Two groups of patients with a grave form of diabetes mellitus type I and II with diabetic foot syndrome have been examined. Group 1 (21 cases) consisted of patients whose foot was amputated. The cause of the necrotic process was ischemia produced by alteration of the arterial vessels aggravated by infection. Patients of group 2 (18 cases) were treated with resultant wound healing and foot preservation. The material was subdivided into two subgroups: 1) tissue from the "infectious" foot with great amount of bacteria and inflammation reaction; 2) tissue from the "ischemic" foot with considerable alterations of microvessels structure. In both groups well developed granulation tissue was observed after the treatment; almost all the cells of this tissue included 3H-uridin and labelling with 3H-thymidine was increased in fibroblasts, endotheliocytes and pericytes.

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