Microfractures and Bone

The above right image is a picture of a bone with heavy amounts of microcracks(which are microfractures of the cortical bone) to the left is the chemical used to contrast microcracks from regular bone(Source: Selective imaging of damaged bone structure (microcracks) using a targeting Supramolecular Eu(III) Compex as a Lanthanide Luminscent contrasting agent).

You can see how microcracks are partial throughout the cortical bone but you can gain height by zig zagging.  One microcrack may be on the left side of the osteon but another microcrack may be on the right side of the osteon leading to an eventual overall height gain.  What is most important is that the bone is distracted when the microcrack occurs so that the microcracks help the osteon maintain some of the distracted state and the bone gradually grows taller and longer over time.

Exercise-induced metacarpophalangeal joint adaptation in the Thoroughbred racehorse.

"We performed a histologic study of the distal end of the third metacarpal[one of the finger bones] bone in two groups of horses: young Thoroughbreds that were actively racing (n = 10) and a group of non-athletic horses (n = 8). The purpose of this study was to determine whether development of articular microcracks was associated with specific alterations to subchondral plate osteocytes[the subchondral plate is the epiphysis so perhaps these epiphyseal osteocytes could be involved in height gain]. Morphometric measurements were made in five regions of the joint surface: lateral condyle, lateral condylar groove, sagittal ridge, medial condylar groove, and medial condyle. The following variables were quantified: hyaline cartilage width; calcified cartilage width; the number of tidemarks; microcrack density at the articular surface; blood vessel density entering articular cartilage; the presence of atypical bone matrix in the subchondral plate; bone volume fraction; and osteocyte density. Adaptation of articular cartilage was similar in both groups of horses. Vascularization of articular cartilage was increased in the group of non-athletic horses[the group of athletic horses likely already had vascularized articular cartilage pre-microcracks]. Microcracks, which typically had an oblique orientation to the joint surface, were co-localized with blood vessels, and resorption spaces. Microcracking was increased in the condylar grooves of athletic horses compared with the other joint regions and was also increased compared with the condylar groove regions of non-athletic horses. Coalescence of microcracks also led to development of an intracortical articular condylar stress fracture in some joints and targeted remodeling of affected subchondral plate[it's possible that specific modeling of the subchondral plate can induce height growth]."

Colacalize means to occur together in the same cell.  A resorption space would be a place in the bone tissue where bone is reabsorbed.  So microcracks tended to occur near blood vessals and where bone tended to be reabsorbed.  Oblique means that the microcracks tended to not have a standard orientation(the study states 45 degress which means that the microcracks when healed could increase both length and height).

The effects of increased intracortical remodeling on microcrack behaviour in compact bone[cortical bone]

"Samples were cyclically loaded to failure and then histological analyses were carried out. Cracks were categorized by length into three groups; short (<100 mum), intermediate (100-300 mum) and long (>300 mum). Numerical crack density (Cr.Dn) of long cracks was greater in controls compared with OVX. Controls also displayed a higher crack surface density (Cr.S.Dn) compared with OVX (p<0.05). The behaviour of short cracks did not differ between old and new osteons, but intermediate and long cracks preferentially stopped at newer osteons compared with older ones (p<0.05). This mechanism may have an important role in terms of prolonging fatigue life. We conclude that recently formed secondary osteons have a unique influence on propagating microcracks compared with older osteons."


OVX controls are sheep that have had surgical menopause induced.  Mum is a micrometer which is one millionith of a meter. Propagate means to multiply which means newer osteons actually caused more microfractures which contributes to the the theory that microcracks occur more in tougher bone.  This would also explain why there are diminishing returns on microcracks with exercise.  There are only so many new osteons and if older osteons are less able to propagate microcracks then there should be less of a benefit when all the new osteons "are used up."

Micromechanics fracture in osteonal cortical bone: a study of the interactions between microcrack propagation, microstructure and the material properties.

"The interstitial bone is modelled as a matrix, the osteons are modelled as fibres, and the cement line is presented as interface tissue. The interaction between osteons and microcracks is evaluated by linear elastic fracture mechanics theory, followed by a determination of the stress intensity factor at the vicinity of the microcrack tips. The results indicate that bone microstructural heterogeneity greatly influences fracture parameters. Furthermore, microstructural morphology and loading conditions affect growth trajectories, the microcrack propagation trajectory deviates from the osteon under tensile loading, and osteon penetration is observed under compressive loads."

So you need to have tensile loading(bone stretching) to achieve the kind of microcracks that can increase height.

Experimental validation of a microcracking-based toughening mechanism for cortical bone.

"Crack initiation and propagation tests were conducted on cortical bone compact tension specimens obtained from the antlers of red deer. For these tests, the main fracture crack was either propagated to a predetermined crack length or was stopped immediately after initiating from the notch. The microcracks produced in both groups of specimens were counted in the same surface area of interest around and below the notch, and crack growth resistance and crack propagation velocity were analyzed. There were more microcracks in the surface area of interest in the propagation than in initiation specimens showing that the formation of microcracks continued after the initiation of a fracture crack. Crack growth resistance increased with crack extension, and crack propagation velocity vs. crack extension curves demonstrated the characteristic jump increase and decrease pattern associated with the formation of microcracks. The scanning electron micrographs of crack initiation and propagation displayed the formation of a frontal process zone and a wake, respectively. These results support the microcrack-based toughening mechanism in cortical bone. Bone toughness is, therefore, determined by its ability to form microcracks during fracture."

Again, the tougher the bone, the more microcracks are formed.

The behaviour of microcracks in compact bone.

"The first study investigated the manner by which microcracks accumulate and interact with bone microstructure during fatigue testing of compact bone specimens. In a series of fatigue tests carried out at four different stress ranges between 50 and 80 MPA, crack density increased with loading cycles at a rate determined by the applied stress. Variations in the patterns of microdamage accumulation suggest that that at low stress levels, larger amounts of damage can build up without failure occurring...  In a third study, the manner by which crack growth disrupts the canalicular processes connecting osteocytes was investigated. Analysis of individual cracks showed that disruption of the canalicular processes connecting osteocytes occurred due to shear displacement at the face of propagating microcracks, suggesting that this may play some role in the mechanism that signals bone remodelling. In a fourth in vivo study, it was shown that altering the mechanical load applied to the long bones of growing rats causes microcrack formation. In vivo microdamage was present in rats subjected to hindlimb suspension with a higher microcrack density found in the humeri than the femora. Microdamage was also found in control animals. This is the first study to demonstrate in vivo microcracks in normally loaded bones in a rat model."

The first bolded statement suggests that we can cause a lot of microfractures without causing a full fracture of the bone.  The second bolded statement suggests that osteocytes react to being displaced so it may be possible to confuse the bone to induce remodeling in a way that increases height.

We have to create microcracks that denature  the bone in such a way as to make it taller.  Microstrain may be the key(microstrain says that bone may be temporarily lengthened).  If you pull a pencil apart hard enough eventually it will microcrack and maintain some of that elongated state.  Since that pencil is a bone that bone can heal in the elongated state.  The current best way to create this microstrain is with lateral synovial joint loading.

Impact may lengthen the bone if the impact you apply the impact to the side of the bone(if you tap the bone with a hammer laterally to the bone).  Microcracks coupled with micro- Tensile Strain are key to increasing height.