I found earlier studies about chondrocyte transdifferentiation into osteoblast such as this.

Essentially, what’s so significant about chondrocyte transdifferentiation into osteoblasts is that it means that the growth plate genetics are maintained in the transdifferentiated-from-chondrocytes osteoblasts.  So if we can induce de-differentiation of these transgene osteoblasts then we can possibly form neo-growth plates.  This is a much more promising for height growth than the view where hypertrophic chondrocytes just undergo apoptosis and no growth plate genetic information would be maintained by apoptosis whereas if hypertrophic chondrocyes transdifferentiate into osteoblasts some of the growth plate genetic information would be maintained info the former-hypertrophic chondrocytes osteoblasts.

Chondrocytes Transdifferentiate into Osteoblasts in Endochondral Bone during Development, Postnatal Growth and Fracture Healing in Mice.

“To investigate whether cells derived from hypertrophic chondrocytes contribute to the osteoblast pool in trabecular bones, we genetically labeled either hypertrophic chondrocytes by Col10a1-Cre or chondrocytes by tamoxifen-induced Agc1-CreERT2 using EGFP, LacZ or Tomato expression. Both Cre drivers were specifically active in chondrocytic cells and not in perichondrium, in periosteum or in any of the osteoblast lineage cells. These in vivo experiments allowed us to follow the fate of cells labeled in Col10a1-Cre or Agc1-CreERT2 -expressing chondrocytes. After the labeling of chondrocytes, both during prenatal development and after birth, abundant labeled non-chondrocytic cells were present in the primary spongiosa. These cells were distributed throughout trabeculae surfaces and later were present in the endosteum, and embedded within the bone matrix. Co-expression studies using osteoblast markers indicated that a proportion of the non-chondrocytic cells derived from chondrocytes labeled by Col10a1-Cre or by Agc1-CreERT2 were functional osteoblasts{maybe we could investigate these other non-osteoblastic chondrocyte derived cells if they can be used for height increase purposes?}. Both chondrocytes prior to initial ossification and growth plate chondrocytes before or after birth have the capacity to undergo transdifferentiation to become osteoblasts. The osteoblasts derived from Col10a1-expressing hypertrophic chondrocytes represent about sixty percent of all mature osteoblasts in endochondral bones of one month old mice{this is a significant proportion which gives a lot of promise about reversing endochondral ossification}. A similar process of chondrocyte to osteoblast transdifferentiation was involved during bone fracture healing in adult mice. In addition to cells in the periosteum, chondrocytes represent a major source of osteoblasts contributing to endochondral bone formation in vivo. ”

I’d recommend visiting the study as there were some images I couldn’t get onto here.

“Endochondral bone is made of an outer compact bone (cortex) and an inner spongy bone tissue within the bone marrow cavity. The conversion from the nonvascular cartilage template to fully mineralized endochondral bones proceeds in distinct and closely coupled steps. The first step is initiated when chondrocytes in the center of the cartilage models undergo hypertrophic differentiation and cells in the perichondrium surrounding the hypertrophic zone differentiate into osteoblasts to form the interim bone cortex (bone collar). Concurrently, the initial vascular invasion occurs in the same region importing blood vessel-associated pericytes, osteoclasts and progenitor cells in the circulating blood”

“Immediately following the onset of bone collar formation, hypertrophic chondrocytes and the mineralized cartilage matrix in the center of the cartilage template are replaced by a highly vascularized trabecular bone tissue as well as bone marrow. Bone trabeculae in the primary spongiosa are formed by deposition of osteoid by osteoblasts on the surface of calcified cartilage spicules.”

“During endochondral ossification, terminally differentiated hypertrophic chondrocytes are eventually completely removed from the initial cartilage template or growth plates. Some of these chondrocytes have been shown to be eliminated through either apoptosis or autophagy (type II programmed cell death). Hypertrophic chondrocytes express osteoblast markers, such as Alkaline Phosphatase (ALPL), Osteonectin (SPARC), Osteocalcin (BGLAP), Osteopontin (SPP1) and Bone sialoprotein (IBSP), implicating potential complex functions of these cell”

“in cell cultures containing ascorbic acid or in organ cultures, hypertrophic chondrocytes, instead of becoming extinct, resume cell proliferation and undergo asymmetric cell division, giving rise to cells with morphological and phenotypic characteristics of osteoblasts capable of producing a mineralized bone matrix in vitro“<-Could this be a perpetual growth plate?

“in embryonic chicks, long bone chondrocytes differentiated to bone-forming cells and deposited bone matrix inside their lacunae”

“After the growth period the Col10a1-Cre induced reporter+ cells were still present in the metaphyseal and cortical regions in 6-month-old mice”<-6-month old mice are pretty old and not really growing based on the breed of mice so this is promising that the transChondro-Osteoblasts could still be around in older humans.

“However, more of these cells were embedded within the bone matrix, and less of them were found on the bone surfaces, compared to the 2- and 3-week-old mice, implying that the number of active osteoblasts derived from chondrocytes was likely reduced after the growth period. At 8-month, there were almost no Col10a1-Cre induced reporter+ cells in the primary spongiosa and very few were on the bone surfaces.”<-This is less promising information.  TransChondro-Osteoblasts on bone surfaces are in a better position to form neo-growth plates.

“Hypertrophic chondrocytes might first dedifferentiate, then proliferate before these cells redifferentiate into osteoblasts. The existence of cells in the bone marrow that were derived from Col10a1-expressing chondrocytes. These cells displayed properties of mesenchymal progenitor cells and were able to differentiate into osteoblasts, chondrocytes and adipocytes in vitro, although we do not know whether these cells had the ability to become osteoblast cells in vivo. “hypertrophic chondrocytes to osteoblasts” transdifferentiation may indeed involve a dedifferentiation and then a redifferentiation process. In juvenile mice the chondrocyte-derived reporter+ cells, which were negative for osteoblast markers, persisted in the primary spongiosa for a considerable amount of time before becoming functional osteoblasts”<-This information doesn’t really hurt the prospects of using the genetic information of these cells to create new growth plates as even if there’s a dedifferentiation stage between chondrocytes becoming osteoblasts the genetic material will still be maintained.

According to Buried alive: How osteoblasts become osteocytes, ” the average half-life of a human osteocyte as 25 years. However, when we consider an overall bone-remodelling rate of between 4 to 10% per year, the life of many osteocytes may be shorter. Furthermore, the lifespan of osteocytes greatly exceeds that of active osteoblasts, which is estimated to be only three months in human bones”<-So we’d only have three months after growth plate fusion to induce dedifferentiation of trans-chondro osteoblasts before they don’t exist anymore.  10-20% of osteoblasts become osteocytes and osteocytes live longer but osteocytes are in a much less advantageous position to form new growth plates.

Here’s a study that mentions alternative theories:

Pubertal growth and epiphyseal fusion

“There are four theories on the cellular mechanism of epiphyseal fusion after the pubertal growth spurt. Apoptosis, autophagy, hypoxia, and transdifferentiation have been considered the causes of epiphyseal fusion”

Apoptosis: “Hypertrophic chondrocytes of the growth plate undergo death by apoptosis, leaving behind a frame of cartilage matrix for osteoblasts that invade and lay down bone.”

Autophagy: “Autophagy is another method of programmed cell death that involves a catabolic process in which the cell degrades its own components through autophagosomes. ”

Hypoxia: “a dense border of thick bone surrounding growth plate remnants [is present] in a human growth plate tissue specimen undergoing epiphyseal fusion.  The dense border might act as a physical barrier preventing oxygen and nutrients from reaching the fusing growth plate, resulting in hypoxia and eventually cell death in a nonclassical apoptotic manner.”

Transdifferentiation: “terminal hypertrophic chondrocytes transdifferentiate into osteoblasts at the chondroosseous junction of the growth plate”