Increase Height with Hyaline Cartilage

Scientists have shown that it is possible to recreate a growth plate within hyaline cartilage using a mesenchymal chondrocarsonoma. Since we know that growth plate fusion doesn't inhibit height growth, we can try to recreate a new cartilagenous growth plate within the epiphyseal fusion.

In vivo restoration of full-thickness cartilage defects by poly(lactide-co-glycolide) sponges filled with fibrin gel, bone marrow mesenchymal stem cells and DNA complexes. 

"A composite construct comprising of bone marrow mesenchymal stem cells (BMSCs), plasmid DNA encoding transforming growth factor-beta1 (pDNA-TGF-beta1), fibrin gel and poly (lactide-co-glycolide) (PLGA) sponge was designed and employed. To improve the gene transfection efficiency, a cationized chitosan derivative N,N,N-trimethyl chitosan chloride (TMC) was employed as the vector. The TMC/DNA complexes had a transfection efficiency of 9% to BMSCs and showed heterogeneous TGF-beta1 expression in a 10-day culture period in vitro. In vivo culture of the composite constructs was performed by implantation into full-thickness cartilage defects of New Zealand white rabbit joints, using the constructs absence of pDNA-TGF-beta1 or BMSCs as controls. Heterogeneous expression of TGF-beta1 in vivo was detected at 4 weeks, but its level was decreased in comparison with that of 2 weeks. After implantation for 12 weeks, the cartilage defects were successfully repaired by the composite constructs of the experimental group, and the neo-cartilage integrated well with its surrounding tissue and subchondral bone. Immunohistochemical and glycosaminoglycans (GAGs) staining confirmed the similar amount and distribution of collagen type II and GAGs in the regenerated cartilage as that of hyaline cartilage. The cartilage special genes expressed in the neo-tissue were closer to those of the normal cartilage. An overall score of 2.83 was obtained according to Wakitani's standard. By contrast, only part of the defects was repaired by the pDNA-TGF-beta1 absence constructs, and no cartilage repair but fibrous tissue was found for the BMSCs absence constructs. Therefore, combination of the PLGA sponge/fibrin gel scaffold with BMSCs and gene therapy is an effective method to restore cartilage defects." 

Well if you want to create a new growth plate this is the way to do it.  For height increase, it's preferable to use the existing hyaline cartilage but inserting new hyaline cartilage and sending bone marrow mesenchymal stem cells(with appropriate genetic expression) can have applications like fixing scoliosis. 

Recombinant human midkine stimulates proliferation of articular chondrocytes.

"Midkine, a heparin-binding growth factor, promotes population growth, survival and migration of several cell types.
Bromodeoxyuridine incorporation and MTT assays were performed to examine the proliferative effect of recombinant human midkine (rhMK) on primary articular chondrocytes. Activation of extracellular signal-regulated kinase (ERK) and phosphatidylinositol 3-kinase (PI3K) was analysed using western blot analysis. Systemic and local delivery of rhMK into mice and rats was preformed to investigate the proliferative effect of rhMK in vivo, respectively. Histological evaluation, including measurement of articular cartilage thickness, cell density, matrix staining and immunostaining of proliferating cell nuclear antigen was carried out. rhMK promoted proliferation of articular chondrocytes cultured in a monolayer, which was mediated by activation of ERK and PI3K. The proliferative role of rhMK was not coupled to dedifferentiation of culture-expanded cells. Consistent with its action in vitro, rhMK stimulated proliferation of articular chondrocytes in vivo when it was administered subcutaneously and intra-articularly in mice and rats, respectively. rhMK stimulates proliferation of primary articular chondrocytes in vitro and in vivo." 

If you have actively proliferating chondrocytes(either by your natural growth or via delivering stem cells to the hyaline cartilage growth plate) and inject the growth factor rhMK then you will grow taller.  More proliferating chondrocytes equals more chondrocytes dying and eventually being invaded by bone cells thus resulting in longer bones. 
Hyaline cartilage is the base for which long bones grow.  Stem cells differentiate into chondrocytes under orders from TGF-beta.  You inject hyaline cartilage into new areas and activate endochondral ossification then you get new growth possibilities.

Here's a patent involving using Midkine for hair growth.  Maybe there's a way to apply it to growth plate chondrocytes.

"MK is known to promote the migration of inflammatory cells such as macrophages and neutrophil, leading to inflammation."

"Pleiotrophin (PTN or HB-GAM) is a midkine family protein having approximately 50% identity at the amino acid sequence level to MK. Both MK and PTN comprise a high content of cysteine and basic residues. All the 10 cysteine residues are conserved in MK and PTN, and structurally, both can be divided into the N-domain and the C- domain. As a result of NMR analysis, it is known that these two molecules have very similar three-dimensional structures. Each domain consists of three β sheets, connected via a flexible linker region. K79, R81 , and K102, considered to be important to the binding of to chondroitin sulfate and heparin, are conserved between the two proteins[So pleiotrophin does bind to chondrogenic factors]. MK and PTN also share three-dimensional structures wherein these basic residues appear in the vicinity of the protein surface. Accordingly, PTN has been disclosed previously for the same medical indications as MK."

There doesn't appear to be an oral form of MK and PTN at this time.


Chondromodulin I and pleiotrophin gene expression in bovine cartilage and epiphysis.

"Pleiotrophin and chondromodulin-I are low molecular weight proteins that are abundant (20 microg/g tissue) in fetal cartilage and difficult to detect in adult cartilage. The results showed that the mRNAs for both proteins were abundant in fetal cartilage and while present in adult cartilage, were at 20-60-fold lower levels. Northern blotting revealed gradients of mRNA for both of these proteins in growth plate cartilage, with the highest levels in the resting zone, and the lowest in the hypertrophic zone. In contrast to pleiotrophin, chondromodulin-1 is down-regulated by retinoic acid with a pattern of expression similar to collagen type II and link protein, and may play a more specific role than pleiotrophin in modulating the chondrocyte phenotype."

"Ptn is upregulated by platelet-derived growth factor"