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 shoul d 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."