Chondrocyte aging is major culprit in OA

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Rheumawire

Mar 15, 2004

Chondrocyte aging is major culprit in OA

San Francisco, CA - Chondrocyte aging may be largely responsible for the

onset of osteoarthritis (OA), according to new research presented at the

71st annual meeting of the American Academy of Orthopaedic Surgeons. But

researchers may one day be able to stop chondrocyte agingparticularly in

patients at high risk of OA.

" Aging compromises the ability of human chondrocytes to maintain and

restore articular cartilage, " says Dr ph A Buckwalter (University of

Iowa, Iowa City).

" Our research shows that human chondrocytes undergo a very dramatic

age-related phenomenon due to the destruction of the DNA information, "

he says.

Chondrocyte aging does not depend on systemic factors; the changes are

caused by changes in gene expression, he explains. With each cell

division, chondrocytes lose telomere length, and eventually the cells

stop working, the joint falls apart, and patients develop OA. Telomeres

basically let cells work. The length of the telomere determines cell

death or senescence.

Chondrocytes are used to an environment with 5% oxygen. " High oxygen

tension damages genetic information in our chondrocytes, " he says. Such

tension arises after severe joint injury or fracture.

A new study, soon to be published in the journal Gerontology, aimed to

put a stop to chondrocyte aging. Buckwalter and colleagues took

cartilage cells from a 21-year-old man and grew them in culture to find

that they divide 20 times and then stop and die.

But when they put telomerase back into the cells, they did up to 45

divisions and lived longer before senescence. If they cut oxygen

tension, the cells divided 60 times.

" We more than doubled the lifespan just by protecting them from

oxidative stressjust protecting them keeps them alive and functioning

twice as long, " he says.

" If we understand how [chondrocyte aging] happens and causes disease, we

are in a much better position to minimize risk, " he says. He is

especially interested posttraumatic OA and determining whether it is

possible to prevent or minimize oxidative damage after an injury to

prevent OA. Altering joint loading may help, he says.

Antioxidants are known to protect against free-radical damage or

oxidative stress, but Buckwalter says, " It would be way out there to say

that taking [the antioxidants] vitamin C and E will prevent OA, " adding,

" We are a ways [from saying that]. "

Maybe, he supposes, " we can take patients at high risk and go after them

in terns of antioxidants and altering mechanical loading. "

Mann

I'll tell you where to go!

Mayo Clinic in Rochester

http://www.mayoclinic.org/rochester

s Hopkins Medicine

http://www.hopkinsmedicine.org