Years ago I was frustrated over the fact that there seemed to be no good real websites or resources on the internet I could turn to for my height increase questions. I remember finding the Height Quest website and finding it too advanced and scientific to read. At the time, I tried just focusing on exercise with little care to the science. I wanted to get taller and I was not sure whether the exercise routine I was doing at the time, which included swimming everyday, stretching, and yoga poses would really work.

After I did gain the 1/4th of an inch to push my height past the socially accepted height of 6 feet tall, I decided that I was tall enough. I moved on to other things.

After being away for almost 3 years, I came back to focus on this issue. Why did I come back to try to figure out something which no physician or surgeon has ever succeeded in before and think that I would be able to find a solution when the thousands of other people before me who did the research couldn’t figure it out?

I came to realize that a person’s life probably can only have true significance when they are in someway really benefiting the world. I looked on the internet and saw that there seemed to ba a resource for almost everything.

No matter what you were interested in, what you wanted to do, or what you wanted to learn, there was someone who had already figured it out and probably posted a great guide on how to do it.

I looked at the internet and found nothing about how to grow taller which was honest, informative, free, and authoritative. Everything was so scattered, and everyone seemes to be arguing, in deep confusion, or trying to sell a scam.

I realized that with my background, my experience, and my experiences, I had the tools to really try to make a good contribution. All my life, my family seemed to emphasize the point that having height is something that was very important. It seems to have cause certain strange psychological issues and dysmorphia in a few of my family members.

Plus, I realized that there were probably millions, if not billions of people out there who expressed the same thoughts and desires to be come taller, even after they stopped growing.

This whole area of the internet is filled with scams and fake products. There are plenty of pills with calcium carbonate and some oriental herbs which are sold as grow taller miracles. There are plenty of E-Books sold which will do nothing except drain the buyer’s wallet. There are hundreds of websites which all seem to link back to the “Grow Taller 4 Idiots” mega-scam. There are back hat SEO tactics used to push the websites higher up in the search engine rankings.

In the last year, I have reviewed at least 30 products, and none of them except maybe 1-2 has any chance of ever working even for growing kids. I have been slowly trying to cut through the B.S. and see every single method and idea proposed looking for any sign or hint of an idea. Some sections of the website has not been updated in since the beginning because I have been focused so much on the research and the content creation.

And now that it is almost an entire year since the beginning in the summer of last year, 2012. I am proud that I can provide a place where people can go to and find useful and informative articles posted which will help them see that there is real research being done. Sure, there will be many ideas and crazy proposed techniques which will lead me nowhere, but each route I go in for research seems to give me a better and better idea of what is really going on in the human body, in the bones themselves, and in the cartilage which is what really seems to make bones larger.

So if you have something in your own life that you are very frustrated about, whether personal or professional, I would like to ask that you create something to try to solve that problem. The most likely thing is that it is not just you that is suffering from that problem. Probably millions of other people have the same problem. Help make the world a better place and build something that you can be proud of even 30 years later.

Be The Change You Wish To See In The World, and Create Something Of Massive Value

So how do we do this? How can we start our own revolution, our paradigm shifting change? I say to become so good that people can no longer ignore you. I want you to start learning about something which you have always wanted to learn about, or you have always had a deep, dark obsession, madness, or passion about. As long as you can do something for free, where the money is not the thing you are really chasing, you will make it into something that people just can’t ignore, because what you have built is just so useful, so powerful, or so influential.

If you produce and create things that are so high in quality that people will instantly see the value in what you do, then the money will come.

As Pat Flynn, the internet marketer puts it which he applies the key concepts everyday…

1. Provide massive value
2. Earning massive trust
3. Learn and understand the needs and wants of your followers
4. Lead and teach by example.

The Steve Martin Autobiography entitled “So Good They Can’t Ignore You” has an amazing phrase. I took it also from the blog by Cal Newport entitled Study Hacks where his main point is for us to become so good that people can’t ignore us.

So become better at something that you know the whole world will love. Become so knowledgeable on something that people will be desperately emailing you asking you for the secret. If may take many years, if not a decade but you will one day prove all the haters and sceptics wrong. They will have to look up since you are going to be noticed by all the rest of the world. Get ready.

This episode & post will be a very long one since a 16 year old male named Matheus from Brazil recently came to me to report about all the research he has been doing on how to possibly increase his own height.

Episode #11: I Review And Outline All The Research And Studies Matheus Has Shown To Me

This podcast episode will focus on where I will be looking at all the research and studies a guy named Matheus from Brazil has shown me since getting in contact with me since last month. I have sent an email to him asking that he come on to the podcast to discuss in his own words what he has been up to but his claim that he has weak English speaking skills means I will again be speaking alone.

Some of the stuff he has found has definitely helped in clearing up a few blind spots me and Tyler have had in our own research.

The thing is that he has been linking to so many articles, studies, and papers that it has been very hard for me to organize and arrange all the information he has thrown out at me so I will try to just break down each individual compound down to whether there are inhibiting or helping increased growth.

Chemical compounds which stimulate increased bone longitudinal growth

Vitamin K2 (aka Menaquinone) – is animal based which increases Testosterone (source)

MGP(Matrix Gla Protein-derived K2) which is produced by Vitamin K2 – inhibits the calcification of tissues and cartilages – is the major inhibitor of human body tissue calcification and seems to have much influence on chondrocytes. (Coordinated expression of matrix Gla protein is required during endochondral ossification for chondrocyte survival)

Ursolic acid – it interacts with the receptors for IGF-1, and increases sensitivity to IGF-1. (Ergo-log.com)

Asthaxanthin – good antioxidant

Cissus quadrangularis – it increases the production of IGF-1 by osteoblasts.

Glutathione – (source: Nitric oxide decreases IGF-1 receptor function in vitro; glutathione depletion enhances this effect in vivo.)

N-Acetylecysteine (NAC) – (source: N-acetylcysteine prevents nitric oxide-induced chondrocyte apoptosis and cartilage degeneration in an experimental model of osteoarthritis.)

Alfalfa (aka Ipriflavone) – (Source: Ipriflavone modulates IGF-I but is unable to restore bone in rats.)

Amomum villosum – (Source: Amomum villosum induces longitudinal bone growth in adolescent female rats.)

Herbal formula HT042 (made of three elements, 1. Astragalus (most important), 2. Eleutherococcus senticosus, 3. Phlomis umbrosa) – (Source: http://www.ncbi.nlm.nih.gov/pubmed/21091251)

Commelina communis – (Source: http://www.naturalheightgrowth.com/2012/12/29/korean-medicine-extracts-hansogdan-phlomis-umbrosa-and-dalgaebi-commelina-communis-in-milk-enhances-height/)

Artemisia Capillaris – (Source: http://www.naturalheightgrowth.com/2012/12/29/kiwoomi-rice-with-eleutherococcus-senticosus-and-artemisia-capillaris-extract-shows-proof-that-it-can-increase-childrens-height-breakthrough/)

Jaoga-Yukmiwon (R) – Effects of Jaoga-Yukmiwon(R), a Korean herbal medicine, on chondrocyte proliferation and longitudinal bone growth in adolescent male rats.

Carnitine – (Supplementation of carnitine leads to an activation of the IGF-1/PI3K/Akt signalling pathway and down regulates the E3 ligase MuRF1 in skeletal muscle of rats.)

Sesamin (a lignan) – (Source: http://www.heightquest.com/search?q=sesamin)

Genistein – (Source: Mechanism involved in genistein activation of insulin-like growth factor 1 receptor expression in human breast cancer cells.)

Daidzein – (Source: Feeding daidzein to late pregnant sows influences the estrogen receptor beta and type 1 insulin-like growth factor receptor mRNA expression in newborn piglets.)

Isoflavone – bind to estrogen receptors shielded them and preventing the binding of the true hormones. Can only bind to the beta receptors. Genistein binds to the alpha receptors. Increases the synthesis of IGF-1 and VEGF, and is 100X less estrogenic than estrodial.

Letrozole -Can decrease the level of estradiol

Niacin – is the precursor to NADPH

Vitamin D3 – increases the expression of VEGF only in bone – Higher serum vitamin D concentrations are associated with longer leukocyte telomere length in women.

Tuarine – (source: http://www.heightquest.com/search?q=taurine)

• IGF-1
• Zinc
• Lactoferrin
• GH
• Androgens 
• Hyaluronic

Chemical compounds which inhibit bone longitudinal growth

Estradiol – Matheus would cite many sources showing that this is very bad for height increase and growth… the effect of estradiol on the growth spurt at puberty is increasing GH and overexpression of VEGF… the effects of estradiol on chondrocyte senescence… reduces the proliferation of chondrocytes and enhances endochondral ossification

Retinoic acid – inhibits the proliferation of chondrocytes.

Accutane / Roaccutane (derived from retinol / vitamin A) – closes the growth plates (used by people w/ acne) Instead, choose the acne treatment with vitamin B5 and Zinc

Nitric Oxide – seems to do many things to decrease chondrocyte proliferation including decrease TGF-Beta production, induce chondrocyte apoptosis, decreases sensitivity of the IGF-1 receptors, decrease IGF-1 receptor function, etc. (Source: Nitric oxide inhibits chondrocyte response to IGF-I: inhibition of IGF-IRbeta tyrosine phosphorylation)

Corticosteroids – examples are Cortisone and Cortisol – decreasing the expression of receptors of IGF-1 and GH, and acting directly on the resting area and decrease the proliferation of chondrocytes

Homocysteine – is responsible for the shortening of telomeres during methylation, and and can also increase the effects of oxidative stress (source: Homocysteine levels and leukocyte telomere length.)

Oxidative stress – leading to senescence not just of the growth plate but of the entire organism… almost always responsible for the shortening of telomeres – a result of accumulation of excess free radicals that are generated during the cell cycle or by high levels of homocysteine – (Source: Potential involvement of oxidative stress in cartilage senescence and development of osteoarthritis: oxidative stress induces chondrocyte telomere instability and downregulation of chondrocyte function.)

Vitamin A – Converted into retinoic acid

About Growth Plate Senescence

The senescence of the growth plate is not genetically programmed…it occurs after the biochemical factors that occur during the growth spurt at puberty

Chondrocytes have an infinite proliferation and they have longer than average telomeres than all the other cells of the body. The that the cells divide, the more free radicals they produce as well as oxidative stress. The chondrocytes in the growth plate seem to proliferate and divide at a much faster rate than any other types of cells in the body. That is why they are one of the first types of cells that go extinct. the other cells don’t go completely out until old age. it seems that oxidative stress is really bad and causes cartilage senescence and chondrocyte telomere instability.

I personally did not want to look through the list of PubMed studies but for anyone who is interested, go right ahead. The truth is that I looked at the titles of this studies and some of them I have already read and am aware of.

• http://www.ncbi.nlm.nih.gov/pubmed/10912528
• http://www.ncbi.nlm.nih.gov/pubmed/7925098
• http://www.ncbi.nlm.nih.gov/pubmed/16614378
• http://www.ncbi.nlm.nih.gov/pubmed/11641457
• http://www.ncbi.nlm.nih.gov/pubmed/18174286
• http://www.ncbi.nlm.nih.gov/pubmed/10912529
• http://www.ncbi.nlm.nih.gov/pubmed/1415528
• http://www.ncbi.nlm.nih.gov/pubmed/21164272
• http://www.ncbi.nlm.nih.gov/pubmed/21865751
• http://www.ncbi.nlm.nih.gov/pubmed/21441345

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• Length of time: 26 mins
• Beginning of actual interview: 1:15 

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Sometimes a new critical study is found which helps me and the other researchers understand a little better just how chondrocytes in cartilage turn into volumetrically growing bones and cartilage like growth plates. This is one of those studies. it may not seem like a lot for the person who just wants the step-by-step manual on how to grow taller, but for the researchers, this study is in my opinion one of the most insightful studies written due to the fact it shows just how the growth plates seem to be formed as a function of the overall volumetric shape or form that they are in.

Study #1: Growth Plate Chondrocytes Dedifferentiate in Monolayer but Redifferentiate in High-Density Pellet Culture, Sequentially Expressing Resting, Proliferative, and Hypertrophic Zone Markers

Center of Molecular Medicine, Department of Women and Child Health, Karolinska Institutet and University Hospital Stockholm, Sweden

Abstract

Longitudinal bone growth occurs at the growth plate, which is located near the ends of long bones. At the growth plate, cartilage expansion, through chondrocyte proliferation, hypertrophy and matrix production results in elongation of the bone. This process is orchestrated by the interaction of a large number of endocrine and paracrine factors. The study of these complex interactions has been limited by the lack of well characterized chondrocyte culture models and that growth plate chondrocytes cultured in mono-layer rapidly de-differentiate into fibroblast-like cells with high expression of Collagen type I (Col1) and minimal expression of chondrocytic markers, Collagen type II (Col2) and X (Col10). Dedifferentiated rat growth plate chondrocytes in monolayer were trypsinized and centrifuged to form high-density pellets. The cells rapidly (within 3 days) redifferentiated into Col2-expressing chondrocytes as evidenced by a more than 200-fold increase in Col2 expression, up to a level of expression similar to that of growth plate chondrocytesin vivo. We then assessed expression of newly identified resting (Sfrp5) and proliferative zone (Prelp) markers. With prolonged culture, these chondrocytes underwent a reproducible differentiation program characterized by an early rise in expression of resting zone marker Sfrp5, followed by a rise in the proliferation marker Prelp, and finally an increase in hypertrophic zone markers Indian hedgehog and Col10 expression. Our findings suggest that growth plate chondrocytes cultured in high-density pellets undergo a sequential differentiation program similar to growth plate chondrocytes in vivo. These findings may thus help to improve in vitro studies aimed at clarifying the interactions of endocrine and paracrine factors in the regulation of longitudinal bone growth at the growth plate.

Analysis

One of the things that keeps happening to us as any type of scientific researchers is that once we reach a certain level (usually extremely) of study, the understanding on how a phenomena of a physical mechanism actually happens is impossible. For the study of how the mechanism of growth plate process work at a microscopic level, it is the same as well. We just don’t know many things.

It does seem however that if chondrocyte cultures and growth plate chondrocytes are made into monolayers, they actually de-differentiate into a type of cell known as fibroblast-like cells with express only Collegen Type I, not the Type II and Type X which is seen in hyaline cartilage and hypertrophic epiphyseal zones.

The researchers either intentionally or accidently did something that resulted in the fibroblast-like cells to re-differentiate back into growth plate chondrocytes found in vivo. They ” trypsinized and centrifuged to form high-density pellets.” So it seems that they added some type of protein or enzyme called trypsin and took the monolayer cell cultures and spinned them until they turned into 3-D pellets that had the cells in a high density concentration.

The process took just 3 days for the fibroblasts-like cells to turn back into chondrocytes. This was checked with analysis of Collagen Type II testing, which showed a 200 times increase.

In addition, the researchers tested for certain “markers” which signify that a certain zone in growth plates were around

• Resting Zone Markers – Sfrp5
• Proliferation Zone Markers – Prelp
• Hypertrophy Zone Markers – indian hedgehog and Collagen Type X

They state, “Our findings suggest that growth plate chondrocytes cultured in high-density pellets undergo a sequential differentiation program similar to growth plate chondrocytes in vivo.”

This shows an important point which we will need to understand if we ever plan to create a type of research program or do any type of laboratory experiments to get a type of cartilage tissue that functions almost exactly like the growth plates found in human bodies.

We need to form 3-D pellets for growth plates to work, not monolayers. Any type of cartilage structure we decide to create must have a 3-D form, not something very thin. 

Pellets with the diameter large enough to be re-implanted into lab rabbits to test to see if they restart the longitudinal growth process will be done first. That was proven to be successful in studies done by a group of researchers in Hong Kond.

Eventually one day that pellet must be big enough in width, and have the right thickness as well as structure strength to be implanted back into an adult human’s tibia or femur to get them to start growing their bone longer again.

Sometimes someone comes along and shows me a study that pushes the endeavor a little further and that is the type of help I hope we as the researchers can get from the readers.

For most of the stuff that the readers show me or direct me to, I look at the material to see if there is anything useful that I and other researchers can use. I am very grateful to the person who showed me the study “Engineering growing tissues” by Eben Alsberg. From just a quick Google search on Dr. Alsberg, it seems that he is cased in the Biomedical Engineering Department at Case Western University, which I remember had a very strong engineering school. I would look through his profile and research to see what other papers he has written about tissue engineering over the years. There are some interesting papers he has been a coauthor to, including…

1. “Spatiotemporal regulation of chondrogenic differentiation with controlled delivery of TGF-β1 from gelatin microspheres in mesenchymal stem cell aggregates”
2. “Stromal-cell-derived factor (SDF) 1-alpha in combination with BMP-2 and TGF-β1 induces site-directed cell homing and osteogenic and chondrogenic differentiation for tissue engineering without the requirement for cell seeding”
3. “Engineered cartilage via self-assembled hMSC sheets with incorporated biodegradable gelatin microspheres releasing chondrogenic growth factor”
4. “Controlled and sustained gene delivery from injectable, porous PLGA scaffolds”
5. “Chondrogenic differentiation of human mesenchymal stem cell aggregates via controlled release of TGF-b1 from incorporated polymer microspheres.”

These studies are the most interesting to me but the last is is particularly attractive to read through. I guess I will get to it in another day.

It is interesting that he does a lot of research in the biomedical application of electrospinning, since I have stated that electrospinning is one of the more likely ways that human cartilage can be grown rather easily for growth plate re-implantation. I wrote a post about this idea entitled “Increase Height And Grow Taller Through Bioprinting And Electrospinning“. At this point, I will move away from Dr. Alsberg research and look at what other university tissue engineering and biomedical engineer professors have been doing research on.

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The 2nd study that he would refer me to showed that there has been even more ways and methods that researchers have done in recent years that allowed for growth plate regeneration.

IGF-I RELEASING PLGA SCAFFOLDS FOR GROWTH PLATE REGENERATION

Sharath Kumar Chinnakavanam Sundararaj – Master’s Theses – May, 5th 2010 – UKnowledge
University of Kentucky, sharath.sundararaj@uky.edu

Abstract

Growth plate is a highly organized cartilaginous tissue found at the end of long bones and is responsible for longitudinal growth of the bones. Growth plate fracture leads to retarded growth and unequal limb length, which might have a lifelong effect on a person’s physical stature. This research is a tissue engineering approach for the treatment of growth plate injury. Insulin-like growth factor I (IGF-I), which can stimulate cartilage formation, was encapsulated within PLGA microspheres that were then used to form porous scaffolds. The release profile of the IGF-I from the PLGA scaffold showed a biphasic release pattern. In vitro studies were done by seeding rat bone marrow cells (BMCs) on the top of IGF-I encapsulated PLGA scaffolds, and the results showed an increase in cell multiplication and glycosaminoglycan content. The final in vivo studies were conducted by creating growth plate injury and implanting scaffolds in the tibiae of the New-Zealand white rabbits. Histological analysis of tissue sections showed regeneration of cartilage, albeit with disorganized structure, at the site of implantation of IGF-I encapsulated scaffolds. This work will be a significant step towards tissue engineering of growth plate cartilage.

KEYWORDS: PLGA, Tissue engineering, growth plate, drug delivery and IGF-I

Analysis #1: I have reviewed multiple Ph. D theses before and it was very mentally tiring work to read through what are usually 200+ pages of scientific data and charts. This Master’s Theses maybe only 70 pages but it still will take a lot of work to get through.

The overall theses is not to actually grow a growth plate from scratch using a seed from an autologous explant, but it is more towards trying to grow a similar physeal cartilage like the growth plate in the fractured area when the growth plate experiences a type of injury that might cause something like a bony bridge.

1. IGF-1 was somehow put inside/encapsulated in microspheres that are made out of PLGA.
2. The microspheres were used to make into porous scaffolds.
3. The IGF-1 will eventually get released from the PLGA microspheres as either the microspheres and/or the scaffold starts to disintegrate
4. The way that the IGF-1 is released is shown to have two phases.

The studies to look at the release profile and release characteristics of the IGF-1 was done AT FIRST in in-vitro environment.

1. Some rat marrow cells were taken out from the actual lab animal (probably using a similar invasive method as a biopsy)
2. The cells were put on top of the scaffold which already has the IGF-1 inside.
3. The result is that there was an increase in glycosaminoglycan content and cell multiplication

The studies were then done AT THE END in vivo

1. Some lab rabbits, of the New Zealand type was taken. 
2. The growth plate in their tibia was broken to create an injury, which left a defect or distracted area where intact, continuous growth plates used to be.
3. The scaffold with the IGF-1 inside was put in the area of empty space left by the growth plate
4. Histological analysis (which is just taking a microscope and looking at the tissue being analyzed to see the cell structure, cell number) of tissue sections showed regeneration of cartilage.
5. The growth plate cartilage that was created however showed a disorganized structure

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What is PLGA? – From Wikipedia – poly(lactic-co-glycolic acid) is a copolymer which is used in a host of Food and Drug Administration (FDA) approved therapeutic devices, owing to its biodegradability and biocompatibility

What is a Copolymer? – From Wikipedia – A heteropolymer or copolymer is a polymer derived from two (or more) monomeric species, as opposed to a homopolymer where only one monomer is used.

What is a Polymer? – From Wikipedia – is a large molecule composed of many subunits, known as monomers…  Polymers range from familiar synthetic plastics such as polystyrene (of styrofoam) to natural biopolymerssuch as DNA and proteins that are fundamental to biological structure and function. Polymers, both natural and synthetic, are created via polymerization of many monomers

What is a Monomer? – From Wikipedia – refers to the organic molecules which form synthetic polymers, such as, for example, vinyl chloride, which is used to produce the polymerpolyvinyl chloride (PVC).

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 So what was the overall message of the Thesis?

(Page 2) Tissue engineering of cartilage is gaining heavy importance in the field of tissue engineering. But most of the research till now is mainly focused on the regeneration of articular cartilage and very little progress has been made in tissue engineering of growth plate. This work was aimed at providing a significant contribution towards tissue engineering of growth plate.

We hypothesized that microencapsulation of IGF-I in PLGA would be an appropriate growth factor delivery system for regeneration of growth plate cartilage both in vitro and in vivo.

THe 5th section of this Master’s Theses is on the Discussion. It is broken up into certain sections

• Release profile of protein encapsulated scaffolds degraded in PBS 
• Release profile of protein adsorbed and protein encapsulated scaffolds
• Release profile of protein-encapsulated scaffolds degraded in cell culture medium 
• Release profile of protein-encapsulated scaffolds degraded in cell culture medium 
• along with macrophages

2nd part: Degradation of PLGA scaffolds

• Mass loss of scaffolds degraded in PBS 
• Mass loss of scaffolds degraded in cell culture medium

3rd part: In vitro cell studies

• Seeding the cells with fibrin glue 
• Confocal imaging of BMC-seeded scaffolds
• Analysis of GAG content from the BMCs

4th part: In vivo studies 

• Scaffold used in the animal surgery
• Radiographic images
• Histology

Last section #6: CONCLUSION 

The main aim of this research was to develop a biodegradable drug delivery device for the treatment of the growth plate injury. The regeneration of the growth plate cartilage in the site of injury has confirmed that the IGF-I was successfully released from the porous PLGA scaffold and induced the formation of chondrocytes and extracellular matrix. The release studies showed that microencapsulation of IGF-I was a suitable method for storage of the drug within the scaffold that is going to be released. The release studies and the in vitro cell studies confirmed that the device was capable of releasing the drug in a required pattern and bioactive state. The IGF-I encapsulated porous PLGA scaffold implanted in the rabbit model for treatment of growth plate injury has successfully regenerated cartilage at the site of injury, even though it was not effective in correcting the defect in the bone angle that was caused due to the injury. The results of this research has shown that using porous PLGA scaffolds with IGF-I encapsulated in the form of microspheres will serve as an appropriate drug delivery system for the cartilage regeneration. This work will be a significant step forward in the tissue engineering of growth plate cartilage.

Analysis #2

It seems that as long as there is some growth plate left in the animal, regeneration is possible using just a scaffold of the right type (this time the right material is PLGA) and some IGF-1. The IGF-1 did result in cartilage being regenerated but it did not manage to fix the defect in the bone angle that was originally induced to create the bone injury.

Me and the other researchers have found this type of thing before, and this theses shows that if some growth plates is missing, we can recreated it. The histological analysis seems to show that the chondrocytes that were in the newly created cartilage were not organized or columnar stacked like how they should be to have the hypertrophic zone which would lead to maximum longitudinal growth rates.

This suggests that while IGF-1 is affective alone in a scaffold, there might be some growth factors which might be better to towards forming chondrocytes that are more organized and in the right position for better growth chances.

Something to realize is that if there is NO growth plate cartilage left, then this method would not work There has to be at least some cartilage left. This method is similar to what we see in techniques which result in articular cartilage layer thickening where some articular cartilage is regenerated on the top surface to decrease osteoarthritis and cartilage degeneration associated with old age.

The problem is that if we are talking about adult human with absolutely no cartilage to start with, then wee need more than just a scaffold and a growth factor as a stimuli.

This study/theses was useful and will be used in future posts to show that it is possible to heal over defects in growth plate cartilage with new cartilage. However it is not enough for people with absolutely no physeal cartilage to start with.