Answer: D

In 1978, Wallace Clark first introduced the term dysplastic nevus in the context of “B-K mole syndrome;” since then, its definition has been debated and its name has changed multiple times.10,12 Despite recommendations by the National Institutes of Health Consensus Development Conference to change the name to atypical mole, dysplastic nevus and dysplastic nevus syndrome are the most commonly used terms in the literature.10 The condition causes debate because it exists in the gray area between common nevi and melanoma.13

The prevalence of dysplastic nevi is estimated to be anywhere from 2% to18%.10 Dysplastic nevi significantly increase a patient’s risk for developing melanoma; accordingly, patients with a history of melanoma have a higher prevalence of dysplastic nevi ranging from 34% to 59%.6,10,12 While this association exists, most dysplastic nevi themselves do not transform into melanoma.6,10,12 Since they are associated with sun exposure, dysplastic nevi begin to appear in puberty or adolescence and can either further develop or regress throughout adulthood.14 A patient may have just 1 or multiple heterogenous dysplastic nevi. Sun-exposed areas such as the trunk and upper back are the most common location for dysplastic nevi to develop.3,6,12

Dysplastic nevi can develop de novo or from previously normal-appearing nevi.6 As mentioned previously, exposure to UV-radiation induces numerous changes in the skin. It can damage DNA, which allows cells to acquire mutations that allow for uncontrolled cell growth. Currently, dysplastic nevi are thought to be precursors to melanoma.7

Common risk factors for developing atypical nevi include fair, sun-sensitive skin types and a history of blistering sunburns lasting more than 2 days.6 Another risk factor is dysplastic nevus-melanoma syndrome, which is a condition that can occur spontaneously or be inherited in an autosomal-dominant fashion.6,7 With this syndrome, patients classically have a triad of a minimum of 100 nevi, 1 nevus ≥8 mm in diameter, and 1 nevus with clinically atypical features.6

Clinically, dysplastic nevi look very similar to melanoma. They were originally defined as symmetric moles ≥5 mm in length with irregular, fuzzy borders and color variability.6,10,14 The current definition of dysplastic nevi states that they are macular lesions with a majority of the following features: pigment irregularity, an ill-defined or irregular border, background erythema, and size >5 mm.10

Several subtypes of dysplastic nevi are known. The lentiginous variant is flat with evenly distributed dark brown to black pigmentation.10 The “fried-egg” or sunnyside-up variant has a raised or flat center with pigmentation different from its flat peripheral border.6,10 The targeted variant presents as variable pigmentation in a concentric pattern.10 The seborrheic keratosis–like variant presents as a dark brown verrucous lesion.10 The erythematous type is pink to red in color.6,10 Finally, the melanoma stimulant subtype resembles melanoma and thus is not determined to be a dysplastic nevus until histologic examination of the biopsied lesion has been performed.10

Dysplastic nevi are characterized by several histologic features. These include architectural disorder without symmetry, papillary dermis fibroplasia, perivascular lymphocytic infiltrate, bridging of rete ridges, and lentiginous melanocytic hyperplasia.12,15 Additionally, dysplastic nevi may show melanocyte atypia confined to the dermal-epidermal junction.15

The differential diagnosis for dysplastic nevi includes malignant melanoma, congenital nevus, and recurrent nevus. Compared with melanoma, dysplastic nevi are more symmetric and have well-defined lateral borders.12 One study found that pathologists misdiagnosed dysplastic nevi as melanoma approximately 21% of the time and that the reverse occurred approximately 12% of the time.10 In order to improve diagnostic accuracy, scientists are developing tools that use nuclear image analysis in conjunction with next-generation sequencing.15 Specific markers for discrimination between melanoma and dysplastic nevi are scarce. One study found 4 (Bim, BRG1, Cul1, and ING4) out of 12 immunohistochemical markers that could differentiate melanoma from dysplastic nevi with nearly 95% sensitivity.16 In contrast, congenital nevi and recurrent nevi cannot be clinically differentiated from dysplastic nevi; the differentiation is made with histologic examination.13

Diagnosis of dysplastic nevi is made clinically; thus, biopsy is unnecessary except in cases of suspected melanoma.10 The likelihood of dysplastic nevi progressing to melanoma is very low, and removing the mole does not significantly lower the risk of developing melanoma.6,10 Dysplastic nevi can be graded as mild, moderate, or severe. Mild and moderate dysplastic nevi can be monitored; however, severely dysplastic nevi should be excised, as they might represent an overlap with melanoma in situ. Patients diagnosed with dysplastic nevi should be followed closely. Recommendations vary, but annual visits are a general guideline, with more frequent visits if the patient prefers.6,10 Patients with familial dysplastic nevi should be seen every 3 months.6 When screening patients during these visits, clinicians should reassess the nevus for concerning changes such as growth, color change, or papule formation within the lesion. Patients should be cautioned to avoid sun exposure as much as possible and to wear protective clothing when outdoors.10 In this case, it was determined that the lesion showed signs of atypia upon examination with dermoscopy. Biopsy of the lesion was performed, the results of which revealed mild atypia; thus it was monitored for changes during future visits.

Eleanor G. Johnson, BA, is a medical student; McKenna E. Boyd, BS, is a medical student; and Christopher Rizk, MD, is a dermatology fellow at Baylor College of Medicine, in Houston, Texas.


  1. Denkler K, Johnson J. A lost piece of melanoma history. Plast Reconstr Surg. 1999;104(7):2149-2153.
  2. Miller AJ and Mihm MC. Melanoma. N Eng J Med. 2006;355(1):51-65.
  3. Garbe C, Peris K, Hauschild A, et al. Diagnosis and treatment of melanoma. European consensus-based interdisciplinary guideline – Update 2016. Eur J Cancer. 2016;63:201-217.
  4. Lee CS, Thomas CM, Ng KE. An overview of the changing landscape of treatment for advanced melanoma. Pharmacotherapy. 2017;37(3):319-333.
  5. Schadendorf D, van Akkooi ACJ, Berking C, et al. Melanoma. Lancet. 2018;392(10151):971-984.
  6. Naeyaert JM and Brochez L. Clinical practice. Dysplastic nevi. N Engl J Med. 2003;349(23):2233-2240.
  7. Goldstein AM, Tucker MA. Dysplastic nevi and melanoma. Cancer Epidemiol Biomarkers Prev. 2013;22(4):528.
  8. McEnroe-Petitte MD. Melanoma. Nursing. 2011;41(5):45-45.
  9. Bolognia J, Jorizzo JL, Schaffer JV, eds. Dermatology. 4th ed. Philadelphia: Elsevier Saunders; 2012:1885-1914.
  10. Farber MJ, Heilman ER, Friedman RJ. Dysplastic nevi. Dermatol Clin. 2012;30(3):389-404.
  11. American Cancer Society. Treating melanoma skin cancer. American Cancer Society. Published 2018. Accessed April 22, 2019.
  12. Clarke LE. Dysplastic nevi. Clin Lab Med. 2011;31(2):255-265.
  13. Duffy K and Grossman D. The dysplastic nevus: from historical perspective to management in the modern era: Part II. Molecular aspects and clinical management. J Am Acad Dermatol. 2012;67(1):19.e11-19.e12.
  14. Halpern AC, Guerry D, Elder DE, Trock B, Synnestvedt M, Humphreys T. Natural history of dysplastic nevi. J Am Acad Dermatol. 1993;29(1):51-57.
  15. Hanna M, Liu C, Rohde G, Singh R. Predictive nuclear chromatin characteristics of melanoma and dysplastic nevi. J Pathol Inform. 2017;8(1):15.
  16. Zhang G, Li G. Novel multiple markers to distinguish melanoma from dysplastic nevi (biomarker in differential diagnosis of melanoma). PLoS One. 2012;7(9):e45037.