Become Taller at your Primary Ossification Center?

Lateral Synovial Joint Loading increases height by initiating growth in the hyaline cartilage growth plate line at the secondary ossification centers.  Is there a method to become taller at the primary ossification center in the middle of the bone?  There's no hyaline cartilage remnant at the primary center of ossification like their is at the secondary centers of ossification.  The identity of stem cells is based on their environment and genetic expression of the surrounding cells.  There's no cartilage in the primary center of ossification(the middle of the bone).  But are there any possibilites at the primary ossification center to aid in growing taller?

[Expression of hypoxia inducible factor-1alpha in long bone development] 

"To observe dynamically the development of fetal long bone and detect the expression and distribution of HIF-1alpha,to investigate the expression pattern and possible effects of hypoxia inducible factor-1alpha (HIF-1alpha)[The best way to induce hypoxia is intense cardiovascular training like High Intensity Interval Training but it's only the high intensity parts that matter] in fetal long bone development of mouse. METHODS: E12.5, E13.5, E14.5, E15.5, E16.5 and E17.5 pregnant C57BL6 mice were sacrificed. After sacrifice, the embryos were delivered by caesarean section. The development of fetal long bone was dynamically observed by stereoscopic microscope, and the distributional expression of HIF-1alpha protein was detected by using method of immunohistochemistry. The expression of HIF-1alpha mRNA and osteoblast marker gene at various stage were also detected by using methods of reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: The cartilaginous long bone began to form and joints outline arised at E13.5, then the primary ossification center was observed at E14.5, showing opaque ossification under stereoscopic microscope,and then the osteogenesis expanded and extended to both sides. Immunohistochemistry demonstrated lots of HIF-1alpha protein positive chondrcytes in the center of primary ossification at E14.5, then they decreased dramatically. HIF-1alpha mRNA expressed at high level from E13.5 to E15.5, and then decreased to low level. CONCLUSION: Fetal long bone development pattern appeared to be endochondral osteogenisis process, existing hypoxia microenviroment may increase HIF-1alpha mRNA expression and thus initiate the cascade of endochondral osteogenisis." 

One of the keys to triggering growth in the primary ossification center is hypoxia(lack of air).  Hypoxia is best induced by intense cardio and not strangulation.  You want the hypoxia to be in your bone cells not in your brain cells. 

The transcriptional cofactor Lbh regulates angiogenesis and endochondral bone formation during fetal bone development. 

"Lbh is thought to act as a transcriptional cofactor and is highly conserved among species. Here we show that Lbh is expressed in chondrocytes, cells of the perichondrium, and the primary spongiosa in fetal growth plates of mice and chickens. Lbh overexpression in chick wings, using the RCAS-retroviral vector strategy, results in shortened skeletal elements and delayed hypertrophic chondrocyte maturation and bone formation. Additionally, osteoclast and endothelial cell invasion are delayed in the Lbh-overexpressing bones. Finally, we find a dramatic suppression of Runx2 and VEGF mRNAs in chondrocytes and osteoblasts that overexpress Lbh. Strikingly, this abnormal bone development in infected limbs can be rescued by concurrent overexpression of Runx2. These results suggest that during endochondral bone formation, Lbh may negatively regulate vascular invasion and formation of the early ossification center at least in part by interfering with Runx2 and/or VEGF expression." 

Runx2 and VEGF(two genes) are responsible for growth in the primary ossification center.  The primary spongiosa is the name for the initial trabecular bone network.  Heterotrophic Ossification may be something worth studying in the future as it is where new bone grows outside existing bone.  It would be interesting to see if Runx2 expression is responsible for this abnormal growth.  If bone can grow off of liver cells then bone can certainly grow back in the primary ossification center. 

Impaired bone development and increased mesenchymal progenitor cells in calvaria of RB1-/- mice. 

"We have previously shown that the retinoblastoma protein (pRb) can activate expression of Runx2-dependent, bone-specific genes in cultured cells. We now show that pRb also plays a role early in osteogenesis, and that in primary RB1(-/-) calvarial cells there is an increased osteoprogenitor pool. To understand pRb's function in vivo, we generated a conditional RB1-KO mouse in which pRb expression is efficiently extinguished in osteoblasts. These animals display an apparent developmental defect in bones, most strikingly in the calvaria. Cultured RB1(-/-) calvarial osteoblasts fail to cease proliferation upon reaching confluence or following differentiation. Re-plating assays of primary RB1(-/-) calvarial cells after differentiation showed a clear adipogenic ability with increased multipotency. RB1(-/-) osteoblasts display a severe reduction in levels of mRNAs expressed late in differentiation. In this study, we present strong evidence that pRb has multiple regulatory roles in osteogenesis. Furthermore, in the absence of RB1(-/-) there is a larger pool of multipotent cells compared with the WT counterpart. This increased pool of osteoprogenitor cells may be susceptible to additional transforming events leading to osteosarcoma, and is therefore key to understanding RB1 as a target in malignancy." 

Retinoblastoma protein can activate the genetic expression of Runx2 and possibility initiate bone growth at the primary center of ossification. 

Regulation of embryonic endochondral ossification by Smurf2. 

"Smurf2 is an E3 ubiquitin ligase that targets TGF-beta receptor activated Smad2 and Smad3 for the proteasome in primary articular chondrocytes, thus stimulating their hypertrophic differentiation. Comparatively, how Smurf2 functions in growth plate chondrocytes in a developing long bone is an open question. In this study, we measured the mRNA levels of endogenous Smurf2 and type X collagen in chick growth plate at different embryonic stages to monitor the correlation between the level of Smurf2 expression and chondrocyte maturational stage. We found that high levels of Smurf2 were associated with the differentiative and proliferative stages, while Smurf2 levels were thereafter decreased as the chondrocytes matured toward hypertrophy. In addition, we injected Smurf2-RCAS into chick wing buds at HH stage 20-23 and examined how the ectopic overexpression of Smurf2 in condensing chondrogenic mesenchyme affects the subsequent process of chondrocyte maturation and ossification during embryonic development. Histological analysis showed that overexpression of Smurf2 in a developing wing bud accelerated chondrocyte maturation and endochondral ossification, which may result from a decrease in TGF-beta signaling in the infected chondrocytes with Smurf2-RCAS." 

It seems like you want your Smurf2 levels in the primary ossification centers to be just right as you don't want chondrocytes to mature too quickly so the chondrocytes have more time to proliferate.  

There doesn't appear to be any special to induce growth in the primary ossification center.  However, there may be remnants of genes left over from earlier development.  New bones can grow from anywhere if the stem cells are there and the proper genetic expression is in place including within the primary center of ossification.