A new hypothesis on the mechanism of atrophic non-union

Abstract

Non-union after bone fracture is rather common with an increasing frequency of incidence rate due to poorly treated early operations, among which the mechanism of atrophic non-union remains unclear. Previous opinions showed that impaired blood supply of affected limbs might mostly contribute to the atrophic non-union, which discriminated it with hypertrophic non-union. Nevertheless, there had been increasingly adequate evidences supporting that normal blood supplies existed in atrophic non-unions, as well as in hypertrophic non-unions or healthy bone fractures. Our hypothesis, based on the newly acquired evidences of atrophic non-union, was that there existed mesenchymal stem cells in the area of atrophic non-union. These mesenchymal stem cells, which remained temporally quiescent, could perform re-ossification under certain growth conditions, such as pressure during callus distraction with external fixator. According to the hypothesis, treatment for atrophic non-union should focus on the stimulation and reactivation of endogenetic mesenchymal stem cells or transplantation of autologous normal mesenchymal stem cells. This hypothesis may shed some light on the mechanism of atrophic non-union.