Philadelphia University + Thomas Jefferson University

Pacifici, Maurizio

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Maurizio Pacifici, PhD

Contact Dr. Pacifici

1015 Walnut Street
Curtis Building, Room 501
Philadelphia, PA 19107

(215) 955-7352
(215) 955-9159 fax


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.


English, Italian


Most Recent Peer-Reviewed Publications

  1. Acquired and congenital forms of heterotopic ossification: new pathogenic insights and therapeutic opportunities
  2. Retinoid roles and action in skeletal development and growth provide the rationale for an ongoing heterotopic ossification prevention trial
  3. Roles of Ihh signaling in chondroprogenitor function in postnatal condylar cartilage
  4. Intervertebral Disc Degeneration in a Percutaneous Mouse Tail Injury Model
  5. Advances in the pathogenesis and possible treatments for multiple hereditary exostoses from the 2016 international MHE conference
  6. The pathogenic roles of heparan sulfate deficiency in hereditary multiple exostoses
  7. Heparan sulfate antagonism alters bone morphogenetic protein signaling and receptor dynamics, suggesting a mechanism in hereditary multiple exostoses
  8. Hereditary Multiple Exostoses: New Insights into Pathogenesis, Clinical Complications, and Potential Treatments
  9. Cell origin, volume and arrangement are drivers of articular cartilage formation, morphogenesis and response to injury in mouse limbs
  10. Genetic and pharmacological inhibition of retinoic acid receptor γ function promotes endochondral bone formation
  11. Unsuspected osteochondroma-like outgrowths in the cranial base of Hereditary Multiple Exostoses patients and modeling and treatment with a BMP antagonist in mice
  12. Epiprofin Regulates Enamel Formation and Tooth Morphogenesis by Controlling Epithelial-Mesenchymal Interactions During Tooth Development
  13. Assessing the general population frequency of rare coding variants in the EXT1 and EXT2 genes previously implicated in hereditary multiple exostoses
  14. Effectiveness and mode of action of a combination therapy for heterotopic ossification with a retinoid agonist and an anti-inflammatory agent
  15. Palovarotene Inhibits Heterotopic Ossification and Maintains Limb Mobility and Growth in Mice With the Human ACVR1R206HFibrodysplasia Ossificans Progressiva (FOP) Mutation
  16. Targeted stimulation of retinoic acid receptor-γ mitigates the formation of heterotopic ossification in an established blast-related traumatic injury model
  17. HhAntag, a Hedgehog Signaling Antagonist, Suppresses Chondrogenesis and Modulates Canonical and Non-Canonical BMP Signaling
  18. Osteophyte formation and matrix mineralization in a TMJ osteoarthritis mouse model are associated with ectopic hedgehog signaling
  19. Excess BMP Signaling in Heterotopic Cartilage Forming in Prg4 -null TMJ Discs
  20. Common mutations in ALK2/ACVR1, a multi-faceted receptor, have roles in distinct pediatric musculoskeletal and neural orphan disorders