Scleroderma (systemic sclerosis), a complex illness, include severe fibrosis, vascular changes, and autoantibodies against several cellular antigens. Incidence rates range from 2.7 cases per million annually during 1947-1968 to 18.7 cases per million annually during 1972-1982. Prevalence estimates in the United States have also fluctuated, ranging from 138 cases per million during 1950-1979 to 286 cases per million in 1985. Though the exact cause of systemic sclerosis is not known, it is widely believed that both hereditary and environmental factors like parvovirus B19, Epstein-Barr, HLA DRB1*1104 and DQB1*0301 virus play a role in its development. The generally accepted classification of scleroderma is divided into two main subgroups: diffuse cutaneous scleroderma and restricted cutaneous scleroderma. Systemic sclerosis was often thought to be a dull fibrotic process, but there is now strong evidence that the pathophysiology of the disease involves an active inflammatory process. The majority of part of systemic sclerosis is determined clinically. When making a differential diagnosis, it is important to take into account a number of different illnesses that can resemble systemic sclerosis. The disease's normal progression cannot be changed by a conclusive treatment or generally accepted disease-modifying substance. Nonetheless, controlling the impacted system or systems has worked well. For better results, early diagnosis is essential. The effectiveness of treatment depends on clinical assessment, organ identification, and disease progression. In order to maximize the quality of life for impacted patients and stop more organ damage.