Benign Melanocytic Lesions

. Melanocytes from neural crest . Spindle shaped clear cells with dark nucleus and dendritic processes . Melanin is synthesized from tyrosine via DOPA . Accumulates in vesicles – melanosomes . When melanocytes leave the epidermis they become nevus cells

Nevus cells vs Melanocytes 1. nevus cells congregates in nests – lost contact inhibition 2. do not have dendritic processes 3. become round rather than spindle shaped

Melanocytic Nevi

Epidermal

Ephelis . small, light brown macules of sun-exposed areas in fair-skinned subjects . normal number of melanocytes producing an increased number of melanin . fades in winter time dermoscopy . absent brown globules . moth eaten edge . uniform pigmented background

Solar lentigo . normal number of melanocytes producing an increased number of melanin in background of actinic dermal changes, elongated rete ridges. dermoscopy . absent brown globules . discrete regular network . uniform lightly pigmented background

Lentigo simplex . increased number of melanocytes producing an increased number of melanin . does not fade . same pathology as café au lait spots (neurofibromatosis, Allbright’s) dermoscopy . absent brown globules . discrete regular network . uniform darkly pigmented background

Becker’s nevus

. dark patch on shoulder . appears during adolescence and may become hairy . due to an overgrowth of the epidermis, melanocytes and hair follicles . acne may develop in the lesion . thought that it is due to a gene defect, which has not yet been identified. . may be triggered by circulating androgens during puberty

Pigmented hairy epidermal nevus syndrome(Becker nevus syndrome) . usually occurs sporadically . Beckers nevus in association with underlying smooth muscle hamartoma and developmental defects such as ipsilateral hypoplasia of breast and skeletal anomalies including scoliosis, spina bifida occulta, or ipsilateral hypoplasia of a limb.

Dermal melanocytic nevi . Thought to result from arrested migration of melanocytes

Blue nevus . Usually acquired after infancy . Two clinically recognized variants of blue nevus exist o Common/classic blue nevus - small, usually extremities o cellular blue nevus – large, usually on buttocks . clinically noted blue color is due to the depth of melanin in the epidermis and the Tyndall effect (preferential absorption of long wavelengths of light by melanin and the scattering of shorter wavelengths, representing the blue end of the spectrum) . Most cases remain entirely benign. Blue nevi usually persist unchanged throughout life and are asymptomatic. . Rare cases of malignant melanoma have been reported arising in association with cellular blue nevi. . Dermoscopy o Homogenous blue pigmentation o Absent network o Absent brown/black globules/dots . Carney syndrome (complex) o AD o rare association of blue nevi with other cutaneous and systemic findings. o Characterised by lentigines, atrial myxomas, mucocutaneous myxomas (neurofibromas), and blue nevi (LAMB)

Mongolian Blue Spot . 90% of Mongoloid infants

Nevus of Ota . Bluish pigmentation of sclera and adjacent periorbital skin . Common in Japanese . 50% of nevus of Ota cases present at birth. . Rare cases of melanoma reported . Glaucoma reported . Pulsed Q-switched laser surgery is unquestionably the current treatment of choice for nevi of Ota and Ito, and it works via selective photothermal and photomechanical destruction of dermal melanocytes and melanophages.

Nevus of Ito . Blue-grey discoloration in shoulder region . Common in Japanese

Naevus cell naevi

1. Congenital a. Congenital melanocytic nevus 2. Acquired a. Junctional nevus b. Compound nevus c. Intradermal nevus d. Spitz nevus e. Halo nevus f. Dysplastic nevus

Spitz Nevus

. Considerable confusion exists in the literature whether a Spitz nevus is a melanoma. . no set of criteria can be used to predict the clinical outcome with absolute assurance. . A Spitz nevus can arise de novo or in association with an existing melanocytic nevus. . 50% of cases occur in children younger than 10 years; 70% of all cases are diagnosed during the first 2 decades of life. . lesion tends to grow rapidly and may reach a size of 1 cm within 6 months. . tend to become static after the rapid initial growth phase; however, color changes may be observed, and bleeding and pruritus are rarely noticed . Single, dome-shaped, red or pigmented papules or nodules are typical. . color may vary from nonpigmented through pink to orange-red. . Some lesions are pigmented, especially those found on lower extremities. . Pigmented lesions in adults are most difficult to distinguish from melanoma . Dermoscopy o Symmetrical pigmentation pattern o Central retiform depigmentation . rare recurrences may mimic metastatic malignant melanoma. . Clinically may also resemble pyogenic granuloma Histology . classic Spitz nevus is predominantly compound, although junctional and intradermal lesions are also observed. . Characterised by presence of large and/or spindle-shaped melanocytes, usually in nests. . Striking symmetry, sharp lateral demarcation, absent (or rare) mitoses, absence of atypical mitoses, presence of eosinophilic and periodic acid-Schiff (PAS)–positive globules (Kamino bodies) and nondisruptive (Indian-file like) infiltration of collagen are important features indicating the diagnosis of Spitz nevi . The epidermis is hyperkeratotic and acanthotic. . Diagnosis equivocal in up to 8% of cases. . 6.5% of cases diagnosed clinically as melanomas were Spitz nevi. Management . Classify Spitz naevi into 3 categories based on clinical presentation and histopathological features. 1. typical clinical presentation vs atypical clinical presentation. o Atypical features include older patient, any ABCD's changes of melanoma, rapid growth, atraumatic ulceration and change in an established lesion. 2. typical histopathological vs atypical histology . Those with typical clinical presentation and typical pathology are classified as low risk. . Those with typical clinical features and atypical pathology and those with atypical clinical features and typical histology are classified under moderate risk. . Patients with atypical clinical presentation and atypical pathology are classified as high risk. . Those with low risk can be managed conservatively after biopsy confirmation. . The high risk ones should have excision with negative margins . those with moderate risk need to be managed based on expert dermatopathological evaluation and consideration of the clinical presentation

Halo nevus

. melanocytic nevi in which an inflammatory infiltrate develops, resulting in a zone of depigmentation surrounding the nevus. . infiltrating cells are predominantly T-lymphocytes - cytotoxic (CD8) lymphocytes outnumber helper (CD4) lymphocytes by a ratio of approximately 4:1 . As seen in vitiligo, melanocytes in the epidermis in the halo component of the nevus are completely absent . in most cases, a dense, somewhat bandlike lymphocytic infiltrate is present in the papillary and often reticular dermis with nests of nevus cells located centrally

Management . Patients should be instructed to monitor the lesion. If changes occur that suggest irregularity or if such symptoms as bleeding, itching, pain, or ulceration develop, the patient should be reevaluated promptly to exclude the possibility of cutaneous melanoma.