Biomechanics of natural Bone Union like u have never seen or read before

Biomechanics of natural Bone Union like u have never seen or read before

The first thing we need to know is that bone union is bone regeneration, not healing; the term healing indicates that the bone heals with secondary intention, and that never happens except pathologically. The bone unites by regenerating, by forming tissue of its own nature and structure, not by fibrous tissue, and if it did, it is called pathological fibrous non-union. Agreeing on all that makes us know, why bone healing is the most common orthopedic misnomer term in use.

But, that doesn’t just pass us by, without asking the important question, why does bone regenerate unlike almost all of the other tissue types, that heal with fibrosis and in secondary intention🙃🙃🙃??? the liver heels by cirrhosis, the kidney heals by scar formation, skin by scar formation, and so on … why bone is the exemption??? It is the very same answer I offered as to why bone must start forming early in enchondral ossification before any other system can develop??? the bone is the strut our soft bodies are hanged over and supported by, if the bone was allowed to just heal by secondary intention, this strut would fail, and eventually, we could just collapse as a shapeless soft heap.

Now, how does bone regenerate?? It needs all the mechanical, biochemical, vascular, and biological factors to be optimized for this regeneration

a) Mechanical factors

For understanding that we have to explore the amazing principle of inter-fragmentary strain🤩🤩🤩🤩

Sadly, this principle is explained in most books in a way that makes orthopedic and biomechanical students completely oblivious to how beautiful it is!! 🙃🙃🙃…when we experience a bone fracture, let’s keep it simple and examine a simple one-line fracture pattern, the bone becomes two segments connected by a fracture hematoma.

This principle states that the smaller the gap between the two segments, the more strains would happen in response to certain defined stress imposed. So the inter-fragmentary strain is inversely proportionate to the size of the gap. The other part of this principle is related to biology, it states that we need interfragmentary strains from 0-2 % for the bone to form, 2-10% for cartilage to form, 10-100 % for fibrous tissue to form; and at any value more than that, no tissue can form at all. That is it!!

The first part is easy, if you held your fingertips closer together, with a little gap between them, and you just moved them as if you are bending them, you would notice that the percentage of strain or elongation of the gap between your fingertips is much more than what would happen if you applied the same degree of bending while holding your fingertips farther apart.

In fig. (a) notice that the moving segment on the right side, is angulated in all three scenarios to the same exact degree and angle. A represents the original length of the gap with no stresses, while B represents the length of the gap after applying the stress. Strain is defined as the change of length compared to the original length so it would be (B-A/A), now notice the difference between the ratios between B&A in all three drawings, the larger the gap, the lower the B/A ratio will be. The larger the gap” the bottom figure”, the lower (B-A/A) for a given amount of stress, compared with what would happen if the gap is small “top figure”

But what does all that mean!! When we have a fracture, it is very natural that during conservatively managing this fracture, some strains will happen as splintage by a slap or even a cast won’t offer absolute stability, those strains will judge and define what kind of tissue can be used to cross the gap between the fractured bone segments.

We first need relative stability afforded by internal as well as external splintage:

  1. Internal splintage: as soon as fracture happens, a hematoma forms, and the surrounding soft tissues become edematous. This increases the hydrostatic pressure around the bone as the bone and its surrounding soft tissues are contained within a relatively non-compliant fascial compartment, splinting it from within; and it is actually useful so long as it can build physiologically accepted pressure values, and doesn’t make the compartment too tight. This mechanism fails in these two coming scenarios:

• It can’t build necessary pressure if it happened in a very large compartment; for it to build this pressure given the vast compartment size, it might compromise the blood volume and risk going into hemorrhagic shock. Femoral shaft fractures are an example; it bleeds too much and doesn’t build pressure as the compartments are too vast. No wonder, Thomas traction splints used nowadays with femoral shaft fractures decreased the high mortality rate associated with this type of fracture before its use, noticeably observed during its introduction during world war two.

• Or it can happen in a tight compartment like around the heel and ankle region, or the hand as examples, if the edema is excessive, it might progress to be a compartment syndrome, or the extracellular edema fluid might raise the epidermis forming bullae and it might even break it.

  1. External splintage: either a makeshift at the scene; or a form of a brace, a slab, or even a cast.

This is not absolute fixation, so strains do happen, how does the body minimize the strains that develop in response to externally applied loads?? It does that by widening the gap by releasing macrophages and osteoclasts at the fracture site, inciting edge necrosis, and through this, widening the gap between the fracture ends.

 Do you remember what widening the gap does; it will decrease the strains that happen in the gap in response to the imposed stress values.

 Now, to the second part and that is where the real beauty is, why these different values for different kinds of tissues ??? And what do those numbers actually represent???🥰🥰🥰🥰

 Do you remember what we said again and again, that our bodies use mass and energy very effectively, now let me ask you a question… will it be wise to create a tissue you know already that it won’t handle the strains imposed and then ultimately break??? …keeping the concept of mass and energy conservation in mind, the answer would simply be IMPOSSIBLE. NOW, those numbers represent the maximum amount of strain these tissues can withstand before grossly failing, GOT IT NOW??? If the bone can fail at 2 % strain values, would you lay down bone with a strain value of 7 % for example??? If you did, it will break!!! So, of course, you will not, you can lay down cartilage instead, it can withstand up to ten percent deformation without breaking. That collectively means that you won’t ever build a tissue where the strains will break it, or else, you would be wasting energy and mass only to be doomed by failure and our bodies can never do that, I hope you got it now.

b) Vascular and biochemical factors

One of the most amazing phenomena in bone is how its bone vascular tree is arranged and structured. it is a story and what a story it is

Let me ask you a question, where do fractures start? On the periosteal or the endosteal surface??? It is a no-brainer of course, on the bone surface as it is the most tensile point when bending the bone “the most common modality of loading”. Ok then, so if cracks started on the periosteal surface, another question should be asked, if you have to supply this “crack starting point” with blood, how would you supply it? Would you make the horizontally penetrating periosteal vessels, large calibered or thin?? High pressure or low pressure?? Again it is a no-brainer if cracks start on this surface, and if I had to supply it by penetrating surface vessels, I would like to penetrate the surface with very narrow vessels with as low pressure as I can manage not to be a crack helper. Only the very unwise would penetrate the periosteal surface with a wide bore vessel, drilling inside the bone by its high-pressure system, as if he is inviting a crack start.

Would you make the surface little tiny canals penetrate the whole width of the cortex or only slightly?? If it runs the entire width of the cortex, cracks can spread along with it and break the whole width, but if it was only part of the way, the cortex would be much less vulnerable to completely crack, right??? 

As for the endosteal circulation. The smart one would tell me, that this surface is relatively immune and relatively not vulnerable, as it is never the starting point of a crack, so I can make the vessels penetrate well deep into the cortex, 2/3 s of the width and if it is high pressure, there is no harm as it can’t start a crack.

This logic-building rationale is how our great creator made our bones. He made the periosteal circulation comprised of so so many numerous branches, very small tiny branches, the collective diameter of all of them is huge, making the volume of blood running through this very wide collective caliber a low pressure and slow system of supplying blood to the bone. Finally, those very narrow, low pressure, and slow flow channels penetrate only through the outer cortical third, substantially limiting the lines of weakness created by them. Inside the bone, however, we have only one nutrient artery, hence the pressure is high and it penetrates the inner two-thirds of the cortical width.

 I can’t really believe that was just a random evolution, nor can any sane person, seeing this beauty and not appreciating and acknowledging the rightfully deserved respect and admiration and thanks to whoever made this amazing beautiful arrangement and structure, I just can’t !!! 

 Is that all?? No, it is not, this arrangement didn’t just protect the bone against being cracked and fractured, but it is the best and ideal arrangement ensuring successful regeneration if the bone failed in a fracture, how is that??

Let’s continue examining the beauty of our bone vascular supply 

The type of tissue that will form in the fracture gap isn’t just dependent on the inter-fragmentary strain, but also on oxygen tension. The higher oxygen tension there is, the more the media is suitable for bone formation. If the environment is ischemic, cartilage rapidly forms as it can sustain this environment but only if the mechanical pre-requisite is fulfilled “strain values”.

Time to question again. When the bone continuity is interrupted, which of those two vascular systems is more prone to serious damage? The very highly segmental and regional source, or the ONLY and one single nutrient artery??? It is, again, weirdly a no-brainer , the periosteal circulation will suffer the least, as there are many regional sources and it is a highly segmental one. Limited periosteal vessels at the site of the fracture will suffer. However, the other nearby numerous periosteal small arteries will remain perfectly normal; at the same time, major damage will come to the nutrient artery with the slightest displacement of the bone segments.

What does that mean, it means mostly after fractures, the periosteal surface will still be a high oxygen media, and the endosteal surface mostly will be ischemic, again what does that mean, it means that cartilage will mostly form inside the bone and bone on the outside, but let’s not forget the timing, which will form first.

Let’s review the whole process to keep being in focus

Bone fractures; the resultant hematoma and edema provide a hydrostatic pressure splint to the fractured bone temporarily tell external splintage is applied; those will decrease the loads and stresses on the bone end; at the same time, the edge necrosis minimizes the magnitude of strains those stresses cause by the principle of interfragmentary strain, ideally to below 10%. Now, it is time for oxygen tension to determine which tissue will form.

The inside of the bone is ischemic, cartilage can rapidly develop withstanding ischemia and with the amount of strain present and so it forms. Cartilage formation serves a much greater function as it holds the ends in an even more stable position, decreasing the strain more and the instant those strains get below 2 %, only then, bone is ready to form. But where it forms ?? Of course in the outer periosteal oxygen-rich environment, even in that, there is much beauty to be seen.

Forming the bone that is initially weak as it forms is easy but protecting it is hard … how to protect it?? We will now use another beautiful biomechanical principle, the principle of the second moment of inertia “areal moment of inertia”, it is a mechanical term describing how the shape of a structure affects the stresses that can develop inside, in response to the externally applied load, our regenerating uniting bone structure is very much like a cylinder

The yield of the second moment of inertia for cylindrical structures is directly proportionate to the fourth power of its diameter, increasing its diameter substantially increases the structure’s second moment of inertia …

So now, stresses inside the construct = externally applied load / very high second moment of inertia”. The second moment of inertia is very high because the bone is laid on the periphery of the construct and the cylinder it forms is wide”. Placing the bone peripherally protected the construct by decreasing the internally generated stresses that can break it.

Without the bone’s very peculiar arrangement of its vascular supply, this whole scenario wouldn’t have been even remotely possible. Just tell me how beautiful that is.

c) The biological environment

That is brought about by the very complex interaction between bone cells, blood cells, growth factors, and inflammatory mediators. All of that organizes, controls, and regulates all those processes just mentioned in the earlier two environments, there is so much wisdom and beauty still to be seen in that but that is beyond the scope of this post.

as I said…it is a story …and it is a very beautiful one indeed…

سبحانك ما خلقت هذا باطلا …🙏🙏🙏🙏

I would like to thank Mostafa el seba3ee, the very talented orthopedic surgeon and medical painter for drawing those drawings … 😍😍

I hope u got it all well, and it was useful…tell we meet again in other posts or videos or whatever…