THE CONTEXT
Inflammatory lesions differ in their exudates, distribution of tissue necrosis, cellular composition, and subsequent repair.
Illustrated inflammatory patterns
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A serous skin blister shows separation of the epidermis from the dermis by a focal collection of serous effusion.
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Fibrinous pericarditis features fibrin deposits on the pericardium, appearing as a pink meshwork over the pericardial surface.
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Purulent inflammation may produce multiple bacterial lung abscesses in bronchopneumonia. An abscess contains neutrophils and cellular debris and is surrounded by congested blood vessels.
Abscess architecture and evolution
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The central region of an abscess contains necrotic leukocytes and tissue cells, usually surrounded by a rim of preserved neutrophils.
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Outside this rim, vascular congestion and parenchymal and fibroblastic proliferation may indicate chronic inflammation and repair.
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An abscess may eventually become walled off and replaced by connective tissue.
Ulcer formation and common sites
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An ulcer is a localized surface defect or excavation caused by shedding of inflamed necrotic tissue.
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Ulceration requires tissue necrosis and the resulting inflammation to lie on or near a surface.
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Common sites include the mucosa of the mouth, stomach, intestines, and genitourinary tract.
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Ulcers also occur in the skin and subcutaneous tissue of the lower extremities when circulatory disturbances predispose to extensive ischemic necrosis, as in peripheral vascular disease.
Acute and chronic changes in ulcers
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Acute and chronic inflammation may coexist in an ulcer.
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The acute stage shows intense polymorphonuclear infiltration and vascular dilation at the margins.
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With time, the margins and base become scarred, and lymphocytes, plasma cells, and macrophages accumulate.