Abstract
Intraosseous pressure measurements (IOP) are not new. Several authors have struggled to interpret static IOP and to understand arthritis and osteonecrosis pathology. This work uses a combination of simple experiments in vivo to reassess bone and joint physiology. Joint replacement needs to take into account the hydrodynamic conditions that are present in bone. Intraosseous pressure measurements were carried out with vascular occlusion, activity and saline injection in experimental conditions and then in man during walking.
RESULTS
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1
Basal IOP has a pulse wave and an underlying respiratory wave (RW).
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2
IOP closely reflects systemic vascular changes.
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3
Proximal arterial occlusion causes loss of IOP (IOPa) and pulse volume (PV).
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4
Proximal vein occlusion causes a rise in IOP (IOPv) with preservation of PV and RW.
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5
Physical loading raises IOP with preservation of PV and RW.
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6
Load with arterial occlusion caused minimal rise in IOP.
Loading with venous occlusion caused an augmented rise in IOP with preservation of the PV.
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7
Simultaneous recordings from the femoral head, condyle and upper tibia during vascular occlusion and loading show that the same effects occur at all sites.
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8
Simultaneous recording from the femoral head, condyle and upper tibia during saline injection shows pressure is transmitted through bone but not across joints.
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9
The Ficat bolus test destroys local circulation. Aspiration is better and preserves local perfusion.
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10
Bone health at the needle tip is better assessed by IOPv – IOPa, the perfusion ‘bandwidth’.
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11
Upper tibial pressure during standing, slow walking and fast walking shows large IOP changes in vivo.
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12
There is probably a physiological subchondral bone blood pump.
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13
Anatomical features are present which support this idea.
CONCLUSIONS
IOP measurement in isolation is meaningless. With arterial and venous occlusion, perfusion at the needle tip can be studied.
Compartment syndrome testing should be similar.
Subchondral bone is a compressible perfused sponge with a ‘pumped’ microcirculation.
Very high pressures arise in subchondral bone during activity.
There are protective modifications of the microcirculation.
Failure of subchondral circulation causes arthritis. Arthritis is mainly a ‘vasculo-mechanical’ disease. This work explains the spectrum of arthritis and osteonecrosis, and Perthes, caisson and sickle cell disease patterns. It explains why osteoporosis might protect against arthritis.
