PA3.1-4,PA4.1 | Inflammation & Healing — Glossary

A localised collection of pus (dead neutrophils + liquefied necrotic tissue) within a cavity lined by a pyogenic membrane and outer fibrous capsule; characteristic of suppurative inflammation.

Histological term describing a background of chronic mononuclear infiltrate with superimposed active neutrophilic infiltration; important pattern in gastric and bowel biopsies indicating ongoing injury.

Rapid-onset inflammation (seconds to days) characterised by vascular changes and neutrophilic exudation; the immediate response to injury.

A hepatic protein synthesis programme triggered by IL-6 during inflammation, producing CRP, fibrinogen, serum amyloid A, complement proteins, ferritin, and hepcidin while reducing albumin and transferrin.

A normocytic normochromic anaemia caused by prolonged inflammation — mediated by hepcidin (sequesters iron in macrophages), reduced erythropoietin responsiveness, and shortened red cell survival.

Complement fragments C3a and C5a that trigger mast cell degranulation (histamine release), vasodilation, and increased permeability; C5a is also a major neutrophil chemoattractant.

Formation of new capillaries from pre-existing vessels, primarily driven by VEGF; essential for delivering oxygen and nutrients to healing tissue.

A class of immunosuppressive drugs (infliximab, adalimumab, etanercept) that block TNF-α; used in RA, Crohn disease, and psoriasis; carry a black-box risk of reactivating latent tuberculosis by disrupting granuloma integrity.

A plasma kinin generated by kallikrein cleavage of kininogen; mediates pain (via B₂ nociceptor receptors), vasodilation, and increased vascular permeability in acute inflammation.

An acute-phase protein produced by the liver in response to IL-6; opsonises bacteria and activates complement; a sensitive clinical marker of tissue inflammation and infection.

A variant of coagulative necrosis seen in granulomas — the necrotic centre appears grossly as pale, crumbling, cheese-like material and histologically as amorphous eosinophilic debris without surviving cell outlines.

Form of coagulative necrosis with a cheese-like (caseous) gross appearance; microscopically amorphous, eosinophilic, and anucleate (no ghost outlines); hallmark of tuberculosis and some fungal infections.

Directed migration of leucocytes along a concentration gradient of chemoattractants (C5a, LTB₄, IL-8, bacterial peptides) toward the injury site.

A prolonged inflammatory response characterised by simultaneous active inflammation, tissue destruction, and repair attempts — dominated by macrophages, lymphocytes, and plasma cells rather than neutrophils.

Characteristic nuclear pattern of plasma cells in which chromatin is arranged in alternating dark and pale segments around the nuclear periphery, resembling a cartwheel or clock face.

Pathological complication of wound contraction in which scar tissue deforms a joint, digit, or eyelid, impairing function; classic consequence of burns across flexor surfaces.

Transmigration of leucocytes through the endothelial wall, primarily by squeezing through inter-endothelial junctions (paracellular route), guided by PECAM-1.

A granuloma in which the dominant cells are epithelioid histiocytes; synonym for the granulomatous pattern of chronic inflammation used in histopathology reports.

A macrophage that has undergone transformation in response to persistent stimulation — characterised by abundant pale eosinophilic cytoplasm and a vesicular nucleus, resembling epithelial cells under microscopy.

A non-specific marker of inflammation measured as the distance red blood cells fall in one hour; elevated by fibrinogen (an acute-phase reactant) which promotes rouleaux formation and faster settling.

Protein-rich inflammatory fluid (>3 g/dL protein, specific gravity >1.020) that leaks through vessel walls due to active increase in vascular permeability.

Eosinophilic protein polymer derived from circulating fibrinogen; deposited in exudates when vascular permeability is high; forms threads or meshwork on H&E.

Pattern of acute inflammation in which large amounts of fibrin form in the exudate, occurring in serosal surfaces; classically produces the 'bread-and-butter' appearance of fibrinous pericarditis.

Acute inflammation of the pericardium with fibrin deposition on both serosal surfaces, producing the characteristic 'bread-and-butter' gross appearance.

A multinucleate giant cell with nuclei randomly scattered throughout the cytoplasm, formed around non-digestible foreign material such as sutures, silica, or talc.

Proliferation of astrocytes to fill a defect in the CNS after neuronal loss; the CNS equivalent of scar tissue; does not restore neural function.

Early repair tissue consisting of new capillaries, proliferating fibroblasts, and loose ECM (type III collagen, fibronectin); pink-red, moist, bleeds easily; the precursor to scar.

A focal aggregate of activated macrophages (epithelioid histiocytes) with surrounding lymphocytes, formed when an indigestible agent cannot be eliminated; the tissue response that defines granulomatous inflammation.

A distinct form of chronic inflammation in which the predominant histological pattern is the presence of granulomas; implies inability of the immune system to eliminate the causative agent.

Pre-formed vasoactive amine stored in mast cell granules; the first mediator of acute inflammation; causes vasodilation and increased vascular permeability via endothelial contraction.

Raised, firm scar that remains within the original wound boundary; contains collagen bundles parallel to the surface; tends to regress over 12-18 months.

Intercellular Adhesion Molecule-1; an endothelial surface glycoprotein upregulated by TNF and IL-1 that serves as the ligand for leucocyte integrins during firm adhesion.

A cytokine secreted by Th1 CD4+ lymphocytes that is the principal signal for classical macrophage activation and is essential for granuloma formation and maintenance.

A protective vascular and cellular response of living tissue to injury or infection, aimed at eliminating the causative agent, clearing dead cells, and initiating repair.

Heterodimeric adhesion molecules on leucocytes (e.g., LFA-1, Mac-1) that bind ICAM-1 on endothelium to mediate firm, stable arrest during the leucocyte recruitment cascade.

Nuclear fragmentation as a form of cell death; seen in degenerate neutrophils at the centre of active inflammatory necrosis; indicates a very destructive process.

Excessive scar that extends beyond the original wound margin; composed of thick, disorganised type I/III collagen; does not regress and frequently recurs after excision; commoner in darker-skinned individuals.

Cells that continuously cycle and maintain a robust stem-cell pool (e.g., skin epidermis, gut mucosa); capable of full regeneration after injury.

A multinucleate giant cell formed by fusion of epithelioid histiocytes, with nuclei arranged in a peripheral horseshoe or ring pattern; classic for tuberculosis and fungal granulomas.

The appearance of immature neutrophil precursors (band forms) in peripheral blood during marked bacterial infection or intense inflammatory stimulation — reflects emergency release from bone marrow.

Arachidonic acid metabolites from the 5-LOX pathway; LTB₄ is a potent neutrophil chemoattractant; cysteinyl leukotrienes (LTC₄/D₄/E₄) mediate bronchoconstriction and vascular permeability (SRS-A).

Pattern of necrosis where enzymatic digestion converts dead tissue to a liquid mass; typical of abscesses and CNS infarcts; distinct from caseation.

Small mononuclear cell with a round, densely basophilic nucleus and scant cytoplasm; the most numerous cell in most chronic inflammatory infiltrates.

A macrophage activated by IFN-γ and microbial products to produce pro-inflammatory cytokines (TNF-α, IL-1, IL-12), reactive oxygen species, and nitric oxide; the dominant effector in granuloma maintenance.

A macrophage activated by IL-4 and IL-13 that promotes anti-inflammatory responses, tissue repair, and fibrosis; prominent in helminth infections and wound healing.

Tissue-resident mononuclear phagocyte derived from circulating monocyte; kidney-shaped nucleus, abundant pale cytoplasm; becomes an epithelioid histiocyte when activated in granulomatous inflammation.

Peripheral movement of leucocytes toward the vessel wall as blood flow slows during stasis in acute inflammation.

Zinc-dependent endopeptidases that degrade ECM components (including collagen) during remodelling; essential for replacing type III with type I collagen in mature scar.

Enzyme in neutrophil azurophil granules that catalyses conversion of H₂O₂ + Cl⁻ to hypochlorous acid — the most potent bactericidal product of the oxidative burst.

Fibroblasts that express α-smooth muscle actin under TGF-β stimulation; contractile cells responsible for wound contraction in secondary intention healing.

Short-lived phagocytic granulocyte with a multilobed nucleus; the first and dominant cell of acute inflammation; its presence defines acute inflammatory exudates.

A granuloma without central necrosis; the epithelioid histiocytes extend to the centre of the aggregate; characteristic of sarcoidosis, Crohn disease, and foreign-body reactions.

A molecule (IgG, C3b, collectins) that coats a pathogen and enhances its recognition and engulfment by phagocytes.

Growth factor released early from platelets and macrophages; recruits fibroblasts and smooth-muscle cells to the wound; initiates the repair signalling cascade.

Terminally differentiated cells that cannot divide post-natally (neurons, cardiomyocytes); defects are filled by scar or gliosis, not regeneration.

Diffuse spreading acute inflammation through tissue planes without localisation or abscess formation; typically caused by organisms producing spreading factors such as streptococcal hyaluronidase.

Terminally differentiated B lymphocyte that secretes antibodies; identified on H&E by an eccentric nucleus with clock-face (cartwheel) chromatin and a pale perinuclear hof.

Healing of a clean, surgically apposed wound with minimal tissue loss; results in a thin scar with limited granulation tissue and brief inflammation.

Lipid mediators derived from arachidonic acid via the COX pathway; PGE₂ mediates fever, pain sensitisation, and vasodilation; targeted by NSAIDs.

Creamy exudate composed of dead and living neutrophils, liquefied necrotic tissue debris, and tissue fluid; the definitive product of suppurative inflammation.

The inner lining of an abscess cavity consisting of viable and degenerate neutrophils, fibrin, and necrotic debris overlying a layer of granulation tissue.

Any substance that causes fever; exogenous pyrogens (bacterial LPS) stimulate macrophages to release endogenous pyrogens (IL-1, IL-6, TNF-α) that elevate the hypothalamic temperature set-point via prostaglandin E2.

Restoration of lost tissue by proliferation of surviving parenchymal cells of the same type, requiring an intact stromal framework; results in normal architecture.

Replacement of lost tissue by fibroblast-derived collagenous scar when regeneration is impossible or insufficient; sacrifices specialised function for structural integrity.

Outcome of acute inflammation resulting in complete restoration of normal tissue architecture; requires brief injury, minimal tissue death, and a tissue capable of regeneration.

Rapid increase in oxygen consumption by activated phagocytes driven by NADPH oxidase, generating superoxide and downstream reactive oxygen species for microbial killing.

Stacking of red blood cells like coins, promoted by elevated fibrinogen coating the cell surfaces; the direct mechanism responsible for elevated ESR in inflammatory states.

Redness, one of the five cardinal signs of inflammation; caused by vasodilation and increased blood flow to the area.

A systemic inflammatory disease of unknown aetiology characterised by non-caseating epithelioid granulomas ('naked granulomas') in multiple organs — most commonly lung and mediastinal lymph nodes — diagnosed by exclusion after negative microbiological stains.

Healing of a large open wound with significant tissue loss; requires abundant granulation tissue, wound contraction by myofibroblasts, and produces a wider, firmer scar.

Cell adhesion molecules (P-, E-, L-selectin) that mediate initial, reversible rolling of leucocytes along the activated endothelium.

Mild inflammatory exudate with a dilute, protein-poor fluid and few cells; occurs in early viral infections and as skin blisters; reversible without fibrosis.

Cells normally quiescent in G0 that re-enter the cell cycle when stimulated (e.g., hepatocytes, fibroblasts); can regenerate if scaffold is intact.

Master fibrogenic cytokine released by platelets and macrophages; activates fibroblasts, promotes collagen synthesis, and inhibits inflammation; drives pathological fibrosis when persistently elevated.

A cytokine produced by activated macrophages that is critical for granuloma structural integrity; pharmacological blockade (anti-TNF biologics) disrupts granulomas and can reactivate latent tuberculosis.

Low-protein fluid (<2 g/dL) accumulating due to haemodynamic imbalance (raised hydrostatic or reduced oncotic pressure); not due to inflammation.

Swelling, a cardinal sign of inflammation; results from exudate accumulation in the interstitium secondary to increased vascular permeability.

Thick, cross-linked collagen fibre predominating in mature scar; provides high tensile strength; replaces type III collagen during the remodelling phase.

Thin, reticular collagen deposited early in granulation tissue; provides provisional scaffold; replaced by type I collagen during maturation/remodelling.

Full-thickness mucosal or epithelial defect produced by necrosis and sloughing; histologically shows four layers: fibrinopurulent exudate, necrosis, granulation tissue, and fibrous base.

Key angiogenic cytokine released by macrophages and hypoxic cells; stimulates endothelial cell proliferation and migration into the wound.

Normal reduction of wound surface area during secondary intention healing, mediated by myofibroblast contraction; beneficial unless it deforms adjacent structures (contracture).

Rupture or separation of a previously closed wound, usually due to infection, haematoma, or impaired collagen synthesis (e.g., vitamin C deficiency, malnutrition).