Acquired Melanocytic Nevi

Origin of Melanocytes

The origin of melanocytic nevi has been debated for a long time. In 1893 Unna suggested that epidermal melanocytes were the source of common acquired nevi and that most nevi started as junctional nevi from which some melanocytes would migrate to the superficial dermis to form compound nevi. He named this process “Abtropfung” (dropping off). Accordingly, it was assumed that purely intradermal nevi result after involution of the junctional component. An alternate theory proposes that dermal melanocytic precursor cells may be the source of many melanocytic nevi and that in compound melanocytic nevi the dermoepidermal junction is populated from below (so-called Hochsteigerung, or climbing up).

Studies on nevi at various ages have shown that compound and intradermal melanocytic nevi outnumber junctional nevi in children. Furthermore, junctional melanocytic nevi occur more frequently in older individuals. It is therefore likely that acquired nevi displaying a predominantly intradermal growth in a pattern that has historically been associated with congenital nevi result from an initiating oncogenic mutation in a dermal melanocyte rather than epidermal melanocyte. It seems less likely that these nevi would have progressed through a junctional phase. The so-called congenital pattern of compound melanocytic nevi is more plausibly explained by a dermal origin of lesional melanocytes. On the other hand, those nevi developing later in life that begin as macular lesions in a sun-exposed distribution are probably derived from a junctional melanocyte and may follow the pattern of “Abtropfung” as proposed by Unna.

Ultraviolet (UV) Radiation and Nevi

Many studies have documented a relationship between exposure to ultraviolet radiation and the development of melanocytic nevi. This includes an association between total nevus counts and/or distribution of nevi with a history of sun exposure. The most common driver mutation in common acquired nevi involves BRAF , which is found in approximately 80% of these nevi. Interestingly, mutations in BRAF are not Ultraviolet B (UVB)-induced DNA photoproducts. Among melanomas, there is a link of UV-related melanomas with particularly intense intermittent bouts of UV and BRAF mutation. However, among nevi, BRAF mutation may be seen in both UV-related and non–UV-related nevi. They are more frequent in compound than junctional nevi.

Although ultraviolet light plays a role in the development of nevi, twin studies have demonstrated a significant heritability component to total nevus counts. Monozygotic twins had significantly greater similarity in total nevus counts compared with dizygotic twins.

Clinical Findings

Common Acquired Junctional Melanocytic Nevi

Common acquired junctional melanocytic nevi are uncommon in childhood and are typically seen in adults. Clinically these are typically flat, circumscribed, small macular lesions with variable pigmentation. By dermoscopy they usually have a reticulated pattern ( Fig. 2.1 ). The reticulation is a result of the accumulation of the pigment along the rete ridges, and the clear spaces between the network correspond to dermal papillae where there is usually less pigment in these lesions.

Common Acquired Compound Melanocytic Nevi

The growth of melanocytes in the dermis typically elevates the overlying epidermis and leads to the formation of papules. The lesions may be pigmented, display the same color as the adjacent skin, or be reddish. They are usually small and circumscribed. Some lesions may be polypoid or pedunculated. The epidermal surface may be smooth or verrucous/papillomatous. Dermal nevi, if pigmented, may have a granular or globular dermoscopic appearance or the appearance of granules on the background of a reticulated network ( Fig. 2.2 ).