The responses as of Thursday, May 28, 1998 follow.

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Hello,

I have been thinking about a particular
research question lately, and could not find
any relevant papers on the topic. I hope
someone can suggest some solutions.
The question is - how do continuously
loaded tissues grow? Two good examples
of these tissues exist: (1) the walls of arteries,
and (2) the periosteum surrounding long bones.
Both of these tissues are continuously loaded,
but must grow. My question does not concern
the actual morphological changes occurring during
growth, but the changes that occur in the
molecular load-bearing components of the
tissue. If the tissue is under continuous load,
then how are new load-bearing elements
added? In the arterial tissue, for example,
the load is carried by microfibrils, elastin,
and collagen. (There are some interesting
developmental and evolutionary aspects
of these elements too, which I may raise
in another message.) How are new elements
added while the wall continues to function?

I want to start answering this question
by looking at a very simple mechancial system –
the locomotor system of a scallop. This
consists of two shells that are pulled together
by a single muscle. The shells are connected
by a hinge. The muscle antagonism is elastic
– created by a compressive spring on the inside
of the hinge, and tensile elements on the outside
of the hinge. Most of the energy storage
occurs in the compressive hinge, which is
composed of an elastomer called abductin.
(This is very similar to elastin.)

When a scallop dies, the shells gape open,
but eventually stop, as the collagenous elements
in the muscle are stretched. However, if you cut
the muscle out of the shell, the shells will gape
even farther, showing that the hinge is continuously
loaded. I want to use this simple system to
examine the general question mentioned above.

If anyone is aware of any previous work
on the broad question, or would like to
comment on it, I would appreciate hearing
from you. I will post all replies in about two weeks.

Thank you in advance for your time.

Cheers

M. Edwin DeMont, Ph.D.
email: edemont@stfx.ca
WWW: ../biomechanics-lab.html

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Great question. I don't have an answer, but I'd love to hear responses. Many
skeletal muscles are always under some (passive) tension, although the
tension may be small. With growth there is serial addition of sarcomeres in
muscle fibres. Perhaps the growth occurs in a way that the load bearing part
(in this case the sarcomere) is relieved of its load bearing role by
parallel elements during the critical parts of its growth. There is now
evidence that muscles are organised so that load bearing structures are
tremndously connected both in series and in parallel. Perhaps the demands of
growth have necessitated this.

Rob Herbert
School of Physiotherapy
University of Sydney

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An interesting question, and one that has, as you suggest, important
consequences for growth of blood vessels. We actually frame the question in
a slightly different way, although it amounts to much the same thing: Since
elastin, one laid down in the extracellular matrix of vessels does not turn
over in any general way (and there is a lot of evidence to show that the
elastin you synthesize in your aorta when you are growing is the same
elastin that is present when you are 8o years old), and since the elastic
lamina are circumferentially continuous in the vessel, how can you have a
vessel increase in diameter with growth without cutting and adding new
elastin into the old matrix. If you are opening up the lamina and adding
new elastin, how can the structural integrity of the vessel be maintained
during this remodelling process. One suggestion that has been made
by a colleague of mine involves a very special and geographically limited
type of remodelling. The elastin lamina in vessels (especially the internal
elastin lamina) contains goles or fenestrae. By increasing the size of the
fenestrae even slightly, the stress/strain properties of the vessel can be
altered such that the same stress level produces an increased strain,
allowing the vesel to expand in diameter. This adjustment in sze can be
locked in place by the addition of new elastin in the area of the fenestra
In that way, the vessel can adjust in size without any general turnover of
the matrix components, but just by local remodelling in the area of the
fenestra. I'm not sure how far this idea will hold up in a biophysical
sense, but it seemed to me to be an interesting suggestion. Whether it
would apply in general to other tissues that have to remodel under load I
am not sure. The conference sounds interesting. I looked at their web site
and might consider it. Send me any other intersting replies you might get

Fred Keeley
Hospital for Sick Children, Toronto

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Dear Dr. DeMont,

I will not attempt to answer your very interesting question, but just
wanted to call your attention to the next conference of the Society for
Physical Regulation in Biology and Medicine. Perhaps, if you can, you
might submit a paper to raise this very issue to a very interested and
capable group of engineers, physicians, physical scientist and biologists.
It would certainly be a great discussion, albeit in real space rather than
cyberspace...

Information may be obtained at the SPRBM website set up for this:

http://WWW.ec.hscsyr.edu/sprbm

--Joe Spadaro

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Joseph A. Spadaro, Ph.D.
Research Associate Professor
Department of Orthopedic Surgery
S.U.N.Y. Health Science Center at Syracuse
750 East Adams St. Syracuse, NY,13210 U.S.A.

e-mail: spadaroj@hscsyr.edu

Fax: 315-464-6638

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