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J. Edward Puzas

Edward Puzas
J. Edward
Donald & Mary Clark Professor of Orthopaedics
University of Rochester Medical Center
Professor, Biochemistry & Biophysics, Pathology & Laboratory Medicine, Oncology, Biomedical Engineering

Activation of undifferentiated mesenchymal stem cells and committed progenitors in the marrow space and periosteum of bone is one of the initial steps in skeletal repair. Recently, much research has been aimed at devising ways to modulate the stromal cells with the ultimate goal of controlling skeletal metabolism, including the processes of fracture repair. With relevance to identifying a new agent to accelerate the healing process, parathyroid hormone (PTH) and parathyroid hormone related peptide (PTHrP) have been documented to be potent in the expansion of progenitor populations and the regulation of differentiation of these cells. An emerging concept regarding the role of PTH/PTHrP in chondrogenesis and endochondral bone formation states that both of these hormones play an important role in regulating the pool of undifferentiated mesenchymal stem cells available for growth plate expansion and fracture callous formation.

Select Publications: 

Zuscik, M.J., Ma, L., Buckley, T., Puzas, J.E., Drissi, H., Schwarz, E.M., O'Keefe, R.J. (2007).  Lead induces chondrogenesis and alters transforming growth factor beta and bone morphogenetic protein signaling in mesenchymal cell populations.  Environ Health Perspect  115(9): 1276-1282.

Ryan, E.P., Holz, J.D., Mulcahey, M., Sheu, T.J., Gasiewicz, T.A., Puzas, J.E. (2007).  Environmental toxicants may modulate osteoblast differentiation by a mechanism involving the aryl hydrocarbon receptor.  Journal of Bone & Mineral Research. 22(10): 1571-80, 2007.

Puzas, J.E., Houck, J., Bukata, S.V. (2006).  Accelerated fracture healing.  J Am Acad Orthop Surg.  14(10 Suppl): S145-151.