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.