Scientists observed for years that lead poisoning delays fracture healing, and now a team at the University of Rochester has discovered how that occurs and a possible remedy to the problem.
In a study in the Journal of Orthopaedic Research, scientists describe how the heavy metal interferes with healing through a cellular signaling pathway known as b-catenin. In lead-exposed mice, researchers noticed smaller fracture calluses and decreased levels of b-catenin during the healing process. Smaller mineralized calluses result in reduced strength and instability, and fewer active bone-forming cells. Normal bone formation requires mature calluses, which is a mix of cartilage and tissue that, over time, changes to normal bone.
Researchers hypothesized that by stimulating b-catenin activity with therapeutic agents, they could boost fracture healing by rescuing the decreases in callus volume. Evidence showed that activation of the b-catenin pathway does, in fact, promote better healing. In addition, researchers characterized the overall effect of lead exposure on bone repair – a process poorly understood until now.
Lead poisoning is still a problem in the U.S. despite greater awareness and measures to curb exposure. The Centers for Disease Control and Prevention estimates that a half-million children suffer from high blood-lead levels, and adults with occupations requiring exposure to lead also sustain hazardous exposure. The study was funded by the National Institutes of Health and conducted in the labs of Regis O’Keefe, M.D., Ph.D.; Michael J. Zuscik, Ph.D.; and J. Edward Puzas, Ph.D.
To read the full study, click here.