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Morphea–a tick transmitted borreliosis of the skin? A contribution to the pathogenesis of circumscript scleroderma.


We report on a 34-year-old patient suffering from erythema chronicum migrans, who developed clinically and histologically typical morphea, which was confined to the area previously involved by the erythema migrans. The patient’s serum antibody level against borrelia burgdorferi spirochetes was significantly elevated. By means of the silver impregnation technique, we were able to identify spirochetal organisms both in the lower dermis and within the septa of the subcutaneous fatty tissue. In frozen sections, spirochetes were demonstrated by the immunoperoxidase method using specific anti-spirochetal antibodies. For a better assessment of the composition of the inflammatory infiltrate in morphea, we applied a panel of monoclonal antibodies to a sensitive two-stage immunoperoxidase technique. Helper-inducer T-cells and a large number of suppressor-cytotoxic T-cells were observed both in the perivascular infiltrate and between collagen fibers in close proximity to the HLA-DR reactive fibroblasts. A large number of mast cells were seen in the dermal infiltrate. The detection of spirochetal organisms in histological sections as well as the demonstration of closely associated helper-inducer T-cells, macrophages, and activated fibroblasts in the dermis strongly suggest that a cell-mediated immune response against borrelia may be the dominant pathogenetic event in this variant of scleroderma. Activated T-lymphocytes and various factors secreted either by activated lymphocytes or mast cells may cause proliferation of fibroblasts, which can lead to increased collagen synthesis and dermal fibrosis.

Z Hautkr. 1989 Aug 15;64(8):661-4, 667-9. Case Reports; English Abstract [1]