CME

Benign and Premalignant Skin Lesions

Erica H. Lee, M.D. Kishwer S. Nehal, M.D. Joseph J. Disa, M.D.
New York, N.Y.

Learning Objectives: After reading this article, the participant should be able to: 1. Clinically describe various cutaneous neoplasms. 2. Identify the corresponding histopathologic findings. 3. Discuss the optimal treatment approach for each entity. Summary: Cutaneous neoplasms are broadly viewed as benign, premalignant, or malignant. In dermatology, lesions are classified based on the primary cell of origin or the component of the skin predominantly affected by the pathologic change (epidermis, dermis, or subcutaneous fat). The diagnosis and treatment of skin lesions rely on understanding the clinical presentation and corresponding histopathology. Surgical treatment is not always indicated and is dependent on multiple variables. This review discusses several benign and premalignant neoplasms frequently encountered by the plastic surgeon. The emphasis is on clinical presentation, histopathologic correlation, and management approach. (Plast. Reconstr. Surg. 125: 188e, 2010.)

enign and premalignant skin lesions are commonly encountered by dermatologists and plastic surgeons for diagnosis and management. Based on their origin in the skin, these lesions are classified into categories such as epidermal, melanocytic, follicular, and dermal. Histologic evaluation illustrates the predominant location of the lesion in the epidermis or dermis and provides insight into its evolution and natural progression. This clinical-pathologic correlation provides vital information and significantly influences management and treatment. There are numerous cutaneous neoplasms; however, some of the most common benign and premalignant lesions are presented in this review. Classic clinical presentation, key histopathologic components, and treatment options are discussed. The arsenal of treatment modalities is vast and ranges from simple techniques to excisional and laser surgery. A thorough understanding of the clinical and histologic presentation can guide the physician in selecting the most appropriate treatment approach.

ically present in older, fair-skinned individuals as erythematous scaly areas (Fig. 1). Other variants include the thicker, hypertrophic actinic keratoses and pigmented actinic keratoses. These precancerous lesions may develop into squamous cell carcinoma and are predictors of future squamous and basal cell carcinoma development.1 An actinic keratosis may regress spontaneously, persist, or transform into an invasive squamous cell carcinoma. The progression to squamous cell carcinoma is estimated at 10 percent.2 Due to the inability to predict transformation, treatment is often advocated. All modalities yield similar success rates but vary in terms of treatment duration and degree of inflammation. Cryotherapy is widely used and ideal for spot treatment in any location, without the need for anesthesia or hemostasis (see Video 1, which demonstrates cryotherapy of actinic keratoses on the dorsal hand treated with liquid nitrogen dispensed from a handheld apparatus, available in the Related Videos section of the full-text article on www.PRSJournal.com). Liquid nitrogen (195.8C boiling point)

ACTINIC KERATOSES
Actinic keratoses, or solar keratoses, are epidermal neoplasms that develop in response to prolonged exposure to ultraviolet radiation. They typFrom the Dermatology Service and the Plastic and Reconstructive Surgery Service, Memorial Sloan-Kettering Cancer Center. Received for publication December 2, 2008; accepted April 1, 2009. Copyright 2010 by the American Society of Plastic Surgeons DOI: 10.1097/PRS.0b013e3181d6e89a

Disclosure: The authors have no financial interest to declare in relation to the content of this article.

Related Video content is available for this article. The videos can be found under the Related Videos section of the full-text article.

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is dispensed from a handheld apparatus with a spray tip. The duration and number of each freeze-thaw cycle determine the level of destruction and subsequent erythema and bulla formation. Topical treatment with 5-fluorouracil (Carac or Efudex) specifically targets actinic damage while sparing normal skin, causing erythema and erosions lasting 3 to 6 weeks. Imiquimod (Aldara), a newer Food and Drug Administrationapproved topical agent, induces the skins immune system and may result in less inflammation. Both are good alternatives to cryotherapy when diffuse actinic damage is present.3 Diclofenac sodium 3% gel (Solaraze) is a topical nonsteroidal anti-inflammatory agent with antineoplastic effects that is used for mild actinic damage.4 Superficial glycolic peels and medium-depth peels, such as trichloroacetic acid and Jessners solution, are useful for diffuse actinic damage5,6 and offer the additional advantage of treating related signs of photodamage, such as lentigines and fine rhytids. Photodynamic therapy is a newer treatment option for diffuse actinic keratoses with the advantage of minimal recovery time. 5-Aminolevulinic acid , a topical photosensitizer, is applied as a 20% solution (Levulan Kerastick) after the area is cleansed and degreased with acetone. Incubation for 1 to 3 hours is followed by exposure to the blue light, long-pulsed pulsed dye laser or intense-pulse light for several minutes (see Video 2, which demonstrates photodynamic therapy, available in the Related Videos section of the full-text article on www.PRSJournal. com; the treatment area is prepared with acetone followed by application of the 5-aminolevulinic acid;

Fig. 1. Actinic keratoses classically present as pink scaly macules (above). On histopathologic analysis (below), there are atypical, pleomorphic keratinocytes in the basal cell layer of the epidermis (arrows) with overlying hyperkeratosis (*). Underlying inflammation may be present in the dermis. Hematoxylin and eosin stain; original magnification, 20.

Video 1. Video demonstrates cryotherapy of actinic keratoses on the dorsal hand treated with liquid nitrogen dispensed from a handheld apparatus, available in the Related Videos section of the full-text article on www.PRSJournal.com.

Video 2. Video demonstrates photodynamic therapy of the face. The treatment area is prepared with acetone followed by application of the 5-aminolevulinic acid. After the incubation period, the treatment area is exposed to blue light for approximately 16 minutes. This video is available in the Related Videos section of the full-text article on www.PRSJournal.com.

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after the incubation period, the treatment area is exposed to blue light for approximately 16 minutes).7,8 Mild erythema and edema similar to a sunburn can last a few days. Ablative lasers, such as the carbon dioxide and erbium:yttrium-aluminumgarnet, are good options for actinic keratoses of the mucosal lip (actinic cheilitis).

DYSPLASTIC/ATYPICAL NEVUS
Dysplastic melanocytic nevi present as clinical variants of melanocytic nevi with irregular appearance in terms of border, symmetry, color, and size (Fig. 3). They occur sporadically or in the setting of a personal or family history of melanoma or atypical moles termed familial atypical multiple mole melanoma syndrome (FAMMM). Dysplastic melanocytic nevi are considered an important risk factor for melanoma; however, the majority are stable with low transformation rates to melanoma.11,12 Management of dysplastic melanocytic nevi is influenced by the number and character of background lesions, personal and family history of melanoma, and history of new or changing lesions. In patients with multiple dysplastic melanocytic nevi, skin self-examinations, interval complete skin examinations with a dermatologist, total body photography, and dermoscopy can aid in surveillance and early detection of changing lesions (see Video 3, which demonstrates total body photography, available in the Related Videos section of the full-text article on www.PRSJournal.com; total body photography and dermoscopy are useful tools to follow and detect changing nevi; saucerized excision of a pigmented lesion is performed following administration of local anesthesia).13 Change in pigmented lesions is a significant feature in early evolving melanomas and is a key component of the ABCDE acronym for melanoma screening.14,15

DERMATOFIBROMA
Dermatofibroma is a benign fibrohistiocytic tumor of the skin with a predilection for the lower extremities of women. It typically presents as a slightly raised to dome-shaped papule ranging in color from pink to light brown to dark brown (Fig. 2). If the lesion is pinched, puckering of the overlying skin, or the dimple sign, occurs. In the solitary presentation, minor trauma is implicated, whereas the eruptive form is associated with immunosuppression, autoimmune diseases, and atopic dermatitis.9 Dermatofibromas are largely asymptomatic and with time may undergo partial regression. If there is no clinical suspicion to prompt removal, it is best to avoid treatment. If necessary, surgical excision with narrow margins is preferred. Cryotherapy is an option, but results vary and multiple treatments may be required. Successful treatment with the 600-nm pulsed dye laser has been reported. A recent report shows that three treatments improve color and symptoms and, in 75 percent, led to complete resolution of the lesion.10

Fig. 2. A dermatofibroma on the lower extremity (left) is histologically characterized by a hyperplastic epidermis (*) overlying a dermal proliferation of spindled-shaped fibroblasts (right; inset). Hematoxylin and eosin stain; original magnification, 2; inset, 10.

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Video 3. Video demonstrates total body photography. Total body photography and dermoscopy are useful tools to follow and detect changing nevi. Saucerized excision of a pigmented lesion is performed following administration of local anesthesia. Physician in video, Dr. Ashfaq Marghoob, Memorial Sloan-Kettering Cancer Center. This video is available in the Related Videos section of the full-text article on www.PRSJournal.com.

error. After infiltration of local anesthesia, a no. 15 blade at an angle almost parallel to the skin surface can be used to shave or saucerize the lesion and leave a shallow defect. Subtle angulation of the blade changes the depth, affecting whether the upper papillary or the deeper reticular dermis is removed. In a punch biopsy, the diameter of the metal barrel of the punch instrument (ranging from 2 to 6 mm) is chosen to encompass a narrow margin around the lesion, and the defect is typically sutured to reapproximate the defect. If on histologic evaluation there is severe melanocytic atypia, recommended margins for reexcision vary from 2 to 5 mm.16

HALO NEVUS
A halo nevus is a pigmented melanocytic nevus surrounded by a ring of hypopigmentation or depigmentation (Fig. 4). One or multiple lesions can be present, and the torso is a common location. The pathogenesis is unclear; however, a cell-mediated immune response is suspected to be involved in the nevus destruction.17 The natural progression is variable, with the central nevus persisting indefinitely or involuting over time. Because the majority of lesions occur before age 20, the onset of multiple lesions in adults older than 40 may signal an occult or remote melanoma, and a comprehensive skin and ocular examination is warranted. A halo phenomenon may also occur around congenital melanocytic nevi and regressing melanoma. Removal or observation of a halo nevus depends on the clinical setting. Atypical features of the central nevus, an asymmetric halo, presence of several atypical

Fig. 3. Multiple dysplastic nevi (above) are characterized by asymmetry, border irregularity, and color variegation (center). The ABCDE acronym also includes diameter greater than 6 mm and evolution or change. Histopathologic analysis (below) shows elongated rete ridges (arrows) and increased melanocytes in a confluent manner at the basal layer of the epidermis (*). Cytologic atypia of the melanocytes is typically present and is designated as mild, moderate, or severe. Hematoxylin and eosin stain; original magnification, 20.

For clinically suspicious lesions, removal with a 2-mm margin is recommended. A full-thickness excision, saucerized removal, or punch biopsy is favored over a partial biopsy to minimize sampling

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Fig. 4. A classic halo nevus (left) with a dense infiltrate of lymphocytes and histiocytes (*) obscuring nests of nevus cells in the dermis (right). Hematoxylin and eosin stain; original magnification, 10.

nevi, or a history of melanoma raises suspicion, and the lesion should be excised for histologic examination. Nevi that appear benign do not require removal.

KERATOACANTHOMA
Keratoacanthoma is an epithelial neoplasm of sun-exposed skin. Classically, a solitary papule rapidly increases in size to become a crater-like nodule with a central keratotic core (Fig. 5). The lesion may spontaneously involute over months. Keratoacanthoma is considered by many to be a variant of

squamous cell carcinoma.18 Chronic ultraviolet radiation, chemical carcinogens, trauma, human papillomavirus, and genetic factors are implicated in its pathogenesis.19 The giant keratoacanthoma and eruptive types have also been described. The treatment modality selection depends on the lesion size, location, and patient comorbidities. Standard excision with a narrow margin allows for histologic evaluation; however, recurrences at the scar margin can occur. Mohs micrographic surgery is preferred for recurrences or areas with limited tissue laxity.20,21

Fig. 5. A classic clinical presentation of a keratoacanthoma (left). On histopathologic analysis, a cup-shaped lesion (solid line) with well-differentiated, glassy-appearing keratinocytes surrounds a large keratin-filled core (right). There is minimal cytologic atypia. Hematoxylin and eosin stain; original magnification, 2.

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Oral retinoids may be considered for eruptive or multiple keratoacanthoma.22 Radiotherapy is also an option but risks poor wound healing if encountered on the lower extremity. Intralesional treatment with 5-fluorouracil and methotrexate is a tissue-conserving, inexpensive, and noninvasive procedure. Approximately one to four injections spaced at an average of 18 days apart can lead to complete resolution. The literature does not support significant adverse effects.23 the lack of tissue laxity is a challenge, and in large lesions, sequential excisions may be performed. Avoiding absorbable sutures around hair follicles and limiting them to the galea may prevent inflammation and subsequent alopecia.27 Shave excision and ablation with the carbon dioxide laser28 are other options but are not very successful.

PILAR CYST
Pilar or trichilemmal cyst is a common scalp lesion originating from the outer root sheath of the hair shaft. Clinically difficult to distinguish from an epidermoid cyst, it presents as one or multiple lesions (Fig. 7). A proliferating pilar cyst or tumor presents as a slow-growing scalp nodule varying from a few millimeters to over 20 cm in size. Malignant changes, aggressive local growth, and nodal metastasis have been reported in proliferating pilar cysts or tumors. In a noninflamed pilar cyst, a small incision followed by tissue dissection, rather than an elliptical excision, successfully removes the cyst without rupture. For a benign proliferating pilar cyst or tumor, a simple excision can be performed; however, local recurrence is common. If the lesion has features of malignant transformation, a wide local excision, nodal evaluation, and other workup may be necessary on a case-by-case basis.29

NEVUS SEBACEUS
Nevus sebaceus is a congenital epidermal hamartoma of sebaceous glands that typically presents as a linear yellowish plaque on the scalp or face (Fig. 6). At birth the lesion is flat, but becomes raised and verrucous during puberty. The development of secondary adnexal neoplasms, most commonly benign but also malignant, is well established.24 The risk of a basal cell carcinoma was initially believed to be high; however, the evidence now shows an incidence of less than 1 percent.25,26 Historically, prophylactic excision was advocated to prevent the development of basal cell carcinoma. Excision is now recommended when secondary neoplasms are present or for cosmetic removal. A conservative excision with 2- to 3-mm margins to the adipose or galea is usually adequate. On the scalp,

Fig. 6. Nevus sebaceus on the scalp (left) with epidermal hyperplasia and papillomatosis (arrows) on histopathologic analysis (right). In the dermis, there are enlarged sebaceous (**) and apocrine glands (*). Hematoxylin and eosin stain; original magnification, 4.

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Fig. 7. A pilar cyst on the vertex of the scalp.

SEBORRHEIC KERATOSES
Seborrheic keratoses are common lesions of the epidermis presenting as well-demarcated papules or plaques (Fig. 8, above). Seborrheic keratoses vary from a light brown to waxy brown-black, develop a verrucous surface with follicular prominence, and appear stuck on. A familial predisposition and sunlight are suggested risk factors. Requests for removal are often for cosmetic reasons or due to irritation. Curettage is most frequently used (Fig. 8, below). A 3- to 6-mm curette is chosen based on the lesion size (see Video 4, which demonstrates curettage, available in the Related Videos section of the full-text article on www.PRSJournal.com; a seborrheic keratosis is anesthetized with local anesthesia and removed by curettage). An advantage of this technique is minimal scarring. A disadvantage is that the removed lesion is fragmented and may not be optimal if histopathologic evaluation is required. Smaller lesions may be treated with light electrodessication using a monoterminal apparatus or cryotherapy with liquid nitrogen in a single freezethaw cycle. Melanocytes are easily destroyed at temperatures of 4 to 7C30; therefore, in darkly pigmented individuals permanent hypopigmentation is common and should be avoided. A superficial shave removal may be indicated for larger lesions.

SOLAR LENTIGO
A solar lentigo is an oval or irregularly shaped brown macule on sun-exposed skin (Fig. 9). Solar lentigines are regarded as the first signs of photoaging, affecting more than 90 percent of Caucasians 50 years of age and older.31 These can be difficult to distinguish clinically from other pigmented lesions, including lentigo maligna and ac-

Fig. 8. A seborrheic keratosis along the jawline (above). Histologic analysis showed epidermal acanthosis (arrow) and hyperkeratosis (*) (center). Invaginations of the epidermis create horned pseudocysts (**), a characteristic feature of this lesion. Curettage is an effective treatment modality to remove seborrheic keratoses. The curette is placed at the base and the lesion is removed in a smooth, firm motion (right). If remnants remain, the process is repeated. Hematoxylin and eosin stain; original magnification, 10.

tinic keratoses; however, histopathology and stains such as Melan-A aid in their differentiation.32 Treatment is divided into destructive and topical therapy. A single freeze-thaw cycle with cryotherapy

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Video 4. Video demonstrating curettage. A seborrheic keratosis is anesthetized with local anesthesia and removed by curettage. This video is available in the Related Videos section of the fulltext article on www.PRSJournal.com.

is simple; however, central hypopigmentation with peripheral hyperpigmentation may occur in darker skin types. Lasers selectively target and destroy melanin due to its broad absorption spectrum (351 to 1064 nm) and are a preferred method of treatment in lighter skin types (see Video 5, which demonstrates laser treatment of solar lentigines, available in the Related Videos section of the full-text article on www.PRSJournal.com; the 595-nm pulsed dye laser without cryogen spray cooling and the compression method are utilized to treat solar lentigines). The Q-switched ruby (694 nm) laser delivers excellent results with no scarring or recurrence after 6 to 8 weeks in a single treatment.33 There is mild post-

Video 5. Video demonstrating laser treatment of solar lentigines. The 595-nm pulsed dye laser without cryogen spray cooling and the compression method are utilized to treat solar lentigines. This video is available in the Related Videos section of the fulltext article on www.PRSJournal.com.

treatment hypopigmentation with the alexandrite laser (755 nm), and transient pigmentary and textural changes with the frequency-doubled neodymium:yttrium-aluminum-garnet laser (532 nm).34 The intense pulsed light, a broadband visible light, results in no hyperpigmentation or scarring in Asians.35 Hydroquinone and tretinoin are the most widely used topical therapies. Other agents used as monotherapy or in combination are mequinol (4-hydroxyanisole) and azelaic acid.34 Double-blind randomized controlled trials show the combination of 2% mequinol and 0.01% tretinoin is superior when

Fig. 9. Multiple solar lentigines on the forehead (left). There is increased basal layer pigmentation, rete ridge elongation (arrows), and variable melanocytic proliferation (right). Solar elastosis is present in the dermis (*). Hematoxylin and eosin stain; original magnification, 20.

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compared with its active components separately or the vehicle. Common side effects are erythema and burning.36 Topical therapy is not ideal for multiple lesions, as compliance with daily application is difficult and several weeks are required for clinical results. Chemical peels improve irregular pigmentation and also treat solar lentigines. Superficial peels, such as glycolic acid, an alpha hydroxyl acid, penetrate into the epidermis and have minimal downtime but require repeated treatments at regular intervals. Medium-depth and deep peels, such as trichloroacetic acid and phenol, penetrate and produce necrosis at the level of the papillary or reticular dermis. These require a minimum of 1 to 2 weeks for healing and carry a higher risk of scarring, infection, and postinflammatory hyperpigmentation. Forty percent trichloroacetic acid with 70% glycolic acid or 30% trichloroacetic acid alone improves the appearance of lentigines with a low risk profile of pigmentary and textural changes in skin types I to III.37 A more indepth review is highly recommended before its initial use.

SPITZ NEVUS
Spitz nevus commonly presents as a homogenous, dome-shaped reddish or dark brown papule (Fig. 10). Spitz nevus is common in children and rare in older adults. The majority occur on the head and neck, but in patients younger than age 40, the thigh is a common location.38 They may occur in an agminated or disseminated pattern or be associated with atypical clinical and histologic features. In melanocytic tumors with spitzoid features, termed atypical spitzoid tumors, a sentinel lymph node biopsy may be performed to determine malignant potential.39 Management of a histologically confirmed Spitz nevus requires observation or reexcision. A classic Spitz nevus does not require further surgery. If reexcision is indicated for residual lesions, there is insufficient evidence and a lack of consensus on optimal margins.40 An algorithm stratifying the lesion into low, moderate, and high risk may help guide therapeutic management.41 Margins approaching or equal to those recommended for melanoma in situ (5 mm) are favored for atypical lesions. Sentinel lymph biopsy may be considered for markedly atypical lesions with a Breslow thicknesses of 1 mm or greater.

Fig. 10. A classic Spitz nevus (above) presents with (below) large nests of epithelioid or spindle cells (*) surrounded by clefts (arrows). Occasional mitotic figures, atypia, and eosinophilic globules, or Kamino bodies can be present. Hematoxylin and eosin stain; original magnification, 4.

SYRINGOMA
Syringoma is a benign neoplasm that most commonly presents as firm, skin-colored to slightly yellowish papules in the lower eyelid area of women (Fig. 11). Lesions may also develop on the upper trunk, genital skin, scalp, palms, and soles. On histo-

Fig. 11. Multiple syringomas along the eyelid.

pathology, well-circumscribed small ducts with eccrine differentiation that resemble tadpolelike structures are confined to the upper dermis.

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Syringomas are familial or sporadic, can present in an eruptive manner, and are more frequent in patients with Down syndrome.42 Due to the syringomas common periorbital location, patients often desire removal for improved cosmesis. Punch excision of larger lesions and a trial of low-voltage electrodessication and trichloroacetic acid are suggested before treating all lesions. In a diffuse presentation, treatment is challenging and laser ablation is an option. Laser ablation with the carbon dioxide laser risks prolonged erythema, pigmentary changes, and scarring. Trichoepithelioma and desmoplastic trichoepitheliomas are benign lesions and do not require further treatment. Lesions are typically on the face, however, and tend to grow in size, becoming an aesthetic concern for patients. A conservative excision or shave removal of solitary lesions is recommended. If there are multiple lesions, ablative lasers may improve their appearance.43 On occasion, rendering a diagnosis of a desmoplastic trichoepithelioma is difficult, as the superficial component on histopathologic examination mimics a morpheaform basal cell carcinoma and microcystic adnexal carcinoma (Fig. 12). A deeper biopsy, conservative excision, or Mohs micrographic surgery is recommended for definitive diagnosis and treatment.
Joseph J. Disa, M.D. 1275 York Avenue New York, N.Y. 10065 disaj@mskcc.org

TRICHOEPITHELIOMA AND DESMOPLASTIC TRICHOEPITHELIOMA

Trichoepithelioma is a neoplasm of follicular differentiation presenting as small, skin-colored or slightly pink papules. They are common on the face, with a predilection for the cheeks, nose, and nasolabial folds. Multiple lesions are seen in the familial form or in association with cylindromas in Brooke-Spiegler syndrome. Desmoplastic trichoepithelioma is an uncommon variant with extensive dermal sclerosis. It presents as an asymptomatic plaque with a central depression on the upper cheek. In contrast to trichoepitheliomas, multiple lesions are rare.

REFERENCES
1. Marks R, Rennie G, Selwood T. The relationship of basal cell carcinomas and squamous cell carcinomas to solar keratoses. Arch Dermatol. 1988;1124:1039. 2. Fuchs A, Marmur E. The kinetics of skin cancer: Progression of actinic keratosis to squamous cell carcinoma. Dermatol Surg. 2007;33:1099. 3. Gold MH, Nestor MS. Current treatments of actinic keratosis. J Drugs Dermatol. 2006;5:17. 4. Fecker LF, Stockfleth E, Nindly I, et al. The role of apoptosis in therapy and prophylaxis of epithelial tumours by nonsteroidal anti-inflammatory drugs (NSAIDs). Br J Dermatol. 2007; 156:25. 5. Marrero GM, Katz BE. The new fluor-hydroxy pulse peel: A combination of 5-fluorouracil and glycolic acid. Dermatol Surg. 1998;24:973. 6. Lawrence N, Cox SE, Cocerell CJ, et al. A comparison of the efficacy and safety of Jessners solution and 35% trichloroacetic acid vs 5% fluorouracil in the treatment of widespread facial actinic keratoses. Arch Dermatol. 1995;131:176. 7. Gold MH, Bradshaw VL, Boring MM, et al. Split-face comparison of photodynamic therapy with 5-aminolevulinic acid and intense pulsed light versus intense pulsed light alone for photodamage. Dermatol Surg. 2006;32:795. 8. Alexiades-Armenakas MR, Dover JS, Arndt KA. The spectrum of lalser skin resurfacing: Nonablative, fractional and ablative laser resurfacing. J Am Acad Dermatol. 2008;58:719. 9. Zaccaria E, Rebora A, Rongioletti F. Multiple eruptive dermatofibromas and immunosuppression: Report of two cases and review of the literature. Int J Dermatol. 2008;47:723. 10. Wang SQ, Lee PK. Treatment of dermatofibroma with a 600 nm pulsed dye laser. Dermatol Surg. 2006;32:532. 11. Fuller SR, Bowen GM, Tanner B, et al. Digital dermoscopic monitoring of atypical nevi in patients at risk for melanoma. Dermatol Surg. 2007;33:1198. 12. de Snoo FA, Kroon MW, Bergman W, et al. From sporadic atypical nevi to familial melanoma: Risk analysis for melanoma in sporadic atypical nevus patients. J Am Acad Dermatol. 2007;56:748.

Fig. 12. On histopathologic analysis, desmoplastic trichoepithelioma is composed of narrow strands of basaloid aggregates (*), horn cysts, and a sclerosing stroma (**) separated by clefts (arrows) from the dermis. In a trichoepithelioma, the basaloid cell aggregates are larger and well circumscribed. Hematoxylin and eosin stain; original magnification, 4.

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