Thursday, May 16, 2013

Growth Plate Regeneration

This is from the Google Preview of the Book Bone: Fracture Repair and Regeneration.  Specifically the chapter: Prospects of Regeneration of Growth Plates in Mammals written in 1992. 

The author Richard M. Libbin is old.  I believe he is still alive in New York but I couldn't find contact info.  The book was available for $8 so I bought it so I'll have more information from it.

Overall the book doesn't have new revolutionary information but it makes several statements that provide evidence for the possibility of height increase by LSJL or other mechanical means.

One interesting theory he presents is that the osseous bridge formed during growth plate fracture decreases height by decreasing blood flow to the growth plate.  Blood flow has been shown to affect growth plate and height growth via genes like HSP90.

The author mentions a regrowth of the hemiephysis occurring in some instances but "physeal regeneration does not occur innately in the distal humerus of the rat."

"Physeal regeneration [sites may be] formed via chondrocyte reorganization within the junctional cartilage."

"Regions of physeal regrowth were observed in the cartilage which had formed distal to the skeletal transection surfaces, and also within the junctional cartilage proximal to them."

"Proliferation of periosteal cartilage similar in morphology to fracture callus is the starting point for physeal regeneration"

"Regeneration of growth plate cartilage does not occur at forelimb amputation sites of rats [because] while exuberant periosteal chondrogenesis rapidly encloses the hindlimb bone ends within a mass of hyaline cartilage, in the forelimb the equivalent process occurs less frequently and less vigrous, newly formed cartilage rarely extending beyond the plane of amputation.  The failure of rat forelimb growth plate cartilage to regenerate may reflect a deficiency in the chondrogenic potential of its periosteum."

On page 274, he mentions an argument that states that regenerative capacity is never completely lost in higher level vertebrates.  In frogs, which can regenerate as tadpoles but not as full frogs the lack regenerative capacity as adults because cells lose the ability to dedifferentiate.  Maybe this relates to genes such as OCT4, Sox2, Klf4, and Myc.  Once dedifferentiation was induced through trauma, regeneration was achieved.  Maybe LSJL can help induce dedifferentiation.  Dedifferentiation may be a key step before neo-growth plates can be formed.

"In [instances of] regrown junctional cartilage, [that cartilage] now contained extended regions of growth plate cytoarchitechture, suggesting that physeal organization is not restricted to the ends of long bones, but may be provoked to occur at other sites as well."

On page 280, it's mentioned that cartilage formed off the periosteum is very similar to the growth plate in terms of cellular organization.

"Any cartilage or cartilage forming tissue may be able to reform a growth plate."<-MSCs and the periosteum is cartilage forming tissue.  The problem with MSCs is the microenvironment of the adult bone.  The goal with LSJL is induce mesenchymal condensation thus allowing MSCs to become cartilage forming tissue.

"Physeal cartilage may be provoked to form anywhere along the length of the bone"

"growth plate cartilage phenotype may be expressed wherever cartilage is present"

"After complete physeal ablation following division of the limb, it is periosteal cartilage which forms the regenerate, the characteristic ordered arrangement of growth plate chondrocytes appearing within an expanse of nonphyseal, hyaline cartilage as had occurred during the development of bone in fetal and neonatal life."

Mention of voluntary muscle at the skeletal end being important to cartilage regrowth.  This is a place of cutoff so when I get the book, I'll analyze it.

Other Chapters:

Synthesis and Stability during Fracture Repair

"[A lack of blood vessals may not lead] to chondrogenesis because some large, sinusoid-like vessels [was detected] in the cartilage of rat tibial fractures."

"[Some] areas of cartilage, or chondroid bone, are transient, persisting for only a few days, and so the proteoglycans may not mature to their normal levels of sulfation."

Regeneration of the growth plate.

"in 5 different series of experiments reported between 1950 and 1986 regeneration of injured parts of growth plates in long bones of rabbits and pigs could be demonstrated. The 1st series implied partial X-ray injury of growth plates in rabbits aged 3–6 weeks.The 2nd series implied autotransplantation of the head of the fibula in rabbits aged 10–21 days. The 3rd, 4th and 5th series implied transplantation of autologous fat grafts into provoked defects of growth plates in rabbits and pigs. The findings show that regeneration of a growth plate occurs when a part of it is injured in such a manner that a bone bridge is not formed between the epiphysis and the metaphysis. Regeneration of a plate is much faster in relation to the growth in length of the bone in the rabbit than in the pig. The 1st and 2nd series suggest that regeneration takes place by interstitial proliferation of cells from the germinal layer of the uninjured parts of the plate. Signs of partial regeneration of growth plates have been seen in radiographs after operation for partial closure of growth plates in children. "

Interesting that fat tissue was implanted to prevent bone fusion.


"rat bone marrow cells (BMCs) [were seeded] on the top of IGF-I encapsulated PLGA scaffolds, and the results showed an increase in cell multiplication and glycosaminoglycan content. "  They were then implanted into injured growth plates.  Of course, the question is what would be the effect of this implantation in a bone with no active growth plate.

"The practical difficulty in the use of IGF-I is due to its short biological half life. Encapsulation of IGF-I with PLGA protects the bioactivity and stability of IGF-I."

"Stacks of chondrocytes were observed in the case of the native growth plate. In the regenerated growth plate the chondrocytes were not found in the usual stacked manner. Single chondrocytes were distributed in the extra cellular matrix in the regenerated growth plate."<-maybe this is due to lack of some chemicals like BMP-2 or Ihh?

Monday, May 13, 2013

Lateral Synovial Joint Loading Supplement Guide

In an earlier post, I estimated that you can gain 1/4" every two months from lateral synovial joint loading.  This seems to be going along with how reported gains of about 0.5 cm for 2 months so about 1/5") and RT(gains of about 1 cm in a month and a half) have reported gaining on the LSJL forum.  Now, what LSJL is good at is good at is inducing chondrogenic differentiation which can cause height growth.  But anything anabolic that can accelerate the rate of cellular proliferation can make this height growth occur faster like HGH.

And incorporating LIPUS and electromagnetic fields(which are important as shown by the pizeoeletric current and the OPG/RANKL gradient).

I'm not going to be going into things like supplement purity and supplement forms(yet).  That's something that will come with time.  Note that all supplements and dosages are at your own risk.  I only study the possible effects of supplements on height increase.  All the information I have on the supplements is based on the studies I present on this blog.  This means that there are possible interactions and side effects that I may overlook.  This list is intended to inspire discussion about the possibility of supplements to increase height and to inspire discussion about possible risks and side effects.  I do not vouch for the safety of any supplements nor do I provide any dosages.  If you want vouches of safety than look to the manufacturer or to an organization such as the FDA.

DNA Protectors like Sam-e may not be necessary with a normal diet but as you do more anabolic activities or take more anabolic supplements your need for these supplements may increase.

I'm will be including supplements like Viagra and Lithium that are only available by prescription.  Because if people are aware of the height increasing potential of certain supplements that might increase the availability.

Dosages of each supplement likely vary based on diet, weight, and activity level.

Basic Lateral Joint Loading Routine(Lateral Loading of the Epiphysis):
-Increases cellular differentiation stem cells to chondrocytes which leads to height growth.
-Increases TGF-Beta, Wnt, and ECM pathways(Hyaluronic Acid).

-Need more TGF-Beta1.  Won't increase height without TGF Beta.
-Increases Aggrecan Expression.
-Inhibits GSK-3Beta increasing cellular proliferation(which is why it makes bone fractures heal faster).

Increases TGF-Beta release.

Axial Loading(Heavy Weightlifting):
-Increases TGF-Beta
-Increases all kinds of anabolic hormones(net gain in cellular proliferation resulting in more need for anti-oxidants and DNA methylaters)
-Increases need for calories

Endurance Training:
-Can increase VO2 max which can lengthen telomeres
-Increases sensitivity to Growth Hormone.

Now the Supplements:

c-Fos inhibitors:


Beta-Catenin inhibitors:


EstrogenReceptorAlpha inhibitors:

-Royal Jelly

ECM(Extracellular Matrix) Protectors:

-As your shear strain increases your need for more ECM increases so endurance training, sprinting or other exercises that cause shear strain on chondrocytes.  You'll notice that your bones will crack more after endurance training(not like a chiropractic crack but more of a dry crack).

So the more you run the more of these you'll need-
-Chondroitin & Glucosamine
-Hyaluronic Acid <-More Important than Chondroitin & Glucosamine for growing taller

Seaweed and Beta-Glycerophosphate:
Beta-Glycerophosphate may play a role in allowing endochondral ossification without periosteum.  Seaweed may help increase ECM levels.

Increases proteoglycan syntehesis and aggrecan mRNA.

Glucosamine may only have benefits if you engage in a lot of joint taxing exercises whereas hyaluronic acid and chondroitin can help you grow taller during puberty or while performing LSJL.

DNA Protectors:

-B6, B12, Folic Acid(<-The need for these increases the more anabolic activities you engage in or the more anabolic supplements intake)

-Folinic Acid may provide additional protection for DNA.  It should also be noted that Folinic Acid produced an observable increase in growth plate morphology and a non-significant increase in longitudinal bone growth.

-Sam-e(<-You only need this if B6, B12, and Folic Acid are not performing their jobs which they do in most people)

-Telomere Length(Astragalus Membranaceous which also doubles as an anti-oxidant)

-Anakrina and Entarnercept(prescription only substances that act to inhibit TNF-alpha and IL-1Beta, those two compounds are produced endogenously by growth plate chondrocytes and reduce growth)

Increase Cellular Proliferation(May not always increase final adult height but results in faster gains in LSJL and doesn't hurt):

-Examples are HGH, Myostatin Inhibitors, IGF-1, Testosterone.  The higher your cellular proliferation rate the more DNA protectors and anti-oxidants you need.  Use all supplements as directed(Niacin must be taken at a specified large dose).  Remember, that anabolic supplements increase non-bone cells as well such as skin cells, muscle cells, etc.  Usually, adipogenic differentiation is inhibited though.

-Creatine(inhibits Myostatin)

-Lactoferrin(increases chondrocyte proliferation, also available in milk)

The below two supplements are testosterone boosters and have a role in the nitric oxide pathway which can increase height growth:

-Tribulus Terristris

-Horny Goat Weed

-Niacin(enhances the bodies response to HGH when taken in large doses)

-Puerarin(increases cellular proliferation by the PI3K pathway)

-Leptin(increases cellular proliferation)

-Increases cellular proliferation and hypertrophy be inhibiting GSK3Beta however may have negative effects on height like stabilizing Beta-Catenin.  However, inactivation of Beta Catenin & overexpression of Sox9 has been shown to reduce height.  Methylation of Sox9 by CARM1 inhibits Beta-Catenin degradation so upregulating Beta-Catenin may not be needed in some circumstances.

Sophorae Beans:
Increases TGF-Beta and IGF-1 levels.

Increases bFGF, IGF-1, and BMP-2 levels.

Increases IGF-1 and Type II Collagen levels.

Growth Plate regulation(Endochondral Ossification Pathways):

Parathyroid hormone antagonizes Ihh, Runx2, and TypeX Collagen differentiation plus upregulates CyclinD1.  So basically Parathyroid Hormone delays terminal differentiation and increases chondrocyte proliferation.  PTH also stimulates Nkx3.2 which increases type II collagen(cartilage) and GAG production. Parathyroid Hormone is pro-chondrogenic.

PDE5 inhibitor and stimulates the Nitric Oxide pathway.  The Nitric Oxide Pathway and CNP both increase cGMP levels thus like CNP may increase longitudinal growth.  Viagra is a far more effective NO pathway stimulator than something like arginine, as Viagra targets a NO pathway inhibitor(PDE5) and so may be less susceptible to negative feedback mechanisms than something like Arginine.

Stimulates NO pathway.

Inhibits NFKappaB which inhibits height growth in active growth plates.  In bones with no growth plates, NF-kappaB may cause apoptosis of bone cells and stimulate stem cells.  So you shouldn't take Harpogoside if you have active growth plates.


Vitamin C:
Vitamin is pro-chondrogeneic.  It is unclear whether levels of Vitamin C above requirements would help increase height however Vitamin C deficiency reduces height. Vitafusion Power C, Gummy Vitamins For Adults, 150-Count.

-Pretty much all anti-oxidants are good except for NAC which inhibits free radicals that are essential for height growth(NADPH).

Increases levels of TGF-Beta in addition to scavenging free radicals.  Note that Melatonin increases levels of CYP1A2 which metabolizes Melatonin.  Therefore it may be necessary to cycle Melatonin.  Also note, that most doses of Melatonin may be too high and may increase CYP1A2 levels higher than a low dose for the same beneficial effects.  Many studies have found 0.3mg of Melatonin to be effective versus the 3mg in most supplement tablets. Here's 0.5mg Melatonin: Pure Encapsulations Melatonin 0.5 mg - 180 capsules.

-Acai Berry has been shown to be a highly effective anti-oxidant and it is available in foods(Acai berry enhanced smoothies)


Silicon Reduced Diet:
-Silicon Deficiency may have possibility to inhibit growth plate closure and increase longitudinal growth.
-Silicon seems to be pro-bone rather than pro-cartilage.  Thus, a silicon deficiency may be favorable to increased chondrogenesis.

So if you want to grow taller faster with LSJL.  First, look at what physically can you do that's anabolic like cardio and weight training.  Then make sure as you increase your activity level increase your levels of chondrocyte protectors as necessary.  Also increase your levels of DNA protectors and anti-oxidants.

With each supplement that's anabolic you try up your anabolic and DNA protector supplement content as well.  For safety, whenever possible go for water soluble supplements like Vitamin C.

Thursday, May 2, 2013

Grow taller with Collagen Hydrolysates

Collagen Hydrolysates are available for sale:
Alfa Vitamins Collegen Hydrolysate Nutrition Supplement, 120 Count

This makes it a very promising supplement but the cost of the dosage ratios recommended would be insane but could be up to 25% additional height.  There are 120 pills for $10.  A 50lb kid would take 25 a day to meet the dosage requirements.  So that would be about $2.50 a day.  Which I guess is not that bad.

Porcine Skin Gelatin Hydrolysate Promotes Longitudinal Bone Growth in Adolescent Rats.

"Collagen hydrolysates (CHs) are mixtures of peptides obtained by partial hydrolysis of gelatin that are receiving scientific attention as potential oral supplements for the restoration of osteoarticular tissues. The aim of this study was to evaluate the effectiveness of CHs for promoting longitudinal bone growth in growing rats. An in vitro study was carried out in osteoblast-like MG63 cells and the most effective CH on bone formation was selected among 36 various CHs. An in vivo study confirmed the functional effects of a selected CH with molecular weight of <3 kDa on longitudinal bone growth. CHs dose-dependently promoted the longitudinal bone growth and height of the growth plate in adolescent male rats, whereas gelatin failed to affect longitudinal bone growth. Insulin-like growth factor-1 and bone morphogenetic protein-2 in the CH treated group were highly expressed in the growth plate."

"Collagen is the major constituent of the connective tissues in vertebrates, comprising 30% of total body protein. The denatured form of collagen is referred to as gelatin and is commonly used in foods, pharmaceuticals, cosmetics, and others. To increase the solubility of gelatin, partially hydrolyzed gelatin products have been prepared and are referred to as collagen hydrolysates (CHs)."

3-Week old male Sprague-Dawley rats were used.

"Longitudinal bone growth in normal adolescent male rats was 404.0±11.6 μm/day, and administration of 50 and 250 mg/kg gelatin failed to promote the longitudinal bone growth. However, treatment with 250 mg/kg of CH significantly increased the longitudinal bone growth exhibiting 468.4±27.4 μm/day."<-The dosage for the alfa vitamins collagen above is 1000mg.  So maybe a human should actually take a larger dosage.  250mg/kg is actually pretty insane dosage in terms of cost but growth was over 25% more. That's 550mg/lb.  So a 200lbs individual would have to take 100 pills a day.  50mg/kg still increased height just not statistically significantly.

Here's the growth plate under Collagen Hydrolysate(growth plate height was increased by 11%).
"CHs with molecular weights <3000 Da that is able to increase IGF-1 and BMP-2 protein expression in growth plate, and consequently promote longitudinal bone growth in growing rats."<-the molecular weight of the supplement above is not listed.  Looking it up Collagen Hydrolysate has an average molecular weight of 2000-5000 Da so it's possible that the molecular weight here is over the threshold but humans may be able to tolerate the higher moleculate rate than rats.

Food consumption doesn't seem to be measured but gelatin could serve as sort of a control to that.

Biological effect of hydrolyzed collagen on bone metabolism

"an increase in the overall metabolism of collagen can lead to severe dysfunctions and a more fragile bone matrix and because orally administered collagen can be digested in the gut, cross the intestinal barrier, enter the circulation, and become available for metabolic processes in the target tissues, one may speculate that a collagen-enriched diet provides benefits for the skeleton."

couldn't get full study

The osteochondral endplate

The osteochondral endplate is the place where the articular cartilage meets the bone.  What we've learned about plastic deformation is that is a threshold strain that must be achieved to induce longitudinal growth in the bone.  Studies with epiphyseal distraction have shown that stretching the growth plate rarely increases height without fracturing the bone.

Directly stretching the growth plate did not increase height unless there was fracture or the distraction caused an increase in growth plate activity.  Since stretching the growth plate region does not directly increase height it is unlikely that the growth plate region increases height by stretching that region.  If growth plate increased height by stretching the bone shouldn't a mechanism of stretching like epiphyseal distraction also increase height?

We also know that the amount of tensile strain to induce a longitudinal stretch in the cortical bone is extreme and unlikely to be generated by the growth.  The growth plates must induce a physical mechanism of growing taller, otherwise cartilage would just transform into bone and your bones would not grow longer.  I propose that this method involves a force against the osteochondral endplate.

The epiphysis is weaker than the diaphysis of the bone.  The epiphysis is not cylindrical shaped so it is less stable.  This is a picture of the tibia:

What if the mechanism of growing taller was just to push away the osteochondral endplate and then the stronger cortical bone grows around it?

The Cartilage-Bone Interface

"Mature articular cartilage is integrated with subchondral bone through a 20 to 250 μmthick layer of calcified cartilage. Inside the calcified cartilage layer, perpendicular chondrocyte-derived collagen type II fibers become structurally cemented to collagen type I osteoid deposited by osteoblasts. The mature mineralization front is delineated by a thin 5 μm undulating tidemark structure that forms at the base of articular cartilage.  Growth plate cartilage is anchored to epiphyseal bone, sometimes via a thin layer of calcified cartilage and tidemark{so the tidemark that is at the same at the osteochondral endplate is similar to that of growth plate cartilage}, while the hypertrophic edge does not form a tidemark and undergoes continual vascular invasion and endochondral ossification (EO) until skeletal maturity upon which the growth plates are fully resorbed and replaced by bone.  The tidemark can be regenerated through a bone marrow-driven growth process of EO near the articular surface."

"In the developing knee, epiphyseal bone will continue to expand into the cartilage anlage until the cartilage interface forms a thin calcified layer that arrests vascular invasion.  Calcified cartilage forms at the base of the articular cartilage, and in certain growth plate reserve zones"

"Growth plate hypertrophic cartilage (HTC) does not form a tidemark. This interface is actually a mixture of cartilage and bone, by definition of the primary spongiosa,where newbone is deposited on the cartilage trabeculae carved out by invading blood vessels and marrow"

"Like articular cartilage, the growth plate hypertrophic zone also contains collagen type X and alkaline phosphatase, but a tidemark is notably absent. The tidemark that forms at the base of mature articular cartilage develops slightly below the region of chondrocytes expressing collagen type X.  Mineral deposits form in the neonatal calcified layer of the articular cartilage in line with the collagen fibers."

According to this diagram the articular cartilage grows by appositional growth so you should be able to grow taller with no growth plates by appositional growth in the articular cartilage.

"A distinct and more advanced EO process is going on during postnatal articular cartilage growth(►Fig. 1E and H). In 3- to 6-month-old rabbit articular cartilage,most chondrocytes are no longer proliferating, and a tidemark has formed at the base ofthehypertrophiczone.23 Bone is not being deposited along cartilage trabeculae,i thas developed layer-by-layer to form a thick osteoid around blood vessels subjacent to the calcified cartilage layer. Only small patches of cartilage persist in the subchondral bone (EO, ►Fig. 1E). The remnants of GAG and collagen type II in trabecular bone are the hallmarks of EO"

"The calcified cartilage layer is semipermeable and permits passage of small molecules (<500 Da) from the subchondral bone to the articular cartilage layer"

"Thickening of the calcified cartilage in OA could be expected to reduce the flow of small solutes from the vascularized subchondral bone to the deep zone chondrocytes."<-Maybe this could be part of the reason that people with osteoarthritis don't grow taller?

"Once formed, the tidemark and calcified cartilage layer persist as dynamic structures that can change and remodel over time. Below mature articular cartilage, the mineralization front is a relatively smooth and undulating plate-like surface"<-Maybe this remodeling of the tidemark and calcified cartilage layer plays a role in height growth

"growth plates develop a relatively stable reserve zone-epiphyseal bone interface, with a purely collagen type II GAG-rich cartilage phase, and a mixture of collagen type I and collagen type II in the newly forming primary spongiosa. Calcified cartilage becomes established at the edges of a “permanent” epiphyseal bone layer (i.e., proximal reserve zone and articular cartilage hypertrophic zone), and the tidemark serves as a barrier to vascular invasion and calcification of hyaline cartilage."<-maybe we can induce tidemarks to prevent growth plate resorption.

"The mineral front at the base of the growth plate corresponds with the vascular bone and newly deposited collagen type I. In the growth plate hypertrophic zone, calcification of the collagen type II matrix is much delayed compared with the articular cartilage calcified layer. This is because after
birth, the mammalian joints require a suitable mechanically stable articular surface, while growth plates in the long bones are continually expanding, even beyond sexual maturity. Cartilage calcification is therefore only occurring at the end-stage of cartilage growth. After reaching skeletal maturity, growth plates are completely resorbed and replaced by collagen type I–positive mineralized bone."<-So it's possible that the tidemark is both the limiting factor for the articular cartilage and the growth plate.

"Calcified cartilage becomes established at the edges of a “permanent” epiphyseal bone layer (i.e.,
proximal reserve zone and articular cartilage hypertrophic zone), and the tidemark serves as a barrier to vascular invasion and calcification of hyaline cartilage."<-So if you cause advancement of the tidemark you may create a signal for the bone to grow longer.

"In the calcified cartilage layer of normal human femoral condyles, chondrocytes are quiescent[not dividing] and present at a much lower density compared with hyaline cartilage (average of 51 cells/mm2 versus 152 cells/mm2).The calcified cartilage layer is flanked by an undulating tidemark, and an even more irregular cement line adjacent to the bone"

"the ratio of calcified cartilage to total cartilage thickness [is] relatively constant."  Calcified cartilage layer thins with age and older adults can experience tidemark advancement.

" Repetitive knee microtrauma in a rabbit model during 9 weeks of loading was shown to lead to a mean 25% increase in the proximal tibial calcified cartilage layer thickness, and tidemark duplication, with no change in mean articular cartilage thickness"

"Tidemark duplication could be related to uneven load-sharing following softening of a focal area of damaged cartilage"

"The tidemark is a 5 μm thick structure that appears at the cartilage-calcified cartilage junction"

"A significant correlation was observed between increasing tidemark duplication, mineral density, and carbonate content in primates. Repetitive knee microtrauma in a rabbit model during 9 weeks of loading was shown to lead to a mean 25% increase in the proximal tibial calcified cartilage layer thickness, and tidemark duplication, with no change in mean articular cartilage thickness"

"chondrogenic foci will spontaneously form in drill or microfracture holes generated in skeletally mature knee cartilage defects"

"In some rabbit cartilage repair models involving complete debridement[removal] of the calcified cartilage layer, subchondral bone plate advancement beyond the native tidemark in flanking cartilage has been observed after 3 to 9 months of repair."<-so it may be the calcified cartilage layer that allows for height growth and not the tidemark

"the calcified layer is undergoing continual resorption and endochondral advancement over time"

"the epiphyseal blood vasculature in skeletally immature knees has active endothelial cell proliferation while adult vasculature has postmitotic endothelia and the subchondral bone no longer contains osteoclasts."<-Can LSJL induce endothelial cell proliferation and osteoclast differentiation in adult epiphysis?

I've always said there is nothing that inhibits the formation of growth plates in adult epiphysis.  This study presents two factors that could inhibit adult growth plate formation: lack of proliferating epithelia and no osteoclasts.

According to Early growth response 2 negatively modulates osteoclast differentiation through upregulation of Id helix-loop-helix proteins., egr2(which LSJL upregulates) downregulates osteoclasts by transactivating Id2 however LSJL downregulates Id2.

"All cartilage-bone interfaces develop from an initially cartilaginous structure that undergoes coordinated invasion by blood vessels and osteoblasts. Formation of a tidemark anatomically stabilizes the cartilage-bone interface and arrests cartilage calcification and blood vessel invasion.  Vascularization of the calcified cartilage layer and subchondral bone plate is an important feature of a healthy cartilage-bone interface."

"Calcified cartilage and osteoid in the adult subchondral bone have a similar mineral level."

"Bone plate advancement could be a consequence of delayed or failed tidemark regeneration during bone marrow-driven EO below hyaline-like repair tissue."

"The growth plate-epiphyseal bone interface sometimes includes a layer of calcified cartilage and a tidemark in the reserve zone (A, proximal trochlea), and in other areas is devoid of calcified cartilage
or tidemark and fused to a more vascular bone (B, distal trochlea). Representative decalcified transverse sections from 4-month-old rabbit trochlear growth plates stained with hematoxylin and eosin are shown, from N ¼ 7 distinct New Zealand white rabbit femurs, 4 months old. TM, tidemark (white arrows); BV, blood vessels; CC, calcified cartilage; EO, endochondral ossification (cartilage remnant)."<-Growth for New Zealand White Rabbits really starts to taper off at 19 weeks of age.

Here's the study related to the advancement of the subchondral bone past the tidemark:

Observations of subchondral plate advancement during osteochondral repair: a histomorphometric and mechanical study in the rabbit femoral condyle.

"Osteochondral defects, 3mm diameter by 3mm deep, were made by controlled drilling through the articular surface into the subchondral bone in femoral condyles of 33 rabbits. The repair response was examined at 8, 16 and 32 weeks post surgery.
At 8 weeks, the level of reparative subchondral bone was 0.79+/-0.36 mm below the native tidemark. By 16 weeks, reformed subchondral plate was irregular, showing that 76.5% of the plate had extended beyond the native tidemark (0.13+/-0.05 mm) whilst 16.9% of the plate remained below (0.19+/-0.15 mm). The repaired surface non-osseous layer became thinner than the adjacent cartilage (0.23+/-0.08 vs 0.38+/-0.11 mm, P<0.05). This persisted up to 32 weeks. The repaired surface layers showed disappearance of safranin-O staining, increased separation splits at the boundary, and eventual degradation. General histological scores were similar across 8, 16 and 32 weeks although the scores of defect filling and restoration of osteochondral junction were decreased from 8 to 16 weeks. Mechanically, repaired defects had lower contact pressure and greater indentation than the normal controls at all time. Indentations of the cartilage adjacent to the defects were also greater than the normal at 8 and 32 weeks."

The bone here is taller!  If this had occurred in all the longitudinal ends of the bone you would have a longer bone.  The arrow is pointing to the subchondral bone advancement.

"In [some osteochondral] defects, new marrow-derived cartilage underwent endochondral ossification, forming bone on the surface of calcified cartilage cores. In the depths of the defects, new bone formed directly from osteoblasts derived from marrow mesenchymal cells. The new bone is initially woven, eventually becoming lamella, with the subchondral region modified to form a compact bone plate and a reformed tidemark. However, histological architecture of the reconstituted bone plate and cancellous bone was not identical to the original, and the new tidemark and subchondral bone advanced beyond the native level."

"contact pressure [is the] pressure between the articular surface and the flat circular surface of the transducer."

"contact pressures of reparative articular surfaces were either higher or lower than normal controls, and suggested these differences were related to thickness variation of repaired surface tissue and the presence or absence of an abnormally thick subchondral plate."

There isn't a tidemark for the hypertrophic chondrocytes of the epiphyseal growth plate.  What if the tidemark serves as both the limiting factor for both the articular cartilage and longitudinal bone growth?  With removal of the tidemark/calcified cartilage layer there was advancement of the subchondral bone.  Thus, maybe the growth plate exerts a force causing an advancement of the tidemark allowing for new longitudinal bone growth.

In this model, growth plates would produce upward force(contact pressure) pushing the tidemark upwards allowing for new bone growth.