Mack Y Qin1, Rex E Atwood1, William A Ketchum2, Stephen A Kaba3, Matthew J Bradley1. 1. Naval Medical Research Center, Regenerative Medicine, Silver Spring, MD, USA; Uniformed Services University of the Health Sciences, Department of Surgery, Bethesda, MD, USA. 2. Uniformed Services University of the Health Sciences, Department of Surgery, Bethesda, MD, USA. 3. Naval Medical Research Center, Regenerative Medicine, Silver Spring, MD, USA; The Henry M. Jackson Foundation for the Advancement of Military Medicine, Inc., Bethesda, MD, USA. Electronic address: stephen.a.kaba.ctr@mail.mil.
Abstract
INTRODUCTION: Endocrine dysregulation's role in heterotopic ossification (HO) remains unexplored. We sought to examine corticosterone and testosterone in established rat models of ectopic bone formation, and correlate to HO formation with CT analysis. METHODS: Fifteen rats were placed into three groups of traumatic injury patterns: Blast and injury (120 kPa blast, femoral fracture and quadriceps crush), injury only, and blast only. Serum corticosterone and testosterone levels were drawn until post-operative day 40. HO was analyzed using CT. RESULTS: Corticosterone levels peaked in the blast and injury group in the shortest time post injury, followed by injury only and blast only groups. Testosterone levels reached nadir in similar fashion. Volume of HO was highest in the blast and injury group, followed by the injury only group. CONCLUSION: Corticosterone and testosterone's contribution to HO formation requires further characterization, but this study suggests that high peaks in corticosterone and a low nadir in testosterone are associated with higher volumes of HO.
INTRODUCTION: Endocrine dysregulation's role in heterotopic ossification (HO) remains unexplored. We sought to examine corticosterone and testosterone in established rat models of ectopic bone formation, and correlate to HO formation with CT analysis. METHODS: Fifteen rats were placed into three groups of traumatic injury patterns: Blast and injury (120 kPa blast, femoral fracture and quadriceps crush), injury only, and blast only. Serum corticosterone and testosterone levels were drawn until post-operative day 40. HO was analyzed using CT. RESULTS:Corticosterone levels peaked in the blast and injury group in the shortest time post injury, followed by injury only and blast only groups. Testosterone levels reached nadir in similar fashion. Volume of HO was highest in the blast and injury group, followed by the injury only group. CONCLUSION:Corticosterone and testosterone's contribution to HO formation requires further characterization, but this study suggests that high peaks in corticosterone and a low nadir in testosterone are associated with higher volumes of HO.