New Insights Into The Impact Of Injury On Cartilage Cells

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Source: Wiley & Sons, Inc.

Posted: April 28, 2006

New Insights Into The Impact Of Injury On Cartilage Cells

Documented in extensive studies, backed by the anecdotal evidence of

professional athletes, impact injury to joints causes degeneration of

cartilage. In most cases, the eventual result is the pain, stiffness,

and compromised mobility of osteoarthritis (OA). Yet, questions

remain surrounding the role of the inflammatory system in the

cartilage destruction following mechanical trauma.

Tissue damage typically stimulates an influx of leukocytes, white

blood cells known for promoting tissue regeneration and healing--to

tissue protecting organs. However leukocytes can be a double edged

sword. In the May 2006 issue of Arthritis & Rheumatism (http://

www.interscience.wiley.com/journal/arthritis), researchers at Baylor

College of Medicine and the E DeBakey Veterans Affairs

Medical Center in Houston, Texas, present the results of a study to

test the hypothesis that leukocytes extend the zone of damage and

cell death in cartilage after an acute injury.

The research team began with a collection of dog bones--the hind knee

joints of 24 fresh young adult cadaver canines. Within one hour after

death, each bone was subjected to impact injury with a metal weight,

determined sufficient to cause cartilage damage without shattering

the bone. A comparable collection of cadaver canine bones was

preserved to serve as controls. All of the knee joints were cultured

with blood leukocytes from the same dogCartilage biopsies were taken

at various intervals between 12 hours and 7 days.

Among the assaulted bones, approximately half of the chondrocytes, or

cartilage cells, died within 7 days. In the uninjured bones, over 90

percent of the chondrocytes survived. A surprising finding was the

reduced viability of cartilage cells located well outside the

vicinity of direct impact. In cartilage samples taken 6 to 9 mm from

the impact site, and even in samples taken 10 mm or more from the

impact site, these critical cells to tissue renewal had largely been

killed off by leukocytes. The real culprit, however, was the

leukocytes' generation of noxious nitric oxide (NO).

Is there a way to stop the leukocyte-mediated murders of

chondrocytes? To explore this critical question, the researchers

conducted more experiments on the dog bone cultures. They found that

the killing of cartilage cells could be averted by desferoxamine,

chemical thay=t blocks production of NO, and by anti-CD18 antibodies,

which block the Velcro-like adhesion molecules that white cells use

to adhere to other cells.

" Our findings have interesting clinical implications, " observes the

study's leading author, Dr. D. M. Green. " First, we have demonstrated

that acute mechanical injury of the articular surface causes death of

chondrocytes located at a distance from the site of trauma. Second,

up-regulation of adhesion molecules on the affected chondrocytes

allows leukocytes to adhere and to extend the zone of injury beyond

the impact site. Thus, the data in this study suggest that therapies

to reduce acute influx of leukocytes into damaged cartilage should be

considered in the future when treating osteochondral injuries. "

http://www.sciencedaily.com/releases/2006/04/060428095206.htm