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INFLAMMATION
(continued)
The neutrophil is ubiquitous across a broad spectrum of reaction patterns including a large number of diseases. It is the basic reacting cell in the “vasculitis” of many examples of immune complex disease; as such
the pattern is characterized as leukocytoclastic vasculitis (S1C16P6-1). In practice, the process of “leukocytoclastic
vasculitis” is a limited neutrophilic collagenosis; the respective vessels often will show relatively little histologic evidence of damage.
The neutrophil is a reacting cell in the epidermal infiltrates of psoriasis. Neutrophils in common lesions of psoriasis are found clustered in the keratin layer and show degenerative changes (Munro microabscess).
In more active lesions (so-called pustular variants), the neutrophils may be found in the superficial unit of the viable epidermis (S1C16P6-2). In the latter location, the cells produce lysis of the cytoplasm of keratinocytes but portions of the keratinized
cell walls persist in lattice-like patterns. The remnants of cell wall outline small defects among the remaining viable keratinocytes; neutrophils collect in these defects; the patterns are spoken of as spongioform
pustules. Spongioform pustules are distinguished from Munro microabscesses not only by the distribution of the neutrophils; the influence of environment impacts on the histologic features. In the keratin layer,
sequestered keratinocytes die; they become dessicated. The degenerating inflammatory cells in zones of parakeratosis in lesions of psoriasis are markers for a phase that, in pustular psoriasis, is a dominant feature
but, in common psoriasis, must be a brief, transient feature.
In S1C16-P6-3, the character of the neutrophilic response at the interface between viable and necrotic tissue in a neurotic
excoriation is represented. Epithelium has regenerated along the interface to produce a sequestrum of the necrotic material. In a later stage, such a lesion will be characterized by a rather inconspicuous zone of
dermal fibrosis, and by an area of epidermal hyperplasia in which the epithelium sits upon the cellular fibrous tissue and the reticular dermis without an intervening papillary dermis.
The color of inflammation histologically is influenced by the amount of destruction of tissue, and by the contribution of cellular debris and blood products to the reactions. In many of the preceding illustrations,
zones of necrosis are distinctly basophilic; the basophilia reflects the release of nucleic acid into the tissue following the breakdown of inflammatory cells, particularly neutrophils. In some reactions, leakage of
blood products into the tissue is followed by precipitation of some of the products, particularly fibrin. Fibrin in tissue imparts a distinctive acidophilia to the affected tissue; the acidophilic deposits are
spoken of as fibrinoid necrosis. Often, the deposits have a fibrillar quality; they form a mesh. In other examples, the fibrin is less distinctly defined, and may be admixed with necrotic tissue such as smooth
muscle; in such instances, the deposits are rather homogeneous (S1C16P6-4).
The basophilia of an area of necrosis in a leukocytoclastic process is evident in S1C16P6-5. This type of necrosis has a
pyodermatous quality; it is collagenolytic.
The histiocyte (macrophage) is a representative of the second line of defense in regard to phagocytic functions, and liberation of catalytic enzymes. Although generally characterized as a wandering, phagocytic cell
(as manifested in S1C11P1-1-3), there are good reasons to also characterize the histiocyte as a secretory cell.
Histiocytes may freely migrate in the site of an inflammatory process (a rounded, wandering cell), it also has the capacity to associate in clusters and, in the process, becomes a “fixed” cell; clusters of
histiocytes constitute a granuloma; a granuloma is an enzyme-rich environment. The ability of clustered histiocytes to release enzymes into the interstitium of connective tissue is clearly evident in the structural
arrangement of a palisaded granuloma. A palisaded granuloma is a collagenolytic zone in which the secretions of histiocytes are confined to a localized area (S1C16P6-6 & 7); the secretions not only digest collagen, but also unmask a mucinous matrix; blood products leak into the
mucinous matrix, and some of the products may polymerize as delicate fibrils (fibrinoid degeneration). In some inflammatory processes, histiocytes and eosinophils interact (S1C16P6-8). In active migrations in search of a target, histiocytes are elongated cells with an elongated, wavy nucleus, and
with scanty cytoplasm (migratory histiocytes) (S1C17P7-1 & 2). The migratory histiocyte should be compared with the
activated, migratory form as seen in (S1C11P1-1-3).
Fibrin in tissue is a variable feature. It contributes the acidophilia of fibrinoid degeneration. If found in the vicinity of vessels, it is a morphologic feature identifying the vascular changes as those of a
vasculitis (S1C18P8-1-3)
Plasma cells are the source of antibodies; in contrast to the cellular intimacy required for a cell-mediated immune response, a plasma cell is an indirect effector cell whose product may be involved in an immune
response well away from the domain of its source. Plasma cells are often the trigger for a resident, who having found them in an infiltrate, will propose that the related process is lues. Plasma cells are common in
the infiltrates of follicular diseases. They may be found in the infiltrates of chronic inflammatory processes, and often tend to be at the periphery of lymphoid infiltrates. In lesions of lues, they are often a
prominent feature, and are associated with a high component of migratory histiocytes (S1C17P7-1 & 2, and S1C18P8-1-3). Plasma cells are uncommon in the infiltrates of discoid lupus erythematosus, but are a feature of lesions of
lupus profundus. They are also a variable feature of lesions of morphea, and lichen sclerosis et atrophicus. They are not a feature of lesions of granuloma annulare, but are found in lesions of necrobiosis lipoidica
diabeticorum.
Mast cells have a role in inflammation. They are a source of enzymes, and inflammatory mediators. Mast cells in tissue may be rounded in outline, or may be dendritic; the former might be characterized as migratory
forms, and the latter as fixed forms. The rounded forms are common in perivascular spaces, and in the reticular dermis among collagen bundles. They are increased in number in the mucinoses. The dendritic forms are
found in perifollicular sheaths; they are common in some forms of adult mastocytosis. The variable morphology of mast cells as seen in hyperplasias and mastocytomas is illustrated in S1C19P9 and S1C20P10. In S1C20P10-3, mast cells have monocytoid qualities; the nuclear grooves provide a monocytoid or histiocytic quality.
Longley J, Duffy TP, Kohn S: The mast cell and mast cell disease. J Am Acad Dermatol 1995;32: 545-61.
Eosinophils are among the most easily recognized of all the inflammatory cells. Residents, studying dermatopathology, as a regular effort, make a search for eosinophils. It is as if the discovery of an eosinophils
will greatly impact on the interpretation of a problem histologic pattern. Such a discovery is usually followed by a diagnosis of either drug eruption, or insect bite reaction. Eosinophils are found in remarkably
varied clinical settings. Eosinophils are sensitive to the cytokines of mast cells. On the other hand, histiocytes often follow eosinophils into areas of inflammation. Parasitic infestations often evoke a tissue
eosinophilia. Infiltrates, that are rich in eosinophils, are likely to be associated with signs of edema (S1C30P20-1).
Clusters of eosinophils may undergo necrosis. In dense fibrous tissue, the breakdown products may accumulate upon collagen bundles; the result is a zone of brightly eosinophilic necrosis with an admixture of
eosinophils, usually at the periphery of the zone of necrosis. Such a lesion may also attract histiocytes; the histiocytes collect in radial patterns at the periphery of the zone of necrosis (flame figure - minature
allergic granuloma) (S1C30P20-4-5). Eosinophilia, with visceral infiltrates, may be seen as a manifestation of a familial
disorder (S1C31P21-1-2).
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