PCI in the Treatment of Scleroderma

Scleroderma is a connective tissue disease of unknown etiology, characterized essentially by progressive fibrosis of the skin. An inflammatory response triggered by the destruction of the epidermis causes the production of parallel oriented thick bundles of collagen, unlike the interlacing network of collagen found in normal skin. Studies have shown that TGF-COPY3 plays a significant role: TGF-COPY16 and TGF-COPY2 promote the formation of scar tissue collagen, while TGF-COPY4 promotes wound regeneration and healing at the expense of collagen closer to physiological. When a parallel is made with the pathogenesis of scleroderma, it is observed that the GFR-β1 and the TGF-β2 are considered the main regulatory factors of both physiological fibrogenesis and pathological fibrosis with pleiotropic activities on several cell types. Thus, it was possible to suggest that the action of PCI on this sclerotic collagen, due to the modification of the inflammatory cascade triggered mostly by TGF-α1 and TGF-α3, would result in skin that looks closer to the physiological.