Abstract

The aetiology of atrophic nonunions is not well understood: they are often thought to be nonreactive and metabolically inactive. Investigation of their biological processes is hampered by the lack of a useful animal model. Current models involve either wide segmental excision of the diaphysis or interposition of Silastic to impede the normal healing processes. neither of which resembles the clinical situation. We therefore aimed to establish a model of atrophic nonunion that more closely resembles the clinical situation and to use this model to evaluate the metabolic activity of the gap tissue of the nonunion. A simple and reliable model of atrophic nonunion has been developed in rabbits. It more closely represents the clinical situation by avoiding large segmental excisions and the interposition of foreign materials. Clinical, radiological, and histological data support the diagnosis of atrophic nonunion in the model. The concentration of adenosine triphosphate in the gap tissue of the nonunion served as a marker of metabolic activity. The gap tissue of established atrophic nonunions had a significantly higher concentration of adenosine triphosphate than did the control specimens. In this model, the gap tissue is metabolically active; therefore, under certain conditions, it may be possible to induce union if the correct stimulus is provided.

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