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."