E. Victor Ross


The lentigo is one of the most common presenting complaints in a cosmetic dermatology practice, the treatment of red and brown dyschromias accounting for up to 50% of first-time patients (VR, unpublished data). Lentigines occur in over 90% of Caucasians, with genetic predisposition, aging, and chronic sun exposure being the most important contributing factors.1 Solar lentigines should be distinguished from ephelides, lentigo simplex, pigmented actinic keratosis (AK), flat seborrheic keratosis (SK), melanocytic nevus, and malignant melanoma. Some lentigines are actually early SKs, and one can make the case that most lentigines evolve into SKs. The lentigo must be differentiated from other types of epidermal pigmentation with sometimes similar clinical presentations. These can be differentiated based on clinical appearance from other types of so-called static hyperpigmentation. The term “static” hyperpigmentation is used to differentiate the lentigo from inflammatory variants of hyperpigmentation, most notably melasma, a more complicated condition in which histological and physiologic properties are different from the lentigo.

Any cosmetic dermatologist must be able to treat these macular lesions in a predictable fashion. In this chapter, we review the range of both physical and topical therapies.


Patients complain of dullness, discolorations, or brown spots to the skin. They may give a history of sudden appearance or worsening of dark spots usually after periods of increased sun exposure. The discolorations involve sun-exposed skin.


Solar lentigines appear to be due to chronic UV radiation-induced epidermal hyperplasia, concomitant melanocyte proliferation, and increased transfer of melanosomes to keratinocytes. UV radiation stimulates keratinocyte production of various cytokines including interleukin 1, which has been shown to lead to keratinocyte growth factor production, stimulating pigment production via tyrosinase expression.2 The melanocortin-1-receptor gene (MCR1) variants have
been identified as “the freckle gene,” and variants in MCR1 are implicated in solar lentigo formation.3

Mutations in other genes causing inherited lentiginosis syndromes also appear to be involved in the pathogenesis of lentigines (eg, PTPN11, STK1, NF1, PRKAR1A, PTEN, and others), but the mechanisms and pathways are still being delineated.

Jun 29, 2020 | Posted by in Dermatology | Comments Off on Lentigines
Premium Wordpress Themes by UFO Themes