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Acute Inflammation
The neutrophil is the primary reacting cell in a wide variety of inflammatory diseases of the skin; it is the primary reacting cell in many infectious processes, and in reactions to
trauma. It functions as both a phagocytic cell, and as a secretory cell; it is a rich source of catalytic enzymes. In many inflammatory diseases, it rapidly appears in sites of injury. The subsequent course of an
inflammatory process often will depend upon the ability of neutrophils to eliminate the offending materials, or organisms. In a common sequence, an unsuccessful response by neutrophils is followed by an influx of
macrophages.
In figures S1C11P1-3, the close relationship between neutrophils and histiocytes is
demonstrated. In addition, the histiocytes are activated and contain cytoplasmic vacuoles. Some of the histiocytes have phagocytyzed fragments of nuclear debris. In figure S1C11P1-4, an infiltrate which is rich in neutrophils shows evidence of early necrosis. This type of reaction is
associated with the release of catalytic enzymes into the tissue, and with destruction of the tissue. In this field, the fibrous component of the tissue is no longer evident.
Neutrophils have the capacity to migrate into preferential sites. In disorders such as bullous impetigo, pemphigus foliaceus, and subcorneal pustular dermatosis, neutrophils may
accumulate in a defect between the granular layer and the keratin layer of the epidermis (S1C12P2-1). In these disorders,
they may not be particularly prominent in the dermal infiltrates. This ability to preferentially seek out sites of injury is an expression of a chemically mediated, directed migration (chemotaxis).
Follicular diseases are commonly expressed in patterns of “acute folliculitis” (neutrophilic folliculitis). In addition, the process is likely to be associated with occlusion of the
involved follicle (follicular occlusive diseases). An infiltrate of neutrophils in the lumen of such a follicle is likely to lead to a perforation of the epithelial wall of the affected follicle. Perhaps for some
examples, external pressure produced by squeezing of an affected follicle produces a perforation, and forces a jet of follicular contents into the neighboring dermis. In the dermis, the exudate is likely to be
associated with a release of enzymes into the interstitium of the dermis; the dermis will be liquefied in the involved area. This type of lysis of fibrous, structural proteins of the dermis commonly initiates a
regenerative response in which epithelium from the region of the perforation follows along the tract produced by the extrusion of follicular contents; it forms a cylinder outlining the exudate, and the digested
tissue (S1C12P2-2-4). The outgrowth of epithelium in this manner is a form of pseudoepitheliomatous hyperplasia
(follicular pseudoepitheliomatous hyperplasia).
Neutrophils are often the preponderant cell in reactions at the dermal-epidermal interface. Lesions in which neutrophils are selectively aggregated at the basement membrane zone of
the epidermis are likely to be vesicular or bullous. Examples include bullous disease of childhood, linear IgA bullous dermatosis, dermatitis herpetiformis, and early lesions of cicatricial pemphigoid. In dermatitis
herpetiformis, the breakdown of neutrophils, and the release of catalytic enzymes into the tissue may result in digestion of the reticular framework of the papillary dermis, and in a loss of cellular details at the
extremities of the affected dermal papillae (S1C12P2-5-7). Neutrophils may be the chief reacting cell in the epidermis in
vesicular (IgA?) pemphigus.
Generally, the response of fibrous components of the dermis to the effects of the catalytic enzymes, as often seen in an acute inflammatory process such as the dermal extremity of a
perforating disorder, is variable depending on the nature of the fibrous component. Generally, elastic fibers are more resistant than are collagen bundles. As a consequence, a defect outlined by epithelium may
contain inflammatory debris, and elastic fibers, but be devoid of collagen bundles. In addition, it might appear that the number of elastic fibers in the defect is greater than that of the neighboring, uninvolved
dermis (S1C13P3-1 & 2). The collapse of the elastic framework, after the collagenous component has been digested
away, results in an apparent local increase in elastic fibers.
For some disorders such as superficial erosive dermatitis (neurotic excoriation), neutrophils, early on, are an important component of the reaction at the dermal-epidermal interface.
The process usually is associated with a zone of necrosis involving the epidermis, and a portion of the dermis; neutrophils collect at the interface between viable and necrotic tissue. Epithelium may regenerate
along the interface between viable and necrotic tissue to produce a sequestrum of the necrotic portion. In some examples, the regenerating epithelium extends into the dermis beyond the zone of necrosis; in its
downward growth, it entraps not only elastic fibers but also collagen bundles (S1C14P4-1-3). The collagen bundles are
so prominent in the epidermal interstitium among keratinocytes that their presence has been cited as the basis for the classification of the related disorder - “reactive perforating collagenosis.”
The process in the perforating disorders has been characterized as transepidermal elimination. The perforating disorders are not restricted to examples in which the material, found in
transit, is preexisting fibrous components of the dermis. In emphasizing a “perforation,” there is an implication that the role of the epithelium is passive. There is also an implication of passivity on the part of
epithelium in characterizing the related process as transepidermal elimination. In fact, the process is an epithelium-mediated sequestration of necrotic debris. The role of neutrophils in the sequestration of
collagen and elastic fibers at the advancing margin of classic, active keratoacanthomas is less apparent, but it has been suggested that the intraepidermal abscesses of a keratoacanthoma are a reaction to
intra-epithelially entrapped connective tissue fibers.
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