Common Acquired Melanocytic Nevi
Christine J. Ko, MD
Key Facts
Clinical Issues
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Majority develop in adolescence
Microscopic Pathology
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Flat surface to slightly raised to polypoid
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Epidermis varies (e.g., thin or seborrheic keratosis-like)
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Well-circumscribed
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Melanocytes arranged in regular clusters/nests, particularly at junction of epidermis and dermis and superficial dermis
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Nest defined as 3-5 clustered melanocytes
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Generally symmetrical from side to side
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Orderly arrangement of nests at junction and in superficial dermis
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Mitoses generally absent
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Melanin pigment often limited to junctional or superficial dermal nests
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Dermal maturation: Type A nevus cells superficially, type B and C nevus cells with descent into dermis
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Type A nevus cells: Epithelioid
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Type B nevus cells: Lymphocytoid
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Type C nevus cells: Spindled, neuroid
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May see pseudonuclear inclusion: Lighter staining round area within nucleus
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Top Differential Diagnoses
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Atypical/”dysplastic”/Clark nevus
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Congenital melanocytic nevus
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DDx of junctional lentiginous melanocytic nevus
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Lentigo (simple)
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DDx of intradermal nevus (especially neurotized)
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Neurofibroma
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TERMINOLOGY
Synonyms
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Benign melanocytic nevus, junctional melanocytic nevus, compound melanocytic nevus, intradermal melanocytic nevus, common mole, common melanocytic nevus, nevocellular nevus
ETIOLOGY/PATHOGENESIS
Exact Etiology Unknown
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Believed by some to arise from intraepidermal melanocytes
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Others suggest that melanocytic nevi arise from nerves or pluripotential cells
Tumor vs. Hamartoma?
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Still debated
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Evidence for tumor
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Studies showing that some nevi are clonal
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Growth advantage of nevus cells over epidermal, dendritic melanocytes in cell culture
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Similar expression of different markers by nevi and malignant melanoma
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Presence of mutations in BRAF oncogene in majority of nevi
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Evidence for hamartoma
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Other proliferative elements: Epidermal, follicular, connective tissue
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Studies showing that some nevi are polyclonal
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CLINICAL ISSUES
Epidemiology
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Incidence
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Number of acquired nevi
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Increases with age up to 3rd decade
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May be related to familial predisposition
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Sun exposure in childhood also linked to development of nevi
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More common in lighter skinned individuals
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Age
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Not present at birth
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Majority develop in adolescence
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Density of nevi generally decreases after 4th decade
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Presentation
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Junctional lesions
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Flat to minimally raised macule/very thin papule
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Generally < 6 mm, but may be larger
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Color often a variation of brown
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Compound lesions
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Slightly raised papule
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Variable color (brown, flesh-colored, pink)
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May contain hair
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Intradermal lesions
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Papule, may be pedunculated
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Variable color (brown, flesh-colored, pink)
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May contain hair
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Natural History
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Abtropfung hypothesis of Unna
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Melanocytes are initially junctional
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With chronologic time (aging), melanocytes “drop off” into dermis, creating compound melanocytic lesions
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With more time, the junctional melanocytes have all “dropped off,” creating intradermal melanocytic lesions
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Intradermal melanocytic lesions may eventually “shed” or become acrochordons
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Degenerative changes include balloon cell change and fatty change
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Alternative hypothesis
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Nevi begin in the dermis
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Not all melanocytic nevi display progressive changes; some arrest at a given stage indefinitely
Treatment
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Not necessary
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Conservative removal (e.g., shave removal) generally sufficient
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Residual dark pigment may remain
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Pigment may recur irregularly within scar (recurrent nevus)
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Prognosis
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Benign
MICROSCOPIC PATHOLOGY
Histologic Features
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Flat surface to slightly raised to polypoid
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Well-circumscribed
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Melanocytes arranged in nests, particularly at junction of epidermis and dermis and superficial dermis
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Nest defined as cluster of at least 3 (some authors) or 5 (other authors) melanocytes
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Generally symmetrical from side to side
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Orderly arrangement of nests at junction and in superficial dermis
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