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Rheumatic Granuloma

Granuloma rheumaticum

For medical students2 min readUpdated 2026-10-10

Rheumatic granuloma (also known as the Aschoff-Talalaev body) is a specific focus of productive inflammation that forms in response to fibrinoid necrosis of microvessel walls and the surrounding perivascular connective tissue. The primary biological function of this lesion is the active phagocytosis of necrotic masses containing immune complex remnants.

SizeRanges from submiliary (15–20 µm) to large (60×300 µm or more)
Common localizationPosterior wall of the left ventricle of the heart
SpecificityAnichkov cells are pathognomonic for rheumatic carditis
ShapeRound, oval, or spindle-shaped with indistinct borders

History of Discovery and Macroscopic-Microscopic Characteristics

Specific myocardial nodules were first discovered by the German pathologist L. Aschoff in 1904 (hence the historical term "Aschoff bodies"). Later, the detailed histogenesis of these lesions was described by V.T. Talalaev, giving the granuloma its dual eponym.

On macroscopic and microscopic examination, granulomas are round, oval, or spindle-shaped. Their sizes vary widely: from very small, submiliary (about 15–20 µm) to quite large (60×300 µm and more). The borders of the nodules are indistinct, and their extensions blend smoothly into the surrounding tissue. With standard hematoxylin and eosin (H&E) staining, cellular clusters and stromal changes are clearly visualized.

Cellular Composition and Structure

The rheumatic granuloma is characterized by a palisading or fan-like arrangement of cells around central masses of fibrinoid. T lymphocytes, B lymphocytes, and plasma cells take an active part in the development of the inflammatory focus.

Two special types of cells give the nodule its specificity:

Stages of Formation and Evolution

The life cycle of the granuloma is closely linked to immune processes: immediate hypersensitivity reactions (Type I/III) are gradually replaced by delayed-type hypersensitivity (Type IV). In the initial (1st) stage, following the phase of serous-fibrinous inflammation, macrophages-histiocytes accumulate around the focus of fibrinoid necrosis and subsequently transform into large epithelioid cells.

Further evolution includes three stages:

  1. "Flowering" (mature) granuloma. In this phase, macrophages are rich in RNA, contain glycogen granules, and actively secrete various cytokines. Microscopic preparations show a prominent cellular response.
  2. "Waning" (resolving) granuloma. Characterized by the appearance of fibroblasts. The amount of fibrinoid detritus begins to decrease noticeably, accompanied by lymphoid infiltration and initial sclerosis of the myocardial stroma.
  3. "Scarring" (fibrotic) granuloma. Complete resorption of the fibrinoid and final sclerosis of the former granuloma site occur.

Topography (Body Localization)

Aschoff-Talalaev bodies most frequently affect the heart. In descending order of frequency, myocardial localization is distributed as follows:

  1. Posterior wall of the left ventricle (LV).
  2. Upper part of the interventricular septum.
  3. Posterior wall of the right ventricle (RV).
  4. Papillary muscles of the LV.
  5. Anterior wall of the RV.
  6. Anterior wall of the LV.
  7. Apex of the heart.

Extracardiac localization includes joint capsules, aponeuroses, peritonsillar connective tissue, and the stroma of other organs. However, extracardiac granulomas do not have the typical appearance of Aschoff-Talalaev bodies because Anichkov cells are completely absent in them.

Mnemonic

To remember the appearance of the Anichkov cell nucleus in cross-sections, picture an owl hunting a caterpillar. If you cut the nucleus transversely, an "owl's eye" looks back at you; if longitudinally, a "caterpillar" is crawling.

Frequently asked questions

What biochemical and structural components make up the masses of fibrinoid necrosis in the center of the nodule?

Fibrinoid necrosis masses consist of a complex substance—fibrinoid—formed as a result of severe connective tissue disorganization. Its components include:

  • Proteins and polysaccharides — breakdown products of collagen fibers and ground substance.
  • Plasma proteins — infiltrating tissue due to increased vascular permeability (primarily fibrinogen converting to fibrin).
  • Nucleoproteins — elements of destroyed connective tissue cells.
  • Fibrin — an obligatory structural component derived from blood plasma.
Who first described rheumatic granulomas and when?

Myocardial nodules were first discovered by L. Aschoff in 1904. Later, their histogenesis was detailed by V.T. Talalaev, which is why the dual eponym is established in medical literature.

What is the primary function of the rheumatic granuloma?

Its main task is the phagocytosis of necrotic masses and immune complex remnants resulting from fibrinoid necrosis of blood vessels and connective tissue.

How do extracardiac rheumatic granulomas differ from those in the myocardium?

Extracardiac granulomas (e.g., in joint capsules or aponeuroses) never contain Anichkov cells, meaning they lack the typical structure of Aschoff-Talalaev bodies.

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