GRANULOMA (granuloma; lat. granulum a kernel + - oma) — the limited center of a productive, productive and exudative or alterativno-productive inflammation which is morphological manifestation of various pathological processes.
Distinguish two main types G.: infectious (virus, infectious and allergic) and noninfectious.
G.'s most develops during various infectious diseases, napr, at tuberculosis, syphilis, a leprosy, a sapa, a rhinoscleroma, a tularemia, a brucellosis, belly and a typhus, rage, malaria, fungal infections, rheumatism, a pseudorheumatism, etc.
Macroscopically G. have an appearance of dense small knots of a various form and the sizes: from hardly distinguishable an eye and to the touch to large, diameter in several centimeters of educations, napr, at an actinomycosis, the started syphilis etc.
At dominance of signs of a productive inflammation color of small knots gray, at development of a necrosis — yellow.
Some G. have special names: At tuberculosis is called a hillock (tuberculoma), at syphilis — a gumma.
G.'s localization can be the most various (skin, hypodermic cellulose, limf, nodes, mucous membranes, muscles, internals, the central and peripheral nervous system, etc.).
Features of a structure of G. are defined by the activator, reactivity of an organism and character of fabric, it develops in a cut.
The microscopic structure of G. at different infectious diseases has much in common. G.'s basis is made by the growths of mesenchymal cells which are transformed in macrophages histiocytes (see), epithelioid and colossal cells (see), fibroblasts. These cellular growths, or proliferata, are usually located in a circle of small vessels, sometimes in a wall of an artery (rheumatism). To mesenchymal cells uniform elements of blood are added: polinukleara, eosinophils, lymphocytes, plasmocytes, monocytes.
The cellular structure of G. can be rather typical for a certain disease that helps diagnosis. At the heart of G. at some diseases (e.g., at a sapa, tooth G., venereal G.) primary growths lie granulyatsionny fabric (cm), an infiltrirovanny polinuklearama, lymphocytes, plasmocytes and others in various ratios. The originality of a microscopic structure of G. can be caused also by their localization: e.g., proliferata from microglial cells in combination with changes of a microcirculator bed and the centers of a necrosis are characteristic of G. of a brain at malaria, viral encephalitis, a sapropyra. In the center of the majority of infectious granulomas it is possible to find the center of destruction. At one diseases (rheumatism, a pseudorheumatism, a sapropyra, malaria, mycoses) G.'s formation begins in a circle of primary center of a necrosis, at others — the necrosis arises for the second time, in the center of already created G. (tuberculosis, a tularemia, a brucellosis) more often. At the same time the activator in G. is defined not always. For its detection special colourings gistol, drugs and careful bacterial, a research of material are required. At viral diseases characteristic intracellular eosinophilic or fuchsinophil inclusions in histiocytes — so-called virus little bodies are observed.
Many infectious (infectious and allergic) G. develop not in a zone of inoculation of the activator, and in the place of fixing of a complex antigen — an antibody with the activated complement. Modern methods gistokhy, and immunochemical researches reflect immunol, reactions of an organism, morfol which manifestation is education of. G.'s cells possess the expressed pyroninophilia. Koons's method (see the Immunofluorescence) opens in their cytoplasm complexes antigen — an antibody, and in infiltrate of synovial membranes and in rhematoid G. — cell-bound immune complexes and a rhematoid factor (e.g., at a pseudorheumatism).
Of any etiology passes certain stages (stages) of development during which its structure and cellular players of inflammatory infiltrate is changed. In process of G.'s «aging» the increasing development is gained by the fibroblastichesky elements leading to scarring of. At some diseases (sap, a leprosy) G.'s suppuration with the subsequent scarring of abscesses is observed.
The complete cycle of development of G. comes to the end in terms from 3 — 4 weeks (sapropyra) up to 4 — 5 months (rheumatism). Duration of development of G. is defined by an etiology, disease severity, reactivity of an organism and efficiency to lay down. actions.
All infectious G. are morfol, manifestation immunol, reactions of an organism, and the nature of their evolution reflects its general immunol, a state.
Noninfectious G. arise at hron, the inflammation caused by penetration into fabrics of nerassasyvayemy or trudnorassasyvayemy materials (e.g., surgical suture materials, metal and glass splinters, etc.).
At an injection of oily substances in hypodermic cellulose there can be paraffinomas (see. Lipogranuloma ). Similar G. develop also owing to a focal necrosis of a fatty tissue of any etiology (traumatic, injection, toxic, etc.). All listed G. belong to so-called G. of foreign bodys of which the abundance of the multinucleate colossal cells of a rassasyvaniye containing foreign debris in cytoplasm is characteristic. G. arising in lungs at some prof. diseases (a silicosis, a berylliosis, an argyrosis, etc.) belong to the same category. However the cellular structure of these G. differs in an originality.
The cellular structure of G. and their feature at some diseases and patol, states are given in the table.
See also Granulomatoses .
Cellular structure of granulomas and their feature at various diseases and morbid conditions
Bibliography Rabukhin A. E., Dobrokhotov M. N. and Tonitrov N. S., Sarcoidosis, M., 1975; Serov V. V. and V. S Spiders. Ultrastructural pathology, M., 1975; Strukova. I. Pathological anatomy, page 147, etc., M., 1971; it, Controversial issues in the doctrine of an inflammation, Arkh. patol., t. 34, No. yu, page 73, 1972, bibliogr.; Khmelnytsky O. K. Histologic diagnosis of superficial and deep mycoses, L., 1973; James D. G. Granuloma formation, Trans, med. Soc. Lond., v. 88, p. 116, J 972; Pathology, ed. by W. A. D. Anderson, v. 1 — 2, St Louis, 1971.
H. K. Permyakov.