When I was originally looking over Tyler’s LSJL method I felt that one part of the method was not completely satisfactorily explained. Or at least I couldn’t understand the step.
The step was from the idea of increasing the hydrostatic pressure in the medullary cavity to allow for more interstitial flow down the diaphysis. The Empirical data says that the measurement of flow was indicated by a voltage drop across the length of the long bone. I am not going to argue with the data and assume that the hydrostatic pressure was increased and there was an increase in flow of fluid through the inside of the bone.
Let’s also assume that because of the increasing flow the mesenchymal stem cells in the marrow area starts to turn into chondrocytes at a far greater rate. However, that still should not explain the longitudinal lengthening of the femur or tibia. The boen is bone, and there is no growth plates to allow for any elasticity in the bone. The tensile strength is suppose to be around 100-150 MPa for long bone so it can’t stretch that much. In a previous post, I had shown that there can be tensile loading to the bone and it will do some deformation in the tensile direction before a clear fracture can be observed resulting in bone breaking. This can cause height increase.
However, my question is how it is possible for microscopic blob-like cells be able to push the cortical bone of the outer later appart from each other to allow for longitudinal lengthening. Can the cells just go to edge of the bone, push past the peristoreum, and push the bones and osteoblasts apart from each other? That just seems so unlike because of the amount of tensile strength ordinary bones seem to have. In a mechanics of materials loading test, the human bone is just as strong and tough as stell!!
This is why my suggestion is that even if the theory of LSJL is right and works, there must have been some fractures createed since cartilage no longer exists in the diaphysis region of the bone. For me, there has to be some bone distraction or bone breaking for height increase to begin.
How about you then: Do You believe bone distraction or bone breaking is always needed to increase height after the plates face turned from cartilage to bone.
The thing is that the growth plates always have to exert a force against the two ends of the bones to grow taller. And in the epiphysis of the bone there isn’t cortical bone only trabecular bone which isn’t as tough.
The theory is that there’s also hydrostatic pressure in the epiphysis not just the medullary cavity of the bone. It’s the chondrocytes in the epiphyseal region that can undergo endochondral ossification and generate force to cause height gain.
And not necessarily fractures but LSJL can generate MMPs that can degrade bone and make it easier to push.
Also can you provide a link to the previous post where tensile strain can cause height gain. I have studied this in the past and would really like to see this.
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