[The histological changes and pathogenesis of an infarct of a long bone in soft-tissue trauma to an extremity with damage to the feeding artery].

Acute disturbances in diaphysial intraosseous circulation secondary to the major nutrient artery intersection are not fully compensated from the potential intraosseous collaterals early in their course, which fact leads to bone infarction, as evidenced by histological and angiomorphological investigations in the experiment in rats. Recovery of ischemic tissues occurs in different time periods, necrotized myelokaryocytes undergo lysis, the bone marrow ischemic necrosis focus gets revascularized, with the reduced blood supply foci being intact, immature hemocytes scanty; necrotized osseous tissue undergoes revascularization and revitalization during the course of long-continued reorganization.