WU team finds why some cells turn bad in bones

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WU team finds why some cells turn bad in bones

By Tinsley H.

Of the Post-Dispatch

07/08/2001 06:53 PM

Tumbling along in everyone's bloodstream are cells poised to

destroy bone tissue. Researchers at Washington University

recently showed that inflamed blood vessels snag these cells

and morph them into evil twins responsible for bone loss in

rheumatoid arthritis and other disease.

The findings may illuminate ways to deliver drugs to silence

those inflamed sites that signal the transformation,

improving current treatments.

Turnover in human bones is a normal process delicately

balanced to replace old tissue with new. When cells that

remove bone tissue go haywire, as in rheumatoid arthritis,

the excess destruction, or resorption, results in

irreversible bone loss.

" The body tries to very carefully couple together bone

resorption and construction so you don't just dissolve

away, " said Collin-Osdoby, research associate

professor in biology at Washington University. She is an

author of the study published in the June issue of the

Journal of Biological Chemistry.

Until now, scientists did not think that blood vessels were

capable of signaling immature cells to become

bone-destroying cells. Large numbers of these destructive

cells congregate at sites inflamed by periodontal disease,

though doctors were at a loss to explain how they got there.

Living bone is hardly a petrified amalgam of calcium and

minerals; it is traversed by many tiny blood vessels that

carry oxygen, nutrients and chemical signals essential for

the bone's survival. Collin-Osdoby and her colleagues

discovered that these passageways also have the ability to

cause bone destruction.

When blood vessels become inflamed, they produce a molecule,

RANKL, that turns the immature cells into bone-destroying

ones. As the cells leak through the vessel wall, RANKL

molecules lie in wait on the other side of the wall and

signal the cells to begin gobbling bone.

Normally, in the balanced cycle of bone regrowth, other

molecules inhibit RANKL so that cells can go to work and

fill in the holes with healthy new bone tissue. In the case

of chronic inflammation, the stimulator of bone destruction

is in higher quantities than the inhibitor, said Bob Jilka,

professor of medicine at the University of Arkansas for

Medical Sciences.

Rheumatoid arthritis is a debilitating chronic inflammatory

disease that destroys bone tissue. Affecting at least 2

million people each year, it is two to three times more

common in men than women. Treatments for rheumatoid

arthritis try to reduce inflammation to stop bone loss.

Knowing that blood vessels also can signal destruction may

aid in the development of new drugs that prevent the

bone-gobbling cells from forming, Jilka said.

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