Smoking slows bone healing in mice

NEW YORK (Reuters Health) - Exposure to cigarette smoke delays the early phases of bone and ligament repair in mice, according to two reports in the Journal of Orthopaedic Research.

Previous studies have linked smoking with delayed healing of fractures in human and animal models, the authors explain, but how smoking causes these deleterious effects remains poorly understood.

In the first study, Dr. Linda J. Sandell and colleagues from Washington University School of Medicine at Barnes-Jewish Hospital, St. Louis, Missouri investigated the effects of cigarette smoke exposure on early events in fracture healing, especially cartilage formation.

Mice were randomly assigned to a control group or to a group in which they were exposed to smoke in a chamber for 6 days per week for a month, before experiment leg fracture under anesthesia.

Smoking significantly reduced cartilage formation, an important step in bone healing. By day 14 after fracture, the report indicates, the cartilage was still developing in the smoke-exposed animals, whereas it had already been replaced by bone in the normal controls.

"Our study demonstrated that cigarette smoke delays (cartilage formation), and thus, fracture healing in mice," the authors 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 (problems) associated with cigarette smoking during fracture healing."

In the second study, the same team of researchers investigated whether smoking cigarettes would interfere with the ability of mice to synthesize support tissue at the site of ligament injury. Ligaments are tough fibrous bands that hold bone to bone, whereas tendons are bands that hold muscle to bone.

Synthesis of the support tissue needed for ligament repair was significantly delayed in the animals exposed to smoke.

SOURCE: Journal of Orthopedic Research, December 2006.