I recommend reading this because it is more informal than typical scientific papers and has some good insights.
The mechanical factors which influence bone growth
“the uptake of dye ‘madder’ by bone [is] only deposited where osteoblast activity was present”
“the shaft of the bone actually expanded, so that the bone cells grew apart as interstitial bone formed. ”
” in a deformed bone the internal structure was radically altered as a response to the static forces working on it. A normal bone will alter to meet a change in its function{But that doesn’t mean that the change will be what you want. The body will adapt to you playing basketball but not the desired effect of growing taller}. If such change in mechanical environment is rectified, the bone will resume its former shape and structure.”
” the assumption of the right posture will be associated with a change of cranial length as the centre of gravity of the cranium is required to rest over the feet.”<-So the predominant poster that a child uses will affect his cranium length.
“The hydroxy-apatite crystals are the pressure absorbing component of bone. The collagen fibres give the bone its tensile strength and elasticity. Compression and elongation give rise to electrical charges at the boundaries of the crystals and seem to produce appositional growth and reabsorption by triggering off the chemical processes leading to the formation of the metabolites which control these processes. Bone thus responds in its structure to the different forces such as compression, tension and torsion. The torsional strength of bone is about a third of its compressive strength, so it is not surprising to find that the tibia and humerus have a spiral arrangement of collagen fibres to protect them from the torsional forces to which they are particularly subjected. The bones of infants have a much lower modulus of elasticity than those of children, as though walking only becomes possible once the bone has stiffened.”<-So if one method to grow taller involves decreasing bone age then it might suggest that the bone age has decreased via weaker bone.
” the individual apatite crystals rather than the long glass rods enable the cracks, which always develop before a material fails under stress, to remain isolated rather than spreading rapidly as they do in fibreglass. Thus any lack or excess of muscle pull or body weight will have a significant effect on bone growth.”
“Sustained pressure on the growth plates of the distal femur and proximal tibia may compress the anterior portion and distract the posterior portion of the upper tibial growth plate”
” a simple piezo-electric effect on the apatite bone crystals [responds] to unusual pressure just as a crystal gramophone needle does. The effect is to stimulate growth on the side compressed by body weight until spontaneous correction occurs.”
“The medial femoral condyle tends to force the upper tibial epiphysis laterally so that the cells which bud off from the epiphysis, on which all longitudinal growth depends, will not only be excessively compressed but also subject to lateral sheer. The result may be a cessation of growth in the area where the abnormal stress is greatest. As the lateral half of the growth plate continues to grow, the result is a steadily increasing deformity and all the changes characteristic of tibia vara develop. The medial portion of the growth plate will become grossly abnormal and the histology shows not the normal beautifully ordered vertical columns of cells but total disorganization. I personally believe that this has a purpose, because the tongue of disordered cartilage and bone which is readily palpable, acts as a claw and, rather like a climber’s hands, holds the epiphysis in place and prevents any further lateral shift.”<-So would it be possible to avoid this and get a longer femur?
Here’s another good more traditional technical paper that’s related but still possible for a layman to understand:
The Developing Bone: Slave or Master of Its Cells and Molecules?
“A large number of molecular, cellular, and epidemiologic factors have been implicated in the regulation of bone development. A major unsolved problem is how to integrate these disparate findings into a concept that explains the development of bone as an organ. Often events on the organ level are simply presented as the cumulative effect of all factors that individually are known to influence bone development. In such a cumulative model it must be assumed that each bone cell carries the construction plan of the entire skeletal anatomy in its genes. This scenario is implausible, because it would require an astronomical amount of positional information. We therefore propose a functional model of bone development, which is based on Frost’s mechanostat theory. In this model the genome only provides positional information for the basic outline of the skeleton as a cartilaginous template. Thereafter, bone cell action is coordinated by the mechanical requirements of the bone. When mechanical challenges exceed an acceptable level (the mechanostat set point), bone tissue is added at the location where it is mechanically necessary. The main mechanical challenges during growth result from increases in bone length and in muscle force. Hormones, nutrition, and environmental factors exert an effect on bone either directly by modifying the mechanostat system or indirectly by influencing longitudinal bone growth or muscle force. Predictions based on this model are in accordance with observations on prenatal, early postnatal, and pubertal bone development. We propose that future studies on bone development should address topics that can be derived from the mechanostat model.”
“the desired effect of bone homeostasis is to keep the mechanically induced deformation of bone (in biomechanical terminology called “strain”) close to a preset level, or set point. The deformation of a bone is a surrogate measure of its strength, because a strong bone will deform less than a weak bone when a mechanical challenge is applied. Bone deformation generates canalicular fluid flow”<-A bone’s goal is to aid strength and not length. So we have to increase bone length in other ways at the stem cell level.
“Longitudinal growth increases lever arms and bending moments and therefore leads to greater bone deformation. Greater muscle force will also increase bone deformation during muscle contraction. Body weight alone puts relatively small loads on bones, but the effect of weight is amplified by muscle action”
