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Melanocytic Nevi Clinical Presentation

Author: Timothy McCalmont, MD; Chief Editor: Dirk M Elston, MD more...
Updated: Jun 3, 2013

History
Melanocytic nevi are common lesions that can be found on the integument of almost all individuals. Some patients
present with few lesions, while others have hundreds. The number on a given individual increases in rough
proportion to the degree of skin pigmentation.
Melanocytic nevi can be broadly divided into congenital and acquired types. Determining if a lesion is congenital or
acquired is generally easily accomplished by direct query of the patient, although, as noted above, some small
congenital melanocytic nevi are tardive and may be perceived by the patient as acquired.
When evaluating the nature of a melanocytic lesion, a number of attributes must be assessed. Further
commentary describing physical attributes can be found in Physical.
Whether a lesion has become symptomatic (eg, itchy, painful, irritated, or bleeding) is considered an
important indicator of potential malignant change.
Not all melanocytic nevi that change are malignant, especially if change is noted in a person younger
than 40 years. However, change that is perceptible over a short time is an indicator of potential
malignancy and designates a lesion deserving of biopsy. An Australian study found that 16% of
benign lesions changed (as measured by sequential digital dermoscopic imaging) over an interval of
2.5-4.5 months. The proportion of benign lesions that changed was higher in persons aged 0-35
years than in those aged 36-65 years but rose again in the elderly (age >65 y).[7]
Acquired melanocytic nevi are typically less than a centimeter in diameter and evenly colored.
Melanocytic nevi most commonly are tan to brown, but coloration can be variable, ranging from skin-colored
(nonpigmented) to jet black. The deep pigmentation associated with dark melanocytic nevi often stems from
associated intracorneal pigmentation. The spectrum of "hypermelanotic" melanocytic nevus includes lesions
with heavy epidermal pigmentation.
Dysplastic melanocytic nevi have also been referred to as Clark nevi. The designation "dysplastic" was
applied to such lesions because of an early belief that such lesions might be biologically unstable and
represent common precursors of melanoma. Further study has not definitively confirmed that this is the
case. Dysplastic nevi present clinically as flattish, pigmented macules or thin papules. Often, a "fried egg"
configuration is apparent, with a central papular area that is flanked by a macular zone of deeper
pigmentation.
Spitz nevi represent another distinctive variant of melanocytic nevus. In decades past, such lesions were
referred to as "juvenile melanomas," but now they are recognized by specific microscopical features and
are believed to be benign.
Although Spitz nevi tend to manifest as pink papules on the head of a child, they can be clinically
indistinguishable from conventional nevi in some instances; they also can be heavily pigmented.
Heavily pigmented Spitz nevi may also be referred to as "Reed nevi" or "pigmented spindle cell
nevi."
Many Spitz nevi exhibit considerable associated vascular ectasia and, thus, display a
hemangiomalike clinical appearance.
Blue nevi represent melanocytic nevi with a dermal distribution of cellularity and spindled cytomorphology
under the microscope. Such lesions are typically heavily pigmented. Because of the presence of deep
pigmentation within a refracting colloidal medium (namely, the skin), the brownish-black pigment present
contributes a bluish cast to such lesions, thereby explaining the name. The optical effect that accounts for
clinical blueness is known as the Tyndall phenomenon. The Tyndall phenomenon is not unique or exclusive
to blue nevi. Any melanocytic nevus with deep pigmentation may present clinically with a blue hue.
Not all blue nevi are blue. Some present with various shades of gray, brown, or black. The clinical
appearance varies depending on the degree of clinical pigmentation. Indeed, some blue nevi may be
wholly amelanotic. Because of the fact that the term blue nevus is not always reflective of the true
clinical appearance of the lesion, some dermatopathologists name blue nevi based on the cellular
morphology present. The terms spindle cell melanocytic nevus or dendritic melanocytic nevus
represent morphological terms that refer to the spectrum of blue nevi.
Despite their variability in coloration, blue nevi are usually relatively small and reasonably symmetric,
as typically is the case in benign lesions. Some blue nevi may be large and nodular with high
cellularity under the microscope. Blue nevi typically occur on the distal extremities or scalp, but they
can occur at any body site.

Physical
Physical examination involves, at a minimum, careful visual inspection of the lesion in question; in some instances,
an examination of the entire skin surface should be performed. Importantly, document the dimensions and
coloration of any lesion evaluated and record its exact location. A simple drawing of the lesion and the overall
topography can be helpful. Many dermatologists use topographic charts to record the location of multiple lesions
that are monitored from visit to visit. Some dermatologists enumerate individual lesions to facilitate follow-up. For
some patients, especially those with multiple melanocytic nevi, photographic documentation of lesions (including
both distant views that demonstrate topography and close views that capture subtle features of a particular lesion)
can be valuable. When examining melanocytic nevi, the physician should examine the scalp (possibly with the aid
of a hair dryer), the palms, the soles, between the toes, and the genitalia.
Congenital melanocytic nevi vary considerably in size and are commonly classified as small (< 1 cm),
intermediate (1-3 cm), or large/giant (>3 cm).
Congenital melanocytic nevi are generally relatively evenly pigmented and tan or brown, especially

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those that are thin. In some congenital nevi, the cells extend from the level of the epidermis to the
subcutaneous fat. These lesions can have an array of colors, and, at times, they cannot be easily
distinguished from melanoma based solely on findings from the clinical evaluation.
Congenital melanocytic nevi are hamartomalike; that is, they contain a predominance of
melanocytes but also seem to have simultaneous accentuation of other cutaneous elements. Thus,
an increase in the number of hair follicles, the presence of follicles of increased size, or an increase
in other appendages may be observed.
Conventional or common acquired melanocytic nevi are generally less than 1 cm in diameter and evenly
pigmented. Some atypical melanocytic nevi (melanocytic nevus of the so-called Clark or dysplastic type)
exceed 1 cm in size, especially when such lesions occur on the trunk.
Junctional melanocytic nevi are macular or thinly papular. Junctional lesions typically range from
brown to brownish-black. The darker coloration of junctional melanocytic nevi stems from the fact
that the surface epidermis is often simultaneously hyperpigmented.
Compound and intradermal melanocytic nevi display elevation relative to surrounding uninvolved
skin. Compound melanocytic nevi are often lighter in color than junctional nevi and range from tan to
light brown. Some compound melanocytic nevi have areas of dark pigmentation, particularly those
that have been recently irritated or traumatized. Many wholly intradermal melanocytic nevi display no
significant pigmentation.
The development of a new area of pigmentation within a long-standing nonpigmented or lightly
pigmented compound or intradermal melanocytic nevus, as shown in the image below, is a cause for
concern. While pigmentary changes could be due to incidental inflammation or recent irritation or
trauma, the possibility of evolving melanoma is also a consideration in the differential diagnosis.
Generally, a biopsy for microscopic examination is warranted in this context.

A conventional (papular) melanocytic nevus occurring within acral skin. Note slight border irregularity, a feature
common in association with acral nevi.

Dysplastic or atypical nevi (also known as Clark nevi) are acquired variants that are relatively flat, thinly
papular, and relatively broad. Often, such lesions exhibit target-like or fried egglike morphology, as noted
above, with a central papular zone and a macular surrounding area with differing pigmentation.
Dysplastic nevi often occur in a familial fashion. Affected individuals may present with dozens or
hundreds of such lesions. Almost invariably, individuals with dysplastic nevi are of northern
European ancestry from the United Kingdom, the Netherlands, Germany, or, occasionally, Poland or
Russia. Most of these individuals have fair skin and other Celtic features. Some individuals have only
a few atypical nevi, and their risk of melanoma may not be much higher than persons without such
nevi. Persons with large numbers of nevi (>100) have a high lifetime risk of melanoma that
approaches unity. Persons with large numbers of nevi and a familial history of melanoma (consisting
of 2 members of the primary family with melanoma) have an extremely high risk of developing
melanoma and deserve vigilant clinical monitoring.
Dysplastic nevi generally grow through lateral extension of the intraepidermal component of the
lesion; therefore, these lesions often assume the clinical configuration of a fried egg, with a central
papular zone and a surrounding macular area of differing pigmentation. The peripheral border is
often perceived as blurred or fuzzy because of this lateral extension of superficial melanocytes.
Some authorities have postulated that Clark (dysplastic) nevi (shown below) are significant or
common precursors to melanoma. The designation dysplastic was chosen to suggest that these
lesions represent an intermediate (unstable) form between conventional nevi and melanoma. This
concept remains controversial. They may represent precursor lesions, markers for an increased risk
of de novo melanoma, or both. Some data suggest that most melanomas in patients with the
dysplastic nevus syndrome occur de novo. While the removal of all dysplastic nevi from an individual
with melanoma is generally not indicated, removal of lesions with a highly atypical appearance is
indicated to be certain that melanoma is not present.

A Clark (dysplastic) nevus with modest variation in pigmentation and irregular borders. Biopsy of the lesion proved no
evidence of melanoma.

A compound Clark (dysplastic) nevus with fried egglike clinical morphology, with a central dark papule flanked by an
eccentric more lightly pigmented macular zone.

Spitz nevi (shown below) vary considerably in size, but they generally are smaller than 1 cm in diameter.
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Many Spitz nevi have a keratosislike quality because of associated epidermal hyperplasia and
hyperkeratosis, and some have an angiomalike appearance because of associated vascular ectasia.
The degree of pigmentation of Spitz nevi also varies; a heavily pigmented, small, spindle cell variant
on the legs of women has been referred to as "pigmented spindle cell nevus" or "Reed nevus"
because the pigmented spindle cell variant was described by Richard Reed.

A heavily pigmented junctional Spitz nevus, also known as pigmented spindle cell nevus. Note that many Spitz nevi are
nonpigmented and may have an angiomalike clinical appearance.

Blue nevi are not always blue, and they are not even always pigmented. The designation blue nevus,
although flawed, has been preserved for historical reasons.
Blue nevi are sometimes larger than other melanocytic nevi, occasionally measuring 2 cm or greater
in diameter. This is particularly true of cellular lesions (cellular blue nevi) that occur at sun-protected
sites, such as the buttocks.
Blue nevi are often firm because of associated stromal sclerosis, and they often have a nodular
quality, a reflection of their deeper position within the skin.
Heavily pigmented blue nevi manifest clinically as blue, black, or gray lesions, whereas blue nevi
with lesser degrees of pigmentation may be tan or brown or strictly the color of surrounding healthy
skin.
Hypocellular blue nevi that cover an extensive clinical distribution have been referred to as "dermal
melanocytic hamartomas" by some authors. This spectrum includes the entities nevus of Ito, nevus
of Ota, and nevus of Sun.

Causes
The etiology of melanocytic nevi remains unknown. No established genetic or environmental influences are known
to contribute to the development of congenital nevi. However, after studying 144 children in Naples, researchers
concluded that development of melanocytic nevi early in life is the result of complicated relationships among nevus
evolution, anatomic location, and environmental and constitutional factors.[8] The specific genetic factors that
contribute to the development of acquired melanocytic nevi also remain unknown. However, data suggest that the
propensity for developing large numbers of nevi, such as multiple dysplastic nevi, might be inherited as an
autosomal dominant trait.
Patients with the familial atypical multiple mole and melanoma syndrome (also known as the dysplastic
nevus syndrome) develop dozens to hundreds of melanocytic nevi and have an elevated lifetime risk for the
development of melanoma. As the name implies, this disorder is believed to have an inherited basis.
As noted previously, population-based evidence suggests that ultraviolet irradiation may trigger the
development of acquired melanocytic nevi. The number of melanocytic nevi in childhood is inversely related
to the degree of skin pigmentation and is high in children with poor sun tolerance. The mechanism of this
induction has not been adequately investigated, but such induction could represent an example of tumor
promotion by ultraviolet light.

Contributor Information and Disclosures

Author
Timothy McCalmont, MD Director, UCSF Dermatopathology Service, Professor of Clinical Pathology and
Dermatology, Departments of Pathology and Dermatology, University of California at San Francisco; Editor-inChief, Journal of Cutaneous Pathology
Timothy McCalmont, MD is a member of the following medical societies: Alpha Omega Alpha, American
Medical Association, American Society of Dermatopathology, California Medical Association, College of
American Pathologists, and United States and Canadian Academy of Pathology
Disclosure: Apsara Consulting fee Independent contractor
Specialty Editor Board
James J Nordlund, MD Professor Emeritus, Department of Dermatology, University of Cincinnati College of
Medicine
James J Nordlund, MD is a member of the following medical societies: American Academy of Dermatology,
Sigma Xi, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.
David F Butler, MD Section Chief of Dermatology, Central Texas Veterans Healthcare System; Professor of
Dermatology, Texas A&M University College of Medicine; Founding Chair, Department of Dermatology, Scott
and White Clinic
David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of
Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for
MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa
Disclosure: Nothing to disclose.
Rosalie Elenitsas, MD Herman Beerman Professor of Dermatology, University of Pennsylvania School of
Medicine; Director, Penn Cutaneous Pathology Services, Department of Dermatology, University of
Pennsylvania Health System

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Rosalie Elenitsas, MD is a member of the following medical societies: American Academy of Dermatology and
American Society of Dermatopathology
Disclosure: Lippincott Williams Wilkins Royalty Textbook editor
Glen H Crawford, MD Assistant Clinical Professor, Department of Dermatology, University of Pennsylvania
School of Medicine; Chief, Division of Dermatology, The Pennsylvania Hospital
Glen H Crawford, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy
of Dermatology, American Medical Association, Phi Beta Kappa, and Society of USAF Flight Surgeons
Disclosure: Abvie Honoraria Speaking and teaching
Chief Editor
Dirk M Elston, MD Director, Ackerman Academy of Dermatopathology, New York
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

References
1. Natarajan K, Arunachalam P, Sundar D, Srinivas CR. Congenital melanocytic nevi: catch them early!. J
Cutan Aesthet Surg. Jan 2013;6(1):38-40. [Medline].
2. Palicka GA, Rhodes AR. Acral melanocytic nevi: prevalence and distribution of gross morphologic
features in white and black adults. Arch Dermatol. Oct 2010;146(10):1085-94. [Medline].
3. Kelly JW, Rivers JK, MacLennan R, Harrison S, Lewis AE, Tate BJ. Sunlight: a major factor associated
with the development of melanocytic nevi in Australian schoolchildren. J Am Acad Dermatol. Jan
1994;30(1):40-8. [Medline].
4. Harrison SL, MacLennan R, Buettner PG. Sun exposure and the incidence of melanocytic nevi in young
Australian children. Cancer Epidemiol Biomarkers Prev. Sep 2008;17(9):2318-24. [Medline].
5. Gallagher RP, Rivers JK, Lee TK, Bajdik CD, McLean DI, Coldman AJ. Broad-spectrum sunscreen use
and the development of new nevi in white children: A randomized controlled trial. JAMA. Jun 14
2000;283(22):2955-60. [Medline].
6. Zalaudek I, Schmid K, Marghoob AA, et al. Frequency of dermoscopic nevus subtypes by age and body
site: a cross-sectional study. Arch Dermatol. Jun 2011;147(6):663-70. [Medline].
7. Menzies SW, Stevenson ML, Altamura D, Byth K. Variables predicting change in benign melanocytic nevi
undergoing short-term dermoscopic imaging. Arch Dermatol. Jun 2011;147(6):655-9. [Medline].
8. Patruno C, Scalvenzi M, Megna M, Russo I, Gaudiello F, Balato N. Melanocytic Nevi in Children of
Southern Italy: Dermoscopic, Constitutional, and Environmental Factors. Pediatr Dermatol. May 31 2013;
[Medline].
9. Khera S, Sarkar R, Jain RK, Saxena AK. Neurocutaneous melanosis: an atypical presentation. J
Dermatol. Jul 2005;32(7):602-5. [Medline].
10. Tran KT, Wright NA, Cockerell CJ. Biopsy of the pigmented lesion--when and how. J Am Acad Dermatol.
Nov 2008;59(5):852-71. [Medline].
11. Ko CJ, McNiff JM, Glusac EJ. Melanocytic nevi with features of Spitz nevi and Clark's/dysplastic nevi
("Spark's" nevi). J Cutan Pathol. Oct 2009;36(10):1063-8. [Medline].
12. Ackerman AB, Milde P. Naming acquired melanocytic nevi. Common and dysplastic, normal and atypical,
or Unna, Miescher, Spitz, and Clark?. Am J Dermatopathol. Oct 1992;14(5):447-53. [Medline].
13. Ackerman AB, Magana-Garcia M. Naming acquired melanocytic nevi. Unna's, Miescher's, Spitz's Clark's.
Am J Dermatopathol. Apr 1990;12(2):193-209. [Medline].
14. [Guideline] The Cancer Council Australia, Australian Cancer Network, Sydney and New Zealand
Guidelines Group. Congenital melanocytic naevi. Clinical practice guidelines for the management of
melanoma in Australia and New Zealand. National Guideline Clearinghouse. 2008.
15. [Guideline] Finnish Medical Society Duodecim. Skin cancer. In: EBM Guidelines. Evidence-Based
Medicine. National Guideline Clearinghouse. May 2005.
16. [Guideline] Scottish Intercollegiate Guidelines Network. Cutaneous melanoma. National Guideline
Clearinghouse. Jul 2003.
17. Harth Y, Friedman-Birnbaum R, Linn S. Influence of cumulative sun exposure on the prevalence of
common acquired nevi. J Am Acad Dermatol. Jul 1992;27(1):21-4. [Medline].
18. Richtig E, Jung E, Asback K, Trapp M, Hofmann-Wellenhof R. Knowledge and perception of melanocytic
nevi and sunburn in young children. Pediatr Dermatol. Sep-Oct 2009;26(5):519-23. [Medline].
19. Carrera C, Puig-Butill JA, Aguilera P, Ogbah Z, Palou J, Lecha M, et al. Impact of Sunscreens on
Preventing UVR-Induced Effects in Nevi: In Vivo Study Comparing Protection Using a Physical Barrier vs
Sunscreen. JAMA Dermatol. May 8 2013;1-11. [Medline].
20. Barnhill RL, Argenyi ZB, From L, et al. Atypical Spitz nevi/tumors: lack of consensus for diagnosis,
discrimination from melanoma, and prediction of outcome. Hum Pathol. May 1999;30(5):513-20.
[Medline].
21. Casso EM, Grin-Jorgensen CM, Grant-Kels JM. Spitz nevi. J Am Acad Dermatol. Dec 1992;27(6 Pt

http://emedicine.medscape.com/article/1058445-clinical

Page 4 of 5

10/6/14, 11:20 PM

1):901-13. [Medline].
22. Cesinaro AM, Foroni M, Sighinolfi P, Migaldi M, Trentini GP. Spitz nevus is relatively frequent in adults: a
clinico-pathologic study of 247 cases related to patient's age. Am J Dermatopathol. Dec 2005;27(6):46975. [Medline].
23. DeDavid M, Orlow SJ, Provost N, et al. A study of large congenital melanocytic nevi and associated
malignant melanomas: review of cases in the New York University Registry and the world literature. J Am
Acad Dermatol. Mar 1997;36(3 Pt 1):409-16. [Medline].
24. Ferrara G, Argenziano G, Soyer HP, et al. The spectrum of Spitz nevi: a clinicopathologic study of 83
cases. Arch Dermatol. Nov 2005;141(11):1381-7. [Medline].
25. Florell SR, Meyer LJ, Boucher KM, et al. Nevus distribution in a Utah melanoma kindred with a
temperature-sensitive CDKN2A mutation. J Invest Dermatol. Dec 2005;125(6):1310-2. [Medline].
26. Gallagher RP, McLean DI. The epidemiology of acquired melanocytic nevi. A brief review. Dermatol Clin.
Jul 1995;13(3):595-603. [Medline].
27. Harrison SL, Buettner PG, MacLennan R. Body-site distribution of melanocytic nevi in young Australian
children. Arch Dermatol. Jan 1999;135(1):47-52. [Medline].
28. James MR, Roth RB, Shi MM, et al. BRAF polymorphisms and risk of melanocytic neoplasia. J Invest
Dermatol. Dec 2005;125(6):1252-8. [Medline].
29. Kincannon J, Boutzale C. The physiology of pigmented nevi. Pediatrics. Oct 1999;104(4 Pt 2):1042-5.
[Medline].
30. Lazova R, McNiff JM, Glusac EJ. Under the microscope. Surgeons, pathologists, and melanocytic nevi.
Clin Plast Surg. Jul 2000;27(3):323-9, vii. [Medline].
31. Mooi WJ. Cutaneous melanocytic naevus versus melanoma: pitfalls, surprises, dilemmas. Eur J Surg
Oncol. Dec 1999;25(6):622-7. [Medline].
32. Murali R, McCarthy SW, Scolyer RA. Blue nevi and related lesions: a review highlighting atypical and
newly described variants, distinguishing features and diagnostic pitfalls. Adv Anat Pathol. Nov
2009;16(6):365-82. [Medline].
33. Sagebiel RW. Pigmented lesion pathology: the specimen and its report. A personal and probably biased
approach. Pathology (Phila). 1994;2(2):281-98. [Medline].
34. Shea CR, Prieto VG. Recent developments in the pathology of melanocytic neoplasia. Dermatol Clin. Jul
1999;17(3):615-30, ix. [Medline].
35. Zaal LH, Mooi WJ, Klip H, van der Horst CM. Risk of malignant transformation of congenital melanocytic
nevi: a retrospective nationwide study from The Netherlands. Plast Reconstr Surg. Dec 2005;116(7):19029. [Medline].
Medscape Reference 2011 WebMD, LLC

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