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Henry C Margolis PhD

Clinical Professor

Dr. Henry Margolis is a clinical professor in the Department of Periodontics and Preventive Dentistry at the University of Pittsburgh School of Dental Medicine, with a secondary appointment in the Department of Oral and Craniofacial Sciences. He also is a faculty member in the Center for Craniofacial Regeneration. Dr. Margolis joined the faculty in 2018.

Dr. Margolis received a BS degree in chemistry from Worcester Polytechnic Institute in 1972, and a PhD in chemistry from the University of Vermont in 1976. Following postdoctoral research at the University of Chicago Department of Chemistry and the Department of Renal Medicine at Michael Reese Hospital (Chicago, Ill.), Dr. Margolis joined The Forsyth Institute (Boston, Mass.) in 1980. Notably, at the Forsyth Institute, Dr. Margolis served as Senior Member of the Staff (1994 – 2017) and Head of the Department/Center of Biomineralization (1995 – 2017). Dr. Margolis also served as associate professor of developmental biology at the Harvard School of Dental Medicine (Boston, Mass.) until 2017.

Education & Training
University of Vermont, PhD, 1976
Research Interests

Dr. Margolis' current research is focused on the exploration of fundamental aspects of biomineralization, through collaborative and interdisciplinary studies on the mechanism of dental enamel formation. In vitro approaches are being used to elucidate the structure and mechanism of formation of higher-order assemblies of enamel matrix proteins and their influence on mineralization and crystal organization. In addition, in vitro approaches are used to provide new understanding of how protein self-assembly, protein phosphorylation, and proteolytic processing of matrix proteins influence dental enamel formation. Protein molecular assembly has been assessed using dynamic light scattering, small-angle x-ray scattering, TEM, and other quantitative and semi-quantitative techniques. Notably, we have extended our NIH-supported work to investigate critical aspects of our developed hypotheses in vivo using mouse models, including a novel knock-in mouse that is phosphorylation defective. Such studies have now shown that amelogenin phosphorylation in essential for proper enamel formation and ameloblast integrity, in part, by enhancing the capacity of amelogenin to stabilize an amorphous calcium phosphate precursor phase. Long term, such information should also provide new insights for the development of bio-inspired materials and novel approaches for hard tissue repair.


Jill Smith