Les lentigos solaires (pour les professionnels)

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Solar Lentigo (For Professionals)

Epidemiology

Occurs mostly in Caucasians phototypes1,2 and 3
Affects worldwide 90% of humans over 70 of age. This amounts today to 600 million aged 65 and over, this will be 2 billion individuals in 2050

Psychological impact

Differential Diagnosis

(Focused): PIH, melasma (chloasma), Seborrheic (Seborrhoeic) Keratosis, reticulated black solar lentigo=ink spot lentigo (melanin unevenly distributed), UVA and PUVA lentigo, sunburn spots (on back, a marker of melanoma presence), ephelides (freckles) (MCR-1 Gene mutation) (not related to sun expression), pigmented seb K, pigmented AK, extensive pigmented AK, Hutchinson’s Melanotic Freckle (HMF) (Dubreuil’s Melanosis) (Lentigo Maligna).

To be complete: juvenile lentigo (lentigo simplex), freckles (epehlides), ink spot lentigo, PUVA-induced lentigenes, Tanning-Bed lentigenes, Seborrheic (Seborroeic) Keratosis, Pigmented actinic keratoses, Large Cell Acanthoma, Junctional Nevomelanocytic nevus, Flat reticular and pigmented seborrheic keratosis, pigmented and pigmented-spreading actinic keratosis, sunburn spot.

Histopathology:

Elongation of reted ridges with bud-like extensions of the epidermis (without cellular atypia) into the dermis except (on the face).

Pathogenesis:

progressive stages: increase of melanocytes, elongation of the rete ridges and increased pigment deposition. Increased melanin synthesis.
Implicated mediators

-SCF (stem cell factor)

-p53

-KGF (Keratinocyte growth factor)

-KGF receptor

-HGF (Hepatocyte Growth Factor)

-Il-1 alpha

-FGFR3 (hyperpigmentation)

-PIK 3CA (hyperpigmentation)

Another observation is that granulated cells expressing FXIIIa are also present in the dermal part of SL (dendrocyte marker). These melanin-laden cells are filled with larger than normal melanosomes (it is not known how the epidermal to dermal trnsfer of melanin takes place).

Treatments in general