center of ossification begin to grow (hypertrophy). They stop secretingcollagen and other proteoglycans and begin secreting alkaline phosphatase, an enzyme essential for mineral deposition. Then calcification of the matrix occurs and apoptosis of the hypertrophic chondrocytes occurs. This creates cavities within the bone. The exact mechanism of chondrocyte hypertrophy and apoptosis is currently unknown.
  • Invasion of periosteal bud: The hypertrophic chondrocytes (before apoptosis) secrete Vascular Endothelial Cell Growth Factor that induces the sprouting of blood vessels from the perichondrium. Blood vessels forming the periosteal bud invade the cavity left by the chondrocytes and branch in opposite directions along the length of the shaft. The blood vessels carry hemopoietic cells, osteoprogenitor cells and other cells inside the cavity. The hemopoietic cells will later form the bone marrow.
  • Formation of trabeculae: Osteoblasts, differentiated from the osteoprogenitor cells that entered the cavity via the periosteal bud, use the calcified matrix as a scaffold and begin to secrete osteoid, which forms the bone trabecula. Osteoclasts, formed from macrophages, break down spongy bone to form the medullary (bone marrow) cavity.

For Secondary Center In Outer Epiphysis Section (taken from Wikipedia)

About the time of birth, a secondary ossification center appears in each end (epiphysis) of long bones. Periosteal buds carry mesenchyme and blood vessels in and the process is similar to that occurring in a primary ossification center. The cartilage between the primary and secondary ossification centers is called the epiphyseal plate, and it continues to form new cartilage, which is replaced by bone, a process that results in an increase in length of the bone. Growth continues until the individual is about 26 years old or until the cartilage in the plate is replaced by bone. The point of union of the primary and secondary ossification centers is called the epiphyseal line.

Let’s now see how Apositional Bone Growth occurs. It seems that the long bones get thicker by forming more bones right underneath the periosteum. On the inside, the osteoclasts degrade the long bone to create the hollow cavity in the middle. Eventually once physical maturity is reached, the rate at which bones are formed underneath the periosteum and the rate which osteoclasts degrade the inner bone is about the same so the thickness of the bone stays constant.

Now let’s remember that the cartilage in the growth plates are the type called hyaline. Let’s look to see what exactly is Hyaline Cartilage

The Epiphyseal Growth Plate (from Wikipedia)

The epiphyseal growth plate has 5 main layers to it, the resting zone, the proliferate layer ,the hypertrophic layer ,the calcification layer, and the ossification layer.

  1. Zone of resting cartilage. This zone contains normal, resting hyaline cartilage.
  2. Zone of proliferation / cell columns. In this zone, chondrocytes undergo rapid mitosis, forming distinctive looking stacks.
  3. Zone of maturation / hypertrophy. It is during this zone that the chondrocytes undergo hypertrophy (become enlarged). Chondrocytes contain large amounts of glycogen and begin to secrete alkaline phosphatase.
  4. Zone of calcification. In this zone, chondrocytes are either dying or dead, leaving cavities that will later become invaded by bone-forming cells. Chondrocytes here die when they can no longer receive nutrients or eliminate wastes via diffusion. This is because the calcified matrix is much less hydrated than hyaline cartilage.
  5. Zone of ossification. Osteoprogenitor cells invade the area and differentiate into osteoblasts, which elaborate matrix that becomes calcified on the surface of calcified cartilage. This is followed by resorption of the calcified cartilage/calcified bone complex.

Hyaline Cartilage (taken from Wikipedia)

Is a type of cartilage found on many joint surfaces. It is pearly bluish in colour with firm consistency and considerable collagen. It contains no nerves or blood vessels, and its structure is relatively simple.

Hyaline cartilage is covered externally by a fibrous membrane, called the perichondrium, except at the articular ends of bones and also where it is found directly under the skin, i.e. ears and nose. This membrane contains vessels that provide the cartilage with nutrition.

If a thin slice is examined under the microscope, it will be found to consist of cells of a rounded or bluntly angular form, lying in groups of two or more in a granular or almost homogeneous matrix.

The cells, when arranged in groups of two or more, have generally straight outlines where they are in contact with each other, and in the rest of their circumference are rounded.

They consist of clear translucent protoplasm in which fine interlacing filaments and minute granules are sometimes present; embedded in this are one or two roundnuclei, having the usual intranuclear network.

The cells are contained in cavities in the matrix, called cartilage lacunae; these are actually artificial gaps formed by the shrinking of the cells during the staining and setting of the tissue for observation. The interterritorial space between the isogenous cell groups contains relatively more collagen fibers, causing it to maintain its shape while the actual cells shrink, creating the lacunae.

This constitutes the so-called capsule of the space. Each lacuna is generally occupied by a single cell, but during the division of the cells it may contain two, four, or eight cells. (see isogenous group)

Hyaline cartilage also contains chondrocytes which are cartilage cells that produce the matrix. Hyaline cartilage matrix is mostly made up of type II collagen and Chondroitin sulfate, both of which are also found in elastic cartilage.

Hyaline cartilage exists on the ventral ends of ribs; in the larynx, trachea, and bronchi; and on the articular surface of bones.

The term “articular cartilage” refers to the hyaline cartilage on the articular surfaces of bones.[edit]Articular Cartilage[1]

Though it is often found in close contact with menisci and articular disks, articular cartilage is not considered a part of either of these structures, which are made entirely of fibrocartilage.

Chondrocytes (taken from Wikipedia)

Chondrocytes are the only cells found in healthy cartilage. They produce and maintain the cartilaginous matrix, which consists mainly of collagen and proteoglycans. Although chondroblast is still commonly used to describe an immature chondrocyte, use of the term is discouraged, for it is technically inaccurate since the progenitor of chondrocytes (which are mesenchymal stem cells) can also differentiate into osteoblasts. The organization of chondrocytes within cartilage differs depending upon the type of cartilage and where in the tissue they are found.

From least- to terminally-differentiated, the chondrocytic lineage is:

  1. Colony-forming unit-fibroblast (CFU-F)
  2. Mesenchymal stem cell / marrow stromal cell (MSC)
  3. Chondrocyte
  4. Hypertrophic chondrocyte

When referring to bone or cartilage, mesenchymal stem cell (mesoderm origin) are undifferentiated meaning they can differentiate into different variance of generative cells (MSC) are commonly known as osteochondrogenic (or osteogenic, chondrogenic, osteoprogenitor, etc.) cell. Undifferentiated mesenchymal stem cell lose their process, proliferate and crowd together in a dense aggregate of chondrogenic cells(cartilage) at the center of chondrification. These condrogenic cells will then differentiate to chondroblasts which will then to synthesize the cartilage ECM(extra cellular matrix). Which consists of ground substance(proteoglycans, glycosaminoglycans for low osmotic potential) and fibers. The chondroblasts then trap themselves in a small space that is no longer in contact with the newly created matrix called lacunae which contain extracellular fluid. The chondroblast is now a chondrocyte, which is usually inactive but can still secrete and degrade matrix depending on the conditions. The majority of the cartilage that has been built has been synthesized from the chondroblast which are much more inactive at a late age (adult hood) compared to earlier years (pre-pubesence)

Chondrocytes undergo terminal differentiation when they become hypertrophic during endochondral ossification. This last stage is characterized by major phenotypic changes in the cell.

Collagen (Wiki)

Collagen is a group of naturally occurring proteins found in animals, especially in the flesh and connective tissues of vertebrates. It is the main component of connective tissue, and is the most abundant protein in mammals, making up about 25% to 35% of the whole-body protein content. Collagen, in the form of elongated fibrils, is mostly found in fibrous tissues such as tendon, ligament and skin, and is also abundant in cornea, cartilage, bone, blood vessels, the gut, and intervertebral disc. The fibroblast is the most common cell which creates collagen.

Collagen occurs in many places throughout the body. Over 90% of the collagen in the body, however, is of type one.

So far, 28 types of collagen have been identified and described. The five most common types are:

  • Collagen I: skin, tendon, vascular ligature, organs, bone (main component of the organic part of bone)
  • Collagen II: cartilage (main component of cartilage)
  • Collagen III: reticulate (main component of reticular fibers), commonly found alongside type I.
  • Collagen IV: forms bases of cell basement membrane
  • Collagen V: cell surfaces, hair and placenta

Amino acids

Collagen has an unusual amino acid composition and sequence:

  • Glycine is found at almost every third residue
  • Proline (Pro) makes up about 17% of collagen
  • Collagen contains two uncommon derivative amino acids not directly inserted during translation. These amino acids are found at specific locations relative to glycine and are modified post-translationally by different enzymes, both of which require vitamin C as a cofactor.
    • Hydroxyproline (Hyp), derived from proline.
    • Hydroxylysine (Hyl), derived from lysine (Lys). Depending on the type of collagen, varying numbers of hydroxylysines are glycosylated (mostly havingdisaccharides attached).

Cortisol stimulates degradation of (skin) collagen into amino acids.

Osteoid (from Wiki)
Osteoid is the unmineralized, organic portion of the bone matrix that forms prior to the maturation of bone tissue. Osteoblasts begin the process of forming bone tissue by secreting the osteoid as several specific proteins. When the osteoid becomes mineralized, it and the adjacent bone cells have developed into new bone tissue.

Osteoid makes up about fifty percent of bone volume and forty percent of bone weight. It is composed of fibers and ground substance. The predominant fiber-type is Type I collagen and comprises ninety percent of the osteoid. The ground substance is mostly made up of chondroitin sulfate and osteocalcin.

Glycogen (from Wikie)

Glycogen is a multibranched polysaccharide that serves as a form of energy storage in animals and fungi. In humans, glycogen is made and stored primarily in the cells of the liver and the muscles, and functions as the secondary long-term energy storage (with the primary energy stores being fats held in adipose tissue).

Glycogen is the analogue of starch, a glucose polymer in plants, and is sometimes referred to as animal starch, having a similar structure to amylopectinbut more extensively branched and compact than starch. Glycogen is found in the form of granules in the cytosol/cytoplasm in many cell types, and plays an important role in the glucose cycle. Glycogen forms an energy reserve that can be quickly mobilized to meet a sudden need for glucose, but one that is less compact than the energy reserves of triglycerides (lipids).

Polysaccharide represents the main storage form of glucose in the body. Found in the liver and muscles, muscle glycogen is converted into glucose by muscle cells, and liver glycogen converts to glucose throughout the body including the Central Nervous System.

In the liver hepatocytes, glycogen can compose up to eight percent of the fresh weight (100–120 g in an adult) soon after a meal. Only the glycogen stored in the liver can be made accessible to other organs. In the muscles, glycogen is found in a low concentration (one to two percent of the muscle mass). The amount of glycogen stored in the body—especially within the muscles, liver, and red blood cells—mostly depends on physical training,basal metabolic rate, and eating habits such as intermittent fasting. Small amounts of glycogen are found in the kidneys, and even smaller amounts in certain glial cells in the brain and white blood cells.

Alkaline Phosphatase


Fibrocartilage (wiki)

White fibrocartilage consists of a mixture of white fibrous tissue and cartilaginous tissue in various proportions. It owes its flexibility and toughness to the former of these constituents, and its elasticity to the latter. It is the only type of cartilage that contains type I collagen in addition to the normal type II.

Fibrocartilage is found in the pubic symphysis, the annulus fibrosus of intervertebral discs, meniscus, and the TMJ. During labor, relaxin loosens the pubic symphysis to aid in delivery, but this can lead to later joint problems.

Formation as a repair mechanism

If hyaline cartilage is torn all the way down to the bone, the blood supply from inside the bone is sometimes enough to start some healing inside the lesion. In cases like this, the body will form a scar in the area using a special type of cartilage called fibrocartilage. Fibrocartilage is a tough, dense, fibrous material that helps fill in the torn part of the cartilage. Yet it’s not an ideal replacement for the smooth, glassy articular cartilage that normally covers the surface of the knee joint.[edit]

Periosteum (taken from Wikipedia)

Periosteum is a membrane that lines the outer surface of all bones, except at the joints of long bones. Endosteum lines the inner surface of all bones.

Periosteum consists of dense irregular connective tissue. Periosteum is divided into an outer “fibrous layer” and inner “cambium layer” (or “osteogenic layer”). The fibrous layer contains fibroblasts, while the cambium layer contains progenitor cells that develop into osteoblasts. These osteoblasts are responsible for increasing the width of a long bone and the overall size of the other bone types. After a bone fracture the progenitor cells develop into osteoblasts and chondroblasts, which are essential to the healing process.

As opposed to osseous tissue, periosteum has nociceptive nerve endings, making it very sensitive to manipulation. It also provides nourishment by providing the blood supply. Periosteum is attached to bone by strong collagenous fibers called Sharpey’s fibres, which extend to the outer circumferential and interstitial lamellae. It also provides an attachment for muscles and tendons.

Cytokines (taken from Wikipedia)

Cytokines are small cell-signaling protein molecules that are secreted by numerous cells and are a category of signaling molecules used extensively in intercellular communication. Cytokines can be classified as proteins, peptides, or glycoproteins; the term “cytokine” encompasses a large and diverse family of regulators produced throughout the body by cells of diverse embryological origin.

Part of the difficulty with distinguishing cytokines from hormones is that some of the immunomodulating effects of cytokines are systemic rather than local. For instance, to use hormone terminology, the action of cytokines may be autocrine or paracrine in chemotaxis and endocrine as a pyrogen. Further, as molecules, cytokines are not limited to their immunomodulatory role. For instance, cytokines are also involved in several developmental processes during embryogenesis

Each cytokine has a matching cell-surface receptor. Subsequent cascades of intracellular signalling then alter cell functions. This may include the upregulation and/or downregulation of several genes and their transcription factors, resulting in the production of other cytokines, an increase in the number of surface receptors for other molecules, or the suppression of their own effect by feedback inhibition.


The effect of a particular cytokine on a given cell depends on the cytokine, its extracellular abundance, the presence and abundance of the complementary receptor on the cell surface, and downstream signals activated by receptor binding; these last two factors can vary by cell type. Cytokines are characterized by considerable “redundancy”, in that many cytokines appear to share similar functions.

Mesenchymal Stem Cells

Mesenchymal stem cells are a type of connective tissue cell that can differentiate into a few different type of cells, specifically bone cells (osteoblasts), cartilage cells (chondrocytes), and fat cells (adipocytes). It is characterized as small cell body,long and  thin, with a large nucleus. It seems that they have a high capacity for self renewal while still being able to keep their ability to differentiate into other types of cells. The actual differentiation can be induced mechanically or chemically. It seems that the ability to multiply and change into other cells seem to decrease as the person grows older. They secrete cytokines.

How Exactly do Bones Heal from Fracture (dislocation, etc) ?

Bone heal first by having a knowledgeable person put the fractured bone area back into the right position or relocation. The position is stabilized and then the natural bone healing process occurs. A fracture ultimately heals through physiological processes.

The healing process is mainly determined by the periosteum (the connective tissuemembrane covering the bone). The periosteum is one source of precursor cells which develop into chondroblasts and osteoblasts that are essential to the healing of bone. The bone marrow (when present),endosteum, small blood vessels, and fibroblasts are other sources of precursor cells. (from Wikipedia)

Phases of fracture healing (from Wikipedia)

There are three major phases of fracture healing, two of which can be further sub-divided to make a total of five phases;

  • 1. Reactive Phase
    • i. Fracture and inflammatory phase
    • ii. Granulation tissue formation
  • 2. Reparative Phase
    • iii. Cartilage Callus formation
    • iv. Lamellar bone deposition
  • 3. Remodeling Phase
    • v. Remodeling to original bone contour


After fracture, the first change seen by light and electron microscope is the presence of blood cells within the tissues adjacent to the injury site. Soon after fracture, the blood vessels constrict, stopping any further bleeding. Within a few hours after fracture, the extravascular blood cells form a blood clot, known as a hematoma. All of the cells within the blood clot degenerate and die. Some of the cells outside of the blood clot, but adjacent to the injury site, also degenerate and die. Within this same area, the fibroblasts survive and replicate. They form a loose aggregate of cells, interspersed with small blood vessels, known as granulation tissue.


Days after fracture, the cells of the periosteum replicate and transform. The periosteal cells proximal (closest) to the fracture gap develop into chondroblasts which form hyaline cartilage. The periosteal cellsdistal to (further from) the fracture gap develop into osteoblasts which form woven bone. The fibroblasts within the granulation tissue develop into chondroblasts which also form hyaline cartilage. These two new tissues grow in size until they unite with their counterparts from other parts of the fracture. These processes culminate in a new mass of heterogeneous tissue which is known as the fracture callus. Eventually, the fracture gap is bridged by the hyaline cartilage and woven bone, restoring some of its original strength.

The next phase is the replacement of the hyaline cartilage and woven bone with lamellar bone. The replacement process is known as endochondral ossification with respect to the hyaline cartilage and bony substitution with respect to the woven bone. Substitution of the woven bone with lamellar bone precedes the substitution of the hyaline cartilage with lamellar bone. The lamellar bone begins forming soon after the collagen matrix of either tissue becomes mineralized. At this point, the mineralized matrix is penetrated by channels, each containing a microvessel and numerous osteoblasts. The osteoblasts form new lamellar bone upon the recently exposed surface of the mineralized matrix. This new lamellar bone is in the form of trabecular bone. Eventually, all of the woven bone and cartilage of the original fracture callus is replaced by trabecular bone, restoring most of the bone’s original strength.

Complications of Fracture Healing

The main complications include:

  1. Delayed Union: Poor blood supply or infection.
  2. Non-Union: Bone loss or wound contamination.
  3. Fibrous Union: Improper immobilization
Other technologies that increase bone healing

Various studies have found that pulsed electromagnetic fields (PEMF) have increased the rate of bone healing.

Low intensity pulsed ultrasound, applied twenty minutes per day, increases the rate of bone healing.

Major Announcement: Shift In Website Focus, Part II (Important)

I was gone for 11 days in China very recently and I only came back 2 days ago. During the time I was staying there, I did not write many articles or posts. When I was writing the posts, there was always a feeling that for me personally, I was sort of spinning the wheels like a hamster. I have currently 396 published posts and very little of it is really worth of great value.

When I copy and paste long articles I thought people were reading these things and I realized that few people who come to the website do what I thought. So here is the plan. I am going to show all of you want my plans are for the next 365 days, because I realize that the endeavor of height increase feels like it is moving too slowly.

For me, I realized that after a certain point in doing all of these articles and writings, I was getting almost nowhere. This is where it is going to change. For us to solve this problem, we have to really focus our attention on this subject and tackle it.

Here are the avenues that I think are the most promising.

1. Stem Cells and Implants

2. Growth Plate implants

3. Bone Morphogenetic Proteins

4. Mesenchymal Stem Cells

5. Transdifferentiation

6. Gene therapy

Here are the topics or article I was supposed to write on but I will not write about…

1. The Implications Of The BMP-7 AND OP-1 Research On Intervertebral Disk Height

2. The Connection Between Noggin Glycoprotein And Height

3. The Connection Between The Parathyroid Hormone-Related Protein (PTHrP) And Height

4. A Study Of The Insulin Growth Factor Receptor, IGF1R

5. Increase Height And Grow Taller Using Hypothalamic Growth Hormone Releasing Hormone

6. The AKT Signaling Pathway

7. Supplement Formulas To Increase Height And Grow Taller

8. Theories On Delaying Puberty To Extend The Growth Period

9. Increase Height And Grow Taller Using Nitric Oxide

10. Increase Height And Grow Taller Using Ghrelin

It is time to get real. it is time to become honest. It is time to get serious.

NOTE: One major thing I will be doing is finding a real medical school textbook on endocrinology and also orthopedics and studying those things to really understand what the hell I am talking about. I want to admit right now that I only understand up to 50% of everything that I have been talking about.

I. Here are the topics that my coworker Nicki has suggested we research into…

I feel that MScs are key to re-opening the growth plates.
androgens (youve touched upon estrogen) need to cover T
indian hedgehog
Fgfs ( i sent you a post on that)
thyroid hormone
i see youve touched upon igf-1 and gh but i feel it needs further understanding
collagen II deff deserves an in depth post on its own
wnt pathway
mesechymal condensation
seperate posts on key processes for growth? chondrogenesis, osteogenesis etc youknow its better organization as well
i see you mention upon controlling stem cells to determine their fate, needs further research
II. Here are the topics that I still have to get through on my blog list of subjects to cover

jagmonan sachdeva – accupresure scam

dit binaural beats article- add theory of how it could possibly work,6dab6d585a096602,5690b6556e9a1a61.html

III. Here are the topics or scientific papers I wanted to review and talk about

IV. From Harald of the Biomedical Growth Research Initiative, I was given a list of scientific articles to look through for ideas which I can’t share on here, yet. 

Me: The truth is that I kind of wanted to start over, and make this site get back to the roots.

Major Change 1: I am going to write only 1 or 2 posts a day but the information in those posts will be of only high quality, the type that you would want to write a comment on and have a heated dissuasion on. I will be challenging the readers to test their intellectual and cognitive ability

Major Change 2: There will be one main page that focuses on the endocrinology of the growth process. There will be another page that focuses on orthopedics.

A. There will be almost no more product reviews since none of the E-products or herbal and amino acid supplements sold on the internet will increase the height of people who are already physically mature. They just don’t work. 

B. There will be almost no more body hacks since since I realize that there are already many websites on the internet that talk about that kind of stuff. This site was created to find a solution to height increase, and that should be what this website should focus on. 

C. Since I do believe that increasing one’s intelligence is important, a few mind hacks for learning how increase one’s intelligence will still be posted. 

D. There will be no more long posts, fewer but in better quality material, and nearly everything that I write will be from my interpretation. Sometimes I will quote small passages from scientific articles or papers but they will be in the italics font with quotations marks around them. My writing will be in normal “times new roman” font.

E. All facts or statement I will try to validate through links, sources, references, and citations. If I make a claim on a scientific principle or idea, I will show you where I got the idea from. 

F. Some old posts will be revised, edited upon, and added upon for future people who manage to find the website to learn and be more informed.
G. The Resources, Useless, Useful, and Complete List of Posts Pages will be always edited and added upon.

That will be all for now. I promise to make this website really worth the time you use to come here and read my material. The late Steve Jobs stated in his most famous delivered 2005 Stanford Commencement Address (found HERE) …

“If you live each day as if it is your last, someday you will most certainty be right…It made an impression on me. Since then, for the past 33 years, I have looked into the mirror every morning and have asked myself ‘If today was the last day of my life, would I want to do what I am about to do today?’…and whenever the answer has been ‘no’ for too many days in a row, I know I need to change something! …Remembering that I will be dead soon is the most important tool I have ever encountered to help me make the big choices in life, because almost everything, all the external expectations, all pride, all fears of embarrassment or failure, these just fall away in the face of death, leaving only what is truly important….”

and finally

“Remembering you are going to die is the best way I know to avoid the trap of thinking that you have something to lose. You are already naked. There is no reason not to follow your heart…”

Me: I remember just 3 weeks when I was sitting at the cafe where I am sitting right, now, only 3 feet from where I am sitting right now typing away on my Macbook Air laptop, and I found myself miserable. I have proclaimed that I would create a website that would help find a solution on height increase and I was not really doing what my original intentions were. I found myself miserable. I dreaded opening up the laptop and trying to grind out another post on the link between height and some chemical compound. I felt like I was running in circles and making no headway. When I asked myself the Steve Jobs question of whether I would do what I wanted to do if that day was the last day of my life, I said no, at least 10 times in a row. I knew something had to change. I had to change. My environment had to change. So I bought ticket to Shanghai and flew there, for rest and to think. I wanted to refocus my energy and gather my thoughts to see what I was doing.

I realized today after coming back to Seoul that I was not being completely honest, not with you the readers or with myself. I wasn’t really making a true contribution to the world. I was only repeating knowledge and information that thousands, if not millions of people before me have already known and repeat as well. How am I expected to make any real contribution and progress in this endeavor if I don’t raise my own standards and o what I said I would. I needed to  raise my own level of thinking, of problem solving. I have to be better.

When I got on that plane to fly out of Seoul nearly two weeks ago, I found myself feeling the same type of uncomfortable dread in the pit of my stomach which I have always felt a little of before fit takes off. I have been afraid of death, and one of the main reasons was that I haven’t made any real contribution to the world. What have I done or given to the world to make it better? What if I die without ever giving my gifts and talent to this world to leave it a better place than when I arrived? I truly believe that if I can make a big contribution in this endeavors, my heart will be a lot lighter the next time I get on the place. I will be less afraid to die.

I’m sure most of you have already seen part or all of the entire video with Jobs before but I think it is worth your time to watch it at least one more time. I believe it is really worth your time.

Product Review XIII: Height Gain HighTole-XL Capsule

From HashmiHealthcare.Com, this is what the product sellers claim on the front page. Also found from

Height increase supplement

  • Boosts natural process of Growth and development of the body.
  • Builds and tones Muscular mass by promoting new cell and tissue growth.
  • Improves Metabolism which further leads to lean body.
  • Strengthens Nervous System.
  • Maintains Cholesterol levels and is a good tonic for Heart.
  • Helps in patients of Insomnia.
  • Slower down’s aging process.
  • Reduces extra fat.
  • Increases memory power.
  • Produces Amino acids that work as a food supplement for Pituitary.
Hight Gain

HighTole-XL Capsule is a no 1 Capsule for height increase, grow taller with the most potent height increase formula on the market today worldwide with results that are guaranteed.This Capsule supplement is 100% natural and safe with no harmful side effects. HighTole-XL Capsule is a height growth supplement.HighTole-XL Capsule is a powerful safe and effective to grow taller formula to help you.HighTole-XL Capsule is a height growth and grow taller supplement which helps people to gain extra inches in their height growth.The product is very much effective and result oriented.

How Hormones help our body to grow taller: As we all know that growth hormone plays key role in any ones height growth. In normal course an Individual’s pituitary gland releases, about 7/10th of a milligram of growth hormone in 24 hour. Where as half of this amount is released within the first hour of sleep and rest of the hormone is released. Sleep is the major stimulator of growth hormone, physical exercise is next in the line. In fact the intensity of Growth hormones peaks higher during exercise as compared to sleep. Several things influence the magnitude and intensity of growth hormone released during exercise.

The intake of HighTole-XL Capsules help body and mind to undergo sound sleep which is a must for repair of cells and production of new cells and harmones. As mentioned above this herbal supplement promotes nervours system, improves Metabolism, help body to enhance making of tissues and also helps in the process of Bone growth.

As this height growth system is based on supplement + Exercise, We recommend some specific type of workouts along with supplement intake. These specific workouts promotes growth by following above mentioned principles of growth.

Grow taller program and Height growth supplement ” HighTole-XL Capsules “

For the last Six years this grow taller program + height growth supplement “HighTole-XL Capsule ” has been considered the best source of safe growth and supplementing worldwide, and provides you with the fastest growing results. HighTole-XL Capsules – A High quality, 100% risk free increase height herbal formulation to help you grow taller and faster by regenerating your bones and cartilages.

Out of the many grow taller programs and height growth supplement out there, why is Grow taller program and height increase supplement HighTole-XL Capsules the safest and ultimate choice? – Because it thoroughly researched grow taller system and it is based on modern and ancient techniques of Yoga and Ayurveda, this herbal formulation comes from natural sources! The revolutionary most potent formula HighTole-XL Capsules not only can increase height, but will help one’s bones recover and grow faster by boosting natural height growth.

Me: You can buy a 1 month supply of the HighTole XL capsule for $73.50 and apparently you can pay for this product buy using your credit card or using Paypal. How convenient. I am really tired today and I don’t want to get into the long scientific discussion on its effectiveness or feasibility. Just read the conclusion.

Conclusion: It is a scam. It will not work for people who are physically mature.

The Link Between Laron Syndrome And Increased Longevity And Cancer Decrease

While I was doing research on Larons Syndrome, I found out about the startling fact that people who have Laron Syndrome which is a lack of the growth hormone receptors to work, seem to have extremely low rates of cancer and diabetes, as well as increase in their lifespan. I don’t want to talk too much about the subject but will let the writers who wrote articles about this phenomena speak.

From the New York Times (source HERE)…

Ecuadorean Villagers May Hold Secret to Longevity

Published: February 16, 2011
  • People living in remote villages in Ecuador have a mutation that some biologists say may throw light on human longevity and ways to increase it.
A 32-year-old community leader and artist who has the rare dwarfism condition, with his bride, 17.

The villagers are very small, generally less than three and a half feet tall, and have a rare condition known as Laron syndrome or Laron-type dwarfism. They are probably the descendants of conversos, Sephardic Jews from Spain and Portugal who were forced to convert to Christianity in the 1490s but were nonetheless persecuted in the Inquisition. They are also almost completely free of two age-related diseases, cancer and diabetes.

A group of 99 villagers with Laron syndrome has been studied for 24 years by Dr. Jaime Guevara-Aguirre, an Ecuadorean physician and diabetes specialist. He discovered them when traveling on horseback to a roadless mountain village. Most such villages are inhabited by Indians, but these were Europeans, with Spanish surnames typical of conversos.

As Dr. Guevara-Aguirre accumulated health data on his patients, he noticed a remarkable pattern: though cancer was frequent among people who did not have the Laron mutation, those who did have it almost never got cancer. And they never developed diabetes, even though many were obese, which often brings on the condition.

“I discovered the population in 1987,” Dr. Guevara-Aguirre said in an interview from Ecuador. “In 1994, I noticed these patients were not having cancer, compared with their relatives. People told me they are too few people to make any assumption. People said, ‘You have to wait 10 years,’ so I waited. No one believed me until I got to Valter Longo in 2005.”

Valter D. Longo, a researcher on aging at the University of Southern California, saw the patients as providing an opportunity to explore in people the genetic mutations that researchers had found could make laboratory animals live much longer than usual.

The Laron patients have a mutation in the gene that makes the receptor for growth hormone. The receptor is a protein embedded in the membrane of cells. Its outside region is recognized by growth hormone circulating through the body; the inside region sends signals through the cell when growth hormone triggers the receptor.

The Laron patients’ mutation means that their growth hormone receptor lacks the last eight units of its exterior region, so it cannot react to growth hormone. In normal children, growth hormone makes the cells of the liver churn out another hormone, called insulinlike growth factor, or IGF-1, and this hormone makes the children grow. If the Laron patients are given doses of IGF-1 before puberty, they can grow to fairly normal height.

This is where the physiology of the Laron patients links up with the longevity studies that researchers have been pursuing with laboratory animals. IGF-1 is part of an ancient signaling pathway that exists in the laboratory roundworm as well as in people. The gene that makes the receptor for IGF-1 in the roundworm is called DAF-2. And worms in which this gene is knocked out live twice as long as normal.

The Laron patients have the equivalent defect — their cells make very little IGF-1, so very little IGF-1 signaling takes place, just as in the DAF-2-ablated worms. So the Laron patients might be expected to live much longer.

Because of their striking freedom from cancer and diabetes, they probably could live much longer if they did not have a much higher than usual death rate from causes unrelated to age, like alcoholism and accidents.

Dr. Longo said he believed that having very low levels of IGF-1 was the critical feature of the Laron patients’ freedom from age-related diseases. In collaboration with Dr. Guevara-Aguirre, he exposed human cells growing in a laboratory dish to serum from the Laron patients. The cells were then damaged with a chemical that disrupts their DNA. The Laron serum had two significant effects, the two physicians reported on Wednesday in Science Translational Medicine.

First, the serum protected the cells from genetic damage. Second, it spurred the cells that were damaged to destroy themselves, a mechanism the body uses to prevent damaged cells from becoming cancerous. Both these effects were reversed when small amounts of IGF-1 were added to the serum.

Dr. Longo said that some level of IGF-1 was necessary to protect against heart disease, but that lowering the level might be beneficial. A drug that does this is already on the market for treatment of acromegaly, a thickening of the bones caused by excessive growth hormone. “Our underlying hypothesis is that this drug would prolong life span,” Dr. Longo said. He said he was not taking the drug, called pegvisomant or Somavert, which is very hard to obtain.

A strain of mice bred by John Kopchick of Ohio University has a defect in the growth hormone receptor gene, just as do the Laron patients, and lives 40 percent longer than usual.

Dr. Longo said that his report had first been submitted to Science, a better-known journal, which turned down the paper because of an adverse report from one reviewer.

Andrzej Bartke, a gerontology expert at Southern Illinois University, said that the new result was “very important” and that the authors had done a fine job in following the patients and generating high-quality data. “This fits in with what we are learning from studies in animals about the relationship of growth hormone to aging, because both cancer and diabetes are related to aging,” Dr. Bartke said.

The longest-lived mouse on record is one studied by Dr. Bartke. It had a defect in its growth hormone receptor gene, just as do the Laron patients. “It missed its fifth birthday by a week,” he said. The mouse lived twice as long as usual and won Dr. Bartke a prize presented by the Methuselah Foundation (which rewards developments in life-extension therapies) in 2003.

Dr. Guevara-Aguirre said he had been struggling to get sufficient IGF-1 to treat 30 of his patients before they reached puberty, at which point it will be too late. He said his group of Laron patients, the largest in the world, had provided essential data for drug companies making IGF-1, and he chided the companies for not reciprocating by providing the drug for his patients.

Dr. Arlan Rosenbloom, a pediatric endocrinologist at the University of Florida who has worked with Dr. Guevara-Aguirre, took a similar position. “Considering that the drug companies needed the initial studies to determine dosage and efficacy, it seems ironic that we should have so much difficulty getting the drug,” he said.

Ownership of the drug has passed through several companies’ hands, so any initial obligation may have been weakened. Dr. Guevara-Aguirre also said he believed that the government of Ecuador should do more to help get the drug for his patients.

Dr. Harry Ostrer, a geneticist at New York University who is exploring the Laron patients’ degree of Sephardic ancestry, said that he had seen several of Dr. Guevara-Aguirre’s patients in Quito, Ecuador’s capital, and that they were “remarkably youthful in appearance.”

A version of this article appeared in print on February 17, 2011, on page A6 of the New York edition.

From the Magazine Scientific American website (source HERE)…

Defective Growth Gene in Rare Dwarfism Disorder Stunts Cancer and Diabetes

A long-term study shows that people with Laron syndrome, a genetically based form of dwarfism, almost never succumb to cancer or diabetes

By Nina Bai

For the past 22 years Jaime Guevara-Aguirre has served as the de facto physician for a truly unique community in Ecuador. His patients stand on average 1.2 meters tall, a result of a rare genetic disorder known as Laron syndrome. Of the approximately 300 people in the world known to have the condition, a third reside in the remote mountainside villages of southern Ecuador. Another remarkable fact about Guevara-Aguirre’s patients: virtually none of them suffer from cancer or diabetes.

The same genetic mutation—an error in thegrowth hormone receptor (GHR) gene—that causes unusually small stature in Laron syndrome also confers seeming immunity from two of the most common diseases that plague mankind. Since 1988 no cases of diabetes and only one case of nonlethal cancer have been diagnosed in 99 Laron’s subjects followed by Guevara-Aguirre. In comparison, fellow villagers without the GHR mutation had a diabetes diagnosis rate of 5 percent and a cancer diagnosis rate of 17 percent over the study period.

GHR-deficient individuals are insensitive to growth hormone and also have abnormally low levels of insulinlike growth factor 1 (IGF1), a hormone that promotes cell proliferation and inhibits programmed cell death. More than two decades of clinical observations by Guevara-Aguirre’s team are now supported by molecular studies linking low levels of IGF1 to cellular protection against cancer and other age-related diseases.

“If we can establish that IGF1 is a risk factor for cancer, then you could imagine that doctors could prescribe IGF1-lowering drugs as we are now doing for cholesterolwith statins,” says Valter Longo of the University of Southern California’s Programs in Biomedical and Biological Sciences, who collaborated with Guevara-Aguirre on a study of the Ecuadorian community published February 16 in Science Translational Medicine.

To investigate the cellular responses to IGF1, researchers bathed isolated human cells in blood serum taken from Laron subjects and from relatives without the mutation. When exposed to a toxin, cells bathed in Laron serum suffered fewer DNA breaks, suggesting that the lack of IGF1 protects against oxidative DNA damage. The protection disappeared when IGF1 was artificially added to the Laron serum.

“I can say that we both came to the same conclusion from different routes—Valter from the basic, and I from the clinical sciences”—says Guevara-Aguirre, who is the medical director at the Institute of Endocrinology, Metabolism and Reproduction in Quito, Ecuador.

The two research teams began their collaboration in 2005. “I realized that nobody was working in humans that had a defect in GHR. We were working on all kinds of model systems,” Longo says.

Previous work on model organisms had suggested the role of IGF1 in cancer prevention and aging. Dwarf mice with the same GHR mutation have low cancer rates, increased insulin sensitivity that protects against diabetes, and extended life span. But it was impossible to study IGF1 in humans in the same way due to the extreme rarity of the naturally occurring GHR mutation.

Meanwhile, Guevara-Aguirre had been studying the distorted body composition in the Laron subjects, but was struck by their unusual resistance to common diseases. “In 1988 I noticed that these patients had no diabetes despite being obese. In 1994 I also noticed they had no cancer. A few years later we documented they were insulin sensitive. These facts were fascinating to me,” he says. When Longo heard about Guevara-Aguirre’s work and his close relationship with such a large population of Laron’s subjects, he realized that it could be the “perfect natural experiment.”

The study represents the first time that the GHR-deficiency mutation has been studied in a human population. Unlike dwarf mice, however, people with Laron syndrome do not seem to experience increased longevity. The effect on life span may have been obscured in this study by the unusually high number of accidents and alcohol-related deaths seen in the Laron subjects. “Being three-and-a-half feet tall, accidents just happen,” Longo says.

Despite the extreme rarity of Laron syndrome, the study findings have important implications for the general population. It is already known that IGF1 can be modulated by diet—specifically, that protein restriction lowers IGF1 levels.

“All the data is coming together now,” says Luigi Fontana who studies nutrition and aging at Washington University in Saint Louis School of Medicine and was not involved in the study. “Put together all the pieces of the puzzle and you see that yes, IGF1 is an important determinant of cancer.” According to Fontana, greater protein intake and higher IGF1 levels contribute to the increasing cancer incidence in recent generations; a similar trend is seen in immigrant populations that move from Eastern to Western diets.

However, Longo cautions, “people shouldn’t make up their own diets to try to extend their life. If you don’t have a clear disclaimer, you will be amazed at what people do.”

Longo suspects the IGF1 pathway may be involved in the great majority of the diseases of aging, including osteoporosis, Alzheimer’s disease and cognitive decline. He hopes to extend the current study but acknowledges that the lower prevalence of these conditions, compared with that of cancer and diabetes, make them more difficult to study in a population of limited size.

Anabolic Steroids And Growth Hormones May Not Increase Muscle Mass

The article I am posting below found from HERE seems to suggest that the GH that bodybuilders have been taking for so long to increase muscle size may not do that either, let alone increase the length of the long bones to grow taller.

I personally found the article to reveal another layer to this mystery of GH. It could be possible that the GH that the experimenters used to test the subjects with was not pure somatropin but a lower quality  synthetic version which is not as effective but I doubt that is the reason. If growth hormones don’t even increase muscle size but bulking up body builders, then the use of growth hormones for adults is very limited.

Research debunks bodybuilding myth: Growth-promoting hormones don’t stimulate strength

Published: Thursday, June 14, 2012 – 15:34 in Health & Medicine

New research from scientists at McMaster University reveals exercise-related testosterone and growth hormone do not play an influential role in building muscle after weightlifting, despite conventional wisdom suggesting otherwise. The findings indicate that bodybuilders who look to manipulate those hormones through exercise routines are wasting their time.

In two separate studies, published in the Journal of Applied Physiologyand the European Journal of Applied Physiology, researchers found anabolic hormones — long thought to be essential for building a muscular frame — do not influence muscle protein synthesis, the process that leads to bigger muscles.

“A popular mindset for weightlifters is that increased levels of hormones after exercise play a key role in building muscle,” explains Daniel West, lead author of both studies and a graduate student in the Department of Kinesiology at McMaster. “That is simply not the case.”

In the first study, researchers examined the responses of both male and female participants to intense leg exercise. Despite a 45-fold difference in testosterone increase, men and women were able to make new muscle protein at exactly the same rate.

“Since new muscle proteins eventually add up to muscle growth, this is an important finding,” says West.

“While testosterone is definitely anabolic and promotes muscle growth in men and women at high doses, such as those used during steroid abuse, our findings show that naturally occurring levels of testosterone do not influence the rate of muscle protein synthesis.”

In the second study, researchers analyzed the post-exercise hormonal responses of 56 young men, aged 18 to 30, who trained five days a week for 12 weeks in total.

The men experienced gains in muscle mass that ranged from virtually nothing to more than 12 pounds, yet their levels of testosterone and growth hormone after exercise showed no relationship to muscle growth or strength gain.

Surprisingly, the researchers noted that cortisol — considered to have the opposite effect of anabolic hormones because it reduces protein synthesis and breaks down tissue — was related to the gain in muscle mass.

“The idea that you can or should base entire exercise training programs on trying to manipulate testosterone or growth hormone levels is false,” says Stuart Phillips, a professor in the Department of Kinesiology. “There is simply no evidence to support this concept.”

The research was funded in part by the Canadian Institutes of Health Research and the Natural Sciences and Engineering Research Council of Canada.

Tiffanie Didonato Suffering From Diastrophic Dysplasia Increases Height 16 Inches From Limb Lengthening Surgery

This is another story I thought was important to be told. The individual is Tiffanie Didonato who had suffered from a type of dwarfism called Diastrophic Dysplasia, which made her only 3 feet 6 inches. Through out my research, this person has gone throughout the most height gain I have ever heard of with over limb lengthening surgery. However, I have known and heard that for people who suffer from type soy dwarfism, limb lengthening surgery gives them the greatest of height increase.

It seems from reading on other forums that people who are only below average in height but is not at the level of dwarf often go to limb lengthening surgery for 3-4 inches in height. Most of the stories I have read about people who suffer from dwarfism who get limb lengthening surgery seem to increase height the most with stories I have heard of being 10 inches, or more. They seem to get the most benefit from this procedure. This story was the most dramatic. The problem with this story is that the numbers don’t really add up.

In there article which was found HERE (ABC News), one of the pictures say that Tiffanie gained 10 inches in height (not shown below). In another section of the article the writer says TIffanie had 14 inches in gained height but they also state that she increased height from 3’6″ to 4’10”, which is not 14, but 16 inches in height difference. This either shows that the writer and journalist was misinformed or really bad in math, forgetting to account for the far that 1 feet is not 10 inches but 12 inches.

Little Person No More

Oct. 13, 2008

For Tiffanie Didonato, nearly everything in the world was out of reach. Things others may take for granted, like flipping a light switch, revving a gas pedal or tackling bathroom basics, Didonato couldn’t do without aid.

That’s because the 27-year-old was born with diastrophic dysplasia, a type of dwarfism. The condition left her with abnormally short arms and legs. By age 15, Didonato was only three-and-a-half feet tall.

“Kids were growing up a lot quicker. They were taller. It was easier to hold their book bags and walk down the hall, and I was basically the size of my book bag,” she said.

A Life Changing Decision

A confrontation with a teacher when she was 15 led her to make a life-altering decision.

“She pulled me in the middle of the classroom, sat me on egg crates and said, ‘I don’t know what kind of disease you have, but obviously you’re a dwarf. Why don’t you tell me what you can and can’t do?’ I’ve never heard the word dwarf be called to me before in my life,” Didonato said.

The interaction was etched in her brain and, shortly afterward, Didonato decided to adapt to life, since life didn’t adapt to her.

She sought to have a controversial surgery to painfully and painstakingly lengthen her arms and legs, not by the recommended four inches but a whopping 10.

The Little People of America organization doesn’t approve of the surgery because it sends the message that there is something wrong with being a little person.

“Most members of the dwarf community believe that no child should undergo surgery unless it is for a treatable medical condition that will improve her or his health. Limb-lengthing surgery, by contrast, does not address any medical condition,” the group said in a statement to “Good Morning America.”

Didonato’s view, though, is, “I don’t judge you, please don’t judge me.”

“I didn’t go through plastic surgery because I didn’t like my face or something like that. I went through it for independence and that’s the main goal,” she said. “I was thinking ahead into the future. I wanted to get married. I wanted to drive. ”

Didonato turned to orthopedic surgeon Dr. Errol Mortimer for help.

“I did have reluctance, but Tiffanie absolutely wanted to get this done as effectively and quickly as possible,” Mortimer said.

How It Works

The bone-lengthening procedure works by taking advantage of the body’s natural ability to heal itself. During surgery, the bone is broken and then slowly stretched one millimeter per day over several grueling months.”Through very small incisions, we insert the screws — two above and two below — the place where we cut the bone,” Mortimer said. “The bone slowly gets pulled apart and as it gets pulled apart the body fills in the gap that is created and ultimately that gap is filled with normal bone.”

During months of recovery, Didonato took solace in writing and visually the things she’d finally be able to do. After 12 surgeries on shins, thighs and arms, Didonato gained 14 inches.

That took her 3-foot-6-inch frame to 4-feet-10-inches.

Didonato was enthused.

“I remember saying to myself, ‘This is going to be the first day of the rest of my life,'” she said. “I’m going to free. I’m going to be independent.”

Now simple chores that caused her so much hassle are much easier. Things like making coffee and emptying the trash bring her joy.

And when she got married over the weekend, the bride was able to stand tall as she made her way down the aisle to her prince, two-time Iraq War veteran Eric Gabrielse.

“I think what she did goes above and beyond any of the physical or mental stuff I’ve done,” said Gabrielse, who met his future wife three years ago as a pen pal. “She dealt with it her all her life and handled it all so amazingly. I’m so proud of her.”

And now Didonato has her happily ever after.