Panel A: Within the frame it is shown a column of cells representative of the organization of a thick collagen cord. To the left side of the frame a well-packed collagen matrix is shown with relative acellularity. Arrows indicate the presence of some disperse vacuoles. Magnification x 40, H&E
Panel B: It shows a collagen matrix with a different aspect to that in panel A. It appears less dense and collagen bundles are not so wavy. Vacuoles are scarce. Note where the arrows, however, the abundant number of cells (possibly fibroblasts) which have lost hematoxylin basophilic affinity, suggesting an irreversible nuclear damage. Magnification x 40, H&E
Figure 1C: Histological aspect of granulation tissue of an ischemic diabetic foot ulcer.
Note the precocious onset of vascular anomalies including wall thickening (thick arrows) and endothelial cells nuclear hypertrophy (thin arrows) within an ischemic granulation tissue of about 10 days. An immuno-inflammatory infiltrate by round cells is typical of these types of wounds (frame). Magnification x 40, H&E staining
Figure 1D: Histological aspect of neuropathic diabetic foot ulcer.
The extracellular matrix here is ordinarily less dense than in ischemic diabetic foot ulcers. Thin collagen fibers appeared interconnected with fibrin material. The frame includes incipient capillaries with wall distortion, luminal occlusion and endothelial nuclear hypertrophy. As indicated by the arrow precocious wall thickening takes along the angiogenic process. As mentioned in the text, at this stage, relative fibroblast scarceness is detected. An apparently active secreting fibroblast is shown in the circle. Magnification x 40, H&E staining.
