Two cases of acquired reactive perforating collagenosis with poorly controlled diabetes mellitus were studied by histochemistry and by electron microscopy. In excoriated wound the necrotic mass on the bottom of the ulcer contained the collagen bundles which were continuous with the collagen bundles in the reticular layer. In the developing stage, the epidermis regenerated between the necrotic mass and the reticular dermis, and the collagen bundles in the reticular dermis were in continuity with those in the necrotic mass through the epithelial tunnels. The collagen in the epidermal channels did not degenerate ultrastructurally. In the mature lesion, collagen bundles being eliminated through the epidermis were surrounded by the fibroblasts at the basal cell layer. Collagen fibers were seen in the cytoplasm of these fibroblasts. From these findings, the mechanisms of the formation of the eruption in acquired reactive perforating collagenosis might be as follow: 1) In the developing stage, the regeneration of epidermis progresses between the necrotic mass and the reticular dermis, and among the collagen bundles. As a result, the collagen bundles remain in the channels of the epidermis. And then, 2) the regenerated epidermis makes the thick horny layer. As a result, the necrotic masses are lifted up and the collagen bundles are pulled up from the dermis through the epidermal channels.
We report an instructive case of a 65-year-old man who presented with a dumb-bell shaped tuberculous abscess across the greater sciatic notch bilaterally compressing both sciatic nerves. Clinical symptoms progressed slowly and mimicked lumbar radiculopathy, thus delaying an accurate diagnosis. Anterolateral retroperitoneal and posterolateral gluteal approaches of the greater sciatic notch as well as the acetabulum on both sides were followed in order to provide safe viewing and resection of the abscess. The abscess wall was adherent to the sciatic nerve and surrounding blood vessels. The symptoms completely disappeared after resection of the abscess.
We have developed a new skin transplantation method, called the skin fenestrating transplantation method, in which the nude mouse skin covering the lesion was removed one week after the transplant was embedded. One week later, transplanted psoriatic skin was biopsied and specimens were examined by electron microscopy. The basal cells and the nuclei of transplanted psoriatic epidermis were long and slender. Projections of basal cells extended to the dermis. Erythrocytes and lymphocytes were seen in the intercellular space. In the spinous cell layer, the cytoplasm and the nuclei were round. In the cytoplasm, mitochondria and endoplasmic reticuli were abundant, and tonofibrillar formation was poor. In the upper part of the epidermis, the cells were horizontally elliptic and, in the cytoplasm, short tonofibril bundles were formed. In the uppermost layers, in the cytoplasm of flat cells, degenerated flat nuclei, low dense lipid droplets and clumps of ribosomes were observed. These findings resembled the findings of intact psoriasis lesions more closely than those obtained by the skin embedding transplantation method.
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