SCLEROSIS (Greek. sklerosis consolidation, hardening) — consolidation of bodies, walls of vessels and fabrics as a result of an atrophy or death of a parenchyma and replacement with its connecting fabric, with adjournment in it of a gnalin and sometimes salts of calcium. Distinguish diffusion and focal Page. At diffusion S. there is a consolidation of all body, the surface to-rogo becomes granular, sometimes hilly. Granularity or tuberosity of body is connected both with uneven development of sclerous changes, and with the phenomena of a compensatory hypertrophy and a hyperplasia of the remained parenchyma. Sometimes S. is followed only by reduction and consolidation of body, the surface to-rogo remains smooth. Focal S. develops most often as a result of the organization of heart attacks, the centers of an inflammation, etc.
Various physiological and pathological processes can be S.'s reasons. So, in fiziol. S.'s conditions develops at involute changes in bodies in senile age (a uterus, ovaries), in a puerperal period (in vessels of a uterus), on site yellow bodies of ovaries, etc. In patol. S.'s conditions develops in the result of inflammatory processes, most often with hron. a current, napr, at syphilis, rheumatism, tuberculosis, an actinomycosis, etc. At a row hron. diseases sclerous changes can develop in heart (see. Cardiosclerosis ), kidneys (see. Nephrosclerosis ), lungs (see. Pneumosclerosis ) both other bodies and fabrics. Besides, S. develops in fabrics at hron. circulatory disturbances (see. Induration ).
Distinguish two main mechanisms of development S. Pervy from them is presented by the following patol. links: damage — an inflammation — a reparative sclerosis. The proliferation of fibroblasts induced by an inflammation leads to increase in mass of collagen in connection with increase of number collagen - the producing cells. The similar mechanism C. is noted also in sites of the organization of heart attacks and the centers of a necrosis, at to-rykh the perifocal inflammation takes place. S.'s development at damage of fabrics for lack of an inflammation is connected with strengthening of collagen-producing function of fibroblasts. The similar (second) mechanism C. is observed at chronic venous stagnation, at Krom the inducing factor of a kollagenogenez is the hypoxia.
Depending on preservation of the general and local regulatory systems of a homeostasis and the autoregulyatorny mechanism of growth of connecting fabric C. it is subdivided on involyutsioniruyushchnn (reversible), stabilized and progressing (irreversible) from the outcome in cirrhosis (see).
Klien, symptomatology at S. is caused by disturbance of functions of body and depends on degree of manifestation patol. process. At an objective research consolidation and deformation of body is noted.
Treatment is based on use of physiotherapeutic methods, and also use fibrolitiches-ky, antiinflammatory and vasodilators. Operational treatment is in some cases shown.
Bibliography: Sarkisov D. S. Regeneration and its clinical value, M., 1970; Serov V. V. and Shekh-of t of e r A. B. Connecting fabric, page 272, M., 1981.
G. M. Mogilevsky.