View Full Version : Osteoporosis, bone metabolism

M Swanepoel
06-29-1998, 05:49 PM
Hi Justin Keogh, Louis Amundsen and others,

On Sunday evening I saw a feature on the use of bone growth
stimulating proteins, presented on the Australian TV science
programme "Beyond 2000". The snippet was on work done at the Bone
Research Unit, attached to the Dept of Orthopaedics of the University
of the Witwatersrand's Medical School. It featured a woman whose
mandible, completely removed due to a tumour, was replaced with a pure
titanium meshwork grille, (quite thin, and presumably mechanically
non-functional), filled with a mixture of healthy bone chips and these
"newly found" bone growth stimulating proteins. The result was absolutely
amazing - a completely new jaw of healthy new bone that replaced
the original item, and which was completely functional in three
months, ready to receive a set of false teeth..

The feature seemed to indicate that the jaw did not have to be extensively
exercised, and that the major role in bone growth was in fact played
by these chemical messengers, which switched osteoblastic and
osteoclastic activity on and off. Now I don't believe that this is
contrary to anything that has been said before, since these protein
growth stimulants are clearly usually produced by cells stimulated by
exercise - exercise is the key. However the feature stated that it
would now be possible for completely new bones to be grown to replace
the originals, and that osteoporotic sufferers would soon be allowed
to receive injections of these bone growth stimulants which would
cure them!

The feature went even further - these protein growth stimulants
apparently also stimulate organ growth, and it seems likely
that soon damaged organs will be capable of being regenerated from
small undamaged fragments. (Is this simply media hype?) I think that
biomechanical engineers working on prostheses should be aware that the
time of genetic and growth stimulant solutions to problems which use to
demand prosthetics is dawning!

I am sure that many of you are also aware of the work of
Helminen, Kiviranta et al. (Finland) and Jill Urban et al. of the University
of Oxford (I'll find and post the references soon!)
on the production of proteoglycans in cartilage, under different
loading regimes. They have found that cyclical loading of
chondrocytes is closely linked to the production of PGs, but it seems that the
ratio of loading to unloading time, and the frequency of loading are
critical. If I remember correctly Prof Currey of the Univ of York
found something similar with bone, loading the ulnas of turkeys. If
he reads this message, it'd be interesting to hear about his work.
Anyhow, the upshot of this is that I am convinced that the repitition frequency,
magnitude, and rate of load change all play a role in determining
bone removal and deposition. It would probably be a good idea to
measure cyclic AMP levels versus load stimulation of bone cells. (The
transduction of the load signal, is of course, a fascinating issue!)

Interestingly the limb bones of many skeletons of South African
antelope which I have looked at, at the Tvl Museum in Pretoria, all
display the removal of bone in tension, and thickening in
compression. The question arises as to whether this is generally
true for all bones, throughout the animal kingdom,
(do the ossicles of the ear, or the iliac wings also obey this rule,
for example?), or whether the location of a bone also plays a role in
determining whether it can continue to exist in a slightly tensile
loading regime. Conversely can collagen happily exist in a
feebly tensile or purely compressive field? (It seems happy enough
in bone!) Is the collagen network placed
under tension in bone, so that the bone is in fact a prestressed
material? If so, how great is this prestressing in MPa, and what is
the significance of prestressing for the mechanical behaviour of
bone? How would the collagen be kept in tension?

Mark W Swanepoel
School of Mechanical Engineering
University of the Witwatersrand
South Africa

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