Microcracks and Height Growth

I sent an email to Dr. Andrew Pitsillides about microfractures and he responded back.  I wanted to discuss a little about what he stated.

Dr. Pitsillides stated that "David Burr studied microcracks in exercising soldiers and that Elwyn Firth examined exercising horses for the presence of microcracks in cortical bone."

Now the David Burr book is 200 dollars so I don't have access to that(Musculoskeletal Fatigue and Stress Fractures).

I searched for Elywn Firth's article and all I could find regarding microcracks was "Mechanical testing to failure of metacarpal mid-diaphysis specimens had a slightly higher toughness, and higher impact strength, which was correlated positively with the amount of microcracking produced during testing. Increased loading was associated with an enhanced ability to microcrack and increase toughness (Reilly et al. 1997)."

So stronger bones are a benefit to creating microcracks.  This contraindicates any sort of plan that might involve cycling to temporarily weaken your bones to be able to cause more fractures(-micro).

In regards to the possibility of microcracks being involved in the expansion of cortical area Dr. Pitsillides stated:

"Loading-induced changes in (re)modelling to increase cortical bone area do not apparently NEED to involve the formation of microcracks. For instance, De Souza et al., showed when he was with me that microcracks could not be found in bones, where increased cortical thickness had been induced in the tibia by loading. Now - we might have been looking in the wrong place and we know that its difficult to know where to look, so we can't, necessarily, completely rule out the involvment of microcracks."

That's great for methods like LSJL being able to help people grow taller as it means that you don't need superhuman loads to induce bone adaptation(we are usually looking for specific activities of osteoblasts and chondrocytes; these activities being capable of increasing height).  But if he had found microcracks in places where tibial thickness increased that would've been a great boon to the tensile strain microcracking method of increasing height.

In regards to the amount of microstrain involved to induce microcracks:

"Not too sure where you've got the 15000 microstrain number from[I got it from mechanostat theory]. In our studies we rarely exceed 3000 microstrain - in fact recent studies have examined changes in bone (re)modelling induced by 1500 microstrain - an order of magnitude lower! It is, therefore, quite possible that 15000 microstrain is high enough to induce this kind of microcrack damage and maybe even fracture - but this is completely outside my comfort zone. "

Microcracks are only one way to grow taller and the microcracks must be caused by tensile strain and not compressive forces.  Microcracks are disadvantageous for our purposes as we can induce bone adaptation and therefore height growth with lower levels of microstrain.  In fact, with LSJL we are not looking for microstrain but we are working towards a lateral compressive force to compress the epiphysis of our bones.  This increases hydrostatic pressure(as the area containing the bone marrow is now smaller) and thereby encourages chondrogenic differentiation.


Living with cracks: damage and repair in human bone.

"Our bones are full of cracks, which form and grow as a result of daily loading activities."

"[Osteoclasts and osteoblasts] combine to form a basic multicellular unit (BMU) — a cavity, about 200 m in diameter, which moves along the length of the bone at a speed of about 40 m per day"

"Compact (cortical) bone is essentially solid material, although spaces for blood vessels and living cells give it a porosity of about 5%; it makes up the majority of our long bones. Spongy cancellous bone is found inside bony structures, especially close to joints{it is here where we try to form new growth plates with LSJL}.  It is essentially the same material as compact bone, but arranged in an open network to create a foam-like structure. At the microscopic scale both materials are made rather like plywood, from sheets of alternating lamellae that can be laid flat, or curved around in circles to protect blood vessels, forming osteons. Inside each lamella, at the ultrastructural level we find fibres of collagen, a soft, polymeric material made from long-chain molecules arranged in a triple helix, and crystals of hydroxyapatite (HA), a hard, brittle mineral material based on calcium. The ultrastructure is highly oriented, creating a strong anisotropy."

"Mechanical loading creates damage; at the microscopic scale one can see small cracks that take the form of planar ellipses, typically having a major axis of length 2c = 400 m oriented approximately parallel to the bone's longitudinal axis, and a minor axis of length 2a = 100 m."

"Microcracks predominate in regions of compression — which constitutes the principal type of loading in our long bones — where they experience shear due to their orientation. In addition to these individual, linear cracks, areas called 'diffuse damage' are also observed, which contain many small cracks, each of the order of a micrometre in size."

"a, Cancellous bone showing examples of microdamage revealed by staining with basic fuschin (pink). The arrows indicate (from left to right): a microcrack (approximately 200 m long), cross-hatching and diffuse damage respectively. b, A microcrack 'C' encounters an osteon 'O', and begins to grow around its cement line (dashed line). The microcrack is approximately 100 m long."

The problem with the microcrack depicted in b is that it's the wrong kind of microcrack for height growth.  The microcrack is lateral to the osteon whereas you'd want the microcrack to be longitudinal for height growth.

"toughness in bone is achieved through bridging of the crack faces by unbroken ligaments of material, inhibiting further crack growth in the same way that reinforcing rods protect concrete."

"Cracks can grow very slowly, over long periods of time, even when their loading conditions are unchanged."

"Flow rates are low in the region of bone immediately ahead of the BMU cavity. Cells die in this stagnant area, possibly because they don't receive enough nutrients, but cell death is deliberate (apoptosis), triggered by a change in the level of nitric oxide released by cells, which acts as a signal indicating the rate of fluid flow. Osteoclasts are attracted to the apoptotic cells and so preferentially eat away the bone in this region."

"Cracks create regions of both high stress (near their tips) and low stress (along their sides) that cancel out, so that from a distance, a crack would be invisible [unless the cells underwent apoptosis]"

We need to find images of microcracks along the longtiduinal axis.

Effect of cyclic loading on the nanoscale deformation of hydroxyapatite and collagen fibrils in bovine bone.

"Cyclic compressive loading tests were carried out on bovine femoral bones at body temperature, with varying mean stresses (-55 to -80 MPa) and loading frequencies (0.5-5 Hz). At various times, the cyclic loading was interrupted to carry out high-energy X-ray scattering measurements of the internal strains developing in the hydroxyapatite (HAP) platelets and the collagen fibrils. The residual strains upon unloading were always tensile in the HAP and compressive in the fibrils, and each increases in magnitude with loading cycles, which can be explained from damage at the HAP-collagen interface and accumulation of plastic deformation within the collagen phase. The samples tested at a higher mean stress and stress amplitude, and at lower loading frequencies exhibit greater plastic deformation and damage accumulation{plastic defomration means greater ability to stretch out the bone}, which is attributed to greater contribution of creep. Cracks are produced during cyclic loading and that they mostly occur concentric with Haversian canals."

"Bone consists of an organic matrix [about 90 % type I collagen with the rest being made up of non-collagenous proteins and lipids], a mineral phase (carbonated hydroxyapatite, HAP) and water "

"Peak compressive stresses (estimated from strain measurements) of −97, −30 and −15 MPa have been recorded in in vivo studies of racing horses, walking dogs and jogging humans"

"Despite the high strength and toughness, bones can fracture due to impact loads and repetitive or sustained loads exerted over long periods of time"

"The fatigue life of cortical bone is greater during compressive cyclic loading than during tensile cyclic loading. The stiffness of bone has been shown to decrease during cyclic loading due to the degradation of the HAP–collagen interface, leading to reduced load transfer"