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Abstract
The term scleroderma traditionally has been utilized to describe the cutaneous changes of a heterogeneous group of disorders involving hardening, tightening, and decreased elasticity of the skin and characterized by deposition of large amounts of collagen. It can be divided into two major groups: localized scleroderma
(LSc)/morphea and systemic sclerosis (SSc).
LSc is a circumscribed sclerosis of the skin and subcutaneous tissue without systemic involvement. It is classified into six types : Plaque, guttate, linear, frontoparietal (segmental), subcutaneous and generalized. SSc is a generalized disorder of the small arteries, microvessels and the diffuse connective tissue. It is characterized by I fibrosis and vascular obliteration in the skin, gastrointestinal tract,lungs and kidneys. Depending on the degree of skin involvement, SSc is frequently categorized as being of the limited cutaneous(ISSc) or the diffuse cutaneous (dSSc) form.
The Pathogenesis of scleroderma may involve interplay between endothelial cell dysfunction and injury, inflammation and autoimmunity, and fibroblast activation. The pathogenesis ofmorphea resembles that of SSc and includes the following:
(A) Endothelial cell dysfunction and injury in !jscleroderma It is the earliest pathological lesions in sclerotic skin. It appears as changes in endothelial cell function and ultrastructure of the
licrovasculature, causing attraction.