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Chronic inflammation is the sum of the responses mounted by tissues against a persistent injurious agent: bacterial, viral, chemical, immunologic, etc. The tissues affected by chronic inflammation commonly show evidence of the following pathologic processes:

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  1. Immune response: Manifestations of the immune response in injured tissue include the presence of lymphocytes, plasma cells, and macrophages (Figure 5-1). Plasma immunoglobulin levels may be elevated.

  2. Phagocytosis: Immune phagocytosis is mediated by macrophages that have been activated by T cell lymphokines, and it involves antigens that have opsonins (immunoglobulins and complement factors) attached to their surfaces. Nonimmune phagocytosis is directed against foreign nonantigenic particles.

  3. Necrosis: Commonly there is some degree of necrosis that may affect only scattered individual cells or may be extensive.

  4. Repair: Repair of tissues damaged by persistent injury is characterized by new blood vessel formation, fibroblastic proliferation, and collagen deposition (fibrosis).

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Figure 5–1.
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Chronic inflammation. Cellular components seen as part of the immune response. In most cases, the persistent injurious agent is antigenic and leads to an immune response involving T cells, B cells, and macrophages. Foreign body granuloma formation, on the other hand, appears to be a direct phagocytic response to inert (ie, nonantigenic) material, and the immune response is not involved. (FGF, fibroblast growth factor; see Table 6-2.)

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Chronic inflammation may follow an acute inflammatory response that fails to vanquish the agent, or it may occur without a clinically apparent acute phase. Chronic inflammation is recognized and defined by its morphologic features (Table 5-1). It is distinguished from acute inflammation by the absence of cardinal signs such as redness, swelling, pain, and increased temperature. Active hyperemia, fluid exudation, and neutrophil emigration are absent in chronic inflammation. It is distinguished pathologically from acute inflammation by being of a duration that is long enough to permit the tissue manifestations of the immune response and repair. Most agents associated with chronic inflammation cause insidious but progressive and often extensive tissue necrosis accompanied by ongoing repair by fibrosis. The amount of fibrosis in the tissues is a function of the duration of chronic inflammation.

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Table Graphic Jump Location
Table 5–1. Differences between Acute and Chronic Inflammation.

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