title: The vascularity of atrophic non-unions.
abstract: The objective of this study was to assess the vascularity of atrophic non-unions using an experimental animal model. Twenty skeletally mature female rabbits were randomly divided into control and experimental groups that were killed 1, 8, or 16 weeks after surgery. The experimental groups underwent surgery to induce an atrophic non-union whereas the control groups underwent a similar operation but which resulted in union. Using immunocytochemical techniques blood vessels were identified in histological sections obtained from the osteotomy site. The concentration of the vessels within the osteotomy gaps was measured, as was the serum concentration of an important angiogenic factor: endothelial cell-stimulating angiogenesis factor (ESAF). The results demonstrated a significant difference between the control and the experimental groups in the concentration of vessels within the gap at 1 week but there was no significant difference between those groups at 8 weeks. There were no significant differences in the ESAF concentration between the groups at any time points. We concluded that established atrophic non-unions can be well vascularised and that measurements of serum levels of ESAF could not distinguish between those osteotomies that would unite and those that would progress to non-union.
authors.affiliation: Nuffield Department of Orthopaedic Surgery, Nuffield Orthopaedic Centre, Oxford OX3 7LD, UK. harry.brownlow@ndos.ox.ac.uk
authors.forename: Harry C
authors.initials: HC
authors.lastname: Brownlow
authors.forename: Anita
authors.initials: A
authors.lastname: Reed
authors.forename: A Hamish R W
authors.initials: AH
authors.lastname: Simpson
mesh_terms: D043925:Angiogenesis Inducing Agents / Q000097:blood; D000818:Animals; D001284:Atrophy; D004195:Disease Models, Animal; D005260:Female; D017102:Fracture Healing / Q000502:physiology; D005599:Fractures, Ununited / Q000097:blood / Q000473:pathology* / Q000503:physiopathology; D007124:Immunoenzyme Techniques; D018919:Neovascularization, Physiologic; D011817:Rabbits; D013977:Tibia / Q000098:blood supply* / Q000473:pathology; D013978:Tibial Fractures / Q000097:blood / Q000473:pathology* / Q000503:physiopathology
chemical_list: D043925:Angiogenesis Inducing Agents