A toxic pollutant spread by oil spills, forest fires and car exhaust is also present in cigarette smoke, and may represent a second way in which smoking delays bone healing, according to research presented today at the annual meeting of the Orthopaedic Research Society in San Francisco.
In 2005, researchers from the University of Rochester Medical Center identified one ingredient in smoke, nicotine, that delays bone growth by influencing gene expression in the two-step bone healing process: stem cells become cartilage; cartilage matures into bone. In the current study, some of the same researchers found that a second smoke ingredient, the polyaromatic hydrocarbon benzo(a)pyrene (BaP), also slows bone healing, but in a different way.
Smoking has been shown to delay skeletal healing by as much as 60 percent following fractures. Slower healing means a greater chance of re-injury and can lead to chronic pain and disability. The obvious solution is for smokers to quit when they get hurt, but studies show that just 15 percent can.
Our results provide the first evidence that BaP prevents stem cells from becoming cartilage cells as part of healing, said Regis J. O'Keefe, M.D., Ph.D., chair of the Department of Orthopaedics and Rehabilitation at the Medical Center and a study investigator. These findings extend our understanding of the impact of cigarette smoke on a process that is critical to fracture repair. Perhaps down the road we will be able to speed bone healing among smokers in more than one way.
Gene expression is the process by which instructions encoded in genes are followed for the building of proteins, the workhorses that make up the bodys organs and carry its signals. In the current study, polymerase chain reaction (PCR), a technique that measures gene expression levels, revealed the genetic changes caused by exposure to BaP in mouse stem cells.
Among the many factors that influ
|Contact: Greg Williams|
University of Rochester Medical Center