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Vascularity in a new model of atrophic nonunion

Botnar Research Centre, Nuffield Department of Orthopaedic Surgery, Nuffield Orthopaedic Centre, University of Oxford, Windmill Road, Headington, Oxford OX3 7LD, UK.

A. H. R. W. Simpson, FRCS, Professor of Orthopaedic Surgery

Musculoskeletal Research Unit, University of Edinburgh, Level 3 Pathology Area, Teviot Place, Edinburgh EH8 9AG, UK.

Correspondence should be sent to Dr A. A. C. Reed.

Our aim was to develop a clinically relevant model of atrophic nonunion in the rat to test the hypothesis that the vessel density of atrophic nonunion reaches that of normal healing bone, but at a later time-point. Atrophic nonunion is usually attributed to impaired blood supply and is poorly understood.

We determined the number of blood vessels at the site of an osteotomy using immunolocalisation techniques in both normally healing bones and in atrophic nonunion. At one week after operation there were significantly fewer blood vessels in the nonunion group than in the healing group. By eight weeks, the number in the atrophic nonunion group had reached the same level as that in the healing group.

Our findings suggest that the number of blood vessels in atrophic nonunion reaches the same level as that in healing bone, but at a later time-point. Diminished vascularity within the first three weeks, but not at a later time-point, may prevent fractures from uniting.