How Smoking Affects Fractures And Ligament Injuries

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How Smoking Affects Fractures And Ligament Injuries

http://www.medicalnewstoday.com/medicalnews.php?newsid=56010

Cigarette smoking, which causes over 8.6 million illnesses annually

in the U.S., has been shown to have harmful effects on a variety of

orthopedic conditions. Studies have shown that the numerous toxins

contained in cigarette smoke can undermine fracture and ligament

repair following injury. In addition, smokers have higher rates of

hip fracture, fracture healing problems and bone infections and

smoking has been shown to impair soft tissue wound healing. Two new

studies, funded by the National Institutes of Health and the

National Football League Charities, examined the effects of smoking

on fractures and ligament healing in mice and found that healing of

both types of injury was delayed. The studies are published in the

December 2006 issue of the Journal of Orthopaedic Research

(http://www.interscience.wiley.com/journal/jor), the official

journal of the Orthopaedic Research Society.

Led by Hossam B. El-Zawawy of the Washington University School of

Medicine in St. Louis, MO the first study involved 35 mice divided

into a smoking group, which was exposed to cigarette smoke 6 days

per week for a month, and a control group. Surgery was performed on

all the mice to achieve a simple fracture. Researchers used type II

collagen expression as a marker of cartilage formation

(chondrogenesis) during healing. They found that smoking delayed

fracture healing and that it began at the early stages of the

healing process, although over time it did not inhibit normal

healing. Specifically, they were able to show that there was a delay

in the development of mature cartilage cells in the mice exposed to

cigarette smoke. This was the first study to analyze the molecular

and cellular mechanisms of fracture healing in mice exposed to

smoke.

The authors note that while the study shows a clear relationship

between smoking and cartilage formation, smoking probably has other

effects on fracture healing, which should be addressed in future

studies. They conclude: " Clinically, if specific events can be

identified, smoking cessation in humans, even temporarily, may

improve or speed the healing process after injury and decrease the

significant morbidity associated with cigarette smoking during

fracture healing. "

In the second study, involving the same group of researchers but led

by Corey S. Gill, researchers examined the effects of smoking on

medial collateral ligament (MCL) injury. They performed MCL surgery

on 40 mice, half of which were exposed to cigarette smoke 6 days a

week for two months. Researchers quantified cellular density at the

site of injury and used Type I collagen gene expression as a marker

for the formation of extracellular matrix, the material outside of

cells that provides tissue support. The results showed for the first

time that cellular density in mice increased between 3 and 7 days

after injury in normal wound healing, and that this was partially

inhibited in mice exposed to cigarette smoke. Based on their

findings, the authors suggest that this delay is due to a difference

in the recruitment of cells to the site of injury.

In addition, the study found that mice exposed to smoke had impaired

or delayed extracellular matrix development, shown by lower collagen

type I gene expression, one week after injury. This may lead to a

delay in restoring biomechanical stability of the healing MCL. The

authors conclude: " Ultimately, a better understanding of the

cellular and molecular mechanisms involved in the MCL healing

process will allow physicians to improve or speed the healing

process, as well as potentially overcome the deleterious effects of

smoking on ligament healing. "