Increase Height with Intramembranous Ossification?

Long bones naturally develop by endochondral ossification whereas short, flat, and irregular bones grow by intramembranous ossification.  Endochondral ossification involves hyaline cartilage and chondrocytes whereas intramembranous ossification does not.  Intramembranous ossification involves mesenchymal stem cells differentiating into osteoblasts which then lay down bone.

This form of ossification is even involved in healing bone fractures as there are stem cells within the trabeculae in the diaphysis of the long bones.  When enough stem cells come together and the appropriate genetic expression is in place the stem cells began to develop into osteoblasts.  The osteoblasts then produce trabecular bone, then the periosteum forms around the network of trabecular bone.  And cortical bone is formed between the trabecular bone and periosteum.

In intramembranous ossification there is no growth plate "fusion".  In some disorders, bone can form anywhere in the body.  Intramembranous ossification is truly organic bone growth.  Humans do not stay the same torso height once intramembranous ossification is complete.  The torso keeps growing due to hormonal changes causing the periosteum to produce new osteoblasts that lay down new cortical bone.  This is referred to as appositional growth.  The cortical bone increases the size of the bone resulting in an increase in height.  Further, intramembranous ossification within already formed bone should increase the number of trabeculae(bone density) as there is already a periosteum formed.  This increase in trabeculae can indirectly increase height by enhancing the periosteum thereby increasing the number of osteoprogenitor cells released as a result of shearing forces on the periosteum.

Appositional bone growth has been shown to be possible in runners.  Most likely due to the constant shearing forces on the periosteum altering genetic expression and releasing osteoprogenitor cells which lay down new cortical bone.  You get appositional bone growth in your spine, hip, pelvis, skull, or calcaneous and you'll grow taller.

Endochondral ossification-Grow taller by Lateral Synovial Joint Loading.  Cause microfractures in the trabecular bone of the epiphysis, increase interstitial fluid flow to send stem cells to hyaline cartilage growth plate line, the genetic expression of the hyaline cartilage growth plate line causes the stem cells to differentiate into chondrocytes

Intramemberanous Ossification-Grow taller by periosteal shear.  Cause shearing forces on the periosteum, like running does on the shin bone except for the spine, pelvic bone, skull bone, and calcaneus.  This shearing force releases osteoprogenitor cells that deposit new compact bone resulting in larger short, flat, and irregular bones resulting in a taller you.

I'm already performing tapping on my calcaneus(heel bone) and haven't really seen any results from it.  I'm going to start performing LSJL on it to see if LSJL can have the same benefits on an irregular bone.

Here's a study that states maybe there's really no such thing as intramembranous ossification and there's always a transitional chondrogenic phase:


Transient chondrogenic phase in the intramembranous pathway during normal skeletal development.


"Calvarial and facial bones form by intramembranous ossification, in which bone cells arise directly from mesenchyme without an intermediate cartilage anlage. However, a number of studies have reported the emergence of chondrocytes from in vitro calvarial cell or organ cultures and the expression of type II collagen, a cartilage-characteristic marker, in developing calvarial bones. Based on these findings we hypothesized that a covert chondrogenic phase may be an integral part of the normal intramembranous pathway. To test this hypothesis, we analyzed the temporal and spatial expression patterns of cartilage characteristic genes in normal membranous bones from chick embryos at various developmental stages (days 12, 15 and 19). Northern and RNAse protection analyses revealed that embryonic frontal bones expressed not only the type I collagen gene but also a subset of cartilage characteristic genes, types IIA and XI collagen and aggrecan, thus resembling a phenotype of prechondrogenic-condensing mesenchyme. The expression of cartilage-characteristic genes decreased with the progression of bone maturation. Immunohistochemical analyses of developing embryonic chick heads indicated that type II collagen and aggrecan were produced by alkaline phosphatase activity positive cells engaged in early stages of osteogenic differentiation, such as cells in preosteogenic-condensing mesenchyme, the cambium layer of periosteum, the advancing osteogenic front, and osteoid bone. Type IIB and X collagen messenger RNAs (mRNA), markers for mature chondrocytes, were also detected at low levels in calvarial bone but not until late embryonic stages (day 19), indicating that some calvarial cells may undergo overt chondrogenesis. On the basis of our findings, we propose that the normal intramembranous pathway in chicks includes a previously unrecognized transient chondrogenic phase similar to prechondrogenic mesenchyme, and that the cells in this phase retain chondrogenic potential that can be expressed in specific in vitro and in vivo microenvironments."

Of course just because there's mesenchymal condensation and that cartilagenous genes are expressed doesn't mean there's a transient cartilage phase.