The pathogenesis of systemic sclerosis (SSc) is extremely complex and heterogeneous. The characteristic pathological changes that occur in SSc are progressive cutaneous and visceral fibrosis, obliteration of small arteries and arterioles, and production of tissue-specific autoantibodies. 1 Extensive research on vasculature, immune response, cytokine profile and fibroblasts (FB) has enabled understanding of major components of pathogenesis of SSc. These include imbalance of immune response, vascular dysfunction, and activation of resident connective tissue cells. 2