Maurizio Pacifici, PhD
Most Recent Peer-reviewed Publications
- HhAntag, a Hedgehog Signaling Antagonist, Suppresses Chondrogenesis and Modulates Canonical and Non-Canonical BMP Signaling
- Common mutations in ALK2/ACVR1, a multi-faceted receptor, have roles in distinct pediatric musculoskeletal and neural orphan disorders
- Osteophyte formation and matrix mineralization in a TMJ osteoarthritis mouse model are associated with ectopic hedgehog signaling
- Palovarotene Inhibits Heterotopic Ossification and Maintains Limb Mobility and Growth in Mice With the Human ACVR1R206H Fibrodysplasia Ossificans Progressiva (FOP) Mutation
- Delayed hypertrophic differentiation of epiphyseal chondrocytes contributes to failed secondary ossification in mucopolysaccharidosis VII dogs
Dr. Pacifici received a PhD in Developmental Biology from the University of Rome. He received a European Molecular Biology Fellowship at the end of which he was appointed Assistant Professor at the University of Rome School of Medicine. He then joined the faculty at the University of Pennsylvania first in the School of Medicine and subsequently in the School of Dental Medicine where he rose to the rank of Professor in 1997. He joined the faculty of Thomas Jefferson University in 2004 as Professor in the Department of Orthopaedic Surgery where he is currently Director of Research. Dr. Pacifici's biomedical research work has been funded continuously by the NIH for over 25 years. He has served and continues to serve on advisory boards, editorial boards and NIH study sections.
Expertise and Research Interests
Dr. Pacifici's biomedical research work focuses on mechanisms controlling skeletal development and growth in fetal and postnatal life. Emphasis is on identification of molecular regulators acting at the nuclear level that direct commitment, determination and differentiation of progenitor skeletal cells. Aim is to target those regulators in gene- and drug-based therapies to repair and reconstruct skeletal tissues affected by pathologies, including osteoarthritis and congenital skeletal defects. Emphasis is also on signaling diffusible factors that normally act within developing skeletal elements to coordinate growth and morphogenesis. When these factors escape skeletal tissues and diffuse into adjacent non-skeletal tissues due to failure of restraining topographical mechanisms, they can trigger pathologies, including heterotopic ossification and multiple exostosis syndrome. Experimental therapies are being tested to restore normal factor-restraining mechanisms and block or reverse those pathologies.