[Durgical](https://durgical.com/en/) › [DurgiPedia](https://durgical.com/en/durgipedia/) › [General pathology](https://durgical.com/en/general-pathology/) › [Skin](https://durgical.com/en/general-pathology/areas/skin/) › Freckles, lentigines and melanocytic nevi # Freckles, lentigines and melanocytic nevi - Lesion Freckles and sun spots are pigment changes; moles are benign clusters of pigment cells. A few atypical moles mark higher melanoma risk. Updated Nov 12, 2026 ## Key points - Freckle (ephelis): more melanin in basal keratinocytes, normal melanocyte number, darkens with sun. - Lentigo: linear increase of melanocytes in the basal layer, elongated rete ridges; does not darken with sun; solar lentigo in old sun-damaged skin. - Nevus evolution: junctional (nests at the junction) to compound to intradermal (nests in dermis only). - Maturation with depth: deeper cells become smaller, less pigmented and neural-like; lack of maturation is a melanoma clue. - Variants: congenital, blue (dermal, dendritic, bluish colour), Spitz (spindle and epithelioid cells, children), halo (lymphocytes destroy the nevus). - Dysplastic nevus: larger, irregular border, variable colour; lentiginous hyperplasia, bridging nests, cytologic atypia, lamellar fibrosis; CDKN2A in familial cases. ## What it is Pigmented lesions range from simple increases in melanin to benign tumours of melanocytes. A freckle has more melanin but normal melanocyte numbers; a lentigo has more melanocytes along the basal layer. Melanocytic nevi are benign clonal proliferations, usually driven by BRAF or NRAS mutations that then stop growing through oncogene-induced senescence. Dysplastic nevi show architectural and cytologic atypia and, in families with many of them, mark a high risk of melanoma. ## Structure - Junctional nevus: nests at the dermoepidermal junction; flat, uniformly dark. - Compound nevus: junctional plus dermal nests; raised. - Intradermal nevus: dermal nests only, often skin-coloured, dome-shaped. - Dysplastic nevus: shoulder of junctional component beyond the dermal part, fused (bridging) nests, random atypia, lymphocytes. - Blue nevus: heavily pigmented dendritic melanocytes deep in the dermis (Tyndall effect gives the blue). ## Step by step - A melanocyte acquires an activating BRAF (often V600E) or NRAS mutation. - The clone proliferates and forms nests at the junction. - Strong oncogenic signalling triggers senescence (p16 rise) and growth stops. - Cells migrate into the dermis and mature. - If additional hits occur (CDKN2A loss, TERT), atypia and eventually melanoma can arise; most nevi never progress. ## Clinical notes - Most melanomas arise de novo, not from an existing nevus. - Dysplastic nevus syndrome: many atypical nevi plus family history; close skin surveillance. - Large congenital nevi carry a small lifetime melanoma risk. ## Memory aid A nevus walks down the stairs as it ages: at the door (junctional), half in (compound), fully inside the house (intradermal), getting smaller as it goes. ## Test yourself Think of the answer, then tap the question to see it. ## What distinguishes a freckle from a lentigo histologically? A freckle has more melanin with normal melanocyte numbers; a lentigo has an increased number of basal melanocytes. ## What is maturation in a melanocytic nevus? Deeper dermal nevus cells become smaller, less pigmented and more neural-like; its absence suggests melanoma. ## Why do most nevi stop growing despite a BRAF mutation? Strong oncogenic signalling induces senescence, with p16 and other checkpoint proteins halting the cell cycle. [Add to my cards (3)](https://durgical.app/estudiar/?add=/en/general-pathology/freckles-lentigines-and-melanocytic-nevi/) [More Pathology questions →](https://durgical.com/en/practice/?f=pathology) ## Elsewhere in DurgiPedia - [Keratinocytes, melanocytes, Langerhans and Merkel cells](https://durgical.com/en/histology/keratinocytes-melanocytes-langerhans-and-merkel-cells/) - [Pigments in tissue: lipofuscin, hemosiderin, melanin, bilirubin, carbon](https://durgical.com/en/general-pathology/pigments-in-tissue-lipofuscin-hemosiderin-melanin-bilirubin-carbon/) - [Dysplasia and carcinoma in situ](https://durgical.com/en/general-pathology/dysplasia-and-carcinoma-in-situ/) ## Connections ## Related 3 - [Melanoma: pathogenesis](https://durgical.com/en/general-pathology/melanoma-pathogenesis/) - [Melanoma: subtypes, Breslow and markers](https://durgical.com/en/general-pathology/melanoma-subtypes-breslow-and-markers/) - [Pigments in tissue: lipofuscin, hemosiderin, melanin, bilirubin, carbon](https://durgical.com/en/general-pathology/pigments-in-tissue-lipofuscin-hemosiderin-melanin-bilirubin-carbon/) ## Related conditions 3 - [Melanocytic nevi and dysplastic nevus](https://durgical.com/en/conditions/melanocytic-nevi-and-dysplastic-nevus/) - [Melanoma](https://durgical.com/en/conditions/melanoma/) - [Melasma](https://durgical.com/en/conditions/melasma/) [← All of general pathology](https://durgical.com/en/general-pathology/) Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given. Sources: [Moles](https://medlineplus.gov/moles.html) (MedlinePlus, US National Library of Medicine, 2025); [Common Moles, Dysplastic Nevi, and Risk of Melanoma](https://www.cancer.gov/types/skin/moles-fact-sheet) (National Cancer Institute, 2025); [Skin Pigmentation Disorders](https://medlineplus.gov/skinpigmentationdisorders.html) (MedlinePlus, US National Library of Medicine, 2025). ## **Spotted a mistake?** We are always improving for the community. Tell us what is wrong and our team will review it. Report a mistake Representative model, for educational purposes only. --- Source: https://durgical.com/en/general-pathology/freckles-lentigines-and-melanocytic-nevi/ License: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Cite as: DurgiPedia (durgical.com), https://durgical.com/en/general-pathology/freckles-lentigines-and-melanocytic-nevi/