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I
in Berlin. This represents the
first elucidation of the molecular
underpinnings of a major disease
of bone formation. The tech-
niques developed for this study
are to be extended to additional
skeletal pathologies, hopefully to
clarify their structural defects
and, perhaps, to eventually find
ways of dealing with them.
The investigation, which ap-
pears in this month's issue of Ma-
trix Biology, was carried out by
Professor Wolfie Traub, Profes-
sor Stephen Weiner and electron
microscopist Talmon Arad of the
Institute's Department of Struc-
tural Biology, in collaboration
with Professor Ulrich Vetter of
the Pediatrics Department of
Humboldt's Charitee Hospital.
The new study
shows that defective
fibers are unable to
mineralize properly.
CH, also known as brittle bone
syndrome, is an inherited conch-
tion caused by the production of
faulty collagen — a major struc-
tural component of bones, ten-
dons, skin and even the eyeball,
all of which can be affected by the
disease. Patients can therefore
suffer from severely misshapen,
brittle bones, multiple fractures,
dwarfism, extremely delicate
skin, deafness and abnormally
blue-hued eyeballs. Depending
on the nature of the collagen de-
fect, CH can range from being ex-
tremely mild to rapidly fatal in
early life. While not common, the
syndrome occurs in most popu-
lations about as often as the bet-
ter-known hereditary disease
hemophilia.
In the first electron microscopy
study of bone samples from OI pa-
tients, the Weizmann and Hum-
boldt researchers revealed some
key aspects of bone malformation
in this disease. One of their ma-
jor findings explains why the dis-
ease is often mild. The
researchers found that despite the
presence of a defective collagen
gene, the majority of collagen
fibers present in the bones of pa-
tients with mild OI were normal.
The scientists believe this occurs
because most of the defective col-
lagen molecules may be destroyed
within the cells manufacturing
them, so that relatively few of
these faulty molecules are incor-
porated into collagen fibers in the
bone. This, however, may also be
the reason why even in the less
severe forms of the disease, the
bones contain substantially low-
er amounts of total collagen than
that in healthy individuals. The
Investigators also found that the
more severe forms of the disease
were characterized by fewer nor-
mal and more abnormbl collagen
fibers than in mild OI.
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