Inadequate theories


Although agreement seems to have been reached on the cellular origin of osteoporosis, in so far as the activity of cells which destroy bone (osteoclasts) is greater than that of the cells which rebuild it (osteoblasts), there are still many unknowns. It was not our original intention to consider this disease which becomes more severe at menopause.

Surgeons are in charge of rebuilding the bones which nature has destroyed. They are therefore at the other end of the chain. They note the importance of bone loss with the severity of the fracture, and the quantity or quality of remaining bone.

If their curiosity should lead them to take a look inside this bone, they would notice, among other destructive events, the number of vascular phenomena. They know that a healthy bone bleeds when it is fractured and that this bleeding is uncontrollable.

They know – empirically – that once the post-fracture haematoma has been evacuated, an osteoporotic femoral neck bleeds relatively little, particularly if the operation is performed some time after the accident, but that it bleeds a lot more when the operation is rapid (independently of ACs).

Several questions come into mind. What is the source of this bleeding? Does the blood come from the wall, inside the bone, muscular tearing or large periarticular vessels?

With trochanter fractures, bleeding comes essentially from the bone if the fracture is simple and not or only slightly displaced, from the bone and soft periarticular parts if the fracture is complex with major displacement. Experience shows that the periarticular arterial circle is almost never broken.

Osteoscopy has revealed the following in the superior femoral metaphysis:

  • There are non-functional vessels, as in any vascular structure. These vessels could be opened to increase blood flow, particularly under mechanical stress
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  • There are functional vessels on the surface of the bone lamellae, along the edges and on the surfaces, carrying blood elements. They are only a few microns apart (approx. 12). These arterial and venous capillaries are very small in diameter and only allow the circulation of one cell visible to the naked eye
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  • There are larger arteries which beat to the rhythm of the pulse
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  • Blood can be seen to flow in the metaphyseal space at a regular rate and continuously, from small diameter vessels
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  • Haematomas can be seen inside the bone.
  • Rigid bony plates can be seen and other which are partly rigid and partly supple.
  • Bone lamellae can be seen, parallel to each other, forming a kind of orderly architecture
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  • Detached bone lamellae can be seen, distributed chaotically.
  • Orthogonally shaped plates can be seen on all four sides. Some have the same transparency or opacity, others contain a clearer oval shape.
  • Some are homogeneous throughout, others are clearer at some points.
  • Some are solid, others are perforated. The hole is in the centre or along the edge of the plate.
  • Certain lamellae have parallel edges, others are swollen in the middle.
  • Some are attached to each other, others are separated and float freely.
  • Brown masses can be seen in the shape of vessels and these resemble micro-thromboses.
  • There are compact masses of adipose cells. In other places, there are isolated cells sprinkled like beads in the optical field.
  • All the bone lamellae are white and remain so.

It is probable that every situation has its own causes. There are an infinite possibility of these. Small vessels may suffer necrosis. The interruption in flow may be due to micro-thromboses, flexible plates may be due to the chemical release of mineral ions. The black spots may be micro-thromboses. Is the destruction of mineral plates only due to cell destruction? Beyond a certain stage, aren't the proteolytic elements of haematomas involved? Don't haematomas play a part in the pain patients suffer after prolonged walking because of the hyperpressure they engender inside the bone? Are bone lamellae of different shapes separated from each other simply by chemical phenomena (rupture at the end of the chain) and/or must mechanical phenomena (such as fatigue microfractures) be included? Does the swollen shape of certain lamellae reflect the microfractures described by Maurice-Michel Forest? Although it is microscopic, this whole macrocosm needs to be elucidated first. A great deal of work has to be done!

We must rely on fundamental researchers – as long as that's all they do – to explain to us what our different brains cannot understand. We must acknowledge our inadequacies with humility. They must inform us clearly with all their expertise. Can they do this?

It is clear, at this stage of destruction, that, unless it is placed in situ, no drug can treat this disease.

If it's true that surgeons – with a few exceptions – cannot learn from the elementary lessons of our old masters (philosophers, mathematicians and physicists), it is even less probable that they can understand the, as yet, poorly understood mysteries of intramolecular life. They shouldn't worry; many physicians – including some of the most highly qualified – are also excluded from the list of the rare few.

On the other hand, surgeons must know all about the technical difficulties they will meet so that they can apply all their expertise to finding solutions. This is within their technical limits. History will not forgive them for missing a technical improvement.

This is not light-years beyond their skill. The solution is here. Filling empty spaces, using a compatible, strong material which will act as a vector, vessel and cell carrier, which the bone needs for its reconstruction. At the same time, they must rebuild the anatomy, i.e. minimise as much as possible the sequelae which will inevitably occur if they forget.

What a challenge! We must hope that our colleagues, particularly the young, become aware that the elderly are our historical memory and it is a duty to thank them for it.

What better gift could we give them than restoring their autonomy for as long as possible.

Conclusion