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the hardening of an organ or tissue in humans and animals caused by connective-tissue overgrowth. Functionally valuable elements of the parenchyma of a sclerosed organ are destroyed and replaced by mature and sometimes coarse-fibered connective tissue, which often contains deposits of amyloid, hyalin, and lime. New connective tissue is usually formed by the reproduction of fibroblasts (connective-tissue cells) and by the intensified formation of collagen molecules by the fibroblasts.
In cases of sclerosis, parenchymal elements may be destroyed by inflammatory processes that are usually chronic in nature, including tuberculosis, rheumatic fever, and syphilis, and by circulatory disturbances, including passive congestion. Parenchymal elements may also be destroyed by involutional changes, for example, the postpartum sclerosis of the corpus lutea, and by changes associated with age and by metabolic disturbances. Sclerosis may be focal or diffuse. The proliferated connective tissue may become corrugated, resulting in the deformation of the organ, or cirrhosis. During cirrhosis, the hardening and reduction of an organ are accompanied by surface changes, including alternating outpouchings and invaginations, such as in a granular kidney or nodular liver.