Section 7 -

Recurrent Melanocytic Nevus Neil Crowson, MD Cynthia M. Magro, MD Martin C. Mihm, Jr., MD

Case # 7. Recurrent Melanocytic Nevus Clinical Features Recurrence of a nevus manifests as repigmentation in the scar at the site of a previous incomplete elliptical, punch or shave excision, electrodessication, or dermabrasion of a melanocytic lesion. The pigmentation within or adjacent to the scar is irregular, stippled or scalloped with a variegated color ranging from tan to dark brown or black (Kornberg and Ackerman, 1975; Sexton and Sexton, 1991). Similar changes appear in nevi partly ablated through trauma of which the patient may be unaware. Recurrent nevi are often flat, reflecting the mainly intraepidermal proliferation; repigmentation occurs within weeks to months of the original excision, unlike recurrent melanoma, where repigmentation occurs years later. Where a skin graft has been applied, showers of tan or black dots may appear in its center. The source of the cells that repopulate the epidermis are those nevus cells that remain in reticular dermal-based adnexal structures, in the deep-seated dermal component, or the adjacent epidermis after incomplete removal (Arrese Estrada et al., 1990; Sexton and Sexton, 1991; Crowson et al., 2001). Histology The original lesion is usually a compound nevus, an intradermal nevus being seen in 32% of cases and a junctional nevus in 5%. Less than 10% of recurrent nevi arise from prior dysplastic nevi, probably as the latter are more aggressively treated ab initio. The recurrent nevus can be easily recognized at scanning magnification by a trizonal arrangement with a high-density intraepidermal melanocytic growth over a dermal scar with a subjacent remnant of benign nevus. Other features help to differentiate it from two other common scenarios associated with dermal fibrosis and an atypical intraepidermal melanocytic growth, namely regressed and/or recurrent melanoma (Blessing, 1999). The intraepidermal growth in recurrent nevi manifests sharp lateral circumscription, whereby the lateral boundaries are defined by the scar from the prior procedure; in some instances the junctional proliferation may be more broad, extending laterally past the confines of the scar, and is often more pronounced than that observed in the original excision (Sexton and Sexton, 1991). The intraepidermal component is cytologically that of a nevus, be it of common acquired, dysplastic, or congenital subtypes. Over the scar, however, the melanocytes are enlarged with epithelioid cytology, round to oval nuclei, abundant cytoplasmic pigment, variable sizes and shapes and conspicuous nucleolation. The chromatin is evenly dispersed and the N/C ratios are not increased. The atypia is mild or moderate in degree; features of high-grade dysplasia such as increased N/C ratios, increased and irregularly distributed chromatin, and angulated nuclear contours are not seen. The melanocytes are in a single-cell and nested array, with confluence of growth, nest variability of shape, location, and orientation, and nest dyshesion (Sexton and Sexton, 1991). The single-cell growth is mainly lentiginous, but there may be some upward pagetoid growth to the suprabasilar epidermis and spinous layer, sparing the granular cell layer. The epidermis may manifest loss of the retiform architecture. There is often intense melanization of keratinocytes. Mitotic activity is seen in less than 10% of cases. Melanocytes may grow along the basal layer of adnexal structures. The dermis demonstrates parallel arrangement of collagen with neovascularization. There may be patchy perivascular lymphocytic infiltrates but lichenoid inflammation is absent. Nucleolated nevomelanocytes similar to those in the epidermis may be seen within the scar, being confined to the superficial dermis and not prominent relative to the intraepidermal component. The cells are usually nested. The recurrent Spitz nevus is typically intradermal in location and may permeate the subcutis. Recurrent Spitz nevi resemble the desmoplastic Spitz nevus by virtue of dermal fibrosis (Stern, 1985). There is a low incidence of recurrence in classical Spitz nevi; one study failed to show any recurrences in 49 such patients during a follow-up period of 5.0 years (Kaye and Dehner, 1990). Recurrent dysplastic nevi manifest cytoplasmic retraction artifact as clear spaces and clefts around nests or individual nevus cells showing variable cytologic atypia indistinguishable from the recurrent common acquired nevus. We emphasize the importance of reviewing the originally excised melanocytic proliferation, as the distinction of recurrent dysplastic nevus from recurrent common acquired nevi is difficult. The exception is those recurrent nevi in which the residual lesion is available for analysis peripheral to the scar. Differentiation from Malignant Melanoma with Regression and Recurrent Melanoma Regressive fibrosis in melanoma is different from a scar, with a delicate pattern of thin collagen fibers in an edematous matrix containing scattered mononuclear cells with prominent ectatic venules oriented perpendicularly to the epidermis. In contrast, a scar is often hypovascular with laminated thick bundles of collagen in a parallel disposition to the epidermis. When vessels are present they are small and may be closely aggregated. In regressed melanoma, there is usually prominent inflammation that may be lichenoid with conspicuous melanophage accumulation. The infiltrate in recurrent nevi is sparse and when present is often localized around blood vessels. In regressed melanoma the epidermis is attenuated and is devoid of melanocytes. In recurrent nevi, the epidermis shows melanocytic hyperplasia and hypermelanosis. In regressed melanoma a severely atypical intraepidermal or dermoepidermal melanocytic proliferation is found outside the areas of regressive stromal fibrosis, in contrast to recurrent nevi where the pattern and cytology of melanocytic growth is often banal. A residual lesion is identified in only 25% of regressed melanomas, versus a much higher frequency in recurrent nevus. The residual lesion identified in melanoma is usually severely atypical, while the residual lesion in a recurrent nevus is not. With respect to differentiating recurrent melanoma from recurrent nevus, if indeed the recurrent melanoma is on the basis of residual primary melanoma rather than representing metastatic disease, we adhere to the following rules: 1) The cytology in recurrent melanoma is that of melanoma. Other supportive features are atypical mitoses and necrosis, neither of which are present in the recurrent nevus. 2) Most recurrences in scar sites of previously excised melanoma are metastases with a constellation of light microscopic findings that, apart from a recurrent Spitz nevus, should not be confused with a recurrent nevus. The hallmarks are nodules of spindle and/or epithelioid cells amidst a scar, coagulative necrosis within the tumor nodules, vascular invasion, and brisk mitotic activity (Yu and Heenan, 1999). Grading Atypia in Recurrent Nevi We do not grade atypia in recurrent nevi; it always looks worse than in the original biopsy and, especially in young children and adolescents, it may be severe with upward migration of melanocytes n the epidermis. Most important is an assessment of the original specimen and the atypia of melanocytes in residual nevus peripheral to the scar. If it is a recurrence of a dysplastic nevus we so indicate following tissue review. 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