Kevin G. Osteen, PhD

Kevin G. Osteen, PhD

Pierre Soupart Chair in Obstetrics & Gynecology

Professor of Obstetrics and Gynecology

Professor of Microbiology, Immunology and Pathology

B-1100 Medical Center North
1161 21ST Avenue South
Nashville 37221
(615) 322-4196


Kevin G. Osteen received his Ph.D. in endocrinology from the Medical College of Georgia in 1980 and subsequently completed his postdoctoral training in reproductive physiology at the University of Maryland School of Medicine in Baltimore. Dr. Osteen came to Vanderbilt University School of Medicine in 1983 as a member of the team that launched the first in vitro fertilization (IVF) program in Tennessee and the fourth program in the United States. He is currently the director of the Women’s Reproductive Health Research Center which includes the International Endometriosis Association Research Program at Vanderbilt. Dr. Osteen is a member of the graduate faculty and has mentored numerous graduate students, postdoctoral research fellows, clinical fellows and junior faculty. He is an active member of several professional societies in the field of reproductive medicine and maintains an active research program funded by the National Institutes of Health (NIH), Industry contracts and private foundations. He has frequently served on NIH study sections and as an adviser to biotechnology and pharmaceutical companies. He has authored more than 100 original scientific papers in the field of reproduction and is a frequent invited speaker at national and international scientific meetings. Dr. Osteen’s research program currently focuses on environmental endocrine disruptors in the pathophysiology of infertility and pregnancy failure. Working within a long established collaboration with Dr. Kaylon Bruner-Tran, their combined research interests include the role that early life exposure to environmental toxicants plays in adult onset diseases affecting reproductive success. Recent research studies have identified inflammation during the preconception period as being an important factor in not only disrupting both male and female fertility but also limiting the capacity of progesterone to support maternal-fetal communication that is necessary for term delivery.