S1C16P6CellTypeMmisc



S1C16P6-1: This is a rather pure infiltrate of neutrophils in the adventitia of a small vessel and in the neighboring interstitium of the reticular dermis. Green arrows identify some of the better preserved neutrophils showing lobated nuclei. The non-descript cells near blue arrows are interpreted as migratory histiocytes. The zone outlined by red arrows has fibrinoid qualities (i.e., fibrinoid necrosis). At the interface between the adventitia of the vessel and the reticular dermis; the actual wall of the vessel is not affected by the fibrinoid change. The widened spaces among collagen bundles is evidence of dermal edema ( leukocytoclastic angiitis).

S1C16P6-2: An almost pure infiltrate of neutrophils is present in the upper portion of the epidermis, and in the keratin layer in this spongioform pustule (pustular psoriasis). Blue arrows identify some of the better preserved neutrophils. The neutrophils have clustered in small defects that are outlined by thin walls in a lattice-like pattern. The thin walls are keratinized, cytoplasmic remnants of walls of keratinocytes in the area of inflammation. The keratinocytes in the area of inflammation have mostly been digested by the enzymes of the neutrophils, but the peripheral rim of keratinized cytoplasm is more resistant; it persists in the pattern of a lattice.

S1P16P6-3: The preceding examples should not lead the reader to the conclusion that neutrophilic infiltrates are peculiar to immune mediated, or genetic disorders. A common lesion in which infiltrates are almost purely neutrophilic is the neurotic excoriation; the characteristic features of an established example are seen in this field. There is a superficial zone of necrosis. This zone of necrosis is not always the base of a true excoriation. Often, it is possible to identify not only an intact epidermis in ghost outlines in the zone of necrosis, but also it is usually possible to trace collagen bundles from the viable dermis into the zone of necrosis. If epithelium regenerates along the interface between the zone of necrosis and the viable dermis, the resultant pattern then will take on the characteristics of “perforating collagenosis.”

S1C16P6-4: This vessel shows fibrinoid necrosis of it wall. Neutrophils and histiocytes (and a few lymphocytes) are the reacting cells; the reacting cells are too poorly preserved to be clearly distinguished. There are scattered extravasated red blood cells. The diagnosis of leukocytoclastic angiitis is often made, even in lesions that show no convincing evidence of fibrinoid necrosis of the wall of the affected vessel.

S1C16P6-5: Neutrophils in the adventitia of a small vessel and in the interstitium of the adjacent reticular dermis have disintegrated in patterns of leukocytoclasia and necrosis. The small, deeply hematoxylinophilic particles are fragments of nuclei. The granular, lavender background represents both cellular debris and disintegrated collagen bundles. The basophilia is contributed in large part by the impregnation of necrotic tissue with the liberated nucleic acids of the fragmented neutrophils. This pattern has pyodermatous qualities. It is a prelude to suppurative necrosis of tissue; it is of a type seen in lesions of pyoderma gangrenosum. Clinically, the lesion in this case was representative of the connective changes of Sweet’s syndrome. The process is necrotizing, neutrophilic collagenosis.

S1C16P6-6: The central area to the left is relatively acellular. At the periphery of the hypocellular zone of connective tissue, cells form palisades; the cells are histiocytes. Zones of increased acidophilia are outlined by blue arrows. These areas of increased acidophilia represent zones of fibrinoid necrosis. This is a characteristic pattern of granuloma annulare (a palisaded granuloma). To then assume, that having stored these virtual images, the observer has gained significant insight into the pathogenesis of this disorder would be an error. This is merely a stage in an evolving life history; greater insights into pathogenesis are to be found in younger lesions than the one illustrated in this field.

S1C16P6-7: With an alcian blue stain, this palisaded granuloma of a lesion of granuloma annulare shows a central, mucinous zone in which surviving collagen bundles are widely spaced and few in number. Histiocytes and giant cells are arranged in palisades at the periphery of the “granuloma.” This pattern is representative of an earlier stage in the evolution of a lesion of granuloma annulare than is the pattern in P6-6. It is easier to appreciate the role of the “histiocytes” in the pathogenesis of the lesion in this field. The histiocytes facilitate the formation of a mucinous matrix; in the process, their lytic enzymes digest the connective tissue in the domain of the granuloma. Collagen bundles are more sensitive than elastic fibers to the catalytic enzymes. Peculiarly, the digestive enzymes are relatively confined by the zone of palisaded cells to the domain of the “granuloma;” the defect is an “enzyme-rich depot.”

S1C16P6-8: Eosinophils are distinguished by the size and intense acidophilia of cytoplasmic granules, and by nuclei which generally are bilobed; such cells have collected in a cluster at the dermal-epidermal infiltrate in this lesion of bullous pemphogoid. They have collected in a lytic defect at the dermal-epidermal interface. The papillary dermis is widened and edematous (pale). The small cells, with thin, elongated nuclei among the eosinophils and lymphocytes, are migratory histiocytes. Histiocytes usually are an important mediator of tissue damage in lesions of bullous pemphigoid. To the right near the bottom of the field, there is a zone in the basal unit of the epidermis showing increased cytoplasmic acidophilia. In this area, cells of the basal unit are degenerating (increased cytoplasmic acidophilia). Necrosis of basal keratinocytes is a common feature of vesiculo-bullous interface disorders.

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