S8C16P3-Polyarteritis Nodosa

S8C16P3-1: Medium-sized vessels tend to be involved in polyarteritis nodosa. Vessels of the skin may be involved as a manifestation of classic generalized disease. In some examples, as in this case, the involvement is limited to the skin (limited or cutaneous polyarteritis nodosa). Blue arrows point to a muscular vessel containing a thrombus. At the bottom of the field, the muscular wall of the vessel is interrupted by an infiltrate of inflammatory cells.

S8C16P3-2: In this area, a muscular vessel is cut in longitudinal section; it shows fibrinoid necrosis of its wall (in areas, the wall is homogeneous, acellular, and bright red). Focally, continuity in the histologic pattern of the vessel is interrupted by dense infiltrates of inflammatory cells; this may be a result of tortuosity of the vessel rather than evidence of disruption of the wall of the vessel by infiltrates of inflammatory cells.

S8C16P3-3: At higher magnification, the zone of fibrinoid necrosis is acellular. Inflammatory cells form palisades along the wall of the vessel at the interface between the zone of necrosis  and the adventitia. To the right of the vessel, the zone of fibrinoid extends into the adventitia.

S8C16P3-4: In cross-section, the rounded outlines of the infiltrates provide a clue as to the nature of the stucture that has been involved by the infiltrates; the rounded outlines would be in keeping with a muscular vessel that has been cut in cross-section. The infiltrates are mixed; they are composed of lymphocytes, histiocytes, neutrophils, and eosinophils (polyarteritis nodosa).

S8C16P3-5: This lesion is a change of pace, but is representative of a process in which neutrophils and necrosis are a feature. This is a section of a “neurotic excoriation” as seen under polarized light. Collagen bundles are bright white (they are birefringent). There is an irregular defect just below the plane defined by the row of green arrows. This defect is the site of a separation between viable and necrotic tissue (the tissue above the row of green arrows is a sequestrum); it consists of  keratin, necrotic epidermis, necrotic papillary dermis, and a thin zone of necrotic reticular dermis (i.e., the bright bundles above the defect provide a marker for a contribution of the reticular dermis to the sequestrum). The present of these collagen bundles in the sequestrum is a clear measure of the level of the defect; birefringent bundles of this type are not a component of the papillary dermis. “Neurotic excoriation” is an inaccurate characterization of the process; although, the designation may have clinical relevance. The process is, in sequence, a response to external trauma, an activation of inflammatory mediators, an infiltration of the zone of damage (in response to trauma) with neutrophils, a release of enzymes, and a digestion of tissue to include the tissue damaged by trauma (this often includes a thin portion of the reticular dermis). Vascular changes, including thrombosis and necrosis, are common adjacent to the site of damage; they probably have a role in defining the area to be infiltrated by neutrophils.

S8C16P3-6: The margin of a denuded “neurotic excoriation” is represented; the sequestrum has been lost. The epidermis on the left, which extends to the margin of the denuded area, is partially necrotic (its keratinocytes are acidophilic; they show pyknosis of nuclei). Along the floor of the defect, there is a thin zone of necrotic reticular dermis (plane between viable and necrotic tissue defined by row of blue arrows). There are perivenular infiltrates of neutrophils; the neutrophils focally extend into the interstitium of the neighboring reticular dermis. There are fragments of nuclear debris.

S8C16P3-7: This is a “neurotic excoriation” late in its evolution. The hyperplastic epidemis is covered by an inflammatory crust containing degenerating neutrophils. The interface between the epidermis and the dermis is irregular; focally, collagen bundles extend into the hyperplastic epidermis (a type of perforating collagenosis as commonly encountered in the setting of pseudoepitheliomatous hyperplasia). A thin zone of newly formed, vascularized fibrous tissue separates the epidemis from the reticular dermis. The fibrous tissue is granulation tissue which formed along the surface of the defect produced by loss of the sequestrum. There are perivenular infiltrates of chronic inflammatory cells. A similar pattern is encountered late in the evolution of the response to shave biopsies.

S8C16P3-8: A vasculitis is present in the dermis just beneath the sequestrum of a “neurotic excoriation.” This pattern of vasculitis is characterized by prominent fibrinoid necrosis (blue and green arrows) and thrombosis (red arrows), but inflammatory infiltrates are not a prominent feature. The infiltrating cells are neutrophils. The changes are livedo vasculitis-like.

 

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