Something that I found today that is really enlightening to me was a published paper I found entitled “Temporal Analysis of Rat Growth Plates: Cessation of Growth with Age Despite Presence of a Physis“. (There is a full free text pdf in the library section as well as the to link above).

From the abstract…

Despite the continued presence of growth plates in aged rats, longitudinal growth no longer occurs. The aims of this study were to understand the reasons for the cessation of growth. We studied the growth plates of femurs and tibiae in Wistar rats aged 62–80 weeks and compared these with the corresponding growth plates from rats aged 2–16 weeks. During skeletal growth, the heights of the plates, especially that of the hypertrophic zone, reflected the rate of bone growth. During the period of decelerating growth, it was the loss of large hydrated chondrocytes that contributed most to the overall decrease in the heights of the growth plates. In the old rats we identified four categories of growth plate morphology that were not present in the growth plates of younger rats: (a) formation of a bone band parallel to the metaphyseal edge of the growth plate, which effectively sealed that edge; (b) extensive areas of acellularity, which were resistant to resorption and/or remodeling; (c) extensive remodeling and bone formation within cellular regions of the growth plate; and (d) direct bone formation by former growth plate chondrocytes. These processes, together with a loss of synchrony across the plate, would prevent further longitudinal expansion of the growth plate despite continued sporadic proliferation of chondrocytes.

This reveals something which I have always been confused and seems to resolve. The studies done by Zhang and Yokota were done on this lab MICE, NOT RATS. However, I as a laymen can’t see any difference between the anatomy and physiology of rats and mice so I would assume that the growth rate and endochondral process of rats and mice are very similar. The first sentence from the study is what really is interesting. It seems that even in aged rats, their physis/growth plates never completely disappear. However, the rats don’t grow any bigger or taller. The researchers state there are 4 reasons, bone bridges, loss of cellularity and problems with resorption of the non-organic material, non-organic bone material encroaching in on the cellular areas, and the chondrocytes turning into bone. If I was to guess, the reason why the growth plates never go away may be from the fact that the load on the cartilage of the limbs are not that high which means that the cartilage were never loaded to the point of accelerated ossification to the point where the rate of cartilage proliferation was overwhelmed by the cartilage to bone process. However, that is only my uneducated guess at this point. This means that the reason why the frequency loading was effective on the mice, even at advanced age can cause some longitudinal growth. I often imagine the dynamic loading at a lateral direction like a hand pushing on on the most sensitive region of a hard cylinder, with a hard region on the top and bottom, but the middle area, where the compression is done, is more sensitive and flexible to external stimuli.

If this is the case, that means that the entire LSJL theory based on the Yokota & Zhang studies is invalid for humans, and should not work on adults with their plates closed. On the LSJL forums there seems to be only one member who has gotten results. st.it, and I wonder whether at the age he started doing the LSJL he still had at least an epiphyseal line. I remember from my old university mechanical engineering and physics courses the application of dynamic loading in in high frequency in the form of shocks or hits done to  objects to see what would be the result. Material science says that any hard hit would cause any fractures or defects already in the material being hit to break and fracture, especially along the lines or areas where the material is the weakest. Maybe the LSJL dyanmic loading caused not epiphyseal cartilage, but closed epiphyseal lines to be split open slightly and leading to new cartilage formation. I note that for men, the age range for growth plate closure and final height age is very large. It could be that the few people who have seen the biggest results were people who still had a slight line available for fracture/distraction to allow the MSCs inside to aggregate and go through one last push in height increase. Due to how the bone remodels and get harder, the only way to possibly lead to more growth, would be to using far higher loads, at higher frequencies, using shorter time intervals, while putting a sharp edge on the most sensitive area to cause a possible horizontal fracture line inside.

One idea that I can give from my Tesla Coil building says is that each type of material in the world has it’s own specific resonance frequency. If the external piezoelectric device can be applied to the bone and it is osscilating at the right frequency, the resonance frequency of the cortical bone, it might cause the bone to shake enough to reveal it’s most weakest areas, and lead to small fractures. Then the piezoelectric material moves to the resonance frequency of the MSCs inside and get them to go through chondrogenesis. Dr. Brighton has already written up a patents which gives a hint of what it could be which is in the library section. This could work but at this point of my research, it is only a theoretical suggestion.